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Physical Therapy of the Shoulder, ed 4 ISBN 0-443-06614-0

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Notice

Physical Therapy is an ever-changing field. Standard safety precautions must be followed, but as new
research and clinical experience broaden our knowledge, changes in treatment and drug therapy may
become necessary or appropriate. Readers are advised to check the most current product information
provided by the manufacturer of each drug to be administered to verify the recommended dose, the
method and duration of administration, and contraindications. It is the responsibility of the licensed
prescriber, relying on experience and knowledge of the patient, to determine dosages and the best
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Previous editions copyrighted 1997, 1991, 1987.

Library of Congress Cataloging-in-Publication Data

Physical therapy of the shoulder / edited by Robert A. Donatelli. – 4th ed.

p. ; cm.
Includes bibliographical references and index.
ISBN 0-443-06614-0 (alk. paper)
1. Shoulder–Wounds and injuries. 2. Shoulder–Wounds and injuries–Treatment.
3. Shoulder–Wounds and injuries–Physical therapy. I. Donatelli, Robert.
[DNLM: 1. Shoulder–injuries. 2. Shoulder Joint–injuries. 3. Physical Therapy
Techniques–methods. WE 810 P578 2004]
RD557.5.P48 2004
617.5¢72044–dc22
2003065163

Acquisitions Editor: Marion Waldman

Developmental Editor: Marjory Fraser
Publishing Services Manager: Pat Joiner
Project Manager: Rachel E. Dowell
Senior Designer: Mark A. Oberkrom

Printed in the United States of America

Last digit is the print number 9 8 7 6 5 4 3 2 1
 Dedication

I would like to dedicate this book to my family—my wife Georgi

Donatelli, my new son, Robby Donatelli, and my daughter, Rachel. They
have added a new meaning of joy and happiness to my life.
CONTRIBUTORS
Mollie Beyers, DPT
Physical Therapist, Biomax Rehabilitation,
Effingham, Illinois
Chapter 11: Frozen Shoulder
Peter Bonutti, MD, FACS, FAAOS,
FAANA
Founder and Director, Bonutti Clinic, Founder and
Director, Bonutti Technology, Effingham, Illinois;
Assistant Clinical Professor, Department of Orthopaedic
Surgery, University of Arkansas, Fayetteville, Arkansas
Chapter 11: Frozen Shoulder
Robert Cantu, MMSc, PT, MTC
Group Director, Physiotherapy Associates, Atlanta,
Georgia; Assistant Professor, University of St. Augustine
for Health Sciences, St. Augustine, Florida
Chapter 16: Myofascial Treatment
Deborah Seidel Cobb, MS, PT
University of St. Augustine for Health Sciences, St.
Augustine, Florida
Chapter 16: Myofascial Treatment
Struan H. Coleman, MD, PhD
Assistant Professor of Orthopaedic Surgery, Hospital
for Special Surgery—Cornell University Medical Center,
New York, New York
Chapter 17: Shoulder Instability
David J. Conaway, DO
Associate Clinical Professor, Department of
Orthopaedics, West Virginia College of Osteopathic
Medicine, Lewisburg, West Virginia; Honorary Clinical
Instructor, Graduate Program in Physical Therapy,
Division of Allied Health Professions, Department of
Rehabilitation Medicine, Emory University School of
Medicine; Past Chairman, Department of Surgery,
Northlake Regional Medical Center; Staff Orthopaedic
Surgeon, Dekalb Medical Center; Northlake Regional
Medical Center; Eastside Medical Center; Atlanta,
Georgia; Orthopaedic Surgeon, Killian Hill Orthopaedic
and Sports Medicine Clinic, Lilburn, Georgia
Chapter 19: Shoulder Girdle Fractures
vii
Jeff Cooper, MS, ATC
Athletic Trainer, Philadelphia Phillies Baseball Team,
Philadelphia, Pennsylvania; Consultant, Physiotherapy
Associates, Memphis, Tennessee
Chapter 3: Throwing Injuries
Robert A. Donatelli, PhD, PT, OCS
National Director of Sports Rehabilitation,
Physiotherapy Associates, Suwanee, Georgia
Chapter 2: Functional Anatomy and Mechanics;
Chapter 4: Differential Soft Tissue Diagnosis; Chapter
10: Impingement Syndrome and Impingement-Related
Instability; Chapter 14: Manual Therapy Techniques
Phillip B. Donley, PT, ATC, MS
Physiotherapy Associates, Chester County Sports
Medicine, West Chester, Pennsylvania; Consultant to the
Philadelphia Phillies Baseball Team, Philadelphia,
Pennsylvania
Chapter 3: Throwing Injuries (Appendix)
Xavier A. Duralde, MD
Peachtree Orthopedics Clinic; Assistant Clinical
Professor of Orthopaedic Surgery, Clinical Instructor,
Emory University School of Medicine, Atlanta, Georgia
Chapter 20: Total Shoulder Replacements
Peter I. Edgelow, MA, PT
Senior Staff Therapist, Physiotherapy Associates,
Hayward, California; Assistant Clinical Professor,
Graduate Program in Physical Therapy, University of
California, San Francisco, California; Graduate
Residency in Orthopaedic Physical Therapy, Kaiser
Permanente, Hayward, California
Chapter 7: Neurovascular Consequences of
Cumulative Trauma Disorders Affecting the Thoracic
Outlet: A Patient-Centered Treatment Approach
viii CONTRIBUTORS
Richard A. Ekstrom, PT, DSc, MS,
OCS
Physical Therapy Department, University of South
Dakota, Vermillion, South Dakota
Chapter 15: Muscle Length Testing and
Electromyographic Data for Manual Muscle Testing and
Exercises for the Shoulder
Todd S. Ellenbecker, MS, PT, SCS,
CSCS
Clinic Director, Physiotherapy Associates-Scottsdale
Sports Clinic, Scottsdale, Arizona
Chapter 12: Etiology and Evaluation of Rotator Cuff
Pathologic Conditions and Rehabilitation
Robert L. Elvey, PT
Senior Lecturer, School of Physiotherapy, Curtin
University of Technology, Perth, Western Australia,
Australia
Chapter 6: Neural Tissue Evaluation and Treatment
Blanca Zita Gonzalez-King, PT, CHT
Physical Therapist, Private Practice, Atlanta, Georgia
Chapter 4: Differential Soft Tissue Diagnosis
John C. Gray, DPT, OCS, FAAOMPT
Lead Clinical Specialist, Department of Physical
Therapy, Sharp Rees-Stealy, Clinical Instructor, Ola
Grimsby Institute; Credentialed Clinical Instructor,
American Physical Therapy Association; Associate Editor,
Journal of Manual and Manipulative Therapy, San Diego,
California
Chapter 5: Interrelationship of the Spine, Rib Cage,
and Shoulder; Chapter 13: Visceral Referred Pain to the
Shoulder
Bruce H. Greenfield, PT, PhD, OCS
Instructor, Division of Physical Therapy, Department
of Rehabilitation Medicine, Emory University School of
Medicine, Atlanta, Georgia
Chapter 8: Evaluation and Treatment of Brachial
Plexus Lesions; Chapter 10: Impingement Syndrome
and Impingement-Related Instability
Ola Grimsby, PT
Chairman of the Board, Ola Grimsby Institute, San
Diego, California
Chapter 5: Interrelationship of the Spine, Rib Cage,
and Shoulder
Toby Hall, PT
Clinical Consultant, School of Physiotherapy, Curtin
University of Technology, Perth, Western Australia,
Australia
Chapter 6: Neural Tissue Evaluation and Treatment
Joseph Herrera, MD
Clinical Instructor, Department of Rehabilitation
Medicine, Hospital for Special Surgery—Cornell
University Medical Center, New York, New York
Chapter 17: Shoulder Instability
Jacob P. Irwin, DPT
Physiotherapy Associates, Suwanee, Georgia
Chapter 4: Differential Soft Tissue Diagnosis;
Chapter 19: Shoulder Girdle Fractures
Scot Irwin, DPT, CCS
Associate Professor, Department of Physical Therapy,
North Georgia College and State University, Dahlonega,
Georgia
Chapter 1: The Guide to Practice
Marie A. Johanson, EdD, PT, OCS
Instructor, Division of Physical Therapy, Department
of Rehabilitation Medicine, Emory University School of
Medicine, Atlanta, Georgia
Chapter 4: Differential Soft Tissue Diagnosis
Michael Lee, MD
Clinical Instructor, Department of Rehabilitation
Medicine, Hospital for Special Surgery—Cornell
University Medical Center, New York, New York
Chapter 17: Shoulder Instability
Kathryn Levit, MA, OTR/L
Private Practice/Consultant, Department of Applied
Developmental Psychology, George Mason University,
Fairfax, Virginia.
Chapter 9: The Shoulder in Hemiplegia

Timothy J. McMahon, PT
Outpatient Program Supervisor for Orthopaedics
and Sports Medicine, The Rehab Results Group,
Decatur, Georgia; Clinical Adjunct Faculty, Division of
Physical Therapy, Department of Rehabilitation
Medicine, Emory University School of Medicine,
Atlanta, Georgia
Chapter 14: Manual Therapy Techniques
Craig D. Morgan, MD
Orthopedic Surgeon, The Morgan Kalman Clinic,
Wilmington, Delaware; Clinical Professor University of
Pennsylvania, Philadelphia, Pennsylvania
Chapter 3: Throwing Injuries (Appendix)
Roy W. Osborn, PT, MS, OCS
Physical Therapy Department, University of South
Dakota, Vermillion, South Dakota
Chapter 15: Muscle Length Testing and
Electromyographic Data for Manual Muscle Testing and
Exercises for the Shoulder
Susan Ryerson, PT
Partner, Making Progress, Alexandria, Virginia;
Adjunct Clinical Faculty, Boston, Massachusetts; General
Hospital Institute of Health Professions, Boston,
Massachusetts; Coordinator/Instructor,
Neurodevelopmental Treatment Association, Inc,
Chicago, Illinois
Chapter 9: The Shoulder in Hemiplegia
Dorie B. Syen, MS, OTR, CHT
Rehabilitation Projects Coordinator, Georgia Baptist
Medical Center, Atlanta, Georgia
Chapter 8: Evaluation and Treatment of Brachial
Plexus Lesions
CONTRIBUTORS ix
Lori Thein Brody, MS, PT, SCS, ATC
Associate Lecturer, Department of Kinesiology,
University of Wisconsin School of Education; Senior
Clinical Therapist, Sports Medicine Center; University
of Wisconsin Clinics Research Park, Madison, Wisconsin
Chapter 10: Impingement Syndrome and
Impingement-Related Instability
Vijay B. Vad, MD
Assistant Professor of Rehabilitation Medicine,
Hospital for Special Surgery—Cornell University
Medical Center, New York, New York
Chapter 17: Shoulder Instability
Joseph S. Wilkes, MD
Associate Clinical Professor, Department of
Orthopaedics, Emory University School of Medicine;
Orthopedist, Southern Orthopedics; Medical Director,
Piedmont Hospital Sports Medicine Institute, Atlanta,
Georgia; Orthopedic Consultant, United States Luge
Association, Lake Placid, New York
Chapter 18: Rotator Cuff Repairs
Michael J. Wooden, MS, PT, OCS
Instructor, Division of Physical Therapy, Department
of Rehabilitation Medicine, Emory University School of
Medicine; National Director, Clinical Research,
Physiotherapy Associates, Memphis, Tennessee
Chapter 19: Shoulder Girdle Fractures
Michael S. Zazzali, DSC, PT, OCS
Co-Director and Partner, Physical Therapy Associates
of New York, New York, New York
Chapter 17: Shoulder Instability
PREFACE
The first edition of Physical Therapy of the Shoulder was published in 1987, and now we are
writing the fourth edition 15 years later. I would like to thank my readers for their support
throughout the years that has made this book successful. The fourth edition has kept up with the
tradition of Physical Therapy Specialization. The shoulder joint is a complicated structure con-
sisting of three synovial joints, the scapula thoracic articulation, and 17 muscles. The shoulder
complex hangs off the rib cage and is connected to the cervical and thoracic spine. The com-
plexity of the shoulder makes many rehabilitation students and clinicians uncertain in assessing
shoulder pathomechanics and in establishing treatment approaches for different shoulder
pathologies.
In keeping up to date with new and innovative treatment techniques, surgical procedures, and
evaluation methods for the shoulder, this fourth edition of Physical Therapy of the Shoulder has
been updated appropriately. There are a dozen new authors and seven new chapters. The fourth
edition is divided into five sections; Mechanics of Movement and Evaluation, Neurologic Consid-
erations, Special Considerations, Treatment Approaches, and Surgical Considerations.
In keeping with the new Guide to Physical Therapist Practice, Scot Irwin has given us an
overview of the Guide, and all the case studies have been rewritten in the Guide format. Chapter
2 was updated with new anatomic and biomechanical information on how the shoulder moves.
Seven fresh cadaver slides have been added to the color plates in the center of the textbook.
Chapter 3 was rewritten by Jeff Cooper with all the new information on the throwing injuries to
the shoulder. Jeff has included new research data that he has collected over the past several
years on professional baseball pitchers. His approach to evaluation and treatment is state of the
art. Chapter 4 finishes the first section with updates on all the new-evidenced-based special tests
for the shoulder. The special tests on the shoulder greatly assist the clinician in the development
of a differential soft tissue diagnosis. The research-based tests are very reliable and accurate in
determining different pathologies of the glenohumeral articulation.
Section 2, Neurologic Considerations, has been updated with new information and references.
John C. Gray, Ola Grimsby, Peter I. Edgelow, and Susan Ryerson completely revised their
chapters.
Section 3, Special Considerations, was highlighted by a new chapter on the Frozen Shoulder
(Chapter 11) written by Mollie Beyers and Peter Bonutti. This chapter features five tables that
provide an excellent summary of the evidence-based research on treatment of frozen shoulder
pathology. In addition, a new shoulder device for treatment of adhesive capsulitis, through static
progressive stretch and stress relaxation, is also featured in this chapter. John C. Gray’s chapter
on Visceral Referred Pain to the Shoulder (Chapter 13), was rewritten, along with important
updates from Todd S. Ellenbecker, Lori Thein Brody, and Bruce H. Greenfield.
In the Treatment Approaches Section, a new chapter was added by Richard A. Ekstrom and
Roy W. Osborn on Muscle Length Testing and Electromyographic Data for Manual Strength Testing
and Exercises for the Shoulder (Chapter 15). Chapter 14, entitled Manual Therapy Techniques,
was updated with additional illustrations of new manual procedures for the shoulder, with a
section on evidence-based manual therapy treatment approaches.
The Surgical Considerations Section was honored with addition of the chapter by Xavier A.
Duralde, a prominent orthopedic surgeon who specializes in shoulder pathology and has devel-
oped his own components for shoulder replacements. In addition, I was also honored by the addi-
tion of a new chapter on Shoulder Instability (Chapter 17). The lead authors—Michael S. Zazzali
and Vijay B. Vad—are affiliated with the Hospital of Special Surgery in New York, NY. The chapter

xi
xii PREFACE

includes state-of-the-art concepts in evaluation and treatment of the Bankart lesion, S.L.A.P
lesions, rotator cuff interval concepts, and thermal assisted capsular shifts. Finally, Jacob P.
Irwin updated Chapter 19 on Shoulder Girdle Fractures.
We are pleased to include a CD-ROM with the fourth edition of Physical Therapy of the Shoul-
der. The CD-ROM compliments the text and enhances the clinical application with excerpts of
an evaluation of a patient using manual therapy treatment techniques of the shoulder. Fresh
cadaver slides and also a link to an electronic image collection that features most of the illus-
trations contained in the book are included on the CD-ROM. This provides instructors with a
useful teaching tool because the images can be downloaded into PowerPoint for presentation in
class. The CD-ROM also features animated movement of the musculoskeletal system for the gleno-
humeral joint and scapula.
Any rehabilitation professional entrusted with the care and treatment of mechanical and patho-
logic shoulder dysfunction will benefit from this book. We trust that the fourth edition will meet
the reader’s expectation of comprehensive, clinically relevant presentations that are well docu-
mented, contemporary, and personally challenging to the student and the experienced specialist
alike.

Robert A. Donatelli, PhD, PT, OCS

Color Plates
Long head of biceps tendon

Head of the humerus

Plate 2-1 Glenoid surface with Glenoid

the labrum.

Labrum

Clavicle

Subscapularis
bursa opening
Plate 2-2 Glenohumeral joint capsule
and surrounding structures.

Anterior inferior Subscapularis tendon

glenohumeral capsule
 Low
er tr
apez
ius
Vertebral border
of the scapula

Spine of the
scapula

Infraspinatus

Teres minor
Serratus anterior

Plate 2-3 Scapula and surrounding muscles.

Coracoacromial
Acromion process
ligament

Supraspinatus tendon

Head of the humerus

Coracoid process

Plate 2-4 Inferiorly subluxed humeral head demonstrating coracoacromial vault.

Inferior angle of Infraspinatus

the scapula

Posterior deltoid

Serratus anterior

Teres minor

Latissimus Teres major

Plate 2-5 Scapula and related muscles.

 Coracoid process

Acromion process

Plate 2-6 Coracoacromial vault. Coracoacromial ligament

Head of the humerus

Area of
impingement

Sternocleidomastoid muscles

Anterior deltoid

Clavicle

Plate 2-7 Anterior chest and cervi- Pectoralis minor

cal spine.

Pectoralis major
Plate 5-1 Muscles with a direct relationship between the spine and the shoulder
girdle. (Copyright 1996. Ciba-Geigy Corporation. From the Ciba Collection of Medical Illustrations,
illustrated by Frank Netter, MD. All rights reserved.)
Plate 5-2 Fascia linking the shoulder to the rib cage. (Copyright 1996. Ciba-Geigy Corporation. From the Ciba Collection of Medical
Illustrations, illustrated by Frank Netter, MD. All rights reserved.)

Plate 5-3 Muscles of the front of the neck. (From Williams PL, Warwick R, Dyson M,
Bammister LH, editors: Gray’s Anatomy, ed 37, Edinburgh, 1989, Churchill Livingstone.)
Plate 5-4 The brachial plexus. (Copyright 1996. Ciba-Geigy Corporation. From the Ciba Collection of Medical Illustrations, illus-
trated by Frank Netter, MD. All rights reserved.)
Plate 13-1 Innervation of viscera. (Copyright 1996. Ciba-Geigy Corporation. From the Atlas of
Human Anatomy, illustrated by Frank Netter, MD. All rights reserved.)
Plate 13-2 Viscera of the abdomen. (Copyright 1996. Ciba-Geigy Corporation. From the Atlas of Human Anatomy,
illustrated by Frank Netter, MD. All rights reserved.)
Plate 13-3 Anatomy of the phrenic nerve and its innervation of the diaphragm. (Copyright 1996.
Ciba-Geigy Corporation. From the Ciba Collection of Medical Illustrations, illustrated by Frank Netter, MD. All rights
reserved.)
Plate 13-4 Pancoast’s tumor. (Copyright 1996. Ciba-Geigy Corporation. From the Ciba Collection
of Medical Illustrations, illustrated by Frank Netter, MD. All rights reserved.)

The Guide to Practice
I n this fourth edition of Donatelli’s Physical Therapy
of the Shoulder, the editor has converted his clinical
cases into the American Physical Therapy Associ-
ation’s (APTA) Guide to Physical Therapist Practice1
(Guide) format. This format was developed and has been
promoted by APTA, which is the largest professional
representative for physical therapists, physical therapy
assistants, and physical therapy students in the United
States.
This chapter is designed to orient the reader to the
origins, purposes, content, and nature of the Guide. In
this way, the intent of this chapter is to encourage clini-
cians and students who use the Donatelli text to incor-
porate the Guide’s language and philosophy into the
examination, evaluation, diagnosis, prognosis, interven-
tion, and outcome provided for their clients with shoul-
der dysfunction.
Origins
To speak at any length about the origins of this docu-
ment would take most of this text. For the abbreviated
yet complete review, the reader is encouraged to read
the Guide.1 Since Mary McMillan first constructed and
presided over the Women’s Physiotherapy Association
in the early 1920s—and until the first edition of the
Guide in 1997—the reconstruction aides, general prac-
titioners, and certified clinical specialists all intuitively
have known the value and importance of rehabilitation
services. Throughout that short but illustrious history,
the association members have professed the uniqueness
and talent within the physical therapy profession to any
who cared to listen. The scientific evidence of this effec-
tiveness, on the other hand, remains to be presented.
3
1
Scot Irwin
There is no defined body of knowledge for physical
therapists. The Guide provides a foundation for devel-
oping the evidence for the effectiveness of physical
therapist interventions. The body of knowledge will be
defined from the evidence that proves the value of the
interventions.
Physical therapy originated from many facets of
health care and health sciences, nursing, physical educa-
tion, medicine, pathology, and rehabilitation—yet we
claim none alone. For most of the decade of the 1980s
and early 1990s, APTA debated the merits and even the
existence of physical therapy diagnoses. The term diag-
nosis is so fraught with interpretations that even within
our own association confusion and debate have con-
sumed an inordinate amount of the association’s gover-
nance time. Finally, the APTA House of Delegates came
to an agreement that physical therapists did diagnose
and that those diagnoses were directed at movement and
movement dysfunction.
The basic premise here is that human movement, like
digestion, is a system. The movement system has normal
behaviors that can become dysfunctional, and a physical
therapist can provide remedies for those dysfunctions.
Eventually, because of a need to better describe the scope
of a physical therapist’s practice for many health care
agencies and the physical therapy profession, APTA
undertook the development of the Guide. From 1992
through the completion of the second edition, a handful
of physical therapists and staff of APTA constructed this
document. For those who have tried to produce anything
by committee, you can imagine the amount of time and
effort required to write the Guide. The authors of the
Guide are too numerous to list, but they are acknowl-
edged within the Guide itself and they deserve the
4 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
respect and thanks of every physical therapist. All of the
authors were chosen for their expertise and knowledge
in a particular practice pattern arena (musculoskeletal,
neuromuscular, cardiovascular/pulmonary, and integu-
mentary). Each of those authors is quick to point out
that this document is not written on a stone tablet. Its
origins come from the cataclysmic changes that have
occurred in health care delivery and reimbursement in
the United States. Those driving forces, along with the
dynamic growth and development of the profession of
physical therapy, created an environment that required
this document’s publication and required that the Guide
be in constant evolution. By the time this textbook is in
print, a third or fourth edition of the Guide may be avail-
able. The challenge for future physical therapists is to
continue to amend and edit the Guide by documenting
errors and omissions and by providing new practice pat-
terns for impairments and functional limitations yet to
be identified or discovered.
Purposes
The list of purposes for the Guide can be found on page
S17 of the second edition of the Guide.1 Throughout the
document, these purposes are reiterated. Each of the
diagnostic patterns described in the Guide uses termi-
nology found in the purposes. Although many readers
find this constant redundancy to be one of the distract-
ing features of the Guide, it is used to demonstrate the
basic constructs of a physical therapist’s approach to
patient management. The authors also used the hy-
phenated patient term throughout the Guide. For this
chapter, the term client is used.
A summary of the purposes is as follows: The Guide
was developed to assist internal (physical therapists) and
external (all others involved in health care delivery and
Table 1-1
NAGI MODEL OF DISABLEMENT
Active Pathology Impairment
Interruption or Anatomic, physiologic,
interference with mental, or emotional
normal processes, and abnormalities or loss
efforts of the organism
to regain normal state
reimbursement) individuals in understanding the scope
of a physical therapist’s practice. As stated in the Guide,
this includes—but is not limited to—practice settings,
roles, terminology, tests and measures, and interventions
used by physical therapists in the delivery of physical
therapy. Perhaps most important, the Guide estab-
lishes preferred practice patterns based upon the Nagi
Model of Disablement.2 A common theme within the
purposes listed in the Guide is the promotion of health,
wellness, fitness, prevention, and appropriate utilization
of physical therapy services as provided by physical
therapists.
The authors of the Guide clearly described what the
Guide is not. To quote the authors: “The Guide does not
provide specific protocols for treatments, nor are the
practice patterns contained in the Guide intended to
serve as clinical guidelines.”1 The authors go on to state
that the Guide is only an initial step in the development
of clinical guidelines. Clinical guideline development
requires evidence from peer-reviewed research. The
second edition of the Guide was not written to provide
that level of information.
Within the Donatelli text, the case examples have
been “Guideisized.” It is the intention that the reader
should become familiar with this system of patient eval-
uation and treatment and incorporate it into his or her
daily practice. It is also hoped that academic and clini-
cal faculty use the Guide approach when instructing
future generations of physical therapists, thus fulfilling
the purpose of the Guide.
Content
The Guide was developed with three key concepts in
mind: (1) the Nagi model of disablement2 (Table 1-1);
(2) physical therapists work in a variety of settings; and
Functional Limitation Disability
Limitation in Limitation in performance
performance at the of socially defined roles and
level of the whole tasks within a sociocultural
organism or person and physical environment
CHAPTER 1 THE GUIDE TO PRACTICE 5

(3) physical therapists provide services through the con-
tinuum of health care.
To understand the Guide, a good understanding of
the disablement model is required. Articles by Guc-
cione3 and Jette4 have provided the background for
understanding disablement. The reader can find these
articles in the Physical Therapy Journal in 1991 and 1994,
respectively. The Nagi model2 was selected by the
authors of the Guide because it provides the best fit for
the development of physical therapy practice patterns
and diagnoses. As Guccione’s diagram so aptly demon-
strates, the Nagi model encompasses the entire spectrum
of health care (Figure 1-1). Pathology and pathophysi-
ology lead to impairment, which can either cause more
pathology or lead to functional limitations. These func-
tional limitations may revert back to impairments or
progress to disability. The domain of a physical thera-
pist’s practice is outlined by the dotted lines in Figure
1-1. The Guide was developed to address the delivery of
health care services by physical therapists from pathol-
ogy to impairment to functional limitation and to dis-
ability with the greatest emphasis on identification and
rectification of impairments and functional limitations.
In effect, the Guide is saying that physical therapists
are the diagnosticians of movement impairments and
provide interventions to prevent, improve, or eliminate
functional limitations and disability.
The Guide goes on to enhance and adapt the Nagi
model by expanding it to include the larger arena of
quality of life (Figure 1-2). This enhancement requires
that the Guide include psychological and social functions
as well as the constructs of the promotion of wellness,
prevention, and fitness.
The actual content of the Guide includes four major
parts. The first part is a description of who physical
therapists are and their approaches to the manage-
ment of clients. The second part of the Guide provides
a description of 24 tests and measures used by physical
therapists as a part of their examination process. The
third part provides definitions and lists of physical ther-
apists’ interventions. The fourth and by far the major
portion of the Guide is made up of preferred practice
patterns.
The section that describes physical therapists pro-
vides information about the prerequisites required to
become a physical therapist; the types of settings in
which they practice; their roles in primary, secondary,
tertiary, and preventive care; the components of a phys-
ical therapist’s episode of care; and the criteria for ter-
mination of physical therapy services. In addition, this
section describes in greater detail the six elements of
patient management: (1) examination, (2) evaluation, (3)
diagnosis, (4) prognosis, (5) intervention, and (6) out-
comes (Figure 1-3). Finally, this section gives a broader
description of the roles of physical therapists in
management, administration, communication, critical
inquiry, and education.
The second part of the Guide provides the list of 24
tests and measures used by physical therapists in their
examination of clients. If a test or measure is not listed
in the Guide, this does not preclude physical therapists
from using that test or measure. It is the intent of the
Guide, however, that any test or measure be valid and
reliable and that each follows the Standards for Tests and
Measurements in Physical Therapy Practice as presented
in the Physical Therapy Journal in 1991.5

Health care

Medical aspects Domain of physical therapist practice Social aspects

Pathology/ Functional
Impairment Disability
pathophysiology limitation

Figure 1-1 Scope of physical therapist practice within the continuum of health care
services and the context of the disablement model. (Modified from the American Therapist Association
from Guccione. AA: Physical therapy diagnosis and the relationship between impairments and function. Phys Ther
71:499-504, 1991.)
6 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
Pathology/
Impairment
pathophysiology
Physical function Physiologic function
Non-health factors
• Economic status
• Individual
expectations
and achievements
• Personal
satisfaction with
choices and life
• Sense of
personal safety
Figure 1-2 Relationship among the disablement model, health-related quality of life,
and quality of life.
The interventions section is provided primarily for
external groups. There are definitions and descriptions
of all of the activities that physical therapists are trained
and required to perform when intervening on behalf of
a client. This list includes coordination, communication,
administration, client education, and the entire spec-
trum of the physical therapists’ interventions from ther-
apeutic exercise to physical agents and modalities.
The bulk of the Guide is dedicated to the practice
patterns. The patterns are broken up into four broad
classifications: (1) musculoskeletal, (2) neuromuscular,
(3) cardiovascular/pulmonary, and (4) integumentary.
All of the client cases described in this edition of
Physical Therapy of the Shoulder can be found in the mus-
culoskeletal and neuromuscular practice patterns. Note
that although the physical therapists’ evaluations direct
them initially to a specific pattern, they do not preclude
them from changing to an alternative pattern if their
examination information leads them to another conclu-
sion. It is also possible for a client to fit into more than
one pattern. In this case, the professional opinion of the
therapist will direct the allocation of resources and time
to the pattern of highest priority.
Functional
Disability
limitations
Social function
Health-related
quality of life
Quality of life
The practice patterns were developed using the Nagi
model2 and the patient management system previously
described.1 This system includes six components. Each
component in the patient management system is found
in every practice pattern. The purpose of this format is to
create a consistent, uniform methodology for patient
examination and treatment. As depicted in Figure 1-3,
each component of this system has specific supportive
parts. Examination includes obtaining a history (Figure
1-4), a review of systems (cardiopulmonary, muscu-
loskeletal, neuromuscular, and integumentary), choice
and administration of tests, measurements of appropri-
ate values, and identification of any need for referral to
another practitioner. The evaluation is the process of
using the information obtained during the examination
to determine a diagnosis or need to refer. This process
proceeds throughout the patient’s contact with the ther-
apist and requires clinical judgments to be made on a
regular and routine basis. The diagnosis is a determina-
tion of which practice pattern is a “best fit” for the previ-
ously gathered examination and evaluation information.
This physical therapist diagnosis relates directly to an
impairment classification in the Nagi model2 and should
CHAPTER 1 THE GUIDE TO PRACTICE 7

DIAGNOSIS
Both the process and the end
result of evaluating examination
data, which the physical therapist
organizes into defined clusters,
syndromes or categories to help
determine the prognosis (including
the plan of care) and the most
appropriate intervention strategies.

PROGNOSIS
(including plan of care)
Determination of the level of
EVALUATION optimal improvement that may be
A dynamic process in which the attained through intervention and
physical therapist makes clinical the amount of time required to
judgments based on data gathered reach that level. The plan of care
during the examination. This specifies the interventions to be
process may also identify possible used and their timing and
problems that require consultation frequency.
with or referral to another provider.

EXAMINATION
The process of obtaining a history,
performing a systems review, and
selecting and administering tests
and measures to gather data about
the patient/client. The initial
examination is a comprehensive
screening and specific testing
process that leads to a diagnostic
classification. The examination
process also may identify possible
problems that require consultation
with or referral to another provider.
INTERVENTION
Purposeful and skilled interaction
of the physical therapist with the
patient/client and, if appropriate,
with other individuals involved in
care of the patient/client, using
various physical therapy methods
and techniques to produce
changes in the condition that are
consistent with the diagnosis and
prognosis. The physical therapist
conducts a re-examination to
determine changes in patient/client
status and to modify or redirect
intervention. The decision to re-
examine may be based on new
clinical findings or on lack of
patient/client progress. The
process of re-examination also
may identify the need for
consultation with or referral to
another provider.

OUTCOMES
Results of patient/client
management, which include the
impact of physical therapy
interventions in the following
domains: pathology/
pathophysiology (disease,
disorder, or condition);
impairments, functional limitations,
and disabilities; risk reduction/
prevention; health, wellness, and
fitness; societal resources; and
patient/client satisfaction.

Figure 1-3 The elements of patient management leading to optimal outcomes.

 TYPES OF DATA THAT MAY BE GENERATED FROM A PATIENT/CLIENT HISTORY

General demographics Medical/surgical history

• Age • Cardiovascular
• Sex • Endocrine/metabolic
• Race/ethnicity • Gastrointestinal
• Primary language • Genitourinary Current condition(s)/
• Education • Gynecological chief complaints
• Integumentary • Concerns that led the patient/
Social history • Musculoskeletal client to seek the services of a
• Cultural beliefs and behaviors • Neuromuscular physical therapist
• Family and caregiver resources • Obstetrical • Concerns or needs of the
• Social interactions, social • Prior hospitalizations, surgeries patient/client who requires the
activities and support systems and preexisting medical and services of a physical therapist
other health-related conditions • Current therapeutic
• Psychological interventions
Employment/work • Pulmonary • Mechanisms of injury or
(job/school/play) disease, including date of onset
• Current and prior work and course of events
(job/school/play), community, • Onset and pattern of symptoms
and leisure actions, tasks or • Patient/client, family, significant
activities other and caregiver
expectations and goals for the
Employment/work therapeutic intervention
(job/school/play) • Patient/client, family, significant
• Current and prior work other and caregiver perceptions
(job/school/play), community, of patient/client’s emotional
and leisure actions, tasks or response to the current clinical
activities situation
• Previous occurrence of chief
Growth and development complaint(s)
• Developmental history • Prior therapeutic interventions
• Hand dominance

Living environment
• Devices and equipment (e.g.,
assistive, adaptive, orthotic, Functional status and
protective, supportive, prosthetic) activity level
• Living environment and • Current and prior functional
community characteristics status in self-care and home
• Projected discharge destinations management, including
General health status activities of daily living (ADL),
(self-report, family report, and instrumental activities of
caregiver report) daily living (IADL)
• General health perception • Current and prior functional
• Physical function (e.g., mobility, status in work (job/school/play),
sleep patterns, restricted bed community, and leisure actions,
days) tasks and activities
• Psychological functions (e.g.,
memory, reasoning ability,
depression, anxiety) Medications
• Role function (e.g., community • Medications for current
leisure, social work) condition
• Social function (e.g., social • Medications previously taken
activity, social interaction, social for current condition
support) • Medications for other conditions

Social/health habits
(past and current) Other clinical tests
• Behavioral health risks (e.g., • Laboratory and diagnostic tests
smoking, drug abuse) • Review of available records
• Level of physical fitness (e.g., medical, education, surgical)
• Review of other clinical
Family history findings (e.g., nutrition and
• Familial health risks hydration)
Figure 1-4 Types of data that may be generated from a patient history.
CHAPTER 1 THE GUIDE TO PRACTICE
lead the therapist to determine the relative level of func-
tional loss the client is experiencing. This in turn directs
the therapist to the appropriate intervention(s) to obtain
the optimal outcome for the client.
The next component is the prognosis. This compo-
nent also includes the plan of care. The prognosis comes
as a natural extension of the diagnosis. Once the diag-
nosis has been made, the therapist should begin to for-
mulate a realistic prognosis and estimate how much
improvement in function can be achieved given the
amount of impairment suffered as a result of the disease.
The logical progression of these interwoven formula-
tions between the Nagi model and the patient manage-
ment system has been formulated in the Guide to create
a continuum of care that leads to improved function or
appropriate referral.
The plan of care is the culmination of all the steps
previously listed and includes the patient goals, the
short- and long-term goals of the therapist, specific
interventions, and the projected outcomes of those
interventions. Included within the interventions and
outcomes should be some projection of the frequency
and duration of treatment required and plans for dis-
charge from therapy.
Perhaps the most important contribution of the
Guide to the clinician is in the intervention segments of
each practice pattern. These suggested interventions are
not cookbooks for care, but rather are listed specifically
as possible physical therapist approaches to achieve-
ment of the desired outcomes for the client. In all
cases, education of the client or supportive personnel is
included as a part of the interventions listed regardless
of the selected practice pattern. Alternative interven-
tions listed under a particular pattern should not be
interpreted by the therapist in terms of trying one or two
interventions and then moving on to the next practice
pattern if they do not work. Each intervention should
be applied as appropriate to the client responses, goals,
needs, and projected outcomes. Nowhere in the Guide is
it suggested that the interventions listed are the only
ones appropriate to a particular practice pattern. But as
the reader will learn in subsequent pages of the Donatelli
text, application of the correct intervention to the client
with shoulder dysfunction has been found to improve
the patient’s functional level and reduce his or her overall
impairment. Notice that in few, if any, cases are the
interventions of the physical therapist directed solely
at the pathology or pathophysiology of the patient’s
9
medical condition. The Guide is a textbook for provid-
ing direction for physical therapists to intervene at the
impairment and functional limitation level without the
use of medication for the most part or surgical inter-
ventions. Intervention also includes the need for the
therapist to interact with the rest of the medical com-
munity involved in the client’s care. This requires coor-
dination and communication with, and documentation
for, all of the physical therapist’s clients.
Inherent in the system of patient management is
that at any point during the patient’s treatment, the
therapist is mandated to provide re-examination. The
re-examination should be performed periodically during
an episode of care in order to ensure that the patient
is progressing according to his or her prognosis and
that short- and long-term goals are being achieved.
During re-examination, the patient management
system steps are repeated as in the original examination
process.
Summary
Why is the Guide titled Guide to Physical Therapists’ Prac-
tice and not Guide to Physical Therapy Practice? That is
the nature of the document. It is intended to describe
the scope, role, and spectrum of the physical therapist’s
activity. Why not physical therapy? Because many other
practitioners who are not physical therapists are legally
allowed to provide and be reimbursed for physical
therapy. APTA and this author believe physical therapy
per se is well described within the Guide, but physical
therapy is really only performed by physical therapists.
Therefore, the Guide correctly describes the physical
therapists’ diagnoses (practice patterns), tests and
measures, interventions, and responsibilities within the
context of the Nagi model.2
The template for defining the body of knowledge of
physical therapy has been produced in the Guide. The
physical therapist community has been challenged to
provide the evidence to prove or disprove the usefulness
of the interventions provided within each practice
pattern. The Guide has provided all physical therapists
with a common language; a patient management system;
and an opportunity to develop definitive, reproducible
methods of optimally improving impairments and func-
tional limitations of a physical therapist’s clients. The
Guide to Physical Therapist Practice is indeed a truly epic
document.
10 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

REFERENCES 4. Jette AM: Physical disablement concepts for physical therapy

1. Guide to physical therapists practice. ed 2, Phys Ther 81:9-744, research and practice. Phys Ther 74:381, 1994.
2001. 5. American Physical Therapy Association, Standards for tests
2. Nagi S: Disability and rehabilitation: Columbus, Ohio, 1969, and measurements in physical therapy practice. Phys Ther
Ohio State University Press. 71:589-622, 1991.
3. Guccione AA: Physical therapy diagnosis and the relationship
between impairments and function. Phys Ther 71:499-504,
1991.

Functional Anatomy
and Mechanics
O ne of the most common peripheral joints to be
treated in a physical therapy clinic is the
shoulder joint. The physical therapist must
have an in-depth understanding of the anatomy and
mechanics of this joint to most effectively evaluate
and design a treatment program for the patient with
shoulder dysfunction. This chapter describes the perti-
nent functional anatomy of the shoulder complex and
relates this anatomy to functional movements, stability,
muscle activity, and clinical application.
The shoulder joint is better called the shoulder
complex, because a series of articulations are necessary
to position the humerus in space (Figure 2-1). Most
authors, when describing the shoulder joint, discuss
the acromioclavicular joint, sternoclavicular joint,
scapulothoracic articulation, and glenohumeral joint.1-4
Dempster relates all of these areas by using a concept of
links. The integrated and harmonious roles of all of the
links are necessary for full normal mobility.5
The glenohumeral joint sacrifices stability for mobil-
ity. It is characterized by its large range of motion. The
shoulder is capable of moving in more than 16,000 posi-
tions, which can be differentiated by 1° in a normal
person.6 The mobility of the shoulder relies upon the
congruent articulating surfaces and surrounding soft
tissue envelope for static and dynamic stability. The
position of the humerus and scapula must change
throughout each movement in order to maintain
stability.6
11
2
Robert A. Donatelli
Osteokinematic and
Arthrokinematic Movement
Analysis of shoulder movement emphasizes the syn-
chronized movement of four joints: the glenohumeral,
scapulothoracic, sternoclavicular, and acromioclavicular
joints.2,4,7,8 As the humerus moves into elevation, move-
ment must occur at all four joints. Elevation of the
arm can be observed in three planes: the frontal plane
(abduction), sagittal plane (flexion), and plane of the
scapula (scaption).8,9 Movement of the long bones of
the arm into elevation is referred to as osteokinematics.
Arthrokinematics describes the intricate movement of
joint surfaces: rolling, spinning, and sliding.10
Osteokinematic Movement
Scaption-Abduction. Abduction of the shoulder
in the frontal or coronal plane has been extensively
researched.4,8,11-17 Poppen and Walker15 and Johnston8
suggest that the true plane of movement in the
shoulder joint occurs in the plane of the scapula. The
plane of the scapula is defined as elevation of the
shoulder in a range between 30° and 45° anterior to the
frontal plane (Figures 2-2 and 2-3).15
Kondo and associates18 devised a new method for
taking radiographs to define scaption during elevation.
The medial tilting angle was used to describe scaption.
Medial tilting angle refers to the tilting of the scapula
toward the sagittal plane. As the medial tilting angle
12 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Figure 2-1 The components of the shoulder joint

complex. 1, Glenohumeral joint. 2, Subdeltoid joint. 3,
Acromioclavicular joint. 4, Scapulothoracic joint. 5,
Sternoclavicular joint. 6, First costosternal joint. 7, First
costovertebral joint.

increases, there is a movement of the scapula around the

thoracic cage. Kondo and colleagues18 demonstrated that
the medial tilting angle was constant at 40° anterior
to the frontal plane throughout a range of 150° of
elevation.
Several authors believe that the plane of the scapula
is clinically significant because the length-tension
relationship of the shoulder abductors and rotators
is optimum in this plane of elevation.8,15 Research has
demonstrated that the length of the muscle determines
the amount of stretch applied to the individual sarco-
meres, enabling them to exert maximum tension.19 The
length tension curves obtained from normal muscles
show that maximum tension is developed when the
muscle length is approximately 90% of its maximum
length.19 Conversely, when the muscle is fully shortened,
the tension developed is minimal.20,21 Therefore, the
optimal lengthened position of the muscle tendon will
facilitate optimal muscle contraction.22
Several studies have compared the torque production
of different shoulder muscle groups when tested in
scaption versus other body planes.23-27 Soderberg and
Blaschak23 and Hellwig and Perrin24 demonstrated no
significant differences in the peak torque of the gleno-
humeral rotators between scaption and other body
Figure 2-2 Elevation in the plane of the scapula.
planes. These studies used 45° and 40° anterior to the
frontal plane, respectively, for the scaption test position.
Greenfield and associates25 reported greater torque in
the external rotators when tested in scaption versus
the coronal plane. Furthermore, Tata and colleagues26
reported higher ratios of abduction to adduction and
external to internal torque when tested in the scapular
plane at 30° and 35° anterior to the frontal plane, respec-
tively. Whitcomb and associates27 found no significant
difference between torque produced by the shoulder
abductors in the coronal and scapular planes, using a
scaption position 35° anterior to the frontal plane.
The studies cited indicate that the external rotators
are the only muscle group that demonstrated a signifi-
cant increase in torque in the scaption plane 30° ante-
rior to the frontal plane. The pectoralis major and the
latissimus muscle groups are not attached to the scapula.
Therefore it would seem reasonable that when
CHAPTER 2 FUNCTIONAL ANATOMY AND MECHANICS
Figure 2-3 Abduction in the plane of the scapula.
comparing the torque output of the internal rotators, the
change in position of the scapula should not influence
the optimal length-tension relationship. Thus the inter-
nal rotators exhibit no change in torque when testing in
different planes of movement.
In addition to optimal muscle length-tension rela-
tionship in the plane of the scapula, the capsular fibers
of the glenohumeral joint are relaxed.8 Because the
capsule is untwisted in the plane of the scapula, mobi-
lization and stretching in this plane may be tolerated
better than in other planes where the capsule is starting
in a twisted position. Poppen and Walker14 demon-
strated that in scaption there is an increase in joint con-
gruity, allowing for greater joint stability. Therefore,
for reasons of glenohumeral stability, minimal scapular
torsion, avoidance of impingement, and balance of
muscle action, scaption may be the plane in which
shoulder trauma is minimal and the most advantageous
plane for mobilization, stretching, testing, and strength-
ening the glenohumeral rotators.
Flexion. The movement of flexion has been inves-
tigated less thoroughly. Flexion is movement in the
sagittal plane. Full flexion from 162° to 180° is possible
only with synchronous motion in the glenohumeral,
acromioclavicular, sternoclavicular, and scapulothoracic
joints.14 The movement is similar to that of abduction.
Arthrokinematic Movement
The motion occurring at joint surfaces is arthrokine-
matic motion, of which there are three types: rolling,
13
gliding, and rotation (Figure 2-4). Rolling occurs when
various points on a moving surface contact various
points on a stationary surface. Gliding occurs when one
point on a moving surface contacts multiple points on a
stationary surface. When rolling or gliding occurs, there
is a significant change in the contact area between the
two joint surfaces. The third type of arthrokinematic
movement, rotation, occurs when one or more points
on a moving surface contact one point on a stationary
surface. There is little displacement between the two
joint surfaces in rotation.
All three arthrokinematic movements can occur at
the glenohumeral joint, but they do not occur in equal
proportions. These motions are necessary for the large
humeral head to take advantage of the small glenoid
articulating surface.16 Saha investigated the contact area
between the head of the humerus and the glenoid with
abduction in the plane of the scapula16 and found that
the contact area on the head of the humerus shifted
up and forward while the contact area on the glenoid
remained relatively constant, indicating a rotation move-
ment. Poppen and Walker measured the instant centers
of rotation for the same movement.15 They found in the
first 30°, and often between 30° and 60°, that the head
of the humerus moved superiorly in the glenoid by
3 mm, indicating rolling or gliding. At more than 60°,
there was minimal movement of the humerus, indicat-
ing almost pure rotation.15
Effective arthrokinematic movements are achieved
by a complex interaction between the various articular
and soft tissue restraints in addition to the dynamic
14 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

action of the rotator cuff muscles. For example, the
rotator cuff muscles center the humeral head in the
congruent glenoid fossa during the midrange of motion
when the capsuloligamentous structures are lax.28 Dys-
function of this complex mechanism would occur with
tightening of the capsule anteriorly, resulting in an ante-
rior restriction and causing an associated posterior shift
in contact of the humerus on the glenoid. The posterior
migration of the humeral head center and glenohumeral
contact are pronounced in shoulder joints with poor
congruence.28 To reestablish harmonious movement
within the shoulder complex, the therapist must reha-
bilitate the connective tissue by restoring its extensibil-
ity and the normal balance of muscles.
Rotations of the Humerus
Concomitant external rotation of the humerus is neces-
sary for abduction in the coronal plane.4,8,10,14,17 Some
investigators have postulated that this motion is neces-
sary for the greater tuberosity to clear the acromion
and the coracoacromial ligament.1,2,17 Saha16 reports that
there is sufficient room between the greater tuberosity
and the acromion to prevent bone impingement. Exter-
nal rotation also remains necessary for full coronal
abduction even after surgically removing the acromion
and the coracoacromial ligament. Saha has reasoned that
external rotation is necessary to prevent the humeral
head from impinging on the glenoid rim.16
Using cadaveric glenohumeral joints, Rajendran29
demonstrated that automatic external rotation of the
humerus is an essential component of active and pas-
sive elevation of the arm through abduction. Even in
the absence of extraarticular influences, such as the
coracoacromial arch and glenohumeral muscles, external
rotation of the humerus was spontaneous. Kn and
associates30 used a magnetic tracking system to monitor
the three-dimensional orientation of the humerus with
respect to the scapula. Appropriate coordinate transfor-
mations were then performed for the calculation of
glenohumeral joint rotation. Maximum elevation in all
planes anterior to the scapular plane required external
axial rotation of the humerus. Browne and colleagues,31
using three-dimensional magnetic field tracking, dem-
onstrated that elevation in any plane anterior to the
scapula required external humeral rotation. Further-
more, maximum elevation was associated with approxi-
mately 35° of external humeral rotation. Conversely,
internal rotation was necessary for increased elevation
posterior to the plane of the scapula.

Figure 2-4 Arthrokinematic motion occurring at the glenohumeral

joint: rolling, rotation, and gliding.
CHAPTER 2 FUNCTIONAL ANATOMY AND MECHANICS 15

Otis and associates32 demonstrated that external glenohumeral articulation in 70% of his subjects. In the
rotation of the humerus allows the insertion of the remaining 30%, the radius of curvature of the humeral
subscapularis tendon to move laterally, resulting in an head was greater than the radius of curvature of the
increase in the distance from the axis of elevation in the glenoid. Thus the joint was not a true enarthrosis.16
scapular plane. An increase in the moment arm enhances Saha16 further described the joint surfaces, especially on
the ability of the superior fibers of the subscapularis to the head of the humerus, to be very irregular and to
participate in scaption. Conversely, internal rotation of demonstrate a great amount of individual variation.
the humerus increases the moment arm of the superior The head of the humerus is a hemispherical convex
fibers of the infraspinatus, enhancing the ability of articular surface that faces superior, medial, and poste-
the muscle to participate in scaption. Flatow and rior. This articular surface is inclined 130° to 150° to the
colleagues33 reported that acromial undersurface and shaft of the humerus and is retroverted 20° to 30°.3 The
rotator cuff tendons are in closest proximity between 60° retroversion, and the posterior tilt of the head of
and 120° of elevation. Conditions limiting external rota- the humerus and the glenoid, cultivates joint stability
tion or elevation may increase rotator cuff compression. (Figure 2-5). This retroversion of the head of the
Rajendran and Kwek34 described how the course of the humerus corresponds to the forward inclination of the
long head of the biceps (LHB) would influence external scapula so that free pendulum movements of the arm do
rotation of the humerus, which in turn prevents tendon not occur in a straight sagittal plane but at an angle of
impingement between the greater tuberosity and the
glenoid labrum, and allows glenohumeral elevation to
move to completion. Brems35 reports that external rota-
tion is possibly the most important functional motion
that the shoulder complex allows. Loss of external rota-
tion could result in significant functional disability.
Walker36 described external rotation of the humerus as
necessary for the greater tuberosity to clear the glenoid,
providing more articular cartilage motion to produce
elevation of the arm.
External rotation is an important component for
active elevation. The author has demonstrated a direct
correlation between passive external rotation, measured
in the adducted position, and active elevation (unpub-
lished study). Therefore when treating patients with
limited active elevation, avoid pushing the joint into
painful elevation activities. Restoring passive external
rotation in the adducted position is a safe and effective
way of restoring extensibility to the capsule and enhanc-
ing active elevation.

Static Stabilizers of the

Glenohumeral Joint
The stability of the glenohumeral joint is dependent on
the integrity of soft tissue and bony structures such
as the labrum, glenohumeral ligaments, capsular liga-
ments, and bony glenoid.37 The glenohumeral joint
contributes the greatest amount of motion to the Figure 2-5 A, Humerus with marker through the
shoulder because of its ball and socket configuration. head-neck and a second marker through the epicondyles.
Saha38 confirmed the ball and socket joint of the B, Retroversion of the humerus as seen from above.
16 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
30° across the body.39 Retroversion of the humeral head
corresponds to the natural arm swing evident in
ambulation.
The head of the humerus is large in relation to the
glenoid fossa. Therefore only one third of the humeral
head can contact the glenoid fossa at a given time.1,39
The glenoid fossa is a shallow structure deepened by the
glenoid labrum. The labrum is wedge-shaped when the
glenohumeral joint is in a resting position, and changes
shape with various movements.40 The glenoid and the
labrum combine to form a socket with a depth up to
9 mm in the superior-inferior direction and 5 mm in the
anteroposterior direction.41 The functional significance
of the labrum is questionable. Most authors agree that
the labrum is a weak supporting structure.40,42 The func-
tion of the labrum has also been described as a “chock
block” preventing humeral head translation.43 Moseley
and Overgaard40 considered the labrum a redundant fold
of the capsule composed of dense fibrous connective
tissue, but generally devoid of cartilage except in a small
zone near its osseous attachment (Plate 2-1).
The glenohumeral joint has been described by
Matsen and associates44 as a “suction cup” because of the
seal of the labrum and glenoid to the humeral head. This
phenomenon is caused by the graduated flexibility of the
glenoid surface, which permits the glenoid to conform
and seal to the humeral head. Compression of the head
into the socket expels the synovial fluid to create a
suction that resists distraction. A negative intraarticular
joint pressure is produced by the limited joint volume.45
Matsen and associates44 illustrated the importance of
an intact glenoid labrum in establishing concavity com-
pression stabilization. The compressive load is provided
by dynamic muscle contraction.
The glenoid fossa faces laterally. Freedman and
Munro46 found that the glenoid faced downward in
80.8% of the shoulders that they studied with radio-
graphs. Saha38 found a 7.4° retrotilt of the glenoid in
73.5% of normal subjects. The retrotilt is a stabilizing
factor to the glenohumeral joint. Both the humeral and
glenoid articular surfaces are lined with articular carti-
lage. The cartilage is the thickest at the periphery on the
glenoid fossa and at the center of the humeral head.16
Anatomy of the Glenohumeral Ligaments
The coracohumeral ligament is the strongest supporting
ligament of the glenohumeral joint. Fibers of the capsule
and coracohumeral ligament blend together and insert
into the borders of the supraspinatus and subscapularis.47
Portions of the coracohumeral ligament form a tunnel
for the biceps tendon on the anterior side of the joint.
The rotator cuff interval, the region of the capsule
between the anterior border of the supraspinatus and the
superior border of the subscapularis muscle, is reinforced
by the coracohumeral ligament.43 The superior gleno-
humeral ligament and the coracohumeral ligament
limit external rotation and abduction of the humerus
and are important stabilizers in the inferior direction
from 0° to 50° abduction.43,48
The superior glenohumeral ligament forms an ante-
rior cover around the LHB tendon and is also part of
the rotator cuff interval.43 The coracohumeral ligament
blends with the superior glenohumeral ligament. The
anatomy of the middle glenohumeral ligament is similar
to that of the superior glenohumeral ligament. The
middle glenohumeral ligament blends with portions of
the subscapularis tendon medial to its insertion on the
lesser tuberosity. The middle glenohumeral ligament
has been shown to become taut at 45° abduction, and
10° extension and external rotation, providing anterior
stability between 45° and 60° abduction.
The inferior glenohumeral ligament complex is a
hammock like structure with attachments on the ante-
rior and posterior sides of the glenoid. The anterior band
of the inferior glenohumeral ligament is attached to the
anterior labrum. At the neutral position (0° abduction
and 30° horizontal extension), the anterior band of the
inferior glenohumeral ligament becomes the primary
stabilizer. The inferior glenohumeral ligament complex
was found to be the most important stabilizer against
anteroinferior shoulder dislocation.43,49
The capsule and ligaments reinforce the gleno-
humeral joint. The capsule attaches around the glenoid
rim and forms a sleeve around the head of the humerus,
attaching on the anatomical neck. A functional interplay
or interdependence exists between the anterior and
posterior, and superior and inferior capsuloligamentous
system. This concept is referred to as the circle theory,
which implies that excessive translation in one direction
may produce damage to the capsule on the same and
opposite sides of the joint.50 The capsule is a lax struc-
ture. The head of the humerus can be distracted one-
half inch when the shoulder is in a relaxed position.48
The anterior capsule is reinforced by the glenohumeral
ligaments noted above. The support these ligaments
lend to the capsule is insignificant51 (Plate 2-2).
CHAPTER 2 FUNCTIONAL ANATOMY AND MECHANICS
Turkel and associates52 described the inferior gleno-
humeral ligament as the thickest and most consistent
structure. The inferior glenohumeral ligament attaches
to the glenoid labrum. Turkel and colleagues52 deter-
mined the relative contribution to anterior stability by
testing external rotation in different positions. The
subscapularis resisted passive external rotation in the
adducted position more than any other anterior struc-
ture (Figure 2-6). In patients with internal rotation
contracture and pain after anterior repair for recurrent
dislocation of the shoulder, surgical release of the
subscapularis increased the external rotation range of
motion an average of 27°.53 Turkel and associates52
demonstrated at 45° abduction that external rotation was
resisted by the subscapularis, middle glenohumeral
ligament, and superior fibers of the inferior ligament
Figure 2-6 External rotation of the humerus in the
adducted position. The most stabilizing structure to this move-
ment is the subscapularis muscle.
17
(Figure 2-7). At 90° of abduction, the inferior gleno-
humeral ligament (Figure 2-8) was restricted by exter-
nal rotation.
Itoi and associates54 concluded that the LHB and
short head of the biceps (SHB) have similar functions
as anterior stabilizers of the glenohumeral joint with the
arm in abduction and external rotation. Furthermore,
the role of the LHB and SHB increased with shoulder
instability. Warner and associates55 studied the capsu-
loligamentous restraints to superior and inferior trans-
lation of the glenohumeral joint. The primary restraint
to inferior translation of the adducted shoulder was the
superior glenohumeral ligament. Abduction to 45° and
90° demonstrated the anterior and posterior portions,
respectively, of the glenohumeral ligament to be the
main static stabilizers resisting inferior translation.
Figure 2-7 External rotation of the humerus at 45°
abduction. The most stabilizing structures for this move-
ment are the middle and inferior ligaments and the subscapu-
laris muscle.
18 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
Figure 2-8 External rotation of the humerus at 90°
abduction. The most stabilizing structure for this movement is
the inferior ligament.
Guanche and associates56 studied the synergistic
action of the capsule and the shoulder muscles. A reflex
arch was identified from mechanoreceptors within the
glenohumeral capsule to muscles crossing the joint.
Stimulation of the anterior and inferior axillary articu-
lar nerves elicited electromyographic (EMG) activity in
the biceps, subscapularis, supraspinatus, and infraspina-
tus muscles. Stimulation of the posterior axillary articu-
lar nerve elicited EMG activity in the acromiodeltoid
muscle.
Between the supporting ligaments and muscles lie
synovial bursae or recesses. Anteriorly, there are three
distinct recesses.57 The superior recess is the subscapu-
lar bursa, which normally communicates with the
shoulder joint. The inferior recess is referred to as the
axillary pouch, and the middle synovial recess lies pos-
terior to the subscapularis tendon. Arthrograms of
frozen shoulders in relatively early stages, before gleno-
humeral abduction is completely restricted, show
obliteration of the anterior glenoid bursa.58
Dynamic Stabilizers of the
Glenohumeral Joint
The major muscles that act on the glenohumeral and
scapulothoracic joints may be grouped into the scapulo-
humeral, axiohumeral, and axioscapular muscles. The
muscles of the scapulohumeral group, which include the
rotator cuff muscles, originate on the scapula and insert
on the humerus. The rotator cuff muscles insert on
the tuberosities and along the upper two thirds of the
humeral anatomic neck.10 The contribution of the
shoulder musculature to joint stability may be caused by
the following mechanisms: muscle bulk acting as a
passive muscle tension; contraction of the rotator cuff
muscles primarily causing compression of the articular
surfaces; joint motion that secondarily tightens the lig-
amentous constraints; barrier or restraint effects of the
contracted muscle; and redirection of the joint force
to the center of the glenoid surface by coordination of
muscle forces.50
The infraspinatus and teres minor control external
rotation of the humerus and reduce anterior-inferior
capsuloligamentous strain. The subscapularis muscle is
the strongest stabilizer of the rotator cuff muscles. It has
the largest amount of muscle mass of the four rotator
cuff muscles.4 Combined contraction of the subscapu-
laris and the infraspinatus forms a force couple, provid-
ing stability throughout the midrange of elevation,
which is from 60° to 150° of abduction.49
Researchers showed that during late cocking by base-
ball pitchers, the glenohumeral joint reaches extreme
external rotation. The subscapularis has the most activ-
ity stabilizer followed by infraspinatus and teres minor.
The supraspinatus has the least activity.50 In addition,
the subscapularis of a professional baseball pitcher is
more active in the propulsive phase than any other inter-
nal rotator.50
Travell and Simons58 believe that a trigger point
within the subscapularis may spur the other shoulder
girdle musculature into developing secondary and satel-
lite trigger points, leading to major restrictions in gleno-
humeral joint motion causing adhesive capsulitis (Plate
2-3).
CHAPTER 2 FUNCTIONAL ANATOMY AND MECHANICS
The rotator cuff muscles have been described as
steering mechanisms for the head of the humerus on
the glenoid.16 The subscapularis, latissimus dorsi, teres
major, and teres minor act as humeral depressors.16,59
The arthrokinematics (rolling, spinning, and sliding) of
the glenohumeral joint result from the action of the
steering mechanisms and the depressors of the humeral
head. Translation of the humeral head is of clinical inter-
est in most shoulder disorders. At the glenohumeral
joint, the amount and direction of translation define the
type of instability. Wuelker and associates60 demon-
strated that translation of the humeral head during ele-
vation of the glenohumeral joint between 20° and 90°
averaged 9 mm superiorly and 4.4 mm anteriorly. Trans-
lation of the humeral head during active elevation may
be diminished by the coordinated activity of the rotator
cuff muscles. This active control of translation forces
provides dynamic stability to the glenohumeral joint.
Perry61 described 17 muscle groups providing a dynamic
interactive stabilization of the composite movement of
the thoracoscapular humeral articulation.
The deltoid muscle makes up 41% of the scapulo-
humeral muscle mass.4 This muscle, in addition to its
proximal attachment on the acromion process and the
spine of the scapula, also stems from the clavicle. The
distal insertion is on the shaft of the humerus at
the deltoid tubercle. The mechanical advantage of
the deltoid is enhanced by the distal insertion and the
evolution of a larger acromion process.4 The deltoid
is a multipennate and fatigue-resistant muscle. This
may explain its rare involvement in shoulder pathologic
conditions.62 The deltoid and the clavicular head of
the pectoralis major muscles have been described as
prime movers of the glenohumeral joint because of their
large mechanical advantage.4 Michiels and Bodem63
demonstrated that deltoid muscle action is not restricted
to the generation of an abduction in the shoulder
joint.
The deltoid provides dynamic stability with the arm
in the scapular plane and decreases stability with the arm
in the coronal plane. The mid and posterior heads of the
deltoid provide more stability by generating more com-
pressive forces and lower shearing forces than the
anterior head. Therefore the mid and posterior heads
of the deltoid should strengthen vigorously in anterior
shoulder instability64 (Plate 2-4).
Itoi and associates54 reported that the biceps muscle
group becomes more important than the rotator cuff
19
muscles as stability from the capsuloligamentous struc-
ture decreases. The anterior displacement of the humeral
head under 1.5 kg force was significantly decreased by
both the LHB and SHB loading in all capsular con-
ditions when the arm was in 60° or 90° of external
rotation and abduction. Abboud and associates50
demonstrated that the LHB in the shoulder neutral
position is anterior to the joint. Internal rotation of the
humerus positions the tendon of the biceps, further
anterior to the joint and external rotation, positions the
biceps tendon posterior to the joint. The forces gener-
ated by the LHB help stabilize the glenohumeral joint
and assist in restricting the translations of the humeral
head. The restrictions in translation of the humeral head
occur as a result of internal and external rotation of the
humerus, allowing the forces generated by the tendon to
change to compressive with a posterior-directed force
and compressive with an anterior-directed force, respec-
tively (Figure 2-9).
The deltoid and the rotator cuff muscles produce
shearing and compressive forces to the glenohumeral
joint. These forces vary as the alignment of the muscles
changes.65 The compressive forces produced by those
muscles acting parallel to the glenoid fossa will stabilize
the humeral head. Muscles acting more perpendicular to
the glenoid produce a translational shear. A larger supe-
rior shear produces impingement while a larger com-
pressive force centers the humeral head in the glenoid,
reducing impingement of the rotator cuff under the
acromion.65 The central position of the humeral head on
the glenoid helps stabilize the glenohumeral joint
(Plates 2-5 and 2-6).
Payne and associates65 simulated rotator cuff, deltoid,
and biceps muscle forces on 10 human cadaver shoul-
ders using transducers within the acromial arch. The
muscle forces that reduce acromial pressure included the
biceps reducing the acromial pressure by 10% in all
the shoulders and 34% in six of the shoulders. Rotator
cuff muscle force, without simulating supraspinatus, was
very effective in reducing the acromial pressure. With
simulation of the subscapularis, infraspinatus, and teres
minor, there was a 52% decrease in the anterolateral
acromion pressure in neutral shoulders with type III
acromion. Without the rotator cuff force, the amount
of deltoid force required to abduct the arm increased
by 17%. According to the Payne study, the action of
the deltoid muscle increased the pressures under the
acromion 1240%.65
20 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
ER
N
IR
A
B C
Figure 2-9 Forces produced by the long head of the
biceps tendon in conjunction with internal and external rota-
tion of the humerus. A, Tendon position neutral and anterior
to joint, ER posterior to joint, IR anterior to joint. B, Forces
are compressive and posterior with internal rotation. C, Forces
are compressive and anterior with external rotation. (Modified
from Pagnani Mj, Xiang-Hua D, Warren RF, et al: Role of the long head
of the biceps brachii in glenohumeral stability: a biomechanical study in
cadavera. J Shoulder Elbow Surg 5:225-262, 1996.)
Sternoclavicular Joint
The sternoclavicular (SC) joint is the only articulation
that binds the shoulder girdle to the axial skeleton
(Figure 2-10). This is a sellar joint, with the sternal artic-
ulating surface greater than the clavicular surface, pro-
viding stability to the joint.10 The joint is also stabilized
by its articular disk, joint capsule, ligaments, and rein-
forcing muscles.5,66 The disk binds the joint together and
Figure 2-10 The upper and lower attachments of the
meniscus and upper and lower ligaments of the sternoclavicu-
lar joint.
divides the joint into two cavities. The capsule surrounds
the joint and is thickest on the anterior and posterior
aspects. The section of the capsule from the disk to
the clavicle is more lax and allows more mobility than
between the disk, sternum, and first rib.10 The inter-
clavicular ligament anteriorly and inferiorly reinforces
the capsule. The costoclavicular ligament connects the
clavicle to the first rib.10 The SC joint gains increased
stability from muscles, especially the sternocleidomas-
toid, sternohyoid, and sternothyroid.66
Acromioclavicular Joint
At the other end of the clavicle is the acromioclavicular
(AC) joint. This articulation is characterized by vari-
ability in size and shape of the clavicular facets and the
presence of an intraarticular meniscus.64 The AC joint
capsule is more lax than the sternoclavicular joint and
thus a greater degree of movement occurs at the AC
joint, which contributes to the increased incidence of
dislocations.66 There are three major supporting liga-
ments for the AC joint. The conoid and trapezoid
ligaments are collectively called the coracoclavicular
ligament and the AC ligament. It is through the conoid
and trapezoid ligaments that scapula motion is trans-
lated to the clavicle.5
Rotation of the clavicle is the major movement at the
AC joint. Steindler67 describes AC joint rotation occur-
ring around three axes. Longitudinal axial rotation, ver-
tical axis for protraction and retraction, and horizontal
axis for elevation and depression are all controlled and
facilitated by the conoid, trapezoid, and AC ligaments
(Figure 2-11).
CHAPTER 2 FUNCTIONAL ANATOMY AND MECHANICS 21

Figure 2-11 Axes of motion of the clavicle. A, Longitudinal axis of

rotation. B, Vertical axis for protraction and retraction. C, Horizontal axis
for elevation and depression. The sternal end of the scapula is on the left.
(From Schenkman M, Rugo de Cartaya V: Kinesiology of the shoulder complex, J Orthop
Sports Phys Ther 8:438, 1987) with permission of the Orthopaedic and Sports Physi-
cal Therapy Sections of the American Physical Therapy Association.

Figure 2-12 Force couple of muscles acting at scapula. A, Axis of scapular rotation from
0° to 30°. B, Axis of scapular rotation from 30° to 60°. FUT , Force of upper trapezius; FLT , force of
lower trapezius; FSA , force of serratus anterior.) (Modified from Schenkman M, Rugo de Cartaya V: Kinesiol-
ogy of the shoulder complex, J Orthop Sports Phys Ther 8:438, 1987) with permission of the Orthopaedic and Sports
Physical Therapy Sections of the American Physical Therapy Association.

Scapulothoracic Joint cave, articulating with a convex girdle.1,61 The scapula is

without bony or ligamentous connections to the thorax,
The scapulothoracic joint is not an anatomic joint, but it except for its attachments at the AC joint and cora-
is an important physiologic joint that adds considerably coacromial ligament. The scapula is primarily stabilized
to motion of the shoulder girdle. The scapula is con- by muscles. The importance of the scapula rotators has
22 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
been established as an essential ingredient to gleno-
humeral mobility and stability (Figure 2-12). The stable
base, and therefore the mobility of the glenohumeral
joint, is largely dependent on the relationship of the
scapula and the humerus. The scapula and humerus
must accommodate the ever-changing positions during
shoulder movement to maintain stability.6 Figure 2-13
demonstrates the force couple of the scapula rotators.
Functional Biomechanics
As previously noted, shoulder elevation is defined as the
movement of the humerus away from the side. It can
occur in an infinite number of body planes.45
Shoulder elevation can be divided into three phases.
The initial phase of elevation is 0° to 60° degrees. The
middle or “critical phase” is 60° to 140°. The final phase
of elevation is 140° to 180°. Specific to each phase of
movement, precise muscle function and joint kinematics
Upper
trapezius
Serratus
anterior
Figure 2-13 Force couple of the scapula rotators.
allow normal, pain-free motion. Analysis of the precise
components critical for each phase of shoulder elevation
will determine the success of clinical management of
shoulder dysfunction.
Initial Phase of Elevation: 0° to 60°
All three arthrokinematic movements occur at the
glenohumeral joint, but they do not occur in equal pro-
portions. These movements—roll, spin, and glide—are
necessary for the large humeral head to take advantage
of the small glenoid articulating surface.16 Saha68 and
Sharkey and Marder69 investigated the contact area
between the head of the humerus and the glenoid with
elevation in abduction and in scaption. The studies
found that the contact area on the head of the humerus
was centered at 30° and superiorly shifted 1.5 mm by
120°. Poppen and Walker14 also studied the instant
centers of rotation for abduction. They reported that in
the first 30° and often between 30° and 60° of abduc-
Levator scapulae
Rhomboideus minor
Middle trapezius
Rhomboideus major
Lower
trapezius
CHAPTER 2 FUNCTIONAL ANATOMY AND MECHANICS
tion, the head of the humerus superiorly moved in the
glenoid by 3 mm, which indicates the occurrence of
rolling or gliding of the head. The EMG activity of the
supraspinatus muscle indicates an early rise in tension,
producing a compressive force to the glenohumeral joint
surface.
The deltoid muscle also demonstrates EMG activity
in the initial phase of elevation. The subscapularis, infra-
spinatus, and teres minor muscles are important stabi-
lizers of the humerus in the initial phase of elevation.3
Kadaba and associates59 report EMG activity of the
upper and lower portions of the subscapularis muscle
recorded by intramuscular wire electrodes. During the
initial phase of elevation, EMG activity of the upper
subscapularis was greater at the beginning of the range,
while the lower subscapularis increased as the elevation
reached 90°.52 A significant amount of force is generated
at the glenohumeral joint during abduction.4,15 In the
early stages of abduction, the loading vector is beyond
the upper edge of the glenoid.70
During the initial stage of elevation, the pull of the
deltoid muscle produces an upward shear of the humeral
head.3 This shearing peaks at 60° of abduction and is
counteracted by the transverse compressive forces of the
rotator cuff muscles.3,15 The primary function of the sub-
scapularis muscle is to depress the humeral head, coun-
teracting the superior migrating force of the deltoid.59
At 60° (abduction), the downward (short rotator) force
was maximal at 9.6 times the limb weight or 0.42 times
the body weight.2,15 The subscapularis, infraspinatus,
and latissimus dorsi muscle have small lever arms that
form 90° angles to the glenoid face, producing com-
pressive forces to the joint.
Movement of the AC and SC joints permits move-
ment of the scapula. Shoulder abduction is accompanied
by clavicular elevation. Sternoclavicular elevation is most
evident during the initial phase of arm elevation. There
is 4° SC movement for each 10° of shoulder abduction.4
The AC joint moves primarily before 30° and after
135°.4
The instantaneous center of rotation (ICR) of the
scapula during the initial phase of elevation is located at
or near the root of the scapula spine in line with the SC
joint.71 The initial phase of arm elevation is referred to
by Poppen and Walker15 as the setting phase; scapula
rotation occurs about the lower mid portion. The rela-
tive contribution from scapular rotation during the
initial phase of elevation is considerably less than from
23
glenohumeral motion. Bagg and Forest71 estimated a
3.29 : 1 ratio of glenohumeral to scapulothoracic mobil-
ity during the initial phase of elevation. The upper
trapezius and lower serratus anterior muscles provide
the necessary rotatory force couple to produce upward
scapular rotation during the early phase of arm
abduction.72
Middle or Critical Phase of Elevation:
60° to 100°
The middle or critical phase of elevation is initiated by
excessive force at the glenohumeral joint. As previously
noted, the shearing of the deltoid muscle is maximal at
60° elevation (Figure 2-14). Wuelker and associates60
simulated muscle forces under the coracoacromial vault.
The forces at the glenohumeral joint were recorded and
applied to the shoulder muscles at a constant ratio
approximating physiologic conditions of shoulder eleva-
tion: deltoid, 43%; supraspinatus, 9%; subscapularis,
26%; and infraspinatus/teres minor, 22% (Figure 2-15).
Peak forces under the coracoacromical vault occurred
between 51° and 82° of glenohumeral joint elevation.
These force values may represent the pathomechanics
of shoulder impingement. Figure 2-16 demonstrates
the compressive and depressive forces generated by the
muscles that provide a parallel force to the glenohumeral
joint to counteract the shearing of the deltoid muscle
group, which is perpendicular to the glenohumeral joint.
Figure 2-14 In the early stages of glenohumeral
abduction, the deltoid reactive force (D) is located outside the
glenoid fossa. The transverse compressive forces of the
supraspinatus (S) and infraspinatus (I) muscles are counter-
acted by this force. The resultant reactive force (R) is there-
fore more favorably placed within the glenoid fossa for joint
stability.
24 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

The resultant acting forces, which help stabilize the

Figure 2-15 Force couple of deltoid and rotator cuff
muscles. Rotatory forces, acting on opposite sides of the axis
of motion, combine to produce upward rotation. Translatory
forces cancel each other out. FRR , Rotatory force of rotator
cuff; FTR , translatory force of rotator cuff; FRD , rotatory force
of deltoid; FTD , translatory force of deltoid. (Modified from
Schenkman M, Rugo de Cartaya V: Kinesiology of the shoulder complex, J
Orthop Sports Phys Ther 8:438, 1987) with permission of the
Orthopaedic and Sports Physical Therapy Sections of the American
Physical Therapy Association.
Acromion
Deltoid
Supraspinatus
joint, are maximal at 90° of elevation,3 with shear and
compressive forces equal.72 As the arm reaches the end
of the critical phase, the resultant and shearing forces of
the deltoid are almost zero.3,15
The balance of shearing and compressive force estab-
lishes dynamic stability of the glenohumeral joint. In the
early part of the critical phase, dynamic stability must be
initiated before further progression of pain-free move-
ment can occur. As previously noted, the lower fibers of
the subscapularis muscle showed more activity at 90° of
abduction.59 The deltoid muscle reaches maximum
EMG activity at about 110° of abduction and maintains
a plateau level of activity.3 Supraspinatus EMG activity
peaks at 100° of elevation and rapidly diminishes there-
after.3 The subscapularis activity decreases substantially
after 130° of elevation, supporting the concept that
anterior ligament stability is critical beyond 130° of
elevation.3
The head of the humerus demonstrates an excursion
of 1 to 2 mm of a superior and inferior glide on the
glenoid surface.14 The movement of the humeral head
in a superior and inferior direction after 60° of elevation
indicates that a roll and glide is occurring in opposite
directions, resulting in a spin of the bone. As previously
noted, external rotation of the humerus is critical for ele-
vation (abduction) of the arm.

Figure 2-16 Forces provided the

Subscapularis muscles that are parallel to the gleno-
Infraspinatus humeral joint. These muscles produce
Lat
iss and Teres minor compressive and depressive forces to help
imu stabilize the glenohumeral joint. The
sd
ors deltoid muscle is perpendicular to the
i
glenohumeral joint.

Biceps
CHAPTER 2 FUNCTIONAL ANATOMY AND MECHANICS
Bagg and Forrest71 examined 20 subjects and found
three distinctive patterns of scapulohumeral movement.
Each pattern had three phases with varying ratios of
humeral to scapular movement. The most common
pattern had 3.29° of humeral motion to every degree of
scapular motion from 20.8° to 81.8° scaption. The
humeral component decreased to 0.71° for scaption
between 81.8° and 139.1°. Therefore the greatest rela-
tive amount of scapular rotation occurs between 80° and
140° of arm abduction.71 The ratio of glenohumeral
to scapulothoracic motion has been calculated to be
0.71 : 1 during the middle phase of elevation.72 Doody
and associates,12 along with Freedman and Munro,46
proposed that the significant role of the scapular
rotators during the critical phase of elevation is
secondary to the relatively long moment arms of the
upper trapezius, lower trapezius, and lower serratus ante-
rior muscles. Therefore during the middle phase of
elevation, the scapular rotators provide an important
contribution to elevation of the humerus in the plane of
the scapula.
Movement of the AC and SC joints permits move-
ment of the scapula. The relative contribution of these
two joints changes throughout the range of motion
depending on where the instant center of rotation (ICR)
lies.71 During the middle phase of abduction, the ICR
of the scapula begins to migrate towards the AC joint.
Clavicular elevation about the SC joint, coupled with
scapular rotation about the AC joint, facilitates normal
scapula mobility. Motion can occur at the AC joint,
with less movement occurring at the SC joint because
of the clavicular rotation around its long axis.4 The
double-curved clavicle acts like a crankshaft, permitting
elevation and rotation at the AC end. The rotation
of the scapula about the AC joint is initiated between
60° and 90° of elevation.72 Clavicular elevation is
completed between 120° and 150° of humeral abduc-
tion.71 Clavicular elevation at the AC joint permits
maximum scapular rotation. At approximately 150° of
elevation, the ICR of the scapula is in line with the AC
joint.71
Final Phase of Elevation: 140° to 180°
During the final phase of elevation, the ratio of gleno-
humeral to scapulothoracic motion is 3.49 : 1, indicating
relatively more glenohumeral motion.71 The ICR of the
scapula has relocated upward and laterally. The rotatory
force arm of the upper trapezius muscle has reduced in
25
length and the role of this muscle is now supportive
of the scapula.72 The new location of the ICR of the
scapula allows the middle trapezius to become a prime
mover for downward scapular rotation.72 The lower
trapezius and the serratus anterior muscles continue to
increase in activity during the final phase of elevation,
acting as an upward rotator and opposing the forces of
the upper and middle trapezius.71
As the humerus elevates towards the end of the ele-
vation range of motion, it must disengage itself from the
scapula. As previously noted, the ratio of glenohumeral
to scapulothoracic motion is 3.49 : 1. Good extensibility
of the teres major and the subscapularis muscles is
important in order to allow the humerus to disassociate
itself from the scapula. Often with passive humeral ele-
vation, a bulge of the scapula is noted laterally. The bulge
is usually the inferior angle that is secondary to increased
protraction of the scapula. Lack of elongation of these
muscles prevents the normally dominant movement of
the humerus at the end of the elevation range. The
author often observes tightness of the subscapularis
muscle, teres major muscle, or both.
Furthermore, observation of limited passive humeral
elevation may exhibit elevation of the chest cavity. If
muscles connecting the humerus and rib cage are not
flexible enough, movement will occur at both ends. The
latissimus and pectoralis major muscles connect the
humerus to the rib cage. Lack of dissociation of the rib
cage from the humerus will result in excessive rib cage
mobility in passive terminal elevation.
Summary of Shoulder Phases of Movement
The initial phase of elevation occurs predominantly at
the glenohumeral joint. A 3-mm superior glide of the
humeral head has been observed in the initial phase of
elevation. The activity of the deltoid muscle produces
this superior shearing at the glenohumeral joint. The
activity of the supraspinatus, infraspinatus, teres minor,
and subscapularis muscles counteracts the forces of the
deltoid muscle, creating a resultant force that helps
stabilize the joint and is necessary for full pain-free
movement to continue. The resultant force in the normal
glenohumeral joint is maximal at 90° of elevation. The
early phase of scapula movement is described as the
setting phase, with the majority of movement occurring
at the glenohumeral joint.
The middle phase of elevation is referred to as the
critical phase. At the beginning of the critical phase,
26 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
maximum shearing forces of the deltoid muscle occur.
The ratio of glenohumeral to scapulothoracic movement
shifts, emphasizing the latter. The increased scapula
movement is established by the activity of the upper and
lower trapezius and lower anterior serratus muscles. The
arthrokinematic movement of the head of the humerus
on the glenoid has been observed as an inferior and
superior glide of 1.5 mm.
During the final phase of elevation, the glenohumeral
joint once again dominates the movement. Good exten-
sibility of the latissimus, pectoralis major, teres major,
teres minor, and subscapularis muscles is necessary to
allow the increased and unconstrained movement of the
humerus away from the scapula.
Summary
Patients with shoulder dysfunction are routinely treated
in the physical therapy clinic. An understanding of the
anatomy and biomechanics of this joint can help provide
the physical therapist with a rationale for evaluation and
treatment. Most studies involving shoulder anatomy
and biomechanics reveal a common pattern along with
a wide variation among subjects. The physical therapist
should keep this variation in mind when treating an
individual patient.
Treatment may be directed toward restoring mobil-
ity, providing stability, or a combination of the two. The
shoulder is an inherently mobile complex, with various
joint surfaces adding to the freedom of movement.
The shallow glenoid with its flexible labrum and large
humeral head provides mobility. At times, this vast
mobility occurs at the expense of stability. The shoulder
relies on various stabilizing mechanisms, including
shapes of joint surfaces, ligaments, and muscles to
prevent excessive motion. Almost 20 muscles act on this
joint complex in some manner and at various times they
can be both prime movers and stabilizers. Harmonious
actions of these muscles are necessary for the full func-
tion of this joint (Plate 2-7).
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28 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
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Throwing Injuries
T o throw a baseball with high velocity and with
great accuracy is a skill that escapes the major-
ity of the population. Those who have ac-
complished this skill often demonstrate a heightened
neuromuscular system and have invested thousands of
hours of sport-specific training. This unique athletic act
has produced a wide array of disabilities that have been
reported in various literature. These disabilities include
neurologic entrapments, arterial and venous thrombosis,
acromioclavicular joint degeneration, primary impinge-
ment, secondary impingement, glenohumeral instabili-
ties, labral lesions, subdeltoid bursitis, biceps tendinitis,
subluxing bicipital tendon, undersurface tears of the
rotator cuff, full-thickness tears of the rotator cuff,
lesions of the humeral head, fracture of the humerus,
fracture of the coracoid, posterior capsular syndrome,
and muscle imbalances among others.1-12
Conte and associates13 reported that of the 3282 dis-
abled players in Major League Baseball between 1989
and 1999, 48.4% of all injuries were to pitchers. This is
not overly alarming given that every club’s pitching staff
comprises from 40% to 46% of the club roster. However,
not all pitchers are active on a game-to-game basis. In
the 5-year period from 1995 to 1999, Conte reports
that 27.8% of disabling injuries to major league players
involved the shoulder. Elbow injuries comprised an
additional 22% of the days of disablement. Thus upper
extremity injuries in this period constituted half of
all Major League Baseball injuries that necessitated the
removal of the athlete from the active roster for a
minimum of 15 days. This is an average loss to Major
League Baseball of 5619 days per year for shoulder
injuries and an additional 4452 days per year for elbow
injuries. On average, each club lost 336 days, or 1.84
29
3
Jeff Cooper
Phillip B. Donley
Craig D. Morgan
years, of service time (182 days constitutes a service year)
to upper extremity injuries.
Lyman and associates14 conducted a prospective
injury study involving 298 youth pitchers over the course
of two seasons. They reported that frequency of shoul-
der and elbow pain was 32% and 26%, respectively. They
suggest that the following were risk factors related to
shoulder pain: decreased self-satisfaction, arm fatigue
during one game pitched, throwing more than 75
pitches in one game, and throwing less than 300 pitches
in a season. Lyman suggests that the risk factors for
reported elbow pain are increased age, increased weight,
decreased height, lifting weights during the season,
playing baseball outside of the league, decreased self-
satisfaction, throwing more than 75 pitches in one game,
and throwing less than 300 pitches or more than 600
pitches during the season.
In a follow-up study, Lyman and associates15 reported
an increased injury risk to young pitchers associated with
throwing breaking balls. Of the 476 youth baseball
pitchers participating in the study, half of the players
reported either shoulder or elbow pain during the com-
petitive season. The study determined that throwing a
curve ball increased the risk of experiencing shoulder
pain by 52% and throwing a slider increased the risk of
elbow pain by 86%. Whether the specific mechanics
of the breaking pitch is the primary offender, or the
increased load placed on the young pitcher trying to
learn a new pitch, it is prudent to be an older teenager
before developing a breaking ball.
Injury to the shoulder complex precipitated by over-
hand throwing is most often the result of a failure in
the kinetic chain manifesting itself in the weakest link.
Most often this weakest link is the glenohumeral joint.
30 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
Macrotrauma injuries, such as a fracture of the humerus,
can often be related to this proximal kinetic chain
failure, which imposes higher demands on distal struc-
tures. Injury to the elbow is often precipitated by a dys-
function of the shoulder complex.16 This chapter focuses
on the underlying causes of the majority of shoulder
injuries and a preventive conditioning program, which
can be applied to the treatment of these injuries in the
overhand-throwing athlete.
Overhand Throwing
The biomechanical and electromyographic activity of
overhand throwing has been investigated17-25 to give us
a relative model of function in a controlled environment.
It is assumed that the forces recorded during data
collections are less than those produced in a competi-
tive arena. Electromyographic sequence activity appears
fairly consistent regardless of generated velocities.
The overhand throw as it relates to pitching has been
divided into the following phases: (1) windup, (2) early
cocking, (3) late cocking, (4) acceleration, and (5)
follow-through.
Windup
The windup is an activity that is highly individualized.
Its purpose is to organize the body beneath the arm to
form a stable platform. As with all overhand activities,
it is vital that the body perform in sequential links to
enable the hand to be in the correct position in space to
complete the assigned task. The hand can be placed
in an infinite number of locations, but it is essential
that the scapulohumeral rhythm place it in an optimal
setting for the task of propulsion. The drawing of the
humerus into the moment center of the glenoid fossa is
accomplished during the first 30° of elevation as the arm
is brought upward by the deltoid and supraspinatus.
Throughout the windup phase, there is no consistent
pattern of muscle activity because of these numerous
individual styles.
Early Cocking
Early cocking is the period of time when the dominant
hand is separated from the gloved hand and ends when
the forward foot makes contact with the mound. The
scapula is retracted and maintained against the chest
wall by the serratus anterior. The humerus is brought
into position of 90° of abduction and horizontal
extension, with a minimal external rotation of approxi-
mately 50°. This is accomplished with the activation of
the anterior, middle, and posterior deltoid. The external
rotators of the cuff are activated toward the end of early
cocking, with the supraspinatus being more active than
the infraspinatus and the teres minor as it steers the
humeral head in the glenoid. The biceps brachii and
brachialis act on the forearm to develop the necessary
angle of the elbow.
As the body moves forward, the humerus is sup-
ported by the anterior and middle deltoid as the poste-
rior deltoid pulls the arm into approximately 30° of
horizontal extension. At this time, the static stability of
the humeral head becomes dependent upon the anterior
margin of the glenoid, notably the inferior glenohumeral
ligament and the inferior portion of the glenoid labrum.
Late Cocking
Late cocking is the interval in the throwing motion
when the lead foot makes contact with the mound, and
ends when the humerus begins internal rotation. The
lead foot applies an anterior shear to slow the lower
extremity and to transfer energy. The foot serves as an
anchor. The forward and vertical momentum is trans-
formed into rotational components. During this time
the humerus is moved into a position more forward in
relation to the trunk and begins to come into alignment
with the upper body. The extreme of external rotation,
an additional 125°, is achieved to provide positioning for
the power phase or acceleration. This is the first of two
critical instances.18
Supraspinatus, infraspinatus, and teres minor are
active in this phase, but become quiet once external rota-
tion is achieved. Deceleration of the externally rotating
humerus is accomplished by the contraction of the sub-
scapularis. It remains active until the completion of late
cocking. The serratus anterior and the clavicular head of
the pectoralis major have their greatest activity during
deceleration. The biceps brachii aids in maintaining the
humerus in the glenoid by producing a compressive axial
load. At the end of this phase, the triceps begins activ-
ity and provides compressive axial loading to replace the
force of the biceps. The capsule becomes wound tight in
preparation for acceleration.
Acceleration
Acceleration is a ballistic action lasting less than one
tenth of a second. The ball is accelerated from 4 mph to
CHAPTER 3 THROWING INJURIES
a speed of 90 mph or higher.17 This rapid acceleration
produces angular velocities that have been reported as
high as 9198°/s.23 The scapula is protracted, rotated
downward, and held to the chest wall by the serratus
anterior. The arm continues into forward flexion and
is marked by the maximal internal rotation of the
humerus. The humerus travels forward in 100° of abduc-
tion, but adducts about 5° just before release. The latis-
simus dorsi and pectoralis major deliver the power to the
forward-moving shoulder. The subscapularis activity is
at maximum levels as the humerus travels into medial
rotation. The triceps develops strong action in acceler-
ating the extension of the elbow.
The forces developed in this instant reflect the body’s
amazing ability to generate power and encase itself in a
protective mechanism. Pappas and associates23 reported
peak accelerations approaching 600,000°/s. Gainor and
colleagues1 reported 14,000 inch pounds of rotatory
torque produced at the shoulder. This torque develops
27,000 inch pounds of kinetic energy in the humerus.
Control of the ball is lost approximately midway
through the acceleration phase, when the humerus is
positioned slightly behind the forward-flexing trunk and
at an angle of about 110° of external rotation. The hand
follows the ball after release and is unable to apply
further force.
Follow-Through
Follow-through begins with the release of the ball.
Within the first tenth of a second the humerus travels
across the midline of the body and undergoes a slight
external rotation before finishing in internal rotation.
The second critical instant occurs during this segment.18
This is a very active phase for all glenohumeral muscles
because the arm is decelerated. The deltoid and upper
trapezius have strong activity as does the latissimus
dorsi. The infraspinatus, teres minor, supraspinatus, and
subscapularis are all active while eccentric loads are pro-
duced. The biceps develops peak activity in decelerating
the forearm and imposing a traction force within the
glenohumeral joint.
The task of documenting the sequence of muscle
activity during the act of pitching has allowed the mus-
culature acting upon the glenohumeral joint to be
divided into two groups.19 The first group of muscles
consists of those that are most active during the second
and third phases of throwing, and early and late cocking.
They are least active during the acceleration phase. The
31
deltoid, trapezius, external rotators, supraspinatus, infra-
spinatus, teres minor, and biceps brachii comprise this
first group.
The second group of muscles consists of those used
primarily for the fourth phase of throwing—accelera-
tion. These muscles are necessary to protract the scapula,
horizontally flex forward and internally rotate the
humerus, and extend the elbow. This group consists of
the subscapularis, serratus anterior, pectoralis major,
latissimus dorsi, and triceps brachii. The first phase of
throwing is not included in either group because of its
nonspecific generalized activity.
Professional Versus Amateur Pitchers
Gowan and associates19 conducted a study to determine
if the muscle-firing sequence of professional pitchers
was notably different from that of amateur pitchers.
No substantial differences were noted in the first three
phases of the pitch: the windup, early cocking, and late
cocking. There were no significant differences in the
follow-through, where muscle activity was described as
general.
During the acceleration phase, professional pitchers
recorded increased activity of the pectoralis major and
latissimus dorsi. There was also increased activity in the
serratus anterior muscle. The professional pitchers had
decreased activity in the supraspinatus, infraspinatus,
and teres minor during the acceleration. Professional
pitchers used the subscapularis predominantly during
acceleration and internal rotation. Activity in the biceps
brachii was also lower in the professionals than in the
amateurs.
Electromyographic Activity in
the Injured Thrower
Those athletes with subacromial impingement demon-
strated differences in their electromyographic studies
compared with uninjured throwers.24 During the second
phase of throwing, early cocking, the injured athletes
continued deltoid activity whereas the healthy athletes
had decreased deltoid activity. A lower level of
supraspinatus activity was also noted during this time
period. During early cocking and late cocking, the inter-
nal rotators, subscapularis, pectoralis major, and latis-
simus dorsi had decreased activity. The serratus anterior
followed this pattern and was less effective. It was the-
orized that the combination of these differences might
lead to increased external rotation, superior humeral
32 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
migration, and impaired scapular rotation. All or some
of these factors may be an underlying cause for the initial
problem or a factor in the continuance of the syndrome.
Throwing athletes who have been hampered by
glenohumeral instabilities were compared with normal
athletes in a similar fashion. This series25 tested the
activity of the biceps, middle deltoid, supraspinatus,
infraspinatus, pectoralis major, subscapularis, latissimus
dorsi, and serratus anterior. Differences were noted in
every muscle except the middle deltoid. The authors
suggest that the mildly increased activity of the biceps
and supraspinatus may be compensatory for the laxity
present in the anterior capsule. The infraspinatus devel-
oped a pattern of activity during early cocking, reduced
activity during late cocking, and increased activity in the
follow-through. As noted with the impingement group,
the internal rotators—consisting of the subscapularis,
pectoralis major, and latissimus dorsi—had decreased
activity, which was recorded in the early cocking phase.
The serratus anterior also showed decreased activity.
The authors concluded that these changes in muscle
activity allowed for the decreased internal rotation force
needed in both late cocking and acceleration. Reduced
activity, demonstrated in controlling the scapula by the
serratus anterior, allowed the glenoid to be placed in a
compromising position during late cocking—increasing
the stress upon the labrum and capsule. Microtraumas
can be associated with deficiencies in a muscle or muscle
group, and fail to aid in the stabilization of the gleno-
humeral joint or fail to become active in the proper
sequence during the distinct phases of throwing. Lack
of flexibility can be a factor leading to disability, par-
ticularly in the deceleration phase when tremendous
eccentric forces are developed.
Capsule
Elsewhere in this volume is a more detailed description
of the function of the capsule of the glenohumeral joint
and its ligaments. Here it is necessary to describe some
works with regard to the capsule in the cocked position
in the overhand-throwing athlete. Harryman and asso-
ciates26 state that oblique glenohumeral translations are
not the result of ligament insufficiency or laxity, but
rather translation results when the capsule is asymmet-
rically tight. They surgically tightened fresh cadaver pos-
terior capsules and found increased anterior humeral
head translation during cross body movement, flexion,
and internal rotation, and increased superior translation
with flexion.
O’Brien and colleagues27 demonstrated that the
posterior band of the inferior glenohumeral ligament
complex, which is a thickening of the posterior capsule,
is the primary restraint to any posterior force when the
arm is positioned at 90° of abduction and internally
rotated. Tightening of the posterior or posterior inferior
capsule causes a posterior superior shift of the gleno-
humeral fulcrum, which allows contact of the labrum in
the posterior-superior glenoid.
Gohlke and associates28 reported on the pattern of
collagen fiber bundles of the capsule. They describe both
the radial and circular components of this structure.
The nature of these patterns lends itself to a dual action
during glenohumeral rotation. Through rotation, the
capsule becomes shortened and produces both a com-
pressive force and a centering of the humerus upon
the glenoid. The role of the glenohumeral ligaments is
dependent upon the humeral position. When the
humerus is abducted to 90°, and the motion of external
rotation is introduced, the anterior band of the inferior
glenohumeral ligament becomes the supporting struc-
ture to resist anterior displacement of the humeral head.
The posterior band of the glenohumeral ligament is now
positioned under the humeral head and resists inferior
displacement. As the humerus is rotated medially into
internal rotation and elevated, the posterior band of the
inferior glenohumeral ligament becomes the structure to
prevent posterior translation, and the anterior portion of
the ligament is now in the inferior position.28
Branch and associates29 investigated the function of
the capsule in its relationship to anterior and posterior
translation of the humerus during internal and external
rotation. An artificially constructed lengthening of the
capsule tissue and its relationship to the changes in ante-
rior-posterior translation were also investigated. Mea-
surements were made at intervals of 20° of internal and
external rotation. They concluded that with an intact
capsuloligamentous complex the humerus translated
maximally in the glenoid when it is between 40° and
100°25 of external rotation. When the glenohumeral
capsuloligamentous complex was increased in length,
translation increased. During internal rotation, the
length of the posterior capsule had a greater influence
on anterior-posterior translation while the anterior
capsule length had a greater influence on external
rotation.
CHAPTER 3 THROWING INJURIES
Weisner and associates30 investigated the anterior
translation and inferior glenohumeral ligament strain in
a simulated scapular protraction. This cadaver study was
conducted with the specimens placed in the position of
apprehension and simulated protraction. With anterior-
directed loads, there is an increasing strain in the
anterior band of the inferior glenohumeral ligament
with increased scapular protraction.
Novotny and colleagues31 used an analytical model
to predict glenohumeral kinematics and to view how
the glenohumeral capsule and bony contact stabilizes
the joint. The simulation was conducted in the cocking
phase of throwing with an abducted extended external
rotated humerus. In this position, the center of the
humeral head translated posteriorly and superiorly
during external rotation. The anterior band of the infe-
rior glenohumeral ligament increased in tension with
external rotation. The axillary pouch and posterior band
decreased in tension. The contact area stress and force
increased with external rotation. The contact area moved
posteriorly and inferiorly in the area of the glenoid.
Kuhn and associates32 investigated the ligamentous
restraints of the glenoid capsuloligamentous complex in
a cadaver study in the late cocking phase of throwing.
This study involved cutting selected structures and
measuring the increase in external rotation. The release
of the entire inferior glenohumeral ligament allowed
the greatest increase in external rotation. Isolating the
loss of the anterior band of the inferior glenohumeral
produced the greatest external rotation when com-
pared with the loss of either the superior or middle
glenohumeral ligaments.
Pollock and associates33 evaluated the mechanical
response of the inferior glenohumeral ligament of
cadaver shoulders that were exposed to different levels
of subfatigue cycle strains. Three groups of subjects
received increased loads and frequency of subfatigue
strains. These repeated loading of the inferior gleno-
humeral ligament–induced laxity. The mechanical
response was reflective of the magnitude of the cycles,
strain, and the frequency of the loading. A ligament
length increase was noted in all specimens, which led the
authors to believe that this could be a mechanism for
acquired glenohumeral instability.
Baeyens and associates34 used a 3D kinematic study
designed to determine the rotation and shift of the
humeral head in the glenoid cavity and the migration of
contact of the articular surfaces. Helical axis parameters
33
of rotation, shift, and direction were compared between
the glenoid and the articulation surface of the humerus.
Calculations were made from the beginning position of
90° abduction and 90° external rotation to full cocking
(full external rotation and horizontal extension).
The humeral head in normal shoulders did not exter-
nally/internally rotate on the glenoid. In shoulders
deemed as having clinically minor anterior gleno-
humeral instability, a larger external rotational compo-
nent was found. Thus, the humeral head of the normal
shoulder translated into the posterior portion of the
glenoid, and the minor anterior instability shoulder
translated centrally in the glenoid. If the anterior part of
the inferior glenohumeral ligament limits anterior trans-
lation and external rotation, then a minor anterior insta-
bility is a dysfunction of the anterior part of the inferior
glenohumeral ligament.
Biceps Tendon Superior
Labral Complex
The role of the long head of the biceps tendon has long
been the stepchild of glenohumeral mechanism. Often
dismissed as only a minor player at the shoulder, as a
humeral head depressor it is clinically recognized for
its role as an elbow stabilizer and decelerator. Since
the shoulder has been thoroughly investigated via the
arthroscope in the past decade, we have gained a new
appreciation for this structure.
Andrews and colleagues2 examined 73 throwing
athletes and observed that 60% of them had tears in the
anterior-superior labrum and 23% had tears in both the
anterior-superior and posterior-superior portions. In a
subgroup of baseball pitchers, this lesion was associated
with a partial tear of the supraspinatus in 73% of the
athletes. A smaller group of 7% demonstrated a partial
tear of the long head of the biceps. Andrews and
associates hypothesized that the incidence of injury
to this region of the glenoid labrum was because of the
tremendous eccentric stresses placed on the biceps in an
attempt to decelerate the arm during the follow-through
phase of the overhand throw.
The study showed that 95% of the subjects reported
pain during the overhand throw, with 45% of them
reporting a popping or catching sensation. On physical
examination, the popping was evident in the position of
full abduction and full flexion because the upper arm was
aligned with the ear in 79% of the athletes. None of the
34 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
subjects demonstrated a notable weakness of either the
rotator cuff or biceps tendon. This lesion gave the athlete
a sensation of instability.
In a retrospective study of 2375 shoulders examined
arthroscopically, Snyder and associates35 reported 140
subjects with injuries to the superior glenoid labrum.
This represented only 6% of the sample population.
Ninety-one percent of this group was male. The involve-
ment of the dominant shoulder versus the nondominant
shoulder was greater than two-to-one. No radiographic
findings could be correlated with the ailments. At the
time no clinical exam was considered to be specific for
the superior labrum. About half of the subjects described
a painful catching or popping, which was consistent with
the findings of Andrews and associates. Only about one
third demonstrated a positive biceps tension test.
Of those shoulders, 55% were categorized as having
a type II superior labrum anterior to posterior (SLAP)
lesion consisting of detachment of the superior labrum
and biceps tendon from the glenoid rim. Only 28% of
those shoulders were isolated from a rotator cuff injury
or other labral problems.
Rodosky and associates36 investigated the role of the
long head of the biceps and its attachment to the supe-
rior labrum in a laboratory model of the glenohumeral
joint positioned in abduction and external rotation as
experienced by the overhand thrower. They hypothe-
sized that the presence of the long head of the biceps
acted to help limit the external rotating of the shoulder.
The biceps compressed the humeral head against the
glenoid, resisting the rotation. The long head of the
biceps withstood higher external rotational forces
without the inferior glenohumeral ligament experienc-
ing a greater strain. This suggested that the biceps play
a role in the provision of anterior stability. The gleno-
humeral joint demonstrated a heightened torsional stiff-
ness because force was increased through the long head.
When a surgical SLAP lesion was created, the tor-
sional rigidity decreased 26% and the strain produced
upon the inferior glenohumeral ligament was increased
by 33%. This model suggests that the shoulder is thus
dependent upon the long head of the biceps to provide
dynamic stability to the glenohumeral joint in the
cocking, acceleration, and follow-through phases. This
dynamic stability ensures a consistent stress upon the
inferior glenohumeral ligament. The long head acts as a
continuous provider of axial tension, and as a protective
mechanism for the humerus and the inferior gleno-
humeral ligament. There is a clear coexistence of shoul-
der instability in the presence of a SLAP lesion.37 Once
the integrity of the glenohumeral joint is reduced
because of a superior labrum disassociation the shoulder
sacrifices stability. The long head of the biceps plays a
large role in the dynamics of stabilizing the gleno-
humeral joint during overhand throwing.
The data of Snyder and associates35 suggest that the
SLAP lesion occurs in a very limited number of cases
among the general population, and the mechanism of
trauma is varied. Maffet and colleagues37 in a review of
712 surgical shoulders with significant biceps tendon–
superior labral abnormalities suggest the occurrences of
these separations are indeed caused by various events.
Recent investigations are providing a clearer picture of
the mechanism of injury to the biceps tendon–superior
labrum complex in the overhand-throwing athlete and
that the mechanism appears to be at the opposite end of
the throwing spectrum first suggested by Andrews. A
SLAP lesion must be among the suspected diagnoses of
the overhand-throwing athlete who complains of insta-
bility or a sense of instability.
Morgan and Burkhart38 have suggested that the
mechanism of injury extending, or potentially produc-
ing, a type II SLAP lesion is that of a torsional force
that “peels back” the biceps and posterior labrum from
the neck of the glenoid. They have suggested that when
the shoulder is placed in extreme abduction, an external
rotation torsion is produced upon the biceps tendon.
Placing the upper extremity in this position of cocking
the biceps has assumed a more vertical and posterior
angle. When a force is applied, a twist is produced at the
base of the biceps and this transmits a torsional force to
the posterior-superior labrum.
Morgan and Burkhart reviewed a group of 102
patients with type II SLAP lesions. Of this group,
53 patients were overhand-throwing athletes and 44 of
these patients were baseball pitchers. A common history
for these individuals was the development of pain in the
cocking phase of throwing. Pain arose either anteriorly
or posteriorly, and decreased performance or decreased
velocity. These symptoms were often described as a
“dead arm.” The clinical examination included the fol-
lowing tests: (1) Bicipital groove tenderness, (2) Speed’s,
(3) O’Brien’s cross arm (the active compression test)39
and (4) Jobe relocation test,40 in which pain and appre-
hension were posteriorly and superiorly relieved by a
force directed posteriorly to the humeral head. These
CHAPTER 3 THROWING INJURIES
clinical findings were then correlated with a further clas-
sification of type II SLAP lesion. In the overhand-
throwing athletes, 19% had anterior-superior lesions;
47% showed posterior-superior lesions; and 34% dis-
played combined anterior-posterior lesions. Thus, 81%
of the SLAP lesions in the throwing group had a pos-
terior component.
When compared with the entire group of 102
subjects, the posterior type II SLAP lesion was three
times more common in the overhead throwing athletes
while the anterior type II SLAP was three times more
common in the nonthrowing trauma group. When the
clinical examination was correlated with the arthro-
scopic findings, it was generally determined that the
Speed test and the O’Brien test were useful in predict-
ing anterior-superior lesions, and the Jobe relocation test
was useful in predicting posterior-superior lesions.
Of the 53 overhand-throwing athletes, 10 displayed
a partial thickness undersurface tear of the rotator cuff
and one had a complete tear. Eighty-seven percent of
the overhand throwers reported an excellent result with
internal fixation of their SLAP lesion. The other 13%
reported a good result. Eighty-four percent returned
to their preinjury level of sports participation.
Sixteen percent reported decreased velocity and control.
Those seven athletes all had associated rotator cuff
injuries.
All overhand-throwing athletes in this study were
measured for internal and external rotation at 90° of
abduction in the plane of the scapula. A noted lack of
internal rotation in the surgical shoulder was present.
On average, there was a loss of 45° of internal rotation
in a range of 35° to 60°. External rotation in the plane
of the scapula had an average gain of 40° in a range of
+20° to +45°.
The final observation in this investigation is the rela-
tionship of the posterior-superior SLAP and rotator cuff
injuries. Thirty-one percent of those with chronic SLAP
had associated undersurface rotator cuff involvement.
It was postulated that the humeral head acquired the
ability to translate superior or sublux because of the lack
of a fixed biceps labrum. This combination of superior
translation and repetitive twisting of the rotator cuff in
the cocking phase of throwing results in fiber fatigue and
failure of the cuff.
Morgan and Burkhart further reinforce their position
in regard to the mechanism of injury of the biceps
tendon–superior labral complex in the overhand-
35
throwing athlete in a following publication.41 Their
model encompasses the following:
1. A type II posterior-superior glenoid labrum tear.
This tear causes anterior pseudolaxity and a positive
arthroscopic drive-through sign.
2. The upper extremity positioned in abduction and
external rotation with a type II posterior-superior
glenoid labrum tear and an unstable biceps anchor
that will cause the biceps superior labral complex to
“peel back” over the posterior-superior corner of the
labrum.
3. A contracted posterior-inferior capsule resulting in
a reduction of internal rotation in abduction. This
clinical finding is present in all overhand-throwing
athletes who are afflicted with posterior-superior
SLAP lesions.
The mechanism is as follows: Because an overhand-
throwing athlete with an acquired tight posterior capsule
places the shoulder in the cocking position of abduc-
tion and external rotation, the posterior capsule inhibits
normal full external rotation. This causes a posterior-
superior shift of the moment center of the glenohumeral
joint. This new center of rotation places the humeral
head in increased contact with the internal impingement
zone, causing increased forces to the biceps tendon–
superior labrum complex through external rotation. This
mechanism produces the SLAP lesion, and the creation
of the SLAP lesion contributes to a posterior-superior
shift or instability.
Asymmetric Scapular
Malposition
Kibler42 describes five roles of the scapula: (1) to be a
stable part of the glenohumeral articulation; (2) to
retract and protract along the thoracic wall; (3) to elevate
the acromion; (4) to be a base for muscle attachment;
and (5) to serve as a link in the proximal-to-distal
sequence energy delivery. A dysfunction in one role or a
combination of dysfunctions in a number of scapular
roles places the throwing athlete at risk.
Normal scapular kinematics is necessary for optimum
upper extremity motion. The glenoid must be continu-
ally repositioned to correlate with the moving humerus
to maintain the stable glenohumeral joint. A malposi-
tioned scapula has been demonstrated to place greater
demands on the anterior capsule.30 The ability of the
scapula to retract places the upper extremity in the “full
36 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
tank of energy” position for throwing. The ability to pro-
tract through the delivery is necessary for the scapula to
follow the moving humerus while providing a stable
platform. Elevation of the acromion increases the sub-
acromial space to prevent impingement of the rotator
cuff. A number of muscular force couples are necessary
to move the scapula through its three axes of motion.
In the active scapular plane, upward rotation has been
reported to be 50° with a standard deviation (SD) of
4.8°; posterior tilting on a medial to lateral axis is
reported to 30° with an SD of 13°; and externally rotated
around a vertical axis reported to be 24° with an SD of
12.8°.43
More often than not, the overhand-throwing athlete
will have an asymmetric malpositioned scapula. This
malpositioned scapula is referred to as scapula infera
coracoid dyskinesis (SICK). A SICK scapula results
from a muscular fatigue syndrome that is composed of
three major components. First, the scapula drops or is
lower when compared with the nondominant scapula.
Second, the scapula is protracted or lies farther laterally
from the spine when compared with the nondominant
scapula. Third, the scapula has an increased abduction
or a greater angle from the spine to the medial scapular
border when compared with the nondominant scapula.
One, any combination, or all of these components can
be displayed at the time of examination.
An athlete often has one or more of the following
symptoms in association with a SICK scapula: (1) pain
located on the medial aspect of the coracoid; (2) pain
located at the superior medial aspect of the scapula; (3)
painful subacromial space; (4) painful acromioclavicular
joint; and (5) thoracic outlet symptoms/radicular pain.
There is usually an insidious onset of these symptoms,
and a careful medical history does not show a one-time
event or rapid progression to disability.
Because components of a malpositioned scapula are
located inferiorly, protected, and abducted, an increased
tension is placed on the coracoid by virtue of a short-
ened pectoralis minor tendon and conjoined tendon.
With repetitive overhand motions, the restrictive nature
of these shortened tendon structures encourages a
tendinopathy, which results in a painful medial coracoid.
Pain located at the superior medial aspect of the
scapula is present in the malpositioned scapula at the
insertion of the levator scapula, upper rhomboids, and
upper trapezius. Because these scapular control muscles
originate from the essentially fixed spine, they are
required to function in an overtensioned pattern refer-
ring pain into the muscle belly. The key indicator in this
sequence is most frequently posterior dominant-side
neck pain. One must recognize that dyskinesis of the
scapula is the primary offender and a treatment proto-
col should be designed to rectify the malposition of the
scapula to resolve the posterior neck symptoms. Any
attempt to stretch the offended musculature adds insult
to the existing injury.
Subacromial pain is often present because of the
infera component of the SICK scapula, which reduces
the subacromial space by essentially lowering the
acromion. This reduction of space hinders the function
of the rotator cuff in all phases of the overhand throw.
The coinciding lack of posterior tilting of the scapula
with elevation increases the impingement symptoms.45,46
A scapular relocation test that provides relief of these
symptoms will also increase the athlete’s ability to
forward flex, which is often restricted and painful.
The acromioclavicular joint becomes symptomatic
because of altered kinematics of the malpositioned
scapula. Because the clavicle is more rigidly secured at
the sternum, stresses caused by the infera, protraction,
and abduction of the scapula are imposed at the distal
clavicular articulation. Thoracic outlet symptoms are
present in a few athletes because of the closing down on
the neurovascular structures by the unsupported scapula
and clavicle.
The challenge for the clinician is to recognize the
subtle changes in the position of the scapula and how
those subtle changes put the glenohumeral joint at risk.
The task of repositioning the scapula is paramount in
the sequence of rehabilitation of the overhand-throwing
athlete (Figures 3-1 to 3-5).
Posterior Capsular Syndrome:
Glenohumeral Internal
Rotation Deficit
Adaptive range of motion changes in overhand-
throwing athletes have been observed for sometime.47,48
Common adaptations occur in horizontal adduction and
external and internal rotation of the glenohumeral joint
at 90° of abduction. Nonsymptomatic pitchers have been
reported to witness an increase of up to 30° gleno-
humeral external rotation in both the frontal and scapu-
lar planes when compared with their nondominant
shoulders.1 Glenohumeral internal rotation deficits of
CHAPTER 3 THROWING INJURIES
Figure 3-1 SICK scapula: right scapula is lower,
protracted, and abducted.
Figure 3-2 Measurement of SICK scapula using the
superior angle of the scapula.
37
Figure 3-3 Passive shoulder elevation limited, sec-
ondary to tight pectoralis minor.
Figure 3-4 Increased passive elevation of the shoul-
der by lifting the scapula, reducing tension on the pectoralis
minor.
15° to 20° have also been associated with nonsympto-
matic pitchers,47,49-52 while symptomatic pitchers have
reported deficits as high as 45°.38 These changes have
been attributed to a number of factors including a pos-
terior inferior capsular restriction, muscular inflexibility
of the external rotators, and osseous adaptations of the
humeral head or glenoid.53-55
Pappas and associates23 reported a significant limita-
tion of glenohumeral internal rotation range of motion
and posterior shoulder tightness as measured by hori-
zontal abduction with the scapular stabilization in
patients with subacromial impingement. Brown and
associates51 recorded the range of motion for multiple
38 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
Figure 3-5 Passive shoulder elevation is within
normal limits, secondary to relocation of the humeral head and
scapula lift.
upper extremity movements in two separate groups of
professional pitchers and other position players. The
pitchers had significant increases of 9° of external rota-
tion in 90° abduction. The pitchers had significant
decreases of 5° of shoulder flexion and 15° of internal
rotation in 90° abduction compared with their non-
dominant side. Position players had a significant increase
of 8° of external rotation in 90° of abduction.
Verna56 measured 137 professional baseball players
bilaterally for internal rotation by fixing the scapula and
medially rotating the humerus while in 90° of abduction
in the supine position. Correlating the internal rotation
deficits of the dominant shoulder with injury histories
showed that pitchers reporting a shoulder or an elbow
problem averaged an internal rotation deficit of 41%.
Position players reporting a shoulder or an elbow
problem averaged a deficit of 43%. Uninjured athletes,
pitchers, and position players averaged an internal rota-
tion deficit of only 24%.
Warner and associates57 demonstrated a notable
limitation of internal rotation range of motion and
posterior shoulder tightness, as measured in horizontal
abduction, in a group of impingement patients com-
pared with instability patients and control subjects.
Kugler and colleagues58 attempted to identify features
that may correlate with shoulder injuries in highly
skilled volleyball attackers, who are engaged in overhand
activity. To measure posterior shoulder tightness, the
researchers measured the distance from the lateral epi-
condyle to the acromion of the opposite shoulder during
maximal horizontal adduction. The researchers did not
report if the scapula was stable. They found that the
dominant posterior shoulder was substantially tighter in
attackers with shoulder pain compared with attackers
without shoulder pain or compared with a control group.
Attackers without shoulder pain were notably tighter
than the control group. Both groups of volleyball players
had an increase in tightness in their dominant shoulder
compared with their nondominant shoulder.
Bigliani and associates49 examined upper extremity
range of motions and glenohumeral joint laxity in a
study of 148 healthy professional baseball players: 72
pitchers and 76 position players. Glenohumeral internal
rotation was recorded as the highest vertebral level
reached via the thumb up the spine.59 This recording was
converted to a number value per the American Shoul-
der and Elbow Surgeons’ standards to permit statistical
comparisons. Shoulder external rotation with the
humerus at 90° of abduction in the frontal plane and
internal rotation, measured as previously described,
both demonstrated statistically significant differences
between the dominant and nondominant shoulders.
For pitchers, the range of motion in the dominant
glenohumeral external rotation averaged 118° (range of
95° to 145°) and the nondominant glenohumeral exter-
nal rotation range of motion averaged 102° (range of 85°
to 130°). The difference was 15.2° or a 13% increase in
external rotation in the dominant extremity. Dominant
glenohumeral internal rotation range of motion for
pitchers averaged 15.5° (T6-T7) (range L3-T2) and
nondominant glenohumeral internal rotation range of
motion averaged 17.6° (T4-T5) (range T8-T2) or a loss
of 14%. Positional players measured in a similar fashion
recorded an average dominant glenohumeral external
rotation range of 109.3° (range 80° to 150°) and an
average nondominant glenohumeral external rotation
range of motion of 97.1° (range 80° to 120°). Positional
players recorded a loss of two levels of vertebrae calcu-
lated to 12.2°, or 11%, of their internal rotation in their
dominant shoulder.
In a similar study,60 152 right-handed professional
baseball pitchers were measured for glenohumeral inter-
nal rotation using three different protocols: vertebrae
level/thumb-up spine; glenohumeral internal rotation
in frontal plane at 90° of abduction with a stabilized
scapula; and glenohumeral internal rotation in the
CHAPTER 3 THROWING INJURIES
scapular plane at 90° of abduction with a stable scapula.
There was a poor correlation between vertebrae
level/thumb-up spine (average loss of 7.8 cm ± 4.8 cm in
the dominant arm) and glenohumeral internal rotation
in the frontal plane (r = 0.176; P £ .03) or a gleno-
humeral internal rotation in the scapular plane (r =
0.226; P £ .005). The vertebrae level/thumb-up spine
may be a test of functionality, but it is not a valid measure
for glenohumeral internal rotation in the overhand-
throwing athlete because of the inability to stabilize
the scapula.
Tyler and associates,52 while describing a proposed
alternate method for measuring posterior shoulder
tightness, recorded bilateral external and internal rota-
tion of the glenohumeral joint with 90° of humeral
abduction in 22 collegiate baseball pitchers. The scapula
was stabilized only by the weight of the subject. The
baseball pitchers recorded significantly more external
rotation bilaterally than the control group. The pitchers’
dominant shoulders recorded an average range of exter-
nal rotation of 109.7° ± 2.4° compared with the control
group’s 95.9° ± 1.6°. The nondominant shoulders of the
baseball pitchers recorded 98.9° ± 1.6° of external rota-
tion and the control group recorded 95.2° ± 1.6°. The
dominant shoulders of the baseball pitchers averaged
50.0° ± 2.0° of internal rotation compared with 46.4° ±
1.3° of the control group. Internal rotation of the base-
ball pitchers’ nondominant shoulders averaged 69.5° ±
2.5° compared with 50.2° ± 1.4° in the control group.
When one further evaluates the data, the pitchers in
this study experienced an average glenohumeral external
rotation gain of 10.8°, or 10.9%, in the dominant shoul-
der versus the nondominant shoulder. The average loss
of glenohumeral internal rotation was 19.5°, or 28%, of
the dominant versus nondominant shoulder. In the
control group, there was essentially no gain in gleno-
humeral external rotation in the dominant shoulder
and an average loss of only 3.8°, or 7.5%, of internal
rotation.
The larger premise of the Tyler study was to intro-
duce an alternate method of measuring posterior
shoulder tightness to the methods of previous investiga-
tors.57,58 This alternate method involved a side-lying
position in which the scapula is manually stabilized and
the humerus is horizontally adducted without rotation
to a firm end feel. The distance from the medial epi-
condyle to the surface of the examination table was
measured in centimeters. Essentially the supine test
39
position had been rotated 90° and a linear measure, like
Kugler, is used instead of a goniometric measure. When
they compared these linear measure data to their inter-
nal rotation data, they reported that every centimeter of
horizontal adduction lost corresponded with 4° of inter-
nal rotation loss in the baseball pitcher.
In a group of 372 professional baseball pitchers, Wilk
and associates61 reported an average total shoulder range
of motion of 129.9° ± 10° of external rotation and 62.6°
± 9° of internal rotation when passively measured at 90°
of abduction. These measurements represent an unsta-
ble glenohumeral joint. When the dominant shoulder
was compared with the nondominant shoulder, there
was a 7° increase in external rotation and a 7° decrease
in internal rotation in the dominant shoulder. This was
coined as the “total motion concept,” in which total
shoulder rotation is equal to the sum of external rota-
tion and internal rotation.
In the previous discussion on the biceps tendon–
superior labral complex, it has been demonstrated that
there is a strong relationship between glenohumeral
internal rotation deficits in the overhand-throwing
athlete and a surgical shoulder. Burkhart and associates51
reported that 53 overhand throwers with SLAP lesions
had an average internal rotation deficit at 90° abduction
of -45° preoperatively. One year postoperatively, inter-
nal rotation deficits were only -15°. The authors empha-
sized that the rehabilitation protocol demanded was an
aggressive stretching program for a tight posterior-
inferior capsule, which had been thought to initially
cause the SLAP lesion.
Morgan62 introduced the “rotational unity rule,”
which states that an overhand-throwing athlete will
maintain normal glenohumeral mechanics if the inter-
nal rotation deficit is less than or equal to the external
rotation gain. A humeral posterior superior shift will
occur if the internal rotation deficit is greater than the
external glenohumeral gain. The author supports this
theory in a study of 124 baseball pitchers surgically
treated for SLAP lesions. This group was equally
divided into thirds: professional athletes, college ath-
letes, and high school or recreational athletes. Preoper-
atively, the group measured in 90° of abduction with a
stable scapula averaged a glenohumeral internal rotation
deficit of 53° (range 26° to 80°). The external rotation
gain was 33° (range 22° to 45°). Thus a larger gleno-
humeral internal rotation deficit was evident in the 124
athletes compared with the external rotation gain.
40 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
As previously stated, factors limiting horizontal
adduction and internal rotation at 90° of abduction
include a posterior-inferior capsular restriction, muscu-
lar inflexibility of the external rotators, and osseous
adaptations of the humeral head or glenoid. The signif-
icant amount of this loss of motion in either plane is
a result of a capsular contracture. This contracture is
the primary offender in the formation of a posterior ex-
ostosis. Long recognized as a problem in a few over-
hand-throwing athletes, this lesion and the “posterior
syndrome” have been an enigma for a quarter century.48
It must be recognized that a posterior exostosis is an
osseous reaction to the extraordinary traction forces
being generated at the scapular attachment of the
capsule from overhand throwing and not necessarily a
response to posterior humeral head subluxation, which
has been postulated. A poor success rate has been attrib-
uted to the excision of this lesion, most likely because of
the treatment of the result instead of the cause.63
Essential-Essential Lesion
In this chapter, a relationship has been suggested
between a glenohumeral internal rotation deficit caused
by a posterior-inferior capsule contraction and the
injured overhand-throwing athlete. The posterior-
inferior capsule often becomes thick and contracted as
a reaction to the tremendous distraction forces placed
upon the glenohumeral joint during deceleration. As
this slow, insidious adaptive change occurs, it dictates an
altered dynamic for the glenohumeral joint by shifting
of the humeral head during the cocking phase of
throwing from its true moment center to a more
posterior-superior position.
Previous studies have indicated an anterior-superior
migration of the humeral head in relation to a posterior-
inferior contracted capsule. However, these investiga-
tions were focused on the motion of forward flexion.18
With the introduction of external rotation at 90° of
abduction, the posterior-inferior capsule is now posi-
tioned inferiorly and becomes the supporting structure of
the humeral head. Once this structure becomes short-
ened, it puts the overhand-throwing athlete’s shoulder at
risk by altering the mechanics of the glenohumeral joint
and begins the potential crescendo of internal impinge-
ment, labral lesions, and undersurface rotator cuff injury.
Additionally, a contracted posterior-inferior capsule
becomes the steering mechanism for the upper quadrant
during the follow-through phase. The moving humerus
begins to dictate the position of the scapula. When the
posterior-inferior capsule is contracted, the scapula is
forced into a more protracted position. Over time, in an
adaptive attempt to normalize its position, the scapula
settles into a depressed position or as infera.42 This com-
bination of an asymmetric scapular malposition and a
glenohumeral internal rotation deficit has the greatest
potential of producing a substantial injury in the upper
extremity of the overhand-throwing athlete.
Preventive Protocol
The knowledge gained during the past decade in the
rehabilitation of the overhand-throwing athlete has
allowed improved design of preventive protocols. These
protocols not only have made an important impact in the
prevention of disabilities, but also have played an impor-
tant role in the reduction of severity and playing-time
loss by the athlete. As the surgeon’s knowledge expands,
and it is supported with the technical tools necessary to
repair previously undiagnosed lesions, a whole genera-
tion of athletes has been given a second opportunity.
Overhand-throwing athletes who were previously
cast aside because of interarticular structural damage
can now entertain surgical options once a period of
conservative care has proven fruitless. Athletes must
understand that a return to play demands that the
rehabilitation will be a continuing process. At no time
should they think that they have obtained a cure. If the
athlete abandons the rehabilitation process, he will
revert to the previous stress cycle, predisposing him to
reinjury.
For an overhand-throwing athlete to be most effi-
cient, he must obtain congruent glenohumeral stability
throughout the full range of motion.64 Because the
scapula must continually reposition itself to maintain
this stability, it is necessary to ensure an unrestricted
range of motion and a number of balanced force couples.
Kibler42 has identified three scapular patterns related to
shoulder injuries: (1) The lack of retraction, resulting in
the loss of the ability to place the scapula in the posi-
tion of full cocking, causes the loss of acceleration;
(2) the lack of protraction, resulting in increased de-
celeration forces on the shoulder and an altered safe
zone for the glenohumeral joint in acceleration; and
(3) excessive protraction resulting in a scapula that is
rotated downward and forward.
CHAPTER 3 THROWING INJURIES
The first objective in our preventive protocol is to
attempt to maintain an anatomically correct position of
the scapula or reposition the asymmetric scapula. This
is accomplished by mobilizing the restrictive structures
that have permitted the humerus and a tethered cora-
coid to dictate the position of the scapula. These struc-
tures are a contracted posterior capsule and a contracted
pectoralis minor and conjoined tendon.
Exercises are then introduced for scapular elevation
and depression; protraction and retraction; and upward
and downward rotation to restore a normal range of
motion. These exercises can be accomplished in a closed
chain manner for glenohumeral joint protection.65
Muscle strengthening should begin with the scapular
pivoters and glenohumeral protectors.66 Special atten-
tion should be paid to the serratus anterior and lower
trapezius, because this force couple is responsible for the
elevation of the acromion.
The training or retraining of the humeral positioners
and rotators is begun with closed chain exercises in
60° of humeral abduction, which is a safe zone for the
rotator cuff. The exercises are progressively elevated to
90° of humeral abduction. Once the scapula can be ade-
quately positioned and stabilized, the humeral position-
ers and humeral rotators can be exercised in an open
chain.
Contained within the following base-exercise proto-
col are six movements identified as core exercises. These
exercises, commonly used by many throwing athletes,
have become popular after two studies from the Kerlan-
Jobe Clinic.67,68 The specifics of these studies are sum-
marized in Appendix 3-1. Because the experimental
models used small weights at low intensities, the full
benefit of these exercises may not be apparent in the
data. First, some of these exercises are not performed in
the arc of greatest benefit if they are limited to what is
commonly referred to as below the plane. Most of the
tested exercises qualify at the extreme of the available
range of motion. Second, a less than adequate resistance
may have been employed to elicit the desired muscle
response. Third, the use of a high repetition program
was not explored using these tested exercises. Fourth,
the exercises lend themselves easily to an eccentric or a
deceleration program. When the concentric component
of the exercise is provided for the athlete, the resistance
of the eccentric component can be greatly increased. It
is paramount that a negative exercise base be established
before the introduction of stretch-shortening exercises.
41
The mass movement patterns contained in the
following protocol are used to choreograph functional
activity so that the scapula is placed in the optimal posi-
tion for the desired activity at the distal segment.
Global-pattern exercises are incorporated not only for
their specific core and shoulder strength training, but
also to elicit a crossover of upper extremity synchrony.
The combination of these exercises moves the athlete
closer to a return to normal activity.
The final step in conditioning or rehabilitating an
overhand-throwing athlete is to train the accelerators.
This is done through a throwing program that builds
upon and emphasizes long throwing. The act of long
throwing enhances acceleration and builds upper
extremity strength in the required rotational pattern. It
provides a step-by-step form to evaluate the coexistent
stretching and strengthening protocol. Long throwing
also provides an excellent base for protective decelera-
tion conditioning. As the neuromuscular system is
trained or retrained, so there is a synchrony of move-
ment, the capsule must be conditioned to withstand
the tremendous traction forces it is exposed to during
deceleration.
As previously stated, injury to the shoulder complex
precipitated by overhand throwing is most often the
result of a failure in the kinetic chain manifesting itself
in the weakest link—the glenohumeral joint. Because
the lower body and trunk account for 46.7% of the
velocity for the throwing arm,69 it is important to focus
upon proximal joint contractures and muscular imbal-
ances in the conditioning of these segments as part of
the entire rehabilitation process. If one maintains
“glenohumeral vision” in the design of preventive or
rehabilitational protocols for the overhand-throwing
athlete, the process is a guaranteed failure.
Measurements
Previously two methods were used to measure a pos-
terior capsular restriction in the overhand-throwing
athlete: horizontal adduction and internal rotation at
90°. One author has attempted to find a correlation
between the two.70 The following are a few suggested
ways of measuring both these motions and external rota-
tion in 90° of abduction. Because the act of overhand
throwing is rotational in nature, the measurements made
with the capsule in a state of rotation are extremely
important. All measurements are made bilaterally and a
42 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Figure 3-6 Figure 3-7

deficit of internal rotation greater than 20% in the dom-

inant shoulder is cause for concern.
The measurement of external rotation in 90° of
abduction is necessary to establish an individual’s “total
motion” or “rotational unity.” It is, however, important
to note that the arc is critical. If the total rotational range
of motion at 90° of abduction is within bounds, a
limit of 120° of external rotation should be considered
the maximum. Passive glenohumeral external rotation
beyond this point may have a negative consequence for
the joint.60

Horizontal Adduction: Supine Figure 3-8

The athlete is positioned supine and the lateral border
of the scapula is stabilized against the chest wall. The
humerus is then adducted in neutral rotation until a firm
end-feel is obtained. A measurement is then made using
a goniometer with an attached level for greater accuracy
(Figures 3-6 and 3-7).
Glenohumeral Internal Rotation in 90° of
Abduction in Frontal Plane: Supine
The athlete is positioned supine and the humerus is
abducted to 90°. A downward force using one hand sta-
bilizes the scapula, while the humerus is rotated medi-
ally until an end-feel is obtained. A measurement is then
made using a goniometer with an attached level for
greater accuracy (Figure 3-8).
Glenohumeral External Rotation in 90° of
Abduction in Frontal Plane: Supine
The athlete is positioned supine and the humerus is
abducted to 90°. The scapula is stabilized with a down-
ward force from one hand, while the humerus is
laterally rotated until an end-feel is obtained. A meas-
urement is then made using a goniometer with an
attached level for greater accuracy (Figure 3-9).
Glenohumeral Internal Rotation in 90° of
Abduction in Scapular Plane: Supine
The athlete is positioned supine and the humerus is
abducted to 90° and horizontally flexed 30° via a wedge.
CHAPTER 3 THROWING INJURIES
Figure 3-9
Figure 3-10
The scapula is stabilized with a downward force from
one hand, while the humerus is rotated medially until
an end-feel is obtained. A measurement is then made
using a goniometer with an attached level for greater
accuracy (Figure 3-10).
Glenohumeral External Rotation in 90° of
Abduction in Scapular Plane: Supine
The athlete is positioned supine and the humerus is
abducted to 90° and horizontally flexed 30° via a wedge.
The scapula is stabilized with a downward force from
one hand, while the humerus is rotated laterally until an
end-feel is obtained. A measurement is then made using
43
Figure 3-11
Figure 3-12
a goniometer with an attached level for greater accuracy
(Figure 3-11).
Glenohumeral Internal Rotation in 90° of
Forward Flexion: Side Lying
The athlete is positioned in a side-lying position and
the humerus is flexed forward 90°. The scapula is sta-
bilized with a downward force from one hand, while
the humerus is rotated medially until an end-feel is
obtained. A measurement is then made using a
goniometer with an attached level for greater accuracy
(Figure 3-12).
44 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Figure 3-14 Stretch: short unstabilized.

Figure 3-13

Glenohumeral External Rotation in 90° of

Forward Flexion: Side Lying
The athlete is positioned in a side-lying position and
the humerus is flexed forward 90°. The scapula is sta-
bilized with a downward force from one hand, while
the humerus is laterally rotated until an end-feel is
obtained. A measurement is then made using a
goniometer with an attached level for greater accuracy
(Figure 3-13).

Glenohumeral Internal Rotation in 90° of

Abduction in Frontal Plane: Prone
The athlete is positioned prone and the humerus is
abducted to 90°. The distal end of the humerus is ele-
vated to take tension off the posterior capsule. Passive
retraction and a downward force from one hand stabi-
lize the scapula. The distal end of the humerus is then
allowed to drop to the length of the posterior capsule.
A measurement is then made using the shaft of the
ulna and the perpendicular table top as references. A
goniometer with an attached level is used for greater
accuracy. These recordings will have a reverse relation-
ship to the numbers obtained from glenohumeral inter-
nal rotation in 90° of abduction frontal plane: supine
(Figures 3-14 and 3-15).
Figure 3-15 Stretch: short stabilized.
Mobilization of the Scapula
Pectoralis Minor/Conjoined Tendon
Stretch: Supine
The athlete is positioned supine with a rigid bolster
place in line with the medial border of his or her scapula
to elevate the shoulder girdle. In a cross-hand fashion,
one hand is placed inferior and medial to the coracoid.
The heel of the other hand is placed on the coracoid. A
downward motion while separating the hands accom-
plishes the stretch (Figure 3-16).
CHAPTER 3 THROWING INJURIES 45

Figure 3-16 Stretch: pectoralis minor.

Protraction/Retraction Stretch: Side Lying

The athlete is placed in a side-lying position with the
shoulder flexed forward to 90° and the elbow flexed 90°. Figure 3-17 Stretch: protraction.
The humerus is stabilized with the hip so that the hands
are free to manipulate the scapula. By grasping the
medial border of the scapula, the scapula is protracted
by moving it laterally against the chest wall. By placing
the heels of the hands on the lateral border of the
scapula, it is moved into retraction by moving it medi-
ally against the chest wall (Figures 3-17 and 3-18).

Upward/Downward Rotation Stretch:

Side Lying
The athlete is placed in a side-lying position with the
shoulder flexed forward to 90° and the elbow flexed 90°.
The humerus is stabilized with the hip so the hands are
free to manipulate the scapula. By grasping the inferior
medial border of the scapula with one hand and the
lateral border with the heel of the other hand, upward
rotation is achieved along the chest wall. Downward
rotation can be achieved by reversing the hands, grasp-
ing the superior medial border of the scapula with one
hand, and placing the heel of the other hand on the infe-
rior lateral border (Figures 3-19 and 3-20).

Retroversion (Posterior Tilting) Stretch:

Side Lying
The athlete is placed in a side-lying position with the Figure 3-18 Stretch: retraction.
shoulder flexed forward to 90° and the elbow flexed 90°.
One hand is placed on the inferior angle of the scapula
46 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Figure 3-21 Stretch retroversion of scapula: side

lying.

Figure 3-19 D rotation.

and the heel of the other is placed on the coracoid. The
scapula is elevated from the inferior angle and pressed
against the chest wall. Once full elevation is achieved,
the scapula is posteriorly tilted by pressure against the
coracoid (Figure 3-21).

Retroversion (Posterior Tilting)

Stretch: Prone
The athlete is placed in a prone position with the shoul-
der abducted to 90° and the elbow flexed 90°. One hand
is placed on the inferior angle of the scapula and the
fingers of the other hand reach under the chest to locate
the coracoid. The scapula is elevated from the inferior
angle and pressed against the chest wall. Once full ele-
vation is achieved, lifting the coracoid posteriorly tilts
the scapula (Figure 3-22).

Posterior-Inferior
Capsule Stretching

Horizontal Adduction: Supine

Figure 3-20 Forward rotation.
The athlete is positioned supine on the table close
enough to the edge to expose the lateral border of the
scapula. The scapula is stabilized with the hip and
the shoulder is moved into horizontal adduction
(Figure 3-23).
CHAPTER 3 THROWING INJURIES
Figure 3-22 Retroversion of the scapula: prone.
Figure 3-23
Abduction 90°/Scapular Plane With Internal
Rotation: Supine
The athlete is positioned supine on the table close
enough to the edge to expose the lateral border of the
scapula. The humerus is abducted to 90° and horizon-
tally adducted to the plane of the scapula. The elbow is
flexed 90°. One hand is under the ulna and is placed on
the anterior aspect of the shoulder. This hand applies a
downward pressure to stabilize the scapula. Applying
downward pressure at the distal end of the ulna medi-
ally rotates the humerus (Figure 3-24).
47
Figure 3-24
Figure 3-25
Forward Flexion With Internal
Rotation: Supine
The athlete is positioned supine on the table close
enough to the edge to expose the lateral border of
the scapula. The humerus is flexed forward 90° and the
elbow is flexed 90°. The scapula is stabilized with the
hip. One hand is slid under the humerus and is placed
on the anterior aspect of the shoulder. This hand applies
a downward pressure to stabilize the scapula. Applying
downward pressure at the distal end of the ulna medi-
ally rotates the humerus (Figure 3-25).
48 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Diagonal With Internal Rotation: Supine One hand is placed on the proximal humerus to assist
The athlete is positioned supine on the table close the body weight in stabilizing the scapula. The other
enough to the edge to expose the lateral border of hand is placed on the posterior aspect of the distal ulna.
the scapula. The scapula is stabilized with the hip. The A downward motion at the distal ulna medially rotates
humerus is flexed forward 45° and internally rotated the the humerus (Figure 3-28).
maximum amount.
Forward Flexion 90° With Internal Rotation:
The elbow is flexed 90°. One hand is placed on the
Side Lying
posterior aspect of the humerus and the other grasps the
distal end of the ulna. Pressure is applied to the poste- The athlete is positioned in a side-lying position with
rior humerus to move it in the direction of the opposite the humerus flexed forward 90°. The elbow is also flexed
hip. The elbow is extended to enhance the stretch 90°. One hand is placed on the proximal humerus to
(Figure 3-26). assist the body weight in stabilizing the scapula. The
other hand is placed on the posterior aspect of the distal
Abduction 90°/Frontal Plane With Internal ulna. A downward motion at the distal ulna medially
Rotation: Prone rotates the humerus (Figure 3-29, A, B).
The athlete is positioned prone on the table so that the
entire length of the humerus is supported when
abducted to 90°.71 The elbow is flexed 90° and the back
of the hand is supported on the table. In a cross-hand
fashion, one hand stabilizes the scapula against the chest
wall and the other is positioned at the distal end of
the humerus. A downward motion while separating the
hands accomplishes the stretch. Note that in the case
of a severe posterior-inferior capsule contracture, this
stretch may have to be accomplished in less humeral
abduction (Figure 3-27, A, B). A

Forward Flexion 70° With Internal Rotation:

Side Lying
The athlete is positioned in a side-lying position with
the humerus flexed forward 70°. The elbow is flexed 90°.

Figure 3-26 Figure 3-27

 CHAPTER 3 THROWING INJURIES 49

Forward Flexion 110° With Internal

Rotation: Side Lying
The athlete is positioned in a side-lying position with
the humerus flexed forward 100°. The elbow is flexed
90°. One hand is placed on the proximal humerus to
assist the body weight in stabilizing the scapula. The
other hand is placed on the posterior aspect of the distal
ulna. A downward motion at the distal ulna medially
rotates the humerus (Figure 3-30, A, B).

Forward Flexion 90° With Internal Rotation:

Side Lying and Roll Over
The athlete adopts a side-lying position with the
humerus flexed forward 90°. The elbow is also flexed 90°.
Figure 3-28 One hand is placed on the proximal humerus to assist
the body weight in stabilizing the scapula. The other

A A

B B

Figure 3-29 Figure 3-30

 50 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
Figure 3-31
hand is placed on the posterior aspect of the distal ulna.
A downward motion at the distal ulna medially rotates
the humerus. At the completion of medial rotation, the
torso is rotated toward the humerus to enhance the
stretch (Figure 3-31, A, B).
Scapular Elevation and Internal
Rotation: Prone
The athlete is positioned prone on the table so that the
entire length of the humerus is supported when abducted
to 90°. The elbow is flexed 90° and is unsupported. One
hand is placed at the inferior angle of the scapula, while
the other grasps the distal end of the ulna. The scapula is
elevated with a superior motion, while lifting the distal
ulna medially rotates the humerus (Figure 3-32).
Figure 3-32
Figure 3-33 Weight: shift start.
Exercise Protocol
Table Top Exercises
Weight Shift With Scapular Movement. Support
your body weight on the edge of a table in a forward
leaning position with shoulders flexed forward and
hands wider than shoulder width. (1) Shift your body
weight over your right shoulder by moving your body
toward the right side. The right scapula retracts as the
left scapula protracts. (2) Shift your body weight over
your left shoulder by moving your body toward the left
side. The left scapula retracts and the right scapula
protracts (Figures 3-33 to 3-35).
CHAPTER 3 THROWING INJURIES
Figure 3-34 Weight: shift right.
Figure 3-35 Weight: shift left.
Seated: Scapular Protraction/Retraction. Sit
with your shoulder abducted with a towel placed
between your hand and the table. Place your opposite
hand behind your head to maintain your posture. Fully
protract your scapula by advancing your hand forward.
Fully retract the scapula by drawing your hand back-
ward. Be careful not to elevate your shoulder during this
exercise (Figure 3-36, A, B).
Seated:Scapular Depression/Elevation. Sit with your
shoulder flexed forward and a towel placed between your
hand and the table. Place your opposite hand behind
your head to maintain your posture. Fully depress your
scapula by advancing your arm forward. Fully elevate your
scapula by drawing your hand backward (Figure 3-37, A, B).
51
Figure 3-36 A, Seated protraction. B, Seated
retraction.
Wall Exercises
Shoulder Flexion: Protraction/Retraction. Stand
with your shoulder in 90° of forward flexion with your
hand placed against the wall.65 Allow your body to lean
towards the wall. Place your opposite hand behind your
head to maintain your posture. (1) Push away from the
wall at your shoulder by fully protracting the scapula. (2)
Lean into the wall at your shoulder by retracting your
scapula. Be certain to pinch your scapula on full retrac-
tion. Be careful not to elevate your shoulder during this
exercise (Figure 3-38, A, B).
Shoulder Abduction: Protraction/Retraction.
Stand with your shoulder in 90° of abduction and with
52 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

A B

Figure 3-37 A, Scapular depression. B, Scapular elevation.

A B

Figure 3-38 A, Wall exercise: shoulder flexion protraction. B, Wall exercise: shoulder flexion retraction.
CHAPTER 3 THROWING INJURIES
your hand placed against the wall. Allow your body to
lean toward the wall. Place your opposite hand behind
your head to maintain your posture. (1) Push away from
the wall at your shoulder by fully protracting the scapula.
(2) Lean into the wall at your shoulder by retracting your
scapula. Be certain to pinch your scapula on full retrac-
tion. Be careful not to elevate your shoulder during this
exercise (Figure 3-39, A, B).
Shoulder Flexion: Elevation/Depression. Stand
with your shoulder in 90° of flexion and your hand
placed against the wall. Allow your body to lean toward
the wall. Place your opposite hand behind your head to
maintain your posture. (1) Completely elevate your
scapula. (2) Completely depress your scapula. While in
full depression, squeeze your scapulae together (Figure
3-40).
Shoulder Abduction: Elevation/Depression.
Stand with your shoulder in 90° abduction and your
hand placed against the wall. Allow your body to lean
A
Figure 3-39 A, Wall exercise: shoulder abduction protraction. B, Wall exercise: abduction retraction.
53
toward the wall. Place your opposite hand behind your
head to maintain posture. (1) Completely elevate your
scapula. (2) Completely depress your scapula. While in
full depression, squeeze your scapulae together (Figure
3-41, A, B).
Shoulder Rotation: Flexion. Stand with your
shoulder in 90° of flexion with your thumb placed
against the wall. Allow your body to lean slightly toward
the wall. Place your opposite hand behind your head to
maintain your posture. (1) Completely internally rotate
your arm by using your thumb as a fulcrum. Obtain full
upward rotation of your scapula. (2) Completely exter-
nally rotate your arm by using your thumb as a fulcrum.
Obtain full downward rotation of your scapula. When
your scapula is in the full downward rotational position,
squeeze your scapulae together (Figure 3-42, A, B).
Shoulder Rotation: Abduction. Stand with your
shoulder in 90° of abduction and your thumb placed
against the wall. Allow your body to lean slightly
B
 54 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

B
A

Figure 3-40 A, Wall exercises: shoulder flexion elevation. B, Wall exercises: shoulder flexion depression.

towards the wall. Place your opposite hand behind your
head to maintain your posture. (1) Completely internally
rotate your arm by using your thumb as a fulcrum.
Obtain full upward rotation of your scapula. (2) Com-
pletely externally rotate your arm by using your thumb
as a fulcrum. Obtain full downward rotation of your
scapula. When your scapula is in the full downward
rotational position, squeeze your scapulae together
(Figure 3-43, A, B).
Prone Exercises: The Six Back72
Prone: 90° Shoulder Abduction With Thumbs
Forward (Neutral Rotation). Lie prone with your
shoulders abducted to 90° and your thumbs forward.65
Horizontally abduct your arms with full scapular retrac-
tion. Squeeze your scapulae together and hold this
position for 6 seconds (Figure 3-44, A, B).
 B
A

Figure 3-41 A, Wall exercises: shoulder abduction elevation. B, Wall exercises: shoulder abduction depression.

A
B

Figure 3-42 A and B, Wall exercises: thumbtack in shoulder flexion.

56 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

B
A

Figure 3-43 A, Wall exercises: thumbtack shoulder internal rotation. B, Wall exercises: thumbtack shoulder exter-
nal rotation.

Figure 3-44 A, Six back 1. B, Six back 1 on ball.

 CHAPTER 3 THROWING INJURIES
A A
B B
Figure 3-45 A, Six back 2. B, Six back 2 on ball.
Prone: 90° Shoulder Abduction With Thumbs Up
(External Rotation). Lie prone with your shoulders
abducted to 90° and your thumbs up. Fully abduct your
arms horizontally with full scapular retraction. Squeeze
your scapulae together and hold this position for 6
seconds (Figure 3-45, A, B).
Prone: 100° Shoulder Abduction With Thumbs
Forward (Neutral Rotation). Lie prone with your
shoulders abducted to 100° and your thumbs forward.
Fully abduct your arms horizontally with full scapular
retraction. Squeeze your scapulae together, and hold this
position for 6 seconds (Figure 3-46, A, B).
Prone: 100° Shoulder Abduction With Thumps Up
(External Rotation). Lie prone with your shoulder
abducted to 100° and your thumbs up. Fully abduct your
57
Figure 3-46 A, Six back 3. B, Six back on ball 3.
arms horizontally with full scapular retraction. Squeeze
your scapulae together and hold this position for 6
seconds (Figure 3-47, A, B).
Prone: 90° Shoulder Abduction With 90° Elbow
Flexion (90/90 Position). Lie prone with your shoul-
ders abducted and your elbows flexed to 90°. Fully
abduct your arms horizontally with full scapular retrac-
tion. Squeeze your scapulae together and hold this posi-
tion for 6 seconds (Figure 3-48, A, B).
Prone: Shoulder Extension. Lie prone with your
arms at your sides and your palms facing down. Lift your
hands away from the table to produce full shoulder
extension. Squeeze your scapulae together and hold this
position for 6 seconds (Figure 3-49, A, B).
A

Figure 3-47 A, Six back 4. B, Six back on ball 4.

Figure 3-48 A, Six back 5. B, Six back on ball 5.

B
A

Figure 3-49 A, Six back 6. B, Six back on ball 6.

CHAPTER 3 THROWING INJURIES 59

Back Exercises
Pillow Squeezes
Place small pillows under arms so that shoulders are in
45° of scaption. Your elbows are to be flexed to 90°.
Squeeze pillows to your sides by retracting your scapu-
lae and externally rotating your shoulders (Figure 3-50,
A, B).
Shoulder Shrugs
Stand with your arms at your sides. (1) Fully retract your
scapulae. (2) Perform a shoulder shrug by elevating your
scapulae toward the back of your neck. Maintain good
posture by avoiding tilting your head forward. Make
certain to keep your scapulae fully retracted throughout
the movement (Figure 3-51).
Scapula Circles
Stand with your arms at your sides. This is a four-count
exercise. (1) Elevate your scapulae. (2) Fully retract your
scapulae. (3) Fully depress your scapulae. (4) Protract
your scapulae to the starting position. Do not protract
your scapulae beyond the neutral starting position.
Scaption: Internal Rotation (Core 1)
Stand with your arms at your sides. Internally rotate your
humerus and move your hands forward into the
plane of the scapula. Elevate your arms in the scapular

Figure 3-50 Figure 3-51 Scapular shrug: 1 rear.

60 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Figure 3-52 Jobes: scaption.

Figure 3-53 Jobes: scaption.

plane. Then return to the starting position in the same

manner. Perform scapular retraction at the end of each
repetition (Figure 3-52).

Scaption: External Rotation (Core 2)

Stand with your arms at your sides. Externally rotate
your humerus and move your hands forward into the
plane of the scapula. Elevate your arms in the scapular
plane until completing the arc. Return to the starting
position in the same manner. Perform scapular retrac-
tion at the end of each repetition (Figure 3-53).

Horizontal Abduction and External

Rotation (Core 3)
Standing, bend forward at the waist until your torso is
parallel with the floor. Bend your knee for balance. You
may place your head on an appropriate height table for
support. Externally rotate your humerus and contract
your abdominal muscles. Horizontally abduct your arms
until they are parallel with the floor. Squeeze your scapu-
lae into complete retraction at the end of the movement.
Return your arms to the starting position (Figures 3-54
and 3-55).

Prone Scapular Rowing

Figure 3-54 Jobes: horizontal abduction.
Lie prone on a table with your shoulder flexed forward
to 90° and your elbow fully extended. Your shoulder
CHAPTER 3 THROWING INJURIES 61

Figure 3-55 Jobes: horizontal abduction.

should be far enough off the table to allow complete

freedom of scapular motion. (1) Fully retract your
scapula while maintaining full elbow extension. (2)
Return to the starting position by protracting your
scapula (Figure 3-56, A, B).
B
Prone Rowing (Core 4)
Lie prone on a table with your shoulder flexed forward
to 90° and your elbow fully extended. Your shoulder
should be far enough off the table to allow complete
freedom of scapular motion. (1) Fully retract your
scapula while maintaining full elbow extension. (2)
Once your scapula is in full retraction extend the shoul-
der and flex the elbow in a rowing motion. (3) Return Figure 3-56
to the starting position by extending the elbow
and forward flexing the shoulder. Protract the scapula
at the completion of the arm movement (Figure 3-57,
A-C).
far enough off the table to allow complete freedom
Supine Scapular Rowing of scapular motion. (1) Extend your elbow while
flexing forward your shoulder until achieving full elbow
Lie supine on a table with your shoulder flexed forward
extension and 90° of shoulder forward flexion. (2)
to 90° and your elbow fully extended. Your shoulder
Fully protract the scapula. (3) Fully retract the scapula.
should be far enough off the table to allow complete
(4) Lower your arm through elbow flexion and
freedom of scapular motion. (1) Fully protract your
shoulder extension to the starting position (Figure 3-59,
scapula while maintaining full elbow extension. (2) Fully
A-C).
retract your scapula while maintaining full elbow exten-
sion (Figure 3-58, A, B). Push-up Plus (Core 5)
Begin in a forward leaning position supported by a table.
Bench Press Plus (1) Lower your chest between your hands by extending
Lie supine on a table with your shoulder fully extended your shoulders and flexing your elbows. (2) Perform a
and your elbow fully flexed. Your shoulder should be push-up by extending your elbows and flexing forward
 62 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

A A

B B

Figure 3-58

C
your shoulders. (3) At the end of this motion, fully pro-
tract the scapulae by pushing the torso farther away from
the table. Progress this exercise to accomplish it on the
floor or tabletop (Figure 3-60, A-C).

Press Ups—Seated Dips (Core 6)

Position your hands on two supports to allow your
Figure 3-57 shoulders to support some of your body weight. (1)
Using your shoulders, lift your body up. (2) Push
yourself farther by depressing your scapulae into a plus
position (Figure 3-61, A, B).
 CHAPTER 3 THROWING INJURIES 63

A
A

B
B

Figure 3-60

Figure 3-59
 64 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
Figure 3-61
Scapula Depression: Unilateral
Stand with arms at your side. (1) Fully retract the scapula
of the shoulder to be exercised. (2) Place your opposite
hand behind your head to maintain your posture. (3)
Using a pulley, tubing, or manual resistance, depress the
scapula. At the end of scapular depression, squeeze the
scapulae together. Be certain to keep your scapula fully
retracted throughout the movement (Figure 3-62).
Scapular Elevation: Unilateral
Stand with arms at your side. (1) Fully retract the
scapula of the shoulder to be exercised. (2) Place your
opposite hand behind your head to maintain your
Figure 3-62 Scapula: depression (elevation).
posture. (3) Using a pulley, tubing, or manual resistance,
elevate the scapula. At the end of scapular elevation,
squeeze the scapulae together. Be certain to keep the
scapula fully retracted throughout the movement
(Figure 3-63).
Scapula Depression: Bilateral
Place yourself in a position so resistance can be provided
from an area forward and above your shoulders. Your
shoulders should be flexed forward approximately 120°
and your elbows fully extended. (1) Retract and depress
the scapulae in one motion. (2) Return to the starting
position using scapular control (Figure 3-64, A, B).
Mass Movement Patterns
Lateral Lunge. Stand with both hands placed on
your chest with your knees slightly bent and feet apart.
(1) Begin the movement by stepping laterally with your
CHAPTER 3 THROWING INJURIES
Figure 3-63 Scapula: scapula elevation.
right foot while moving the right hand in a sweeping
motion down from the chest into a laterally elevated
position. This motion should occur in the plane of the
scapula. The exercise should concentrate on the move-
ment of the scapula. (2) Return to your starting position
by reversing the sequence of movements, sweeping your
right hand down, and drawing it to your chest while
stepping back to your original position. (3) Perform
scapular retraction at the midpoint of this exercise. (4)
Complete the exercise by performing the movement to
your left (Figure 3-65, A-C).
Forward Lunge. Stand with your right shoulder in
90° to 100° of abduction and full horizontal extension.
Retract the scapula. The elbow should be flexed to 90°.
Place your left hand on your chest and step backward
with your left foot. (1) Step forward with your left foot
while moving your right arm in a fully extended posi-
65
tion with full scapular protraction. Internally rotate the
humerus toward the end of the movement. (2) Reverse
the movement by stepping backwards with your left foot
to its beginning position. Draw the right arm back into
horizontal extension and full scapular retraction. The
elbow returns to its flexed position. (3) Perform scapu-
lar retraction at the midpoint and end of each repetition.
At the completion of the assigned number of repetitions,
the exercise is then performed using the left shoulder
and right foot (Figure 3-66, A, B).
Diagonal Pull. Stand with your right shoulder
abducted to 90° to 100°. Your elbow should be in full
flexion. Place your left hand on your chest. Your feet
should be placed a shoulder width apart. (1) Squat to
about 45° while moving your hand down in a diagonal
movement across your body toward the outside of the
left knee. Internally rotate your humerus toward the end
of the movement. (2) Return to the starting position by
extending your knees and drawing your hand back across
your chest. (3) Perform scapular retraction at the end of
each repetition. At the completion of the assigned
number of repetitions, the exercise is then performed
using the left shoulder (Figure 3-67, A, B).
Same Side Pull. Stand with your right arm at your
side. Place your left hand on your chest. Your feet should
be placed a shoulder width apart. (1) Squat to about 45°
while fully depressing the scapula. (2) Extend your knee
to a full standing position while elevating your scapula.
Simultaneously move the humerus into an abducted
position of 90° to 100° with elbow flexion. Fully retract
the scapula. (3) Change the motion of the upper extrem-
ity by moving your hand across your midline, bringing
the shoulder into horizontal adduction and full elbow
extension. Internally rotate the humerus toward the end
of this movement. (4) Return to the starting position by
retracting your movements. Be certain to include full
scapular retraction before lowering the hand to the start-
ing position. At the completion of the assigned number
of repetitions, the exercise is then performed using the
left shoulder (Figure 3-68, A-E).
Bilateral Lunge. Stand with both shoulders in
extension with elbows flexed. Retract your scapulae. Step
backward with your nondominant foot to establish the
beginning position. (1) Step forward with the nondom-
inant foot while moving your shoulders into a forward
66 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

A
B

Figure 3-64 A, Scapula: scapula pull down 1. B, Scapula: scapula pull down 2.

flexed position of approximately 150°. Your elbows
should be fully extended. (2) The final forward move-
ment should be of full scapular protraction and humeral
internal rotation. (3) Complete the exercise by stepping
back with the nondominant foot and moving the shoul-
ders back into the position of extension with elbow
flexion. (4) Retract the scapulae at the end of the
repetition. Nondominant hip stability can be enhanced
by the use of a step-up (Figure 3-69, A-C).
Global Supine Incline: Abduction. Position your-
self on a stability ball supine with your hips lower than
your shoulders. Your hands should be resting on your
anterior thighs. (1) Sweep your hands away from your
CHAPTER 3 THROWING INJURIES 67

Figure 3-65 A, Lunge: lateral start front. B, Lunge: lateral right front. C, Lunge: lateral left front.
68 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Figure 3-66 A, Lunge: forward lunge start side. B, Lunge: forward lunge middle side.

midline in the plane of the scapula until the arc is com-
pleted. (2) Move your hands back to the starting posi-
tion by adducting them along your midline. Perform a
scapular retraction at the end of each repetition (Figure
3-70, A-D).
Global Supine Incline: Adduction. Position your-
self on a stability ball supine with your hips lower than
your shoulders. Your hands should be resting on your
anterior thighs. (1) Elevate your hands along your
midline until you reach full forward flexion. (2) Sweep
your hands in an arc toward the starting position by
adducting your shoulders in the plane of the scapula.
Perform a scapular retraction at the end of each repeti-
tion. Reverse the abduction pattern.
Global Supine Level: Abduction. Position yourself
on a stability ball supine with your shoulders level
with your hips. Your hands should be resting on your
anterior thighs. (1) Sweep your hands away from your
midline in the plane of the scapula until the arc is com-
pleted. (2) Move your hands back to the starting posi-
tion by adducting them along your midline. Perform a
scapular retraction at the end of each repetition.
Global Supine Level: Adduction. Position your-
self on a stability ball supine with your shoulders level
with your hips. Your hands should be resting on your
anterior thighs. (1) Elevate your hands along your
midline until you reach full forward flexion. (2) Sweep
your hands in an arc toward the starting position by
CHAPTER 3 THROWING INJURIES 69

Figure 3-67 A, Lunge: lawn mower lunge start front. B, Lunge: lawn mower lunge end front.
70 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

B
A

Figure 3-68 A, Lunge: same side lunge 1 front. B, Lunge: same side lunge 2 front.
Continued
CHAPTER 3 THROWING INJURIES 71

C
D

Figure 3-68, cont’d C, Lunge: same side lunge 3 front. D, Lunge: same side lunge 4 front.
Continued
72 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
E
Figure 3-68, cont’d E, Lunge: same side lunge
5 front.
adducting your shoulders in the plane of the scapula.
Perform a scapular retraction at the end of each repeti-
tion. Then reverse the abduction pattern.
Stability Ball: Prone Exercise Pattern of Move-
ments. Position yourself on a stability ball prone with
your arms in the adducted position. Extend your shoul-
ders forward in the plane of the scapula. With your
shoulders horizontally extended and your elbow flexed
to 90°, extend your arm in front and return to the start-
ing position. (1) Horizontally abduct your shoulders and
retract your scapulae. (2) Externally rotate your humerus
(Figure 3-71, A-D).
A
Figure 3-69 A, Lunge: bilateral lunge 1 rear.
Continued
Stability Ball: Dynamic Hug. Position yourself on
a stability ball73 supine with your shoulders horizontally
extended and your elbow flexed to 90°. (1) Move your
hands toward your midline in the same plane without
changing the angle of your elbows (Figure 3-72, A, B).
Stability Ball: Mass Movements. These exercises
are to be performed as rapidly as possible in a given
amount of time. They should be accomplished in linear
and diagonal patterns (Figures 3-73 to 3-78).
Text continued on p. 77.
CHAPTER 3 THROWING INJURIES 73

B C

Figure 3-69, cont’d B, Lunge: bilateral lunge 2 rear. C, Lunge: bilateral lunge 3 rear.
74 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

B D

Figure 3-70
A C

B D

Figure 3-71

Figure 3-72 A, Globe: dynamic hug front 1. B, Globe: dynamic hug front 2.
76 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Figure 3-73 Figure 3-76

Figure 3-74 Figure 3-77

Figure 3-75 Figure 3-78

CHAPTER 3 THROWING INJURIES
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Guidelines for Off-Season
Upper Extremity Conditioning
Protocol
T his conditioning protocol has been designed
into three, 5-week blocks. The first block relies
on a 3-day workout to reestablish the upper
extremity exercises you have used this past season. This
will be your active rest period. The second block will be
a strength-building period with workouts three times a
week using a five-repetition, five-set format with con-
trolled 3-minute rest periods. The third block, beginning
after 1 week of rest, moves to a 4-day-a-week format
with increasing repetitions.
You must determine the weight that you will begin
with and when to increase that weight. Generally, you
begin with half the weight that you were using at the
conclusion of the season and begin the second and third
blocks with half the weight that you will be using at the
conclusion of the previous block.
At the conclusion of the third block, there is 1 week
of modified activity followed by 1 week of activity that
mimics your spring training protocol. A suggested
throwing protocol is included.
Block One: Weeks 1 to 5
• Progress through this period beginning with 16
repetitions and ending with 20.
• Six back begins with one set of three repetitions and
progresses to one set of six repetitions.
• Global Patterns begin with three repetitions per
position per direction. Three supine positions
(incline, level, and decline) for a total of 18
79
Appendix
3-1
repetitions. Three prone positions (incline, level, and
decline) for a total of 18 repetitions.
• The dynamic hug and reverse fly are included in the
Global Patterns because of the use of the physioball.
Repetitions should follow the 16 to 20 formats.
• Add weight as necessary to ensure maximum
benefit.
Block Two: Weeks 6 to 10
• Range of motion exercises are done in 1 set of 25
repetitions.
• Core/base/movement patterns are done in a five-
repetition, five-set sequence.
• Once the first exercise is completed in a group a
clock is started for 3 minutes.
• The remaining exercises are completed to finish
the first set. The second set is not begun until the
3-minute period has elapsed.
• The timing continues through each of the five sets.
• The dynamic hug and reverse fly are accomplished
in 1 set of 25.
Recovery Week 11
• Recovery week: range of motion exercises
Block Three: Weeks 12 to 16
• Range of motion, core, and base exercises return to a
1 set of 20 format.
Text continued on p. 84.
80 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Table A-1

BLOCK ONE: WEEKS 1 TO 5

Week 1: Day 1 Week 1: Day 2 Week 1: Day 3

ROM Exercises 1*16 ROM Exercises 1*16 ROM Exercises 1*16

Six Back 1*4 Six Back 1*4 Six Back 1*4
Core Exercises 1*16 Core Exercises 1*16 Core Exercises 1*16
Base Exercises 1*16 Base Exercises 1*16 Base Exercises 1*16
Movement Patterns 1*16 Movement Patterns 1*16 Movement Patterns 1*16
Global Patterns 3 per position Global Patterns 3 per position Global Patterns 3 per position

Week 2: Day 1 Week 2: Day 2 Week 2: Day 3

ROM Exercises 1*17 ROM Exercises 1*17 ROM Exercises 1*17

Six Back 1*5 Six Back 1*5 Six Back 1*5
Core Exercises 1*17 Core Exercises 1*17 Core Exercises 1*17
Base Exercises 1*17 Base Exercises 1*17 Base Exercises 1*17
Movement Patterns 1*17 Movement Patterns 1*17 Movement Patterns 1*17
Global Patterns 3 per position Global Patterns 3 per position Global Patterns 3 per position

Week 3: Day 1 Week 3: Day 2 Week 3: Day 3

ROM Exercises 1*18 ROM Exercises 1*18 ROM Exercises 1*18

Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*18 Core Exercises 1*18 Core Exercises 1*18
Base Exercises 1*18 Base Exercises 1*18 Base Exercises 1*18
Movement Patterns 1*18 Movement Patterns 1*18 Movement Patterns 1*18
Global Patterns 4 per position Global Patterns 4 per position Global Patterns 4 per position

Week 4: Day 1 Week 4: Day 2 Week 4: Day 3

ROM Exercises 1*19 ROM Exercises 1*19 ROM Exercises 1*19

Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*19 Core Exercises 1*19 Core Exercises 1*19
Base Exercises 1*19 Base Exercises 1*19 Base Exercises 1*19
Movement Patterns 1*19 Movement Patterns 1*19 Movement Patterns 1*19
Global Patterns 4 per position Global Patterns 4 per position Global Patterns 4 per position

Week 5: Day 1 Week 5: Day 2 Week 5: Day 3

ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20

Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20
Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20
Movement Patterns 1*20 Movement Patterns 1*20 Movement Patterns 1*20
Global Patterns 5 per position Global Patterns 5 per position Global Patterns 5 per position
APPENDIX 3-1 GUIDELINES FOR OFF-SEASON UPPER EXTREMITY CONDITIONING PROTOCOL 81

Table A-2

BLOCK TWO: WEEKS 6 TO 10

Week 6: Day 1 Week 6: Day 2 Week 6: Day 3

ROM Exercises 1*25 ROM Exercises 1*25 ROM Exercises 1*25

Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 5*5 Core Exercises 5*5 Core Exercises 5*5
Base Exercises 5*5 Base Exercises 5*5 Base Exercises 5*5
Movement Patterns 5*5 Movement Patterns 5*5 Movement Patterns 5*5
Global Patterns 5 per position Global Patterns 5 per position Global Patterns 5 per position
50 throws at 60 ft 50 throws at 60 ft 50 throws at 60 ft

Week 7: Day 1 Week 7: Day 2 Week 7: Day 3

ROM Exercises 1*25 ROM Exercises 1*25 ROM Exercises 1*25

Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 5*5 Core Exercises 5*5 Core Exercises 5*5
Base Exercises 5*5 Base Exercises 5*5 Base Exercises 5*5
Movement Patterns 5*5 Movement Patterns 5*5 Movement Patterns 5*5
Global Patterns 6 per position Global Patterns 6 per position Global Patterns 6 per position
60 throws at 60 ft 60 throws at 60 ft 60 throws at 60 ft

Week 8: Day 1 Week 8: Day 2 Week 8: Day 3

ROM Exercises 1*25 ROM Exercises 1*25 ROM Exercises 1*25

Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 5*5 Core Exercises 5*5 Core Exercises 5*5
Base Exercises 5*5 Base Exercises 5*5 Base Exercises 5*5
Movement Patterns 5*5 Movement Patterns 5*5 Movement Patterns 5*5
Global Patterns 6 per position Global Patterns 6 per position Global Patterns 6 per position
70 throws at 60 ft 70 throws at 60 ft 70 throws at 60 ft

Week 9: Day 1 Week 9: Day 2 Week 9: Day 3

ROM Exercises 1*25 ROM Exercises 1*25 ROM Exercises 1*25

Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 5*5 Core Exercises 5*5 Core Exercises 5*5
Base Exercises 5*5 Base Exercises 5*5 Base Exercises 5*5
Movement Patterns 5*5 Movement Patterns 5*5 Movement Patterns 5*5
Global Patterns 6 per position Global Patterns 6 per position Global Patterns 6 per position
80 throws at 60 ft 80 throws at 60 ft 80 throws at 60 ft

Week 10: Day 1 Week 10: Day 2 Week 10: Day 3

ROM Exercises 1*25 ROM Exercises 1*25 ROM Exercises 1*25

Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 5*5 Core Exercises 5*5 Core Exercises 5*5
Base Exercises 5*5 Base Exercises 5*5 Base Exercises 5*5
Movement Patterns 5*5 Movement Patterns 5*5 Movement Patterns 5*5
Global Patterns 6 per position Global Patterns 6 per position Global Patterns 6 per position
90 throws at 60 ft 90 throws at 60 ft 90 throws at 60 ft
 Table A-3

RECOVERY: WEEK 11

Week 11: Day 1 Week 11: Day 2 Week 11: Day 3

ROM Exercises 1*25 ROM Exercises 1*25 ROM Exercises 1*25

100 throws at 60 ft 100 throws at 60 ft 100 throws at 60 ft

Table A-4

BLOCK THREE: WEEKS 12 TO 16

Week 12: Day 1 Week 12: Day 2 Week 12: Day 3 Week 12: Day 4

ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20
Six Back 1*6 Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20
Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20
Movement Movement Movement Movement
Patterns 2*12 Patterns 2*12 Patterns 2*12 Patterns 2*12
Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6
75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft
25 throws at 90 ft 25 throws at 90 ft 25 throws at 90 ft 25 throws at 90 ft

Week 13: Day 1 Week 13: Day 2 Week 13: Day 3 Week 13: Day 4

ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20
Six Back 1*6 Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20
Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20
Movement Movement Movement Movement
Patterns 2*14 Patterns 2*14 Patterns 2*14 Patterns 2*14
Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6
75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft
25 throws at 120 ft 25 throws at 120 ft 25 throws at 120 ft 25 throws at 120 ft

Week 14: Day 1 Week 14: Day 2 Week 14: Day 3 Week 14: Day 4

ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20
Six Back 1*6 Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20
Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20
Movement Movement Movement Movement
Patterns 2*16 Patterns 2*16 Patterns 2*16 Patterns 2*16
Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6
75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft
25 throws at 150 ft 25 throws at 150 ft 25 throws at 150 ft 25 throws at 150 ft
APPENDIX 3-1 GUIDELINES FOR OFF-SEASON UPPER EXTREMITY CONDITIONING PROTOCOL 83

Table A-4

BLOCK THREE: WEEKS 12 TO 16—cont’d

Week 15: Day 1 Week 15: Day 2 Week 15: Day 3 Week 15: Day 4

ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20
Six Back 1*6 Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20
Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20
Movement Movement Movement Movement
Patterns 2*18 Patterns 2*18 Patterns 2*18 Patterns 2*18
Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6
75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft
25 throws at 180 ft 25 throws at 180 ft 25 throws at 180 ft 25 throws at 180 ft

Week 16: Day 1 Week 16: Day 2 Week 16: Day 3 Week 16: Day 4

ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20
Six Back 1*6 Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20
Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20
Movement Movement Movement Movement
Patterns 2*20 Patterns 2*20 Patterns 2*20 Patterns 2*20
Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6
75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft
25 throws at 210 ft 25 throws at 210 ft 25 throws at 210 ft 25 throws at 210 ft

Table A-5

WEEK 17

Week 17: Day 1 Week 17: Day 2 Week 17: Day 3 Week 17: Day 4

ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20
Movement Movement Patterns Movement Patterns Movement Patterns
Patterns 2*25 2*25 2*25 2*25
Global Patterns 1*3 Global Patterns 1*3 Global Patterns 1*3 Global Patterns 1*3
75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft 75 throws at 60 ft
25 throws at 240 ft 25 throws at 240 ft 25 throws at 240 ft 25 throws at 240 ft
84 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION

Table A-6

WEEK 18

Week 18: Day 1 Week 18: Day 2 Week 18: Day 3 Week 18: Day 4

ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20 ROM Exercises 1*20
Six Back 1*6 Six Back 1*6 Six Back 1*6 Six Back 1*6
Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20 Core Exercises 1*20
Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20 Base Exercises 1*20
Movement Patterns Movement Patterns Movement Patterns Movement Patterns
2*25 2*25 2*25 2*25
Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6 Global Patterns 1*6

Begin Mound Work

• Six back and global exercises remain at 1 set of 6.
• The dynamic hug and reverse fly are 1 set of 20.
• Movement patterns break into two sets. One set is
to be accomplished after the range of motion
exercises and before the other exercises. The second
movement pattern set is performed at the conclusion
of the workout.
Week 17
• Range of motion exercises remain 1 set of 20.
• Core and base exercises are eliminated.
• One set of 25 movement patterns precedes global
patterns.
• One set of 75 movement patterns follows global
patterns.
Week 18
• Return to block three format.
• Movement patterns remain at 2 sets of 25 as in the
previous week.
Add the peak activity arc (PAA) Chart (degrees)
 Appendix

3-2
Nine-Level Rehabilitation
Throwing Program

level with each outing. It is preferred that a number of

T his program is designed for athletes to work at

their own pace to develop the necessary arm
strength to begin throwing from a mound. The
athlete is to throw 2 days in a row and then rest for 1
day. It is not important to progress to the next throwing
outings at the same level be completed before progress-
ing. It is important to throw with comfort, which may
necessitate moving back a level occasionally.

Table B-1

LEVEL THROWS FEET THROWS FEET THROWS FEET

One 25 25 25 60
Two 25 25 50 60
Three 25 25 75 60
Four 25 25 50 60 25 90
Five 25 25 50 60 25 120
Six 25 25 50 60 25 150
Seven 25 25 50 60 25 180
Eight 25 25 50 60 25 210
Nine 25 25 50 60 25 240

85

Rehabilitation Protocol
Arthroscopic Repair of a SLAP
Lesion in a Throwing Athlete
U nder optimal conditions, early healing occurs
at 3 weeks and progresses to a soft union at 6
weeks. Remodeling and continued strengthen-
ing of the repair continues for 8 to 12 months in most
cases. Fine tuned athletic performance may take up to 18
months. Upper quadrant strength, flexibility, and sound
body mechanics are critical to prevent a recurrence.
Week 1: Acute Stage
• Objectives: Prevent causing a compression, traction,
or shearing force on the repaired labrum. Prevent
stress to the biceps. Prevent painful limited range of
motion. Full passive shoulder flexion should be
achieved by the end of week 3.
• Wear a sling until first postoperative visit.
• Pendulum 3 to 4 times per day in flexion/extension,
abduction/adduction.
• PROM in pain-free range followed with ice and
TENS.
• Sets and reps to the patient’s tolerance
• May perform very light pendulum exercises in
flexion/extension/abduction/adduction
Weeks 2 to 3: Stitches Removed
• Sling for sleeping and as needed during the day.
Elbow may be flexed and extended for light ADLs.
86
Appendix
3-3
Craig D. Morgan
Phillip B. Donley
• Full elbow, wrist, and hand motion for ADLs
• Rope and pulley for ROM with elbow in 90° to 45°
degrees of flexion and 90° of abduction with no
external rotation. Include pendulums.
• Increase the ROM so that by the end of 3 weeks
there is full flexion.
• Shoulder shrugs and circular rotation
• Hand and wrist isometrics and isotonics performed
in the sling
• Ice as necessary
Goals: Full Flexion, 45° of External Rotation and 15° of
Horizontal Adduction After 3 Weeks
Clinical Protocol
• In scaption, PROM stretching with gentle
contract/relax techniques in painful arc
• Week 3: Isometrics with 0° of abduction for
adduction, extension, and internal and external
rotation
• Week 3: Active assistive ROM for abduction and
flexion to 90°
• Scapular isotonics in four directions with no load on
the arm
• Passive capsular ligament stretch
• Emphasis on posterior rotator cuff mobilization
• Myofascial stretching for superficial structures of the
anterior and posterior shoulder
APPENDIX 3-3 REHABILITATION PROTOCOL
Weeks 4 to 6: Subacute Phase:
Discontinue Sling
• Continue the ROM pulley and pendulum if not full
passive flexion
• Protraction and retraction exercises
• Continue overall fitness for uninvolved arm and
lower extremities.
• Do not load the elbow.
• Stretch the posterior rotator cuff in horizontal
adduction with shoulder in 45° to 90° of flexion.
Hold only for 30 seconds.
• Wrist and hand isotonics and isometrics, avoid
loading biceps by keeping elbow in flexion. Wrist
curls: forward and reverse
Goals: Full ROM in Supine Position
• Focus on posterior rotator cuff stretching because
this may be a causative effect of an injury to the
labrum.
Clinical Protocol
• Wrist/hand strengthening without loading the
biceps
• Continue scapular isometrics in 60° to 90° of flexion
and abduction
• Full antigravity ROM with no external loads
• Isometrics: emphasize adduction and extension in
pain-free positions.
• Posture/gait training: cervical and thoracic
• Conduct closed chain rotator cuff exercises by week
6.
• Pelvic and trunk stabilization exercises
• Isotonics lower extremities
• Build endurance with stationary equipment, bicycle
• Flexibility for all body parts
Weeks 6 to 12: Intermediate Program
• Begin progressive resistive exercises with progression
to help: strengthen all upper quadrant motions and
carry light loads pain free.
• Continue progression of flexibility of posterior
rotator cuff and scapula motions
• Protect labrum with low velocity motions
• No throwing or racquet use
Goals
• Throwers should have 90° of external rotation in 90°
of abduction.
87
• At end of week 12: jogging off treadmill
• Overall body conditioning: scapula/thoracic,
wrist/hand, cervical/thoracic, lower extremities,
uninvolved extremity conditioning
• Full range of motion
Clinical Protocol
• Isotonic strengthening in all planes using free
weights and tubing. Emphasize high repetitions
with low weight in full range of motion.
• Continue to emphasize stretching of the posterior
rotator cuff and increasing scapular motion
• Begin treadmill jogging
• PNF patterns (D1 and D2) at week 10
• Stretching with contract/relax in both scaption and
neutral
• UBE with progressive endurance loads
• Start biceps loading
• Increase loads and repetitions with all activities
• Lower extremity agility and functional activities
• Internal and external rotation: multiple sets and
varying degrees of abduction
• Emphasize proprioceptive activities for the shoulder
• Pelvic and trunk stabilization
Weeks 13 to 18: Strengthening Phase
• At 16 weeks, begin tossing a ball.
• Eliminate any mechanical flaws in throwing:
coordination and timing for the entire body
Goals
• Full painless range of motion
• Strength equal to 80% of the uninvolved side
Clinical Protocol
• Pool with no overhand strokes: shoulder
press/punch, paddles or gloves, breaststroke.
• At 16 weeks, begin physioball: activities (with
shoulder rebounder if available)
• Isokinetic (45° of abduction of IR/ER) at no less
than 90° per second
• Increase free weights with machines for all planes of
shoulder with high repetitions
• Rubber tube exercises: include diagonal planes with
physioball.
• UBE in both directions with shoulder arc at 90° to
110° flexion
88 SECTION I MECHANISMS OF MOVEMENT AND EVALUATION
• Begin physioball exercises, one hand on wall dribble,
two-hand push pass, overhead pass, and lateral pass
• Begin impulse machine at 14 weeks
Weeks 18 to 24
Goals
• Return to full activity with no restrictions.
• Strength 80% to 90% of the uninjured side
Clinical Protocol
• Begin Rehabilitation Throwing Program when 75
throws can be successfully completed
• Initiate sports-specific simulation activities including
plyometrics
• Initiate isokinetic testing
• Remember: A tight posterior capsule is a primary
cause of a SLAP lesion. Maintain posterior capsule
flexibility.
Weeks 24 plus
• Full return to presurgical activities per physician’s
orders
• Preventive maintenance program
• Continue regular posterior capsule stretching
program as long as overhead motions are continued
It is VERY Important to Maintain Posterior Cuff and
Posterior Capsule Stretching while Continuing to
Perform Overhead Activities.

Differential Soft
Tissue Diagnosis
E fficient and effective patient care is always
dependent on the clinician’s ability to perform
a systematic evaluation. The evaluation serves
to identify all tissues involved in dysfunction; the current
stage and progression of the dysfunction; and the base-
line parameters on which to judge treatment efficacy.
Soft tissue diagnosis of the shoulder joint includes eval-
uation of the glenohumeral, sternoclavicular, acromio-
clavicular, and scapulothoracic articulations, as well as
the cervical spine and related upper-quarter structures.
We discuss each component of the shoulder evalua-
tion, including the patient interview, cervical screen-
ing, observation, mobility, musculotendinous strength,
palpation, and special tests. The soft tissue diagnosis is
derived from assessment of information obtained from
each component of the evaluation. The chapter con-
cludes with a case study that illustrates the ongoing
assessment process that accompanies each component
of the evaluation.
Patient Interview
The purpose of the patient interview is to identify the
patient’s symptoms, determine the history of the
patient’s current problem, identify coexisting medical
factors that may affect either the current problem or its
treatment, and establish the probable irritability level of
the problem. The irritability level is a measure of how
easily symptoms may be provoked and relieved.1 The
89
4
Robert A. Donatelli
Jacob P. Irwin
Marie A. Johanson
Blanca Zita Gonzalez-King
two major components of the patient interview are: (1)
the history of the patient’s problem(s), and (2) the loca-
tion, nature, and behavior of symptoms. It is important
to ask the patient what reproduces the pain.
History
The clinician initially must establish the onset and
progression of the patient’s problem by asking when the
problem started and how it began. The problem will
likely fall into one of two major categories: macrotrauma
or microtrauma. A macrotrauma is an injury resulting
from a specific trauma. A microtrauma is an injury
resulting from repetitive stress to tissues, and is charac-
terized by an insidious onset of symptoms. The catego-
rization of macrotraumas and microtraumas serves to
guide the clinician most efficiently through the remain-
der of the history and the physical exam.
Whenever a macrotrauma is suspected, the clinician
must determine the mechanism of injury to aid in the
identification of the injured structure(s). Awareness of
possible gross disruption of tissue, such as fractures
and dislocations, may alert the examiner to use caution
during passive range of motion and special tests, thus
preventing further trauma to the injured tissues. Many
postoperative patients may be grouped by macrotrauma
injuries.
When a microtrauma is suspected, the clinician
must identify the patient’s daily activities and postures
to determine both intrinsic and extrinsic factors that
90 SECTION I MECHANICS OF MOVEMENT AND EVALUATION

may contribute to the problem. Intrinsic factors are
physical characteristics that predispose an individual to
microtrauma injuries, such as a hooked (or type III)
acromion process2 or strength deficits of the rotator cuff
muscles.3,4 Extrinsic factors are external conditions under
which an activity is performed that predispose an indi-
vidual to microtrauma injuries, such as training errors.
The patient interview should also identify demo-
graphic information that may aid in the soft tissue diag-
nosis, and past and present medical conditions that may
affect the current problem or its treatment. Additionally,
it should be ascertained whether any current medica-
tions may mask pain or otherwise affect the patient’s
current problem. Because many disease processes may
result in referral of pain to the shoulder region (most
notably, diseases of the cardiovascular, pulmonary, and
gastrointestinal systems),5-7 the clinician can ill afford
exclusion of medical conditions that may explain shoul-
der pain (Table 4-1). Finally, the clinician should estab-
lish any previous treatment received by the patient and
its effect on the frequency and intensity of symptoms
and functional abilities.
Location, Nature, and Behavior of Pain
Defining boundaries of the patient’s pain and other
symptoms establishes the extent of the examination. All
injured structures that potentially produce pain within
the boundaries of the patient’s pain need consideration,
whether the pain is local or referred.
The nature of the pain may assist in identifying the
structures at fault. This can be determined by asking
the patient to describe the pain or symptoms. Deep,
dull, and poorly localized pain has been attributed to
visceral structures and deep ligamentous, deep muscular,
and bony structures.5 A superficial pain described
as sharp or burning in quality has been attributed to
skin, tendon, or bursal tissue.8 A patient may report
“throbbing” or “pulsing” pain when suffering from a
vascular injury. Reports of such symptoms as paresthe-
sias or numbness may indicate irritation or injury of a
nerve.
Although subjective reports of the nature of pain
are not usually reliable enough for consideration, when
combined with the location of pain some patterns may
assist in differentiating local and referred pain. Re-
ferred pain is suspected when the patient reports a deep
burning or deep aching pain with indefinite boundaries,
while local pain is suspected when the pain is superficial
within clear boundaries.8
The behavioral pattern of pain may assist in identi-
fying injured structures, and it also can predict the irri-
tability level resulting from the problem. The following
are routine questions to be asked in exploring the
behavior of pain:
1. Is the pain constant?
2. What activities or positions provoke or increase the
pain?
3. What activities and positions relieve or decrease the
pain?
4. Does the pain level vary with the time of day or
night?
Cyriax8 recommends three questions regarding the
location and behavior of pain in order to establish the
irritability level of a shoulder dysfunction:

Table 4-1

MEDICAL CONDITIONS THAT MAY REFER PAIN TO THE SHOULDER COMPLEX

Body System Right Shoulder Left Shoulder Right or Left Shoulder

Cardiovascular Typical angina pectoralis Atypical angina pectoralis

Myocardial infarction Pericarditis
(rarely may refer to
right shoulder)
Pulmonary Pleurisy
Gastrointestinal Gallstones Pancreatitis Pulmonary neoplasm
Acute or chronic Pancreatic carcinoma
cholecystitis
Hepatitis Hiatal hernia
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS
1. Does it hurt to lie on the affected side at night?
2. Does the pain extend below the elbow?
3. Is there pain at rest?
According to Cyriax,8 affirmative answers to all three
questions indicate a high irritability level. Affirmative
answers to one or two of the questions indicate a mod-
erate irritability level, while negative answers to all
three questions indicate a low irritability level. The
irritability level may be used to predict the tolerance
of the patient to subsequent evaluation and treatment
procedures.
Maitland1 recommends a specific set of questions
regarding the behavior of pain to establish the irritabil-
ity level of the problem. Once an activity or position that
provokes symptoms has been identified, the following
queries address the specific activity or position:
1. How long can the activity or position be
maintained before the pain begins or increases
(time 1 or T1)?
2. How long can the activity or position be continued
before the pain level becomes unbearable and the
activity or position must cease (T2)?
3. How long does it take for the pain to return to its
baseline level after cessation of the activity or
position (T3)?
Relatively short periods for T1 and T2, coupled with
a relatively long period for T3, indicate a high irritabil-
ity level. Conversely, relatively long periods for T1 and
T2, coupled with a relatively short period for T3, indi-
cate a low irritability level.
Mechanical-musculoskeletal pain generally varies
throughout the day and is related to activities or posi-
tions. Therefore constant pain may alert the clinician to
pain associated with a medical disease.
Cervical Screening
The prevalence and pain referral patterns associated
with cervical spine problems necessitate the inclusion
of routine screening for cervical pathologic conditions
during examination of any shoulder patient. Cervical
radiculopathy caused by irritation or compression of the
C5 spinal nerve root often results in referred pain over
the lateral aspect of the proximal arm. Because the C5
and C6 spinal nerves innervate most glenohumeral joint
structures, the lateral-proximal aspect of the arm is also
a very common pain location for a patient with shoul-
der dysfunction. (A notable exception is the acromio-
91
clavicular joint, which is innervated by the C4 spinal
nerve. An injury to this joint usually results in pain
specifically over the AC joint.) Therefore it is impera-
tive to examine every patient for both shoulder and cer-
vical dysfunction.
A cervical spine screening begins with active cervical
movements. If active movements are normal, passive
pressures are used at the end of active movements. The
clinician determines if pain is being produced during
these tests, and if so, locates the source. Compression
and distraction tests of the cervical spine can be done
to confirm suspicion of changeable shoulder pain
potentially referred from the cervical spine. Neurologic
screening may further inform the examiner of the
integrity of the cervical spinal nerves9-11 (Table 4-2) and
spinal cord. Additionally, palpation of structures within
the anterior and posterior triangles of the cervical spine
may provide information on referral of pain from
muscular structures common to the cervical spine and
shoulder complex, or from cervical articular structures.
(Palpation is discussed later in the chapter.) See Chapter
5 for further discussion of the interrelationship between
the cervical spine and the shoulder.
Observation
Observation of the patient in both static and dynamic
situations can reveal information about the patient’s
condition. The three basic components of examination
by observation are assessment of (1) symmetry, (2)
posture, and (3) dynamic activities of daily living, sports,
and work activities.
Symmetry
An assessment of symmetry can give clues to areas of
dysfunction, although the clinician must be aware that
some degree of asymmetry is normal. Generally, an
assessment of symmetry includes both soft tissue and
bony contours.
Anteriorly, the clinician can observe changes in the
thoracic inlet area (e.g., bony abnormalities of the clav-
icle, acromioclavicular, or sternoclavicular joint, or areas
of ecchymosis or edema in the supraclavicular fossa),
and in the muscle contours of the deltoid and pectoral
muscle groups. Posteriorly, muscle atrophy of the
supraspinatus, infraspinatus, and teres minor may be
seen, and gross differences may be noted in the position
of the scapula. Because of specific sports activities, some
92 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
Table 4-2
NEUROLOGIC SCREENING OF CERVICAL SPINAL NERVES
Segment Motor
C1-B2 Neck flexion
C3 Neck side bending
C4 Scapular elevation
C5 Shoulder abduction, elbow flexion
C6 Elbow flexion, wrist extension
C7 Finger extension, elbow extension
C8 Finger flexion
T1 Finger abduction
individuals may have hypertrophied muscles on their
dominant side, resulting in the appearance of muscle
atrophy on the nondominant side.
Posture
An assessment of posture includes scrutiny of the ante-
rior, posterior, and lateral views in the standing position,
and identification of the patient’s sitting and sleeping
postures.
Anterior View. From an anterior view, the clini-
cian can assess the position of the head on the neck in
the frontal and transverse planes (cervical-side bending
or rotation) and the superior-inferior position of the
glenohumeral joint. A relative inferior position of the
humeral head on one side may be seen from this view,
although atrophy of the deltoid can give a false impres-
sion of inferior subluxation.
Lateral View. From the lateral side, the positions
of the head on the cervical spine and of the cervical spine
relative to the torso may be seen; the degree of thoracic
spine kyphosis assessed; and sagittal plane position of
the glenohumeral joint (anteroposterior position of the
humeral head) observed. Two common problems most
easily seen from this view are an anteriorly displaced
position of the humeral head and forward head posture.
Forward head posture is characterized by excessively
protracted and laterally rotated scapulae, internal rota-
tion of the glenohumeral joint, increased kyphosis of the
upper thoracic spine, decreased lordosis of the midcer-
vical spine, and increased backward bending of the upper
cervical spine.12 Forward head posture is more prevalent
Sensory Reflex
Skull None
Lateral neck and jaw None
Top of shoulder None
Proximal lateral arm Biceps
Thumb and index finger Brachioradialis
Middle finger Triceps
Ulnar aspect of forearm and hand None
Medial arm None
in patients with microtrauma shoulder injuries than in
the uninjured population.13 The increase in scapular pro-
traction that occurs with forward head posture decreases
the subacromial space,14 and may predispose an individ-
ual to some shoulder dysfunctions such as impingement
syndrome.
Posterior View. From the posterior view, the clini-
cian can again ascertain the position of the head on the
cervical spine and the cervical spine relative to the torso
in the frontal and transverse planes. The positions of the
scapulae may be compared as to superior-inferior and
medial-lateral placement, and in degree of “winging.”
Scapular winging is defined as the movement of the
medial border of the scapula away from the chest wall.11
The position of the scapula can be further assessed by
palpation of the bony landmarks, such as the inferior
angle. (See the section on palpation elsewhere in the
chapter.)
Objective Clinical Measures of Scapular Position.
Diveta and associates15 evaluate protraction of the
scapulae by taking two linear measurements with a
string (Figure 4-1). The distance in centimeters from the
root of the scapular spine to the inferior angle of the
acromion (scapular width) is divided into the distance
from the third thoracic segment to the inferior angle
of the acromion (scapular protraction). The resulting
ratio provides a measurement of scapular protraction
corrected for scapular size (normalized scapular
protraction). A larger ratio indicates a greater degree of
scapular protraction.
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 93

Figure 4-1 A, Measurement of scapular width. B, Measurement of

scapular protraction.

Diveta and associates15 report good to excellent
intrarater reliability of the scapular width and scapular
protraction measurements (ICCs of 0.94 and 0.85,
respectively), and fair intrarater reliability of the normal-
ized scapular protraction measurement (ICC of 0.78).
However, some controversy in the literature regarding
the reliability of the normalized scapular protraction
measurement has subsequently emerged. Neiers and
Worrell16 report good to excellent intrarater reliability of
the scapular width and scapular protraction measure-
ments, but poor intrarater reliability of the normalized
scapular protraction measurement (ICC of 0.34). Gibson
94 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
and colleagues17 report excellent intrarater and interrater
reliability of the scapular protraction measurement (ICCs
of 0.91 to 0.95) but did not study the normalized scapu-
lar protraction measurement. Greenfield and associates13
compared the clinical method of measuring normalized
scapular protraction described by Diveta and associates15
with identical measurements taken from radiographs. No
statistically significant differences in values obtained
between the two methods were reported, lending cre-
dence to Diveta’s clinical measurement of normalized
scapular protraction. Greenfield and colleagues13 also
reported excellent intrarater and interrater reliability of
the normalized scapular protraction measurement (ICCs
of 0.97 and 0.96, respectively).
The position of the scapula in the frontal plane (rel-
ative degree of scapular abduction or lateral rotation) can
be obtained using the first of three test positions that
comprise the lateral slide test described by Kibler.18 (See
the section on musculotendinous strength elsewhere in
the chapter.)
Mobility
Examination of mobility in the shoulder complex gener-
ally begins with a scrutiny of active range of motion
(AROM) in the cardinal planes, in the plane of the
scapula, and during functional movements, followed by
passive range of motion (PROM) and accessory motion.
Information derived from mobility testing includes
extensibility of contractile and noncontractile tissues,
functional capabilities, irritability level, and differentia-
tion of muscle weakness and/or pain from joint or muscle
restrictions.
Active Range of Motion
The evaluation of AROM encompasses multiple com-
ponents of function. When AROM is limited, one or
more of the following is possible: limited joint mobility,
muscle weakness, or unwillingness of the patient to com-
plete the motion because of pain, apprehension, or other
reasons. Therefore, diagnosis of soft tissue dysfunction at
the shoulder from active movements alone is difficult, as
the examiner is unable to isolate the contribution of spe-
cific muscle groups and joints of the shoulder complex to
the limitation in movement.
Active range of motion can reveal abnormal move-
ment patterns, and can predict what functional abilities
and disabilities the patient is likely to exhibit.
Generally, AROM of the involved side is compared
to the uninvolved side, although some degree of asym-
metry may be normal. Often the dominant side exhibits
less AROM than the nondominant side.11 Conversely,
apparent symmetry in AROM may be achieved by
excessive movements in adjacent joints to compensate
for the restriction of a given joint. (See the sections on
cardinal planes and the plane of the scapula.)
Cardinal Planes. Cardinal plane active move-
ments of the shoulder complex yield less information
regarding specific patterns of joint restrictions than do
cardinal plane passive movements. However, significant
decreases in AROM compared with PROM in the car-
dinal planes can distinguish weakness or pain as a
primary functional limitation from true joint restriction.
Normal ROM in the cardinal planes is 160° to 180° of
flexion; 45° to 60° of extension; 170° to 180° of abduc-
tion; 70° to 80° of internal rotation; 80° to 90° of exter-
nal rotation; 30° to 45° of horizontal abduction; and 135°
to 140° of horizontal adduction.19
Cyriax8 advocated active abduction testing to discern
the presence of a “painful arc.” Cyriax8 defines a painful
arc as “pain encountered midrange that disappears before
the end of range” and indicates compression of subacro-
mial structures. Painful arcs are often used clinically to
assist in the diagnosis of impingement syndromes.20,21
When observing AROM, the examiner must be
careful to identify abnormal patterns of movement even
when the gross quantity of movement is normal. For
example, a patient may substitute excessive scapular
adduction for active glenohumeral external rotation in
0° of abduction (Figure 4-2), or substitute excessive
scapular elevation and external rotation for gleno-
humeral elevation during active elevation (Figure
4-3).
Plane of the Scapula. Active elevation in the plane
of the scapula offers an excellent assessment of scapulo-
humeral rhythm and scapular stability. In order to facil-
itate the evaluation of active elevation, the movement
can be grossly observed through the three phases of ele-
vation (see Chapter 2) for symmetry and the expected
biomechanical events.
Initial Phase of Elevation (0° to 60°). Some oscillation
of the scapula is normally observed through the first 30° to
60° of motion. After 30° to 60°, the scapula should stabilize
against the thoracic wall and begin to laterally rotate.
Movement of the glenohumeral joint should exceed
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 95

Figure 4-2 Excessive left scapular adduction exhibited by a patient with limited
left glenohumeral external rotation at 0° of abduction during active range of motion
testing.

Figure 4-3 Excessive left scapular elevation and external rotation exhibited by
a patient with limited glenohumeral elevation during active range of motion testing.
96 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
movement of the scapulothoracic joint through the initial
phase of elevation.4,22 An inability to complete the initial
phase of elevation most often indicates severe restrictions
of the glenohumeral joint; severe pain and/or apprehension
reported by the patient; and in rare cases severe restriction
of the sternoclavicular joint.
Middle Phase of Elevation (60° to 140°). The middle
phase of elevation is clinically the most common phase
of dysfunction. During this phase, the amount of scapu-
lar rotation exceeds the amount of glenohumeral
motion.22 Because of deltoid muscle activity, upward
shear at the glenohumeral joint peaks and is counter-
acted by activity of the rotator cuff musculature.23,24 If
scapular rotation is decreased on the patient’s involved
side, it may be due to limitation at the acromioclavicular
and/or sternoclavicular joints, which restrict clavicular
elevation and rotation. A limitation of scapulothoracic
rotation may also be due to tightness of the levator
scapulae muscle; weakness of the serratus anterior and
upper and lower trapezius muscles; or both. Weakness
of the scapular muscles, or “scapular instability,” is most
often apparent during the eccentric phase of elevation,
and may be observed as winging or excessive oscillations
of the scapula. This may become more accentuated after
multiple repetitions of elevation.
Excessive scapular rotation on the involved side may
indicate weakness of the rotator cuff muscles (inability
to counteract the upward shear of the anterior deltoid)
or restrictions of the anterior and inferior glenohumeral
capsule. During the middle phase of elevation, the pres-
ence of a painful arc may indicate impingement of sub-
acromial structures.
Final Phase of Elevation (140° to 180°). During the
final phase of elevation, movement of the glenohumeral
joint significantly exceeds that of the scapulothoracic
joint.22 Therefore, the examiner can observe a “disasso-
ciation” of the humerus from the scapula that requires
good extensibility of the teres major, subscapularis, teres
minor, and infraspinatus muscles. The pectoralis major
and the latissimus may also restrict elevation in the final
phase.
Functional Movements. Three functional move-
ments can predict the patient’s ability to perform the
activities of daily living. As with AROM, active func-
tional movements concurrently test joint mobility,
muscle strength, and willingness of the patient to com-
plete the motion.
Hands Behind Neck. Combined glenohumeral ele-
vation and external rotation, and scapular rotation into
the middle phase of elevation are required to complete
this movement. Inability to perform this movement
indicates inability to groom, shave the axilla, manipulate
overhead objects, and throw.
Hands Behind Back. Combined glenohumeral
extension, adduction, and internal rotation, and scapu-
lar distraction are required to complete this movement.
Limitation indicates the inability to fasten a brassiere,
zip clothes, tuck in shirts or blouses posteriorly, and
reach back pockets.
Hand to Opposite Shoulder. Combined gleno-
humeral flexion and horizontal adduction are required to
complete this movement. Limitation indicates an inabil-
ity to manipulate objects across the body or provide
adequate follow-through with many sports maneuvers
such as a golf swing, tennis forehand, or baseball pitch.
Passive Range of Motion
Passive range of motion allows the examiner to identify
specific restrictions at each joint, to distinguish muscle
restriction from restriction of noncontractile tissue, to
evaluate the quality of resistance at the end of the range
of motion (end-feel), and to discern patterns of restric-
tions that may indicate specific soft tissue problems.
Additionally, the probable irritability level of the patient
can be established and serve as one guide in the selec-
tion of initial stretching or strengthening techniques.
Differences in PROM between the involved and
uninvolved sides are generally good indications of
abnormal mobility. As with AROM, the examiner must
be alert for motions of the involved side that only appear
to have full mobility because of excessive motion at adja-
cent joints. For example, when the subscapularis, pec-
toralis major, and latissimus dorsi muscles lack flexibility
or when the inferior glenohumeral capsule is restricted,
the patient may substitute excessive lateral rotation of
the scapula (Figure 4-4) or excessive extension of the
trunk (Figure 4-5) to achieve full shoulder elevation.
Passive glenohumeral extension may also obscure a lim-
itation in passive glenohumeral internal rotation at 90°
of abduction (Figure 4-6). These gross adaptations may
be observed in a high level athlete such as a professional
baseball pitcher.25
Irritability Level. Cyriax8 advocates use of
the sequence of pain and resistance during passive
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 97

Figure 4-4 Excessive lateral rotation (lateral “bulge”) of the right scapula during
passive range of motion testing in abduction exhibited by a patient with glenohumeral
capsular restriction.

movement testing to establish indications and con-
traindications for stretching of a joint. If pain is encoun-
tered in the range of motion prior to resistance, a high
level of irritability is likely, and stretching is contraindi-
cated. If pain and resistance are encountered at the same
time, a moderate irritability level is likely, and any
stretching should be performed gently and with caution.
If resistance occurs during passive movement before
pain, or if no pain is encountered, then a low irritability
level is likely and the patient is expected to tolerate
stretching well. The clinical use of Cyriax’s sequence of
pain and resistance has not been well studied. One
recent study of the use of the sequence in patients diag-
nosed with osteoarthritis of the knee showed poor reli-
ability. The authors attributed this to very short intervals
between onset of pain and resistance, which precluded
clinical measurement through manual palpation.26 Reli-
ability of the pain and resistance sequence in other
patient populations is unknown.
Maitland1 also advocates a method to establish the
irritability level during PROM testing. The method is
somewhat more complex and requires the examiner to
graph the following four occurrences during PROM
testing:
1. The point in the range of motion where resistance
is first detected (resistance 1 or R1)
2. The point in the range of motion where no further
movement can be achieved due to passive resistance
(R2)
3. The point in range of motion where pain is first
reported by the patient (pain 1 or P1)
4. The point in range of motion where no further
movement can be achieved due to pain (P2)
Maitland1 asserts that when pain is the patient’s
primary problem, P1 precedes R1, and pain rather than
resistance usually limits the motion. When pain is the
patient’s primary problem, mobilization techniques to
increase joint mobility are contraindicated. Conversely,
when stiffness is the patient’s primary problem, pain may
or may not be encountered before resistance, but resist-
ance rather than pain limits the motion. When stiffness
is the patient’s primary problem, mobilization and
stretching techniques to increase mobility are indicated.
End-feel. The use and interpretation of end-feel
are controversial due to individual variation and ques-
tionable reliability.26 Cyriax8 describes 6 end-feels (3
normal and 3 abnormal) and Paris and Loubert27
98 SECTION I MECHANICS OF MOVEMENT AND EVALUATION

Figure 4-5 A, Excessive extension of the trunk during passive elevation

testing in a patient with subscapularis muscle tightness. B, Same patient after exten-
sibility of the subscapularis is restored.
 CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS
A patterns of passive restrictions may assist in the soft
B tightness is often found in patients with anterior gleno-
Figure 4-6 A, Substitution of glenohumeral extension
for glenohumeral internal rotation in a patient with restriction
of the posterior capsule. B, Same patient after extensibility of
the posterior capsule is restored.
99
describe 15 end-feels (5 normal and 10 abnormal).
However, clinicians may more simply define a normal
end-feel as an expected resistance of muscle or periar-
ticular tissue at the end of full PROM, and define abnor-
mal end-feel as an unexpected passive resistance of
intraarticular or extraarticular structure(s), or no end-
feel if pain limits PROM prior to the expected end
range.
Specific Patterns of Restrictions. Several specific
tissue diagnosis of shoulder problems. Arguably the
most often cited is Cyriax’s capsular pattern of restric-
tion that aids in the diagnosis of frozen shoulder.8 (See
the chapter on Adhesive Capsulitis.)
Frozen Shoulder or Adhesive Capsulitis. As
described by Cyriax,8 the capsular pattern of restriction
is characterized by a restriction of the glenohumeral
joint that is greatest in external rotation, lesser in abduc-
tion, and least in internal rotation. The authors have
observed a modification of Cyriax’s capsular pattern.
The greatest restriction at the glenohumeral joint is
external rotation in 0° of abduction. Abduction to 90°
combined with external rotation is the next most
restricted range. Internal rotation at 90° of abduction is
the next most restricted range and the least restricted is
internal rotation in 0° of abduction.
Tight Posterior Capsule. Limited glenohumeral
internal rotation and horizontal adduction indicate a
restriction of the posterior capsule. Posterior capsule
humeral instability with secondary impingement at the
glenohumeral joint.28
Subscapularis Muscle Tightness. Subscapularis
tightness results in a greater limitation of glenohumeral
external rotation in 0° of abduction than in 45° to 90° of
abduction.29
Middle and Inferior Glenohumeral Ligament Tight-
ness. Restriction of the middle and inferior gleno-
humeral ligaments and capsule results in greater
limitation of glenohumeral external rotation in 45° to
90° of abduction than in 0° of abduction.29
Accessory Motion
An assessment of accessory motion at the sterno-
clavicular, acromioclavicular, scapulothoracic, and gleno-
humeral joints identifies the presence and direction
of hypomobilities and hypermobilities of the noncon-
100 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
tractile structures (primarily the capsule and ligaments)
of a joint. When hypomobilities are identified,
mobilization techniques to restore the mobility may
be employed (see Chapter 17). For hypermobilities,
strengthening exercises may be employed to improve
joint stability.
Musculotendinous Strength
A careful assessment of the musculotendinous structures
is of vital importance for soft tissue diagnosis. This is
particularly true of the glenohumeral and scapulotho-
racic joints, because they function with little stability
provided by inert structures relative to other joints.
Unless contraindicated following known rupture or
surgical disruption of tendon or muscle, an assessment
of musculotendinous strength generally includes resis-
tive tests, manual muscle testing, and often scapular
stability tests. Isokinetic strength testing may also be
included if more specific information is desired regard-
ing absolute strength values, comparison of involved to
uninvolved strength values, and strength ratios of muscle
groups.
Resistive Tests
Resistive tests may be defined as isometric muscle tests
for strength and provocation of pain. Cyriax8 advocates
six resistive tests to assess shoulder dysfunction, all
performed with the glenohumeral joint in a neutral posi-
tion: shoulder adduction, abduction, external rotation
and internal rotation, and elbow flexion extension.
Many clinicians include shoulder flexion and extension
as well. According to Cyriax,8 pain that occurs during
muscle contraction is more likely to indicate a lesion
within a muscle belly, while pain that occurs upon release
of the contraction is more likely to indicate a lesion
within a tendon. Additionally, each possible combination
of pain and weakness can aid in soft tissue diagnosis
(Table 4-3).
When one or more resistive tests are strong and
painful, Cyriax8 also advocates identifying the muscle
or tendon at fault. This is done by confirming or exclud-
ing a given muscle/tendon with other resistive tests that
also activate the same contractile unit (Table 4-4).
According to Cyriax,8 resistive tests of the primary
function of a muscle are expected to produce the most
pain.
Table 4-3
DIAGNOSIS BASED ON RESISTIVE TESTS
Finding of
Resistive Test Lesion
Strong and painless Normal
Strong and painful Minor muscle lesion
Minor tendon lesion
Weak and painful Gross macrotraumatic
lesion such as fracture
Partial rupture of muscle
or tendon
Weak and painless Muscle or tendon rupture
Neurologic dysfunction
Adapted from Cyriax.8
Manual Muscle Testing
Manual muscle testing provides information regarding
the degree of resistance that a musculotendinous unit
is able to generate. The reader is referred to texts on
manual muscle testing for specific protocols.30,31 Some
of the classic manual muscle testing positions for the
shoulder musculature have been modified in recent years
in response to electromyography (EMG) studies identi-
fying positions that optimally recruit a given muscle.
Test positions for the supraspinatus muscle are one
example (see the section on special tests elsewhere in the
chapter).
Muscle imbalances are a common intrinsic factor in
shoulder microtrauma injuries.3,4 A muscle imbalance
may be defined as a weak agonist, a tight agonist, or a
combination of the two. Janda and Schmid32 and Jull and
Janda33 believe that muscles respond in a predictable
pattern to an altered state of mechanics in both micro-
trauma and macrotrauma. Jull and Janda33 developed a
classification system of skeletal muscle based on response
to dysfunction. Muscles that shorten and tighten in dys-
function are classified as postural muscles, while those
that lengthen and weaken in dysfunction are classified as
phasic muscles. This classification system can expedite
the evaluation of shoulder musculature by predicting
which muscles to routinely manually muscle test and
which to routinely evaluate for flexibility (Table 4-5).
A muscle imbalance of the rotator cuff generally
involves tightness of the subscapularis and weakness of
the infraspinatus, teres minor, and supraspinatus. This
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 101

Table 4-4

IDENTIFICATION OF SPECIFIC MUSCLE/TENDON LESION WITH RESISTIVE TESTS

Positive Resistive Findings of Additional

Test Muscle/Tendon Resistive Tests

Shoulder abduction Deltoid Positive flexion (anterior deltoid)

Positive extension (posterior deltoid)
Supraspinatus Negative flexion
Negative extension
Shoulder adduction Pectoralis major Positive flexion
Positive horizontal adduction
Teres minor Positive external rotation
Latissimus dorsi Positive extension
Positive internal rotation
Teres major Positive extension
Positive internal rotation
Shoulder external rotation Teres minor Positive adduction
Infraspinatus Negative adduction
Supraspinatus Positive abduction
Shoulder internal rotation Subscapularis Negative adduction
Pectoralis major Positive adduction
Positive horizontal adduction
Latissimus dorsi Positive adduction
Positive extension
Teres major Positive adduction
Positive extension

Modified from Cyriax.8

Table 4-5

RESPONSE OF SPECIFIC UPPER QUARTER MUSCLES TO DYSFUNCTION

Muscle Group Postural Muscles (Tighten) Phasic Muscles (Weaken)

Axioscapular muscles Upper trapezius Rhomboid major and minor

Levator scapulae Middle trapezius
Pectoralis minor Lower trapezius
Serratus anterior
Scapulohumeral muscles Subscapularis Deltoid
Supraspinatus
Infraspinatus
Teres minor
Axiohumeral muscles Pectoralis major (clavicular portion)
Cervical and stomatognathic Sternocleidomastoid Longus colli
muscles Suboccipitals Longus capitis
Scaleni Infrahyoid
Suprahyoid

Data from Janda and Schmid32 and Jill and Janda.33

102 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
results in anterior instability of the glenohumeral joint
when in a position of external rotation and abduction.34
Muscle imbalance of the scapula often involves both
tightness of the levator scapulae and weakness of the ser-
ratus anterior and lower trapezius muscles; combined,
these limit elevation of the acromion and potentially
contribute to an impingement syndrome.
Scapular Stability Tests
Normal function of the shoulder complex demands
adequate scapular stability. Thus in addition to manual
muscle testing, specific scapular stability tests may assist
in soft tissue diagnosis.
Lateral Slide Test. Kibler18 described the lateral
slide test to evaluate the function of the muscles that sta-
bilize and/or externally rotate the scapula (upper and
lower trapezius, serratus anterior, and rhomboid major
and minor). A measurement is taken from the inferior
angle of the scapula to the nearest thoracic segment in
three different glenohumeral joint positions (Figure 4-
7). Kibler18 asserts that a difference of 1 cm or greater in
the second and third positions is associated with micro-
trauma injuries of the shoulder. Gibson and associates17
studied the reliability of the lateral slide test by measur-
Figure 4-7 Lateral slide test. Measurement of distance from inferior angle of
scapula to the nearest thoracic segment. A, Patient’s arms resting at sides.
ing with a string from the T8 segment to the inferior
angle of the scapula, and reported intrarater ICCs of
0.81 to 0.94 and interrater ICCs of 0.18 to 0.69. There-
fore, although a useful measurement for each clinician,
the lateral slide test may not be suitable for comparison
between clinicians.
Functional Tests of Scapular Winging. Direct
observation of scapular winging is not possible in the
classic supine position for manual muscle testing of the
serratus anterior muscle.30,31 The examiner may observe
scapular winging caused by weakness of the serratus
anterior muscle by observing active elevation (see the
section on mobility elsewhere in this chapter), wall
push-ups (Figure 4-8), or sitting press-ups (Figure 4-9).
Proprioception And
Kinesthesia
Until recently, proprioceptive and kinesthetic abilities
received more attention in rehabilitation of lower
extremity injuries than upper extremity injuries. Propri-
oception is defined as the ability to perceive position,
weight, and resistance of objects in relation to the body.
Kinesthesia is defined as the ability to sense the extent,
Continued
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 103

Figure 4-7 cont’d B, Patient’s hands on hips (thumbs pointing posteriorly).

C, Glenohumeral joints 90°47,53 abducted and internally rotated.
104 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
Figure 4-9 Sitting press-up. Patient with long thoracic
nerve palsy exhibits severe winging of left scapula.
Figure 4-8 Wall push-up.
Patient with mild left serratus anterior
muscle weakness exhibits mild winging
of left scapula.
direction, or weight of body movement. In addition to
visual, vestibular, and cutaneous input, receptors in the
joint capsule, ligaments, and labrum provide proprio-
ceptive and kinesthetic information.
Published studies on shoulder proprioceptive and
kinesthetic testing have used specialized testing appara-
tus.35,36 Davies and Dickoff-Hoffman37 advocate clinical
angular joint replication testing with an electronic digital
inclinometer. For normal males, they report average
mean differences of plus or minus 2.4° to 3.0° for seven
shoulder joint positions between known angles and
subject replication of known angles.
Because proprioception and kinesthesia are compro-
mised following anterior shoulder dislocation,35,38
exercises designed to improve proprioception and kines-
thesia seem logical—at least in rehabilitation of macro-
traumatic injuries that are likely to disrupt the capsular,
ligamentous, or labral structures.
Palpation
Direct manual palpation of specific structures is
performed to evaluate tissue tension, structure size,
temperature, swelling, static position, crepitus, and
provocation of pain. A systematic procedure for palpa-
tion of tissues is advised to facilitate an efficient, yet
comprehensive, evaluation. In general, palpation of the
anterior and posterior cervical triangles may be more
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 105

Table 4-6

PALPATION OF UPPER QUARTER STRUCTURES

Soft Tissue Injury

Region Structure or Postural Fault Finding

Anterior cervical Suprahyoid muscles FHP Tight, TPs

triangle Infrahyoid muscles FHP TPs
Anterior tubercles of FHP Tender (insertion of anterior scalene)
transverse processes
Longus colli FHP TPs
Posterior Sternocleidomastoid muscle FHP Tight, TPs
cervical Anterior and middle scalene FHP Tight, TPs
triangle muscles TIS Tight, tender, edema
FHP
First rib FHP Elevated, tender
Upper trapezius muscle Scapular instability
Tight, TPs
Cervical facet joints Facet strain
Posterior tubercles of FHP Tight, TPs
transverse processes Tender, edema, thickened
Scapular protraction Tender (attachment of levator scapulae
muscles)
Clavicle Elevated

FHP, Forward head posture; TP, trigger point; TIS, thoracic inlet syndrome.

important in patients with postural abnormalities, while Glenohumeral Stability Tests

palpation of glenohumeral articular structures may be
more important when glenohumeral macrotrauma is
suspected. Because many structures of the shoulder
complex are normally tender to palpation, comparison
of findings to the uninvolved side is crucial. Addition-
ally, similar palpation findings are common to many
shoulder dysfunctions, so palpation may be the least
valuable component in diagnosis of soft tissue dysfunc-
tion. Structures commonly palpated by region are shown
in Tables 4-6 and 4-7, along with the possible dysfunc-
tion(s) when palpation findings are positive.
Special Tests
Special tests may be included in evaluation of the shoul-
der complex to confirm or exclude the presence of spe-
cific shoulder soft tissue dysfunctions. In this section we
describe the more commonly performed special tests for
glenohumeral instabilities, labral tears, impingement
syndrome, musculotendinous dysfunctions, and rupture
of the transverse humeral ligament.
Glenohumeral stability tests are performed to assess the
integrity of the capsular and ligamentous structures. The
tests may be used to confirm both unidirectional and
multidirectional instabilities.
Apprehension Test. The patient is placed in a
supine position. The shoulder is then positioned in
90° of abduction and full external rotation (Figure
4-10). The examiner provides overpressure into
external rotation. Provocation of pain and apprehension
indicates anterior instability.39-41 The apprehension test
may also be performed with the patient in a sitting
position.
Jobe Subluxation Test. The patient is placed in a
supine position. The arm is then positioned off the edge
of the examining table and the glenohumeral joint is
placed in 90° of abduction and 90° of external rotation
(Figure 4-11). The examiner grasps the patient’s forearm
with one hand to maintain the test position and the
posterior humeral head with the other hand. The exam-
iner then gently applies an anteriorly directed force to
 Table 4-7

PALPATION OF STRUCTURES OF THE SHOULDER COMPLEX

Soft Tissue Injury or

Region Structure Postural Fault Finding
Scapular region Acromion process Impingement syndrome Tender
Inferior angle of scapula Scapular elevation or protraction
Suprascapular notch Scapular abduction Elevated
Spine of scapula Lateral
Levator scapulae insertion Scapular protraction
on scapula Suprascapular nerve entrapment Elevated
Supraspinatus muscle Scapular protraction Tender
Infraspinatus and teres FHP Excessively angled in
minor muscles Cervical strain frontal plane
Quadrangular space Tight, TPs
Rhomboid major/minor muscles Decreased scapular rotation
Lower trapezius muscle All rotator cuff pathologies Tight, TPs
Suprascapular nerve entrapment Tight
Anterior instability Atrophy
All rotator cuff pathologies Atrophy
Supraspinatus nerve entrapment
Anterior instability Atrophy
Atrophy
Axillary nerve entrapment Atrophy (infraspinatus)
Scapular instability Atrophy
Scapular instability Tender
Atrophy, TPs
Atrophy
Axillary region Pectoralis major muscle Scapular protraction Tight
Pectoralis minor muscle Tight
Coracoid process Frozen shoulder Tight, tender, TPs
Subscapularis muscle Scapular protraction
Scapular protraction Tender (insertion of
TIS pectoralis minor)
Muscle imbalance rotator cuff Tender
Tight, tender, TPs
Articular Sternoclavicular joint Dislocation Malalignment
structures AC joint Sprain
Coracoacromial ligament Dislocation Tender
Coracoclavicular ligaments Malalignment
Humeral head Sprain
Lesser tubercle humerus Impingement syndrome Tender
Greater tubercle humerus Tender
Long head biceps tendon AC joint sprain
AC joint sprain Tender
Anterior subluxation Tender
Positioned anteriorly
Tight posterior capsul Positioned anteriorly
Tight subscapularis
Tender
Subscapularis bursitis Tender
Impingement syndrome Tender, thickened
Subacromial bursitis
Supraspinatus or infraspinatus Tender, edema, thickened
tendonitis Tender, thickened
Tender, edema, thickened
Bicipital tendinitis

FHP, Forward head posture; TP, trigger point; TIS, thoracic inlet syndrome; AC, acromioclavicular.
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 107

Figure 4-10 Apprehension test.

the posterior humeral head. Pain and apprehension indi-

cate a positive test for anterior instability.42 Provocation
of pain without apprehension may denote either primary
impingement or mild anterior instability with secondary
impingement.42

Jobe Relocation Test. This test may aid in the dif-

ferentiation of a primary impingement from a primary
instability with a secondary impingement.42 The shoulder
is positioned in 90° of abduction and 90° of external
rotation, which is identical to the apprehension test. If
pain and apprehension are provoked, the examiner then
applies a posteriorly directed force to the anterior aspect
of the humeral head (Figure 4-12). Reduction of pain
and apprehension while “relocating” the humeral head
posteriorly is considered a positive test, and indicates
primary anterior instability rather than primary
impingement.

Anterior Release Test. The anterior release test is

performed with the patient in the supine position and
the affected shoulder over the edge of the examining
table. The patient’s arm is abducted 90° while the exam-
iner places a posterior force with his or her hand on the
patient’s humeral head. The posterior force his or her
maintained while the patient’s arm is brought into
extreme external rotation (Figure 4-13, A). Then the
Figure 4-11 Jobe subluxation test. humeral head is released (Figure 4-13, B). The test is
 Figure 4-12 Jobe relocation test.

A B

Figure 4-13 Anterior release test.

CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS
positive if the patient experiences sudden pain or a
distinct increase in pain, or if the patient’s symptoms are
reproduced. The anterior release test is a reliable and
reproducible test for the detection of an unstable
shoulder.43
Glenohumeral Load and Shift Test. The patient is
seated and the examiner is positioned behind the patient
on the ipsilateral side (Figure 4-14). The examiner sta-
bilizes the scapula with the proximal hand and grasps
the humeral head with the distal hand. The humeral
head is directed superiorly and medially to approximate
the glenoid fossa “loaded.” While maintaining the
loaded position, both anterior and posterior stresses are
applied and the amount of translation is noted.41,44
Abnormal displacement of the humerus may be catego-
rized as follows:
1. 5 to 10 mm of displacement: the humeral head rides
up the glenoid slope, but not over the rim.
Figure 4-14 Glenohumeral load and shift test.
109
2. 10 to 15 mm of displacement: the humeral head rides
up and over the glenoid rim, but spontaneously
reduces when stress is removed.
3. More than 15 mm of displacement: the humeral head
rides up and over the glenoid rim and remains
dislocated when the stress is removed.
Sulcus Sign. The patient is seated with the arm at
the side in a neutral position (Figure 4-15). The exam-
iner applies a distraction force to the humerus.45 Exces-
sive inferior translation with a sulcus defect between the
acromion and humeral head indicates a positive test. The
patient may report a subjective response of subluxation
as well. The sulcus sign is indicative of multidirectional
instability and is reported in centimeters of humeral
head displacement from the inferior surface of the
acromion.
Sulcus Sign at 90°. The patient is in a seated posi-
tion and the arm is abducted to 90° and placed on the
Figure 4-15 Sulcus sign.
110 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
Figure 4-16
examiner’s shoulder (Figure 4-16). The examiner applies
a caudal force to the proximal humerus. Excessive
inferior translation with the sulcus defect between the
humeral head and acromion constitutes a positive test
and indicates inferior glenohumeral instability.46
Labral Integrity Tests
Labral tests are performed to detect tears in the anterior
or superior labrum. Several studies have been published
that demonstrated the reliability and validity of special
tests for labral tears. The recently published studies for
labral integrity tests include the Crank test, the
O’Brien’s test, the New Pain Provocation test, and the
Biceps Load test.
Clunk Test. The patient is supine and the humerus
is shifted anteriorly and posteriorly while simultaneously
circumducting the humerus and bringing the humerus
into full abduction (Figure 4-17). During these maneu-
vers, a “clunk” sound and pain, usually located between
90° of abduction and full abduction (anteroinferior
aspect of glenohumeral joint), are positive clinical signs
of a Bankart lesion.47,48
Crank Test. The patient is supine and the humerus
is elevated in the plane of the scapula 160°. The elbow
is flexed to 90° and the examiner applies a compressive
force to the glenohumeral joint through the long axis of
Sulcus sign at 90°.
the humerus and forearm. As the compressive force is
applied with one hand, the other hand is applying exter-
nal rotation, (Figure 4-18, A) and internal rotation
(Figure 4-18, B) of the humerus. The test is positive if
pain, with or without a click, is produced (usually with
external rotation). The patient experiences pain or
“catching” during athletic or work activities. The crank
test is highly accurate for the diagnosis of glenoid labral
tears.41,49
Active Compression Test—O’Brien’s. The patient
is requested to stand with the arm at 90° of flexion,
adducted 10° to 15°, with the elbow fully extended. The
arm is internally rotated so that the thumb points down.
The examiner then applies a downward force to the arm.
With the arm in the same position, the palm is fully
supinated and the maneuver is repeated. The test is con-
sidered positive if painful clicking is elicited with the
first maneuver and reduced or eliminated with the
second maneuver. The examiner asks the patient if the
painful clicking is deep (labral abnormality SLAP) or
superficial pain (acromioclavicular joint strain)50
(Figures 4-19 and 4-20).
New Pain Provocation Test. The patient is sitting
with the arm held at 90° to 100° of abduction, the elbow
is in 90° of flexion, and the shoulder is externally rotated
by the examiner. The examiner moves the forearm from
 Figure 4-17 Clunk test.

A B

Figure 4-18 Crank test.

112 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
Figure 4-19 Active compression test—O’Brien’s.
Position one arm adducted 10° to 15° thumb down.
supination (Figure 4-21, A) to pronation (Figure 4-21,
B). The new pain provocation test is considered positive
for a superior labral tear (SLAP) when pain is elicited
with pronation of the forearm or when pain is
more severe in pronation than with the forearm in
supination.51
Superior Labrum Anteroposterior (SLAP) Lesion
Test-Speeds Test. The patient is sitting with the
humerus in 90° of abduction, the elbow extended, and
the forearm fully supinated. Resistance to abduction
is applied (Figure 4-22). Pain, a clunking sound, or
pseudo-catching may implicate a SLAP lesion with a
possible tear of the long head of the biceps tendon.46,52
Biceps Load Test. The shoulder is placed at 90° of
abduction, externally rotated; the forearm is supinated.
The patient is asked to flex the elbow against the resist-
Figure 4-20 Active compression test—O’Brien’s.
Position two arms adducted 10° to 15° supination of forearm.
ance of the examiner (Figure 4-23). The test is consid-
ered positive if the patient complains of pain during
the elbow flexion. The biceps load test is an effective
diagnostic test for SLAP lesions.53,54
Impingement Tests
Impingement tests are designed to approximate the
greater tubercle of the humerus and the acromion,
thus compressing the subacromial structures. Common
special tests that assist in the confirmation of a diagno-
sis of impingement syndrome include the locking test,
the Neer and Welsh impingement test, and the Hawkins
and Kennedy impingement test.
Locking Test. As described by Maitland,55 the
examiner stabilizes and depresses the scapula with the
proximal hand while the distal hand internally rotates
and slightly extends the humerus. The humerus is then
A B

Figure 4-21 New pain provocation test. External rotation of shoulder, elbow 90° flexion, forearm supinated.

Figure 4-22 Superior labrum anteroposterior (SLAP)

lesion test. New pain provocation test—forearm pronated.
114 SECTION I MECHANICS OF MOVEMENT AND EVALUATION

Figure 4-23 Biceps load test.

Figure 4-24 Locking test.

abducted until firm joint resistance is detected (Figure of the greater tuberosity and the acromion (Figure 4-
4-24). Provocation of pain indicates a positive test or 25).57 Pain implicates impingement of the supraspinatus
impingement of the supraspinatus tendon.49 and long head of the biceps tendons.

Neer and Welsh Impingement Test. The patient is Hawkins and Kennedy Impingement Test. The
seated while the examiner stands. Scapular external rota- patient may either be sitting or standing. The humerus
tion is blocked with one hand while the other hand is placed in 90° of flexion and then internally rotated
raises the arm in forced flexion, causing approximation (Figure 4-26).52,58 The maneuver is accomplished by
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS
Figure 4-25 Neer and Welsh impingement test.
exerting force through the forearm to bring the distal
glenohumeral joint into internal rotation. Pain impli-
cates supraspinatus tendon impingement.
Yocum’s Test for Impingement. The patient may be
either sitting or standing. The humerus is placed in 90°
of flexion and the patient is asked to place his or her hand
on the opposite shoulder. The examiner then elevates the
arm by forcing the elbow into elevation. The patient can
also actively elevate the elbow while maintaining a hand
on the opposite shoulder (Figure 4-27). Pain implicates
impingement of suprahumeral structures.59
Musculotendinous Unit Tests
Musculotendinous unit tests are designed to identify
dysfunction of specific muscles and tendons. Tests
specifically for bicipital tendinitis include Yergason’s
test and Ludington’s test. The supraspinatus tests,
Gerber’s lift off test, and Patte’s test serve as resistive
115
Figure 4-26 Hawkins and Kennedy impingement
test.
tests that isolate the rotator cuff muscles, thereby eval-
uating both musculotendinous strength and pain provo-
cation. The Gilcrest sign and the Drop Arm test both
assess the function of multiple muscles and tendons.
Yergason’s Test. The patient is seated, the elbow is
placed in 90° of flexion, and the forearm is pronated
(Figure 4-28). The examiner palpates the long head of
the biceps tendon with the proximal hand while resisting
supination and elbow flexion with the distal hand.52,60
Provocation of pain over the anteromedial aspect of the
shoulder is a positive sign of bicipital tendinitis.
Gilcrest Sign. The Gilcrest sign evaluates the
eccentric activity of the biceps, supraspinatus, and
deltoid muscles. The patient fully flexes the arm while
holding 5 lb, and then lowers the arm in the frontal plane
in an externally rotated position (Figure 4-29). Pain and
 Figure 4-28 Yergason’s test.
Figure 4-27 Yocum’s test.

Figure 4-29 Gilcrest sign.

CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS
inability to control the arm motion are positive signs
of dysfunction of the long head of the biceps, the
supraspinatus, or the deltoid muscle.52,61
Ludington’s Test. The patient’s hand is placed on
top of the head, forcing the glenohumeral joint into
abduction and external rotation (Figure 4-30). The
Figure 4-30 Ludington’s test.
Figure 4-31
117
patient contracts the biceps muscle isometrically by
pressing the hand against the head. Symptom repro-
duction in the bicipital groove is a positive sign for bicip-
ital tendinitis.52,62
Drop Arm Test. The patient may be either seated
or standing. The arm is passively raised above 90° of
abduction. The patient then actively lowers the arm to
90° of abduction in internal rotation (Figure 4-31). If
the patient’s arm approaches 90° and “drops,” the test is
positive for a full-thickness rotator cuff tear.63,64
Supraspinatus Test. The humerus is placed in 90°
of elevation in the plane of the scapula and full internal
rotation (Figure 4-32). The examiner applies resistance
to elevation while the patient attempts to maintain the
position.65,66 The examiner then grades the strength of
the supraspinatus muscle and notes any pain provoked
by the test.
Alternate Supraspinatus Test. The patient is
prone, with the arm to be tested resting off the side of
the plinth. The patient horizontally abducts the arm at
100° of abduction in external rotation and the examiner
applies resistance at the end of the range (Figure 4-33).67
The examiner then grades the strength of the supra-
spinatus muscle.
Drop arm test.
118 SECTION I MECHANICS OF MOVEMENT AND EVALUATION

Figure 4-32 Supraspinatus test.

Figure 4-33 Alternate supraspinatus test.

CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS
Gerber’s Lift Off Test. The patient is asked to
place the hand against the back at the level of the waist
with the elbow in 90° of flexion. The examiner pulls the
hand away from the back approximately 5 to 10 cm while
maintaining the 90° bend in the elbow. The patient is
then asked to hold the position without the examiner’s
help. The test is positive if the patient cannot hold the
position, detecting a rupture of the subscapularis tendon.
The test is also positive for pain and/or weakness of the
subscapularis as the examiner applies force attempting
to push the hand to the back (Figure 4-34).59,68
Patte’s Test for Infraspinatus and Teres Minor.
The examiner supports the patient’s elbow in 90° of
forward elevation in the plane of the scapula while the
patient is asked to rotate the arm laterally against resist-
ance by the examiner (Figure 4-35).59,69
Figure 4-34 Gerber’s test.
119
There are three types of responses for the supraspina-
tus test, Gerber’s test, and Patte’s test: (a) absence of
pain, indicating that the tendon is normal; (b) the ability
to resist despite pain, denoting tendinitis; (c) the inabil-
ity to resist with gradual lowering of the arm or forearm,
indicating tendon rupture.
Transverse Humeral Ligament Tests
Special tests are also prescribed to identify ruptures of
the transverse humeral ligament. One common test is
the Lippman test.
Lippman’s Test. The patient’s elbow is placed in
flexion and the examiner palpates the long head of the
biceps tendon within the bicipital groove (Figure 4-36).
The examiner then attempts to displace the long head
of the biceps tendon by exerting lateral and medial
Figure 4-35 Patte’s test.
120 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
Figure 4-36
manual forces to the tendon.11 Ability to displace the
tendon from the bicipital groove indicates a rupture of
the transverse humeral ligament. A sharp pain without
tendon displacement indicates bicipital tendinitis.
Clinical Tests for Rotator Cuff Rupture
Lag Signs
ERLS—The External Rotation Lag Sign. The
patient is sitting with his or her back to the examiner.
The elbow is flexed to 90° and the shoulder is elevated
to 20° in the POS and near maximum external rotation
(-5° to avoid elastic recoil in the shoulder). The patient
is then asked to actively maintain the position of exter-
nal rotation when the examiner releases the wrist while
maintaining support of the limb at the elbow (Figure 4-
37, A,B). The magnitude of lag is recorded to the near-
est 5°.70
The Drop Sign—Infraspinatus. The patient is
seated with his or back to the examiner, who holds the
affected arm at 90° of elevation in the POS and
maximum external rotation, with the elbow flexed to 90°
(Figure 4-38, A,B). In this position the maintenance of
the external rotation position is a function of the infra-
spinatus.70 The patient is asked to actively maintain this
position as the examiner releases the wrist while sup-
Lippman test.
porting the elbow. The sign is positive if a lag or drop
occurs. The magnitude of the lag is recorded to the
nearest 5°. Both the ERLS and the drop sign are posi-
tive if a massive rotator cuff tear is present.
Internal Rotation Lag Sign—Subscapularis. The
patient is seated with the arm placed behind the back and
the dorsum of the hand resting on the lumbar region.
The examiner passively lifts the hand away from the
lumbar region while maintaining the internal rotation of
the shoulder. The patient is then asked to actively main-
tain this position as the examiner releases the wrist while
supporting the elbow (Figure 4-39, A,B). The magnitude
of the lag is then recorded. An obvious drop of the hand
may occur with large tears of the subscapularis.70
Case Study
This case study demonstrates the use of each
component of evaluation on a specific patient. A general
plan of care concludes the case study. However, the
reader is referred to subsequent chapters for more
specific descriptions of treatment programs. Although
specific diagnoses are withheld until the exam is com-
plete, assessment is an ongoing process and therefore a
summary of ongoing assessments is included following
each portion of the evaluation.
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 121

A B

Figure 4-37 ERLS—the external rotation lag sign. Integrity of the supraspinatus and infraspinatus.

GENERAL DEMOGRAPHICS: PMH:

The patient is a 47-year-old English speaking, Cau-
casian female with left shoulder pain.
SOCIAL HISTORY:
She is married and has two teenage children that live
at home. She does not smoke and drinks less than once
per week. She walks approximately 1 mile every other
day.
EMPLOYMENT AND ENVIRONMENT:
A.S. is a flight attendant, which requires overhead
lifting of heavy baggage.
GROWTH AND DEVELOPMENT:
She has no abnormalities and is left-hand dominant.
LIVING ENVIRONMENT:
A.S. lives in a two-story home with her husband and
two children.
The patient has a 20-year history of irritable bowel
syndrome for which she takes an antispasmodic med-
ication (Bentyl). She also reports occasional bilateral
neck pain and stiffness for which she takes Advil. No
other problems are reported.
History of Chief Complaint:
The patient reports an onset of left shoulder pain
beginning approximately 4 months ago. She is unable
to identify a specific mechanism of injury. Her routine
activities include carrying and storing luggage as a part
of her occupation, and recreational tennis and swim-
ming. The patient moved to a new home with a swim-
ming pool 6 months ago and began swimming laps
(free-style) two or three times per week. The patient
describes the arm pain as aching in nature and the
122 SECTION I MECHANICS OF MOVEMENT AND EVALUATION

A B

Figure 4-38 The drop sign. Integrity of the infraspinatus.

scapular pain as tightness and soreness. The arm pain
is intermittent. The pain is provoked by swimming,
serving and backhand strokes in tennis, reaching behind
her back, and lifting luggage overhead for storage while
working. She reports waking with aching in the left arm
after sleeping on the shoulder. During freestyle swim-
ming, the pain begins towards the end of her 30-minute
swim, but does not stop her from finishing. Resting the
arm by the side eases the pain after about 10 minutes.
The patient reports pain over the lateral aspect of the
proximal half of the arm. The pain never extends below
the elbow or above the subacromial area. Some discom-
fort in the medial left scapular area extends distally to
the T4 level, proximally to the C5 level, does not cross
the midline, and extends laterally to the acromial area
of the scapula. The patient normally alternates between
sleeping on the right and left sides, with the arm in an
adducted position. She now attempts to stay mainly
on the right side because she awakes with discomfort
when lying on her left side. Arm swing during ambula-
tion is normal. The patient keeps the left shoulder
near its neutral position when donning or doffing
clothing to avoid a combination of abduction and exter-
nal rotation. A videotape of her tennis lessons taken
by her coach demonstrates lack of follow-through on
her tennis forehand and poor positioning for her
backhand.
Medications:
She is currently taking a nonsteroidal anti-
inflammatory medication (Daypro) for her shoulder
problem, and reports some improvement in her symp-
toms with this medication.
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 123

A B

Figure 4-39 Internal rotation lag sign. Integrity of the subscapularis.

Conclusions Based on Patient Interview:
1. The pain stems from microtrauma, based on the
history of the problem’s onset and the introduction
of a new activity (swimming) 2 months before the
onset of pain.
2. Irritability level is generally low because the patient
meets only one of Cyriax’s8 three criteria for high
irritability, and because she reports a relatively long
T1, no T2, and relatively short T3, based on Mait-
land’s1 criteria.
3. The coexisting medical problem of irritable bowel
syndrome is not known to refer pain to the shoul-
der and is unlikely to need further consideration.
Coexisting cervical symptoms need special atten-
tion during the subsequent examination, owing to
common referral of pain to the shoulder region and
common involvement in upper-quarter dysfunction.
4. Progressive degenerative joint dysfunctions are
common in the patient’s age group.
5. Improper biomechanics of tennis strokes may be
either an extrinsic factor in her dysfunction or a
compensation for the dysfunction.
Cervical Screening:
Compared to left rotation and left-side bending, cer-
vical right rotation and right-side bending are slightly
limited, with reports of stiffness at the end range.
Forward bending is full with stiffness at end range.
Backward bending, left rotation, and left-side bending
are within normal limits. Passive overpressures into cer-
vical right rotation and right-side bending provoke mild
124 SECTION I MECHANICS OF MOVEMENT AND EVALUATION

discomfort on the left side of the midcervical region, but Functional movement tests demonstrate the ability
there is no left-arm or scapular pain. Cervical compres- of the patient to put her left hand behind her neck,
sion does not provoke pain. although there is mild arm discomfort during the
Conclusions Based on Cervical Screening: maneuver. The patient is unable to put her hand behind
1. Muscle tightness or cervical facet restriction is her back (left thumb reaches the sacroiliac joint com-
likely, limiting right cervical rotation and right-side pared to the T7 segment on the right side), and is unable
bending. to put her left hand on the opposite shoulder. She
2. Cervical spine tests do not reproduce left-arm or reports left lateral arm pain during both maneuvers.
scapular symptoms. Passive Range of Motion:
3. Palpation of the anterior and posterior triangles of Cardinal plane PROM of the left glenohumeral joint
the cervical spine should be included in the palpa- exhibits limitation of internal rotation to 60° (Figure 4-
tion portion of the examination. 40) and horizontal adduction to 115°. External rotation
Observation of Symmetry and Posture: in 0° of abduction is slightly limited compared to the
Anteriorly, a slight left head tilt and mild atrophy of right side. Other motions are full, with mild left lateral
the left deltoid can be observed. Laterally, moderate arm pain at the end range of external rotation in 90° of
forward head posture, apparent excessive protraction of abduction.
the left scapula, and a slight anterior position of the left During passive internal rotation, resistance is
humeral head are noted in comparison to the right side. encountered prior to pain—and resistance, not pain,
Posteriorly, a slight left head tilt, a slight depression of
the left scapula, and mild atrophy of the left infraspina-
tus and teres minor muscles are observed.
Clinical Measure of Scapular Position:
A measurement of scapular protraction using the
method described by Diveta et al15 (Figure 4-1) demon-
strates an 0.5 cm difference in scapular protraction that
is greater on the left side.
Conclusions Based on Observation:
1. Forward head posture supports the previous deci-
sion to include evaluation of the upper quarter in
the ongoing assessment.
2. Left head tilt supports the previous assessment of
possible left-cervical facet or muscular tightness.
3. The 0.5 cm difference in scapular position is
unlikely to be clinically significant.
4. Depression of the left scapula is likely normal
because this is the patient’s dominant side.
Active Range of Motion:
Cardinal plane movements exhibit limitation in
internal rotation and horizontal adduction to 50° and
110°, respectively, with pain at end ranges over the lateral
arm. A painful arc is present during active abduction.
In the plane of the scapula, normal glenohumeral to
scapulothoracic rhythm is observed during concentric
activity through all three phases of elevation. After seven
or eight repetitions, some mild winging of the left
scapula and some oscillations of the left scapula are seen
in the middle phase of elevation during eccentric Figure 4-40 Passive testing for internal rotation in
activity. the POS and relocation (posterior glide) of the humeral head.
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS
prevents further movement. During passive horizontal
adduction, pain and resistance are encountered concur-
rently at 110°. Pain and muscle guarding (rather than
joint resistance) are felt to further limit movement at
115°.
Accessory Motions:
When compared with the right side, anteroposterior
gliding of the left humerus is mildly restricted and pos-
teroanterior gliding is slightly increased. During acces-
sory mobility testing, caution is taken to begin the tests
with the humeral head in a neutral position, because the
patient’s left humeral head is slightly anteriorly posi-
tioned when compared to the right side. If this care is
not taken, a false-positive restriction of the anterior
capsule and a false-positive laxity of the posterior
capsule may result. Passive scapular distraction is slightly
limited on the left.
Conclusions Based on Mobility:
1. Limited active and passive internal rotation and
horizontal adduction of the glenohumeral joint
indicate tightness of the posterior capsule.
2. With repeated movements, apparent scapular insta-
bility during the eccentric phase of elevation in the
plane of the scapula may indicate weakness of the
scapular rotators and/or stabilizers.
3. Limitations of functional movements indicate that
the patient is unable to perform daily activities such
as fastening a brassiere, tucking in blouses posteri-
orly, or performing tennis strokes with correct body
mechanics. The functional movement limitations
correlate to AROM findings of limited gleno-
humeral internal rotation and horizontal adduction.
4. PROM findings indicate that joint restriction,
rather than muscle weakness or pain, primarily
limits glenohumeral internal rotation and horizon-
tal adduction. The PROM findings correlate with
the functional movement limitations.
5. Irritability level is low (based on internal rotation
PROM) and moderate (based on horizontal adduc-
tion PROM), using the method of assessing irri-
tability from either Cyriax8 or Maitland.1
6. Posterior capsule tightness and mild anterior
capsule laxity may predispose the patient to an
impingement syndrome.28
7. A muscle imbalance of the rotator cuff is likely due
to probable tightness of the subscapularis muscle
(based on the PROM limitation of external rota-
tion in 0° of abduction concurrent with full external
125
rotation in 90° of abduction), and the slight restric-
tion of passive scapular distraction.
Midline Resisted Tests:
Resisted shoulder external rotation and abduction are
weak without pain.
Manual Muscle Testing:
Significant findings during manual muscle testing are
as follows:
Left Right
H external rotators 4/5 4+/5
GH abductors 4/5 (pain) 4/5
Supraspinatus 3+/5 (pain) 4/5
Serratus anterior 4/5 5/5
Lower trapezius 4/5 (pain) 5/5
Scapular Stability Testing:
During the third component of the lateral slide test,18
a 1.5 cm greater measurement is obtained on the left side
(see Figure 4-7). Mild left scapular winging is observed
during wall push-ups (see Figure 4-8).
Isokinetic Testing:
The shoulder external and internal rotators are tested
in 30° of elevation in the plane of the scapula to avoid
pain that may be encountered if tested in 90° of abduc-
tion. Test speeds of 60° and 180° per second are chosen.
The peak torque ratio of the external rotators to inter-
nal rotators is 40% on the left and 60% on the right at
60° per second.
Conclusions Based on Musculotendinous Strength
Testing:
1. According to Cyriax,8 weak and painless resistive
tests indicate a muscle or tendon rupture or neuro-
logic dysfunction (see Table 4-3). However, based on
this patient’s generally low irritability level and rela-
tively high functional level, it is most likely that the
neutral position for resistive testing does not provoke
the patient’s pain, and that muscle atrophy rather
than gross macrotrauma explains the weakness.
2. There is a muscle imbalance of the rotator cuff
based on the weakness of the external rotators and
supraspinatus found with resistive tests, manual
muscle testing, and isokinetic testing, combined
with the previous finding of probable subscapularis
muscle tightness.
126 SECTION I MECHANICS OF MOVEMENT AND EVALUATION
3. The patient exhibits weakness and instability of
the scapular muscles based on the lateral slide test,
manual muscle testing, and previously observed
oscillations of the scapula during the middle phase
of elevation (with repeated testing of eccentric
activity).
Palpation:
There are no significant findings to palpation of the
structures within the anterior triangle of the cervical
spine. Palpation of the posterior triangle of the cervical
spine reveals tightness and tenderness of the left ante-
rior and middle scalene muscles; tightness and trigger
points of the left upper trapezius muscle; and tenderness
of the left posterior tubercles of the transverse processes
of C3 and C4.
During palpation of the scapular region, positive
findings included a depressed left acromion and inferior
angle of the scapula; tightness, tenderness, and trigger
points at the insertion of the left levator scapulae muscle;
and atrophy of the left supraspinatus, infraspinatus, and
teres minor muscles. At the axillary region, mild tight-
ness and trigger points are palpable over the left sub-
scapularis muscle. Palpation of the articular structures
shows tenderness over the anterior aspect of the left
acromion; a slightly anteriorly positioned left humeral
head; tenderness over the lesser and greater tubercles of
the left humerus; and tenderness over the left long head
of the biceps tendon.
Conclusions Based on Palpation:
1. The findings support previous conclusions of
imbalance of the rotator cuff muscles and
mild anterior subluxation of the left humeral
head.
2. Tenderness over the greater and lesser humeral
tubercles, anterior acromion, and long head of the
biceps tendon is consistent with impingement
syndrome.
3. Tightness and tenderness of the levator scapulae;
anterior and middle scalene; and upper trapezius on
the left are consistent with forward head posture;
left head tilt; limited left cervical rotation and side
bending; and subjective tightness at the end range
of cervical flexion.
Special Tests:
Stability test results are a positive left apprehension
test, a positive relocation test, and a mildly positive
left anterior load-shift test. The Neer and Welsh50
and Hawkins and Kennedy51 impingement tests are
positive. In this case, the locking test48 is deferred due
to painfully restricted glenohumeral internal rotation
PROM. The supraspinatus test57,58 is positive for pain
and weakness. The Gilcrest sign is also positive on the
left.47,53
Conclusions Based on Special Tests:
1. The previous assessment of slight laxity of the
anterior glenohumeral joint capsule is further sup-
ported by the load-shift test.
2. Impingement tests are positive.
3. The apprehension and relocation tests suggest that
the patient’s impingement is secondary to a mild
anterior glenohumeral subluxation.39-41
4. Pain and weakness of the supraspinatus support the
findings of impingement and muscle imbalance of
the rotator cuff.
5. Positive Gilcrest sign may suggest the involvement
of both the long head of the biceps tendon and the
supraspinatus tendon in the impingement syndrome.
Assessment:
1. Microtrauma injury characterized by anterior sub-
luxation of the glenohumeral joint with secondary
impingement.39-41
2. Intrinsic factors in this patient’s microtrauma injury
include muscle imbalance of the rotator cuff (weak-
ness of the posterior cuff muscles results in failure
to counteract the upward shear of the deltoid
muscle);23,24 tightness of the posterior glenohumeral
capsule and mild laxity of the anterior gleno-
humeral capsule (decreases the subacromial space);28
and weakness of the scapular external rotators
(weakness of the lower trapezius and serratus ante-
rior muscles may alter the plane of the surface of
the glenoid and change the length-tension relation-
ship of the rotator cuff muscles).
3. Extrinsic factors in this patient’s microtrauma
injury include initiation of a freestyle swimming
program (repetitive elevation in internal rotation
that may predispose to impingement), recreational
tennis (tennis serves involve positioning of the
shoulder in combined abduction and external rota-
tion, and combined flexion and internal rotation),
and an occupation that requires overhead lifting.
Treatment:
Sequential treatment goals and a general treatment
plan to accomplish the goals are shown in Table 4-8. The
reader is referred to subsequent chapters for specific
treatment programs.
CHAPTER 4 DIFFERENTIAL SOFT TISSUE DIAGNOSIS 127

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Interrelationship of
the Spine, Rib Cage,
and Shoulder
O ne of the most difficult and challenging
aspects of the orthopedic physical therapist’s
work is to determine the primary tissue
responsible for their patients’ complaints of pain, or the
nociceptive generator. This is particularly true when
evaluating the shoulder. Pain and dysfunction in the
shoulder may arise from intrinsic pathologic conditions
in the shoulder or extrinsic pathologic conditions in the
spine, rib cage, or viscera. The therapist needs to recog-
nize that pain may be referred directly to the shoulder
from cervical, thoracic, or rib injuries, and that dysfunc-
tions anywhere in the spine or rib cage can precipitate
and exacerbate shoulder dysfunction. For these reasons,
it is important to understand the interrelationship
between the spine, ribs, and shoulder. Central sensitiza-
tion also plays an important role in the maintenance of
chronic shoulder pain and dysfunction. This chapter
reviews the musculoskeletal, biomechanical, postural,
occupational, and neurologic relationships between the
spine, ribs, and shoulder. It will also briefly review
musculoskeletal syndromes that contribute to pain and
dysfunction in the shoulder. In addition, the chapter
will review spine and rib injuries that are capable of
causing shoulder pain and dysfunction. Finally, this
chapter closes with a case study to illustrate the impor-
tant preceding concepts.
133
5
John C. Gray
Ola Grimsby
Musculoskeletal Relationship
One of the most direct relationships between the spine
and the shoulder girdle is through muscle, tendon,
and fascial attachments. Seven muscles of the shoulder,
the rotator cuff group plus the deltoid, teres major,
and latissimus dorsi, are thought to be related morpho-
logically. Their origins appear to be from cervical
myotomes.1
Shoulder Muscles and Fascia With a Direct
Relationship to the Spine
The trapezius muscle originates from the medial third
of the superior nuchal line and the external protuber-
ance of the occipital bone. The muscle also extends from
the ligamentum nuchae and spinous processes of the
seventh cervical and all of the thoracic vertebrae and the
intervening supraspinal ligament (Plates 5-1 and 5-2).2,3
Insertion for this muscle is the lateral third of the
clavicle, the medial border of the acromion, and the
upper border of the crest of the spine of the scapula.2,3
The trapezius assists in suspending the shoulder girdle;
pulling or extension movements of the arm; abduction
of the arm; and upward rotation of the scapula.2,3 With
the shoulder fixed, the trapezius may bend the head and
neck posterolaterally.2,3
134 SECTION II NEUROLOGIC CONSIDERATIONS
The latissimus dorsi muscle originates medially from
tendinous fibers that attach to the lower six thoracic
spines. The muscle also originates from the thora-
columbar fascia, which has attachments to the lumbar
and sacral spines; supraspinous ligaments; and the pos-
terior portion of the iliac crest (see Plate 5-1).2,3 It also
originates, via muscular attachments, from the outer lip
of the iliac crest; the lower three or four ribs; and the
inferior angle of the scapula.2,3 This broad muscle sub-
sequently inserts into the floor of the intertubercular
groove of the humerus.2,3 The latissimus dorsi muscle is
active in adduction, extension, and medial rotation of
the humerus.2,3 It helps support the weight of the body
during ambulation on crutches and is typically active
with swimming, pulling movements, coughing, sneez-
ing, and deep inspiration.2,3
The levator scapulae muscle originates via four sep-
arate tendons from the transverse processes of the first
three or four cervical vertebrae (see Plate 5-1).2,3 The
origin of this muscle often has various accessory attach-
ments that may include the mastoid process, occipital
bone, first or second rib, scaleni, trapezius, and serrate
muscles.3 It inserts into the medial border of the scapula
from the superior angle to the spine.2,3 The levator
scapulae works with the rhomboids to control scapula
motion and to stabilize the position of the scapula. The
levator scapulae, working with the rhomboids and pec-
toralis minor muscles, assists in the downward rotation
and depression of the scapula. It works with the trapez-
ius and assists in elevation of the scapula.3 With the
distal attachments to the scapula fixed, the levator
scapulae will produce ipsilateral side bending of the
cervical spine.3
The rhomboideus minor muscle originates from the
lower part of the ligamentum nuchae, the spinous
process of the last cervical and first thoracic vertebrae,
and the associated segment of the supraspinal ligament
(see Plate 5-1).2,3 It inserts into the medial border of
the scapula at the root of the scapular spine.2,3 The
rhomboideus major muscle originates from the spinous
processes of the second to the fifth thoracic vertebrae
and the corresponding segment of the supraspinous lig-
ament.2,3 It inserts into the medial border of the scapula
below its spine.2,3 The rhomboideus minor and major
muscles work together with the serratus anterior muscle
to hold the scapula firmly to the chest wall.2,3 The
trapezius and rhomboid muscles are the primary movers
for scapula retraction.2,3 Rotating and depressing the
scapula requires the coordinated efforts of the rhom-
boids, levator scapulae, and pectoralis minor muscles.2,3
The deep cervical fascia, internal to platysma, is
fibroareolar tissue between muscles, viscera, and vessels.3
Its superficial layer is continuous with the ligamentum
nuchae and periosteum of the seventh cervical spine.3 It
covers the trapezius and sternocleidomastoid muscles
and adheres to the symphysis menti and the body of
the hyoid bone.3 The deep fascia is attached to the
acromion, clavicle, and manubrium sterni, fusing with
their periostea (see Plate 5-2).3
Shoulder Muscles With a Direct
Relationship to the Rib Cage
The sternocleidomastoid (SCM) muscle originates from
the lateral aspect of the mastoid process and, by a thin
aponeurosis, to the lateral half of the superior nuchal line
(Plate 5-3).3 It inserts into the upper anterior surface of
the manubrium sterni and the medial third of the clav-
icle.3 The SCM muscle side bends the head ipsilaterally
and rotates it contralaterally.3 It also assists in flexion of
the cervical spine.3 With the head fixed, the muscles
work together to aid thoracic elevation and inspiration.3
The suprahyoid muscles (i.e., digastric, stylohyoid,
mylohyoid, and geniohyoid) are important in that they
work in coordination with the infrahyoid muscles (i.e.,
sternohyoid, sternothyroid, thyrohyoid, and omohyoid),
which have direct attachments to the shoulder girdle.
(See Plate 5-3.)3 The suprahyoid muscles are active in
mandibular depression, hyoid elevation, swallowing, and
chewing.3 The infrahyoid muscles are active in hyoid
depression, elevation and depression of the larynx,
speech, and mastication.3 The omohyoid, one of the
infrahyoid muscles, has two bellies that meet at an angle
as an intermediate tendon (see Plates 5-1, 5-2, and 5-
3). The superior belly originates from the lower border
of the hyoid bone and descends into the intermediate
tendon.3 This tendon is ensheathed by a band of deep
cervical fascia that descends to the clavicle and first rib.3
The inferior belly descends from this tendon to attach
to the upper scapular border, near the scapular notch,
and occasionally to the superior transverse scapular lig-
ament.3 Its actions include hyoid depression with pro-
longed inspiratory efforts and tensing of the lower deep
cervical fascia.3
The pectoralis major muscle originates from the
sternal half of the clavicle, a region approximating the
first through seventh ribs along half of the anterior
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
sternum and costal cartilages, and the aponeurosis of
the abdominal external oblique (see Plates 5-1 and
5-2).2-4 Variations include a slip of muscle that blends in
with the SCM. The insertion site for this muscle is the
lateral lip of the intertubercular sulcus along the upper
anterior portion of the humerus.2-4 The pectoralis major
muscle primarily adducts and internally rotates the
humerus. It can also assist in flexion of the shoulder, in
deep inspiration, and in supporting the weight of the
body during ambulation on crutches.2-4
The pectoralis minor muscle originates from the
superior margins and outer surfaces of ribs three to five
(sometimes ribs two to four) near the cartilage and from
the fascia overlying the respective intercostal muscles
(Plate 5-4) (see also Plate 5-2).2-4 The insertion site for
this muscle is the medial border and superior surface of
the coracoid process of the scapula.2-4 Variations include
insertion extending along the coracoacromial ligament
or along the coracohumeral ligament to the humerus.
The pectoralis minor muscle primarily tilts the scapula
anteriorly and assists the serratus anterior in bringing
the scapula forward around the thorax. Along with the
levator scapulae and the rhomboids, the pectoralis minor
will assist in rotating the scapula and depressing the
shoulder.2-4 The pectoralis minor muscle may also assist
in extreme inspiration.
The subclavius muscle originates from the junction
of the first rib and its cartilage, anterior to the costo-
clavicular ligament, and inserts on the inferior surface
of the middle third of the clavicle (see Plates 5-2 and
5-4).2,3 Variations include insertion extending to the
coracoid process. The subclavius muscle may participate
in pulling the shoulder down and forward. It may also
be active in stabilizing the clavicle against the sterno-
clavicular disk.2,3
The serratus anterior muscle originates from the
outer surfaces and superior borders of the upper 8 to
10 ribs (see Plates 5-1 and 5-4).2-4 Variations include
a blended origin with the external intercostals or the
abdominal external oblique muscle. A blended insertion
with the levator scapulae muscle has also been noted.
The insertion site for this muscle is the costal surface of
the medial border of the scapula.2-4 The serratus ante-
rior muscle primarily abducts and rotates the scapula so
that the glenoid fossa faces superiorly; will assist in ele-
vation or depression; is able to move the thorax posteri-
orly when the humerus is fixed (push-up); and may assist
in forced inspiration.2-4
135
The platysma is a broad muscular sheet that spreads
from its fascial attachments over the upper parts of the
pectoralis major and deltoid muscles and ascends medi-
ally across the clavicle to the side of the neck.3 Attach-
ment sites include the symphysis menti, lower border of
the mandibular body, lateral half of the lower lip, and
muscles at the modiolus near the buccal angle.3 The
platysma wrinkles the nuchal skin obliquely; may assist
in mandibular depression; helps express horror and sur-
prise; is active in sudden deep inspiration; and is notably
contracted in sudden violent efforts.3
Fascia of the Shoulder With a Direct
Relationship to the Rib Cage
The clavipectoral fascia, underneath the clavicular
portion of the pectoralis major, fills in the gap between
the pectoralis minor and subclavius muscles. (See Plate
5-2.)2,3 The fascial attachments include the clavicle, sur-
rounding the subclavius muscle and blending with the
deep cervical fascia that connects the omohyoid to the
clavicle; the first rib and the fascia over the first two
intercostal spaces; the coracoid process; and the axillary
fascia.2,3 Special features of this fascia include the costo-
coracoid membrane, which lies superior and medial to
the pectoralis minor muscle; the costocoracoid ligament,
with attachments from the coracoid process to the first
rib; and the suspensory ligament of the axilla, which lies
inferior and lateral to the pectoralis minor muscle (see
Plate 5-2).2,3 The axillary fascia blends with the fascia of
the serratus anterior muscle and the brachial fascia.2
This fascia blends anteriorly with the pectoral and
clavipectoral fascia; it blends posteriorly with the fascia
of the scapula muscles.2
Bones of the Shoulder With a Direct
Relationship to the Rib Cage
Clavicle. The clavicle is attached to the rib cage via
fascia (as noted above), the sternoclavicular joint capsule
and associated ligaments (see Plate 5-2).5 The ster-
noclavicular joint is sellar and contains a fibrocartilagi-
nous disk. Ligamentous attachments of the clavicle to
the sternum and first rib include the anterior and pos-
terior sternoclavicular ligaments; the interclavicular lig-
ament, which is continuous with the deep cervical fascia;
and the costoclavicular ligament that attaches to the first
rib and its costal cartilage.5
Scapula. The scapulothoracic articulation, though
not a true joint, has been described as a functional joint
136 SECTION II NEUROLOGIC CONSIDERATIONS
because of its close interaction with the rib cage.6 The
main components between the scapula and the ribs (ribs
2-7 in the resting position) are the scapulothoracic
bursa, the serratus anterior muscle, and the subscapularis
muscle.6 The scapula does, however, have direct fascial
and ligamentous connections to the rib cage: the costo-
coracoid membrane and the costocoracoid ligament (see
Plate 5-2).
Biomechanical Relationship
The shoulder is designed to be extremely mobile. One
of its primary functions is to allow the hands to be used
to their greatest advantage. All movements of the shoul-
der involve the direct or indirect participation of the cer-
vical, thoracic, and lumbar spine, and ribs (Figure 5-1).
Most of the movement of the shoulder occurs between
the head of the humerus and the glenoid fossa, with
notable and important contributions from the sterno-
clavicular, acromioclavicular, scapulothoracic, and
subdeltoid joints. What is often less appreciated is the
motion that must occur throughout the spine and rib
cage in order for the shoulder and upper extremity to
attain the maximum amount of reach possible. It is
important for clinicians to realize that the spine (cervi-
cal to lumbar) and ribs are not held completely rigid
during active flexion or abduction of the arm. Although
it is well known that distal mobility (shoulder/upper
extremity) requires proximal stability (spine/rib cage),
proximal stability does not preclude carefully controlled
motion of the spine and ribs.
Lifting the arm from the side of the body and up
overhead, abduction (normal range of 180°) involves all
the joints of the shoulder. The primary muscles involved
are the trapezius, levator scapulae, serratus anterior,
deltoid, and rotator cuff muscles. The rhomboid major
and minor muscles simulate the activity of the middle
trapezius and are most active in abduction as a stabiliz-
ing synergist via eccentric contraction during upward
rotation of the scapula.7 A force couple is formed using
the upper trapezius and upper serratus anterior muscles
to produce upward rotation and elevation of the
scapula.7 These two muscle segments, in concert with
the levator scapulae muscle, will also support the shoul-
der against the downward pull of gravity.7 A second force
couple, active in the same task, uses the lower trapezius
and lower serratus anterior muscles.7
Besides the activity of muscles originating from the
spine, direct involvement of the joints of the spine occurs
with end range (usually greater than 150°) of abduction.
As the shoulder and arm are abducted beyond approxi-
mately 150°, there is a component motion of contralat-
eral side bending (usually coupled with rotation in the
opposite direction) and extension of the thoracic spine.8
When both arms are raised, there is a necessary increase
in the lumbar lordosis through activity of the lumbar
erector spinae muscles.8 Lumbar lordosis may also be
increased secondarily to a tight latissimus dorsi muscle.
Full flexion of the shoulder is usually achieved in concert
with extension of the thoracic and lumbar spine and
with some degree of elevation and expansion of the ribs
towards the end of range of motion (ROM). Persons
with adhesive capsulitis, or other chronic conditions that
limit shoulder mobility, will necessarily put more stress
on regions of their spine (cervical, thoracic, and lumbar)
and ribs in order to achieve the ROM they need for a
particular task. If any particular task is repeated over and
over in this manner, then hypermobilities or overuse
injuries may occur in the spine or ribs. The thora-
columbar junction, especially during repeated overhead
activities, is particularly vulnerable to overuse stress in
this manner. During functional activities of daily living
(ADL), the mobility of the spine and ribs is as impor-
tant as mobility in the shoulder for a particular task or
activity to be successful (see Figure 5-1). If normal
mobility is not present in the spine and ribs, then more
stress may be directed at the shoulder to complete the
task. Again, if any particular task is repeated over and
over in this manner, then hypermobilities, impingement,
or overuse injuries (bicipital or rotator cuff tendinosis)
may occur in the shoulder.
To ensure full functional recovery of the shoulder and
prevent future overuse or overstrain injuries, it is impor-
tant to treat all relevant spine and rib dysfunctions that
may be placing excessive stress and strain on the tissues
of the shoulder. It is not enough to simply measure
the gross osteokinematic motion of the shoulder. It
is also necessary to know how the shoulder gets to its
end ROM. You must also know what is happening
arthrokinematically in the relevant joints of the spine and
ribs. Even though your patient may appear to have
normal AROM at the shoulder, they may have
thoracic and rib hypomobilities that have resulted in
the development of glenohumeral hypermobility. Or
conversely, they may have hypomobility in their
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 137

A B

Figure 5-1 Activities of daily living that demonstrate

the shoulder’s dependency on the spine and ribs for normal
C
pain-free function.
138 SECTION II NEUROLOGIC CONSIDERATIONS
glenohumeral joint and be compensating with a thora-
columbar hypermobility. In addition, it is not enough to
simply evaluate your patient’s ability to achieve full
goniometric AROM in a static posture. Their ability to
achieve full functional ROM during repeated ADL,
work, sports, and hobbies should also be of great concern.
Postural Relationship
A forward head and rounded shoulder posture can be
common among healthy persons that do not have phys-
ical complaints.9 Unfortunately, poor posture can also be
a source of neck and shoulder pain.9-13 Normal postural
alignment, starting at the external auditory meatus of
the skull, will allow a line of gravity to pass through the
odontoid process, anterior to the axis of motion for
flexion and extension of the occiput; posterior to the
midcervical spine; through the glenohumeral joint; ante-
rior to the thoracic spine; and posterior to the lumbar
spine (Figure 5-2).14
A B
Figure 5-2 Normal postural alignment in standing.
In a person with good postural alignment, elevation of
the arm is free to proceed through a full 160° to 180° of
motion without impingement of soft tissues in the sub-
acromial space (Figure 5-3, A). In the patient with the
classic forward head, rounded shoulders, and increased
thoracic kyphosis, the scapula rotates forward and down-
ward, depressing the acromion process and changing
the direction of the glenoid fossa. Now as the patient
attempts to elevate the arm, the supraspinatus tendon
and/or the subdeltoid bursa may become impinged
against the anterior portion of the acromion process (see
Figure 5-3, B). Repeated motions of this nature may
accelerate overuse injuries or cumulative trauma disor-
ders and lead to early changes consistent with tendinitis
and/or bursitis.15 At least one study has found a signifi-
cant relationship between severe thoracic kyphosis and
Figure 5-3 Elevation of the arm. A, Person with good
postural alignment. B, Same person, now demonstrating the
effect of poor posture on elevation of the arm.
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 139

interscapular pain; forward head and interscapular pain;
and rounded shoulders and interscapular pain.9
Sitting postures with the whole spine flexed will
result in high levels of electromyographic (EMG) activ-
ity in the neck and shoulder muscles. Neck and shoul-
der muscle activity is lowest in a sitting posture of slight
thoracolumbar extension with a vertical cervical spine
(Figure 5-4).16 Standing postures associated with a
forward head will demonstrate an increase in the cervi-
cal and lumbar lordosis, and an increase in thoracic
kyphosis. In addition, the forward head posture forces
the midcervical spine into hyperextension, with subse-
quent narrowing of the intervertebral foramina and
increased weight bearing of the facet joints, especially at
the C4-5 and C5-6 segments (Figure 5-5).11,17 This may
lead to irritation of the C5 and C6 spinal nerve roots,
respectively.11,17,18 It may also lead to irritation of the
dorsal root of C1, vertebral artery symptoms, or
entrapment of the suprascapular and dorsal scapular
nerves.19 Headaches are a common sequelae of chronic
poor posture. One source of these headaches is the
increased stress on the C2-3 facet joints and the associ-
ated intervertebral foramen. Headaches originating
from the C2-3 facet joints or the C3 dorsal ramus are
fairly common in patients with chronic neck pain and
headaches.20,21
The cervical facet joints are at risk because of the
increased weight bearing stress encountered in the
forward head posture. The articular cartilage, synovial
capsule, and meniscoid of the facet joint will be exposed
to persistent and recurrent trauma.22 This may lead to
arthritic changes and restrictions within the involved
joints.22 Any injury or irritation to these facet joints will
contribute, via type I mechanoreceptor damage, to dis-
orders involving the static postural reflexes of the spine
and upper extremities.23,24 Finally, the intervertebral

A B

Figure 5-4 Sitting postures. A, Poor sitting posture at a workstation. B, Good postural alignment with the
appropriate use of ergonomic design for a person seated at a visual display terminal.
140 SECTION II NEUROLOGIC CONSIDERATIONS
Figure 5-5 Schematic of a forward head posture
resulting in nerve and facet joint compression with increased
shearing at the disks.
disks are put at risk because of the increase in shearing
as a result of increasing the cervical lordosis (see Figure
5-5). The normal lordosis in the cervical spine allows for
an adequate balance of compressive forces with shear-
ing. If the spine were to straighten, then there would be
greater compressive forces and lesser shearing on the
disks.
Additional consequences of the forward head posture
are a shortening of the sternocleidomastoid, upper
trapezius, and levator scapulae muscles, which will result
in an elevated scapula.19,25 The subsequent increase in
thoracic kyphosis will abduct the scapula, allowing for
a lengthening of the rhomboids and lower trapezius
muscles in association with a shortening of the serratus
anterior.19 In addition, this posture will cause shorten-
ing of the latissimus dorsi, teres major, subscapularis,
and pectoralis major and minor muscles, which will pull
the humerus into an internally rotated position.19 This
posture will alter the normal scapulohumeral rhythm
and may precipitate impingement within the subacro-
mial space (subdeltoid bursa, biceps tendon—long head,
and/or supraspinatus tendon) during elevation of the
arm (see Figure 5-3, B).19 An abducted scapula may have
additional sequelae, such as increased acromioclavicular
joint compression, a shortened conoid ligament with a
lengthened trapezoid ligament, and a posterior glide of
the proximal clavicle that results in a shortening of the
anterior capsule of the sternoclavicular joint.19
Scoliosis will also affect the postural relationship of
the scapula to the spine. The scapula will be elevated on
the convex side and depressed on the concave side of the
scoliosis.14 There may also be a slight winging over a rib
hump secondary to ipsilateral rotation of the spine at
that level.14 For example, left side bending will normally
be accompanied by right rotation in the erect thoracic
spine, so that the right scapula will be elevated and
winged slightly.
Occupational Relationship
The spine and the shoulder are inseparable with regard
to their coordinated functions in job-related tasks.
Holding a prolonged and abnormal posture of the neck
and shoulder is a major cause of cumulative trauma
disorder (CTD).26,27 Cumulative trauma disorder in-
volves repetitive microtrauma to specific musculoskele-
tal tissues over a period of time at a faster rate than the
body can heal itself.26 If the damage continues to exceed
the repair process, then it will eventually lead to pain,
decreased work performance, and loss of function.26 Jobs
that require sustained elevation of the arms may cause
supraspinatus tendinitis because of the compression of
the humeral head against the coracoacromial arch as
the head of the humerus migrates cranially because of
rotator cuff fatigue, and as a result of sustained tension
in the muscle that can inhibit venous circulation.28
Bicipital tendinitis can occur with similar working pos-
tures because of repeated friction between the synovial
sheath of the tendon (long head) and the lesser tuberos-
ity of the humerus.28 The physical work demands that
lead to CTD are repetitive motion and holding a sus-
tained posture (Figure 5-6).26,27 Forward head posture is
a major risk factor in CTD.26 The shifting forward of
the weight of the head makes the neck and upper back
muscles work harder.26 This stressful posture can upset
nerve control and circulation to the arms.26 Poor posture
is as much a problem in CTD as is repetitive motion.26
Repetitive motion jobs are often carried out in pro-
longed sitting or standing positions.26,27 The posture
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 141

A B

C D

Figure 5-6 Examples of occupations that require repetitive or sustained postures of the shoul-
der and spine. A, Administrator. B, Administrative assistant. C, Carpenter. D, Electrician.
Continued
142 SECTION II NEUROLOGIC CONSIDERATIONS
E F
Figure 5-6, cont’d. E, Mechanic. F, Musician.
assumed by the neck and shoulder determines how well
the arm, wrist, and hand will tolerate the demands of
work.27
The neck and shoulder are dynamic structures that
are mobile by design.26 The neck and shoulder, however,
are often required to perform static work as the hands
perform a skilled task (see Figure 5-6).26,27,29 Maintain-
ing a sustained work posture of the neck, in associa-
tion with repetitive movements of an elevated shoulder,
can restrict circulation to the working tissues of the
arm and hand.29 This can be a major hurdle for persons
trying to return to work following a musculoskeletal
injury. Patients with chronic neck and shoulder pain,
following a whiplash injury in a motor vehicle accident
for example, have shown a decreased ability to achieve a
normal increase in blood flow to the upper trapezius
muscle during progressive workloads.30 Myofascial dis-
orders of the trapezius, sternocleidomastoid, or infra-
spinatus muscles are capable of referred autonomic
phenomena, including vasoconstriction.31 Jobs that
require holding a sustained posture for a prolonged
period of time can restrict circulation to working tissues,
resulting in early fatigue and a slower rate of repair of
microtraumas to the musculoskeletal system.26
Occupational neck and shoulder disorders are usually
the result of prolonged flexion and/or abduction of
the shoulders, repetitive arm work, high-speed work,
poor head posture, and a maintained static muscle
load.12,18,27,28,32-34 A high level of static muscle activity is
one reason for the high incidence of neck and shoulder
disorders in persons working with cash registers or com-
puter keyboards.12,27,33,34 Working in a posture with the
shoulder flexed and/or abducted will increase the EMG
activity levels in the upper trapezius, cervical, and tho-
racic erector spinae muscles.16,27,32 One solution is to
have the cashier stand rather than sit, which will put
less stress on the trapezius, infraspinatus, and thoracic
erector spinae muscles.27 When seated at a desk or table,
the forward head posture may be secondary to one or
more of the following: a seat height that is too high, a
table or visual display terminal height that is too low,
and/or a seat that is too far away from the table (see
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 143

Figure 5-4, A).32 For computer keyboard operators,
ergonomically designed chairs with foot and arm rests
are available (see Figure 5-4, B). The top portion of the
visual display terminal should be at eye level.
Ergonomic solutions to CTD include correcting
both sitting and standing posture (see Figure 5-2);
adjusting seat, table, and visual display terminal heights
to allow for a supportive posture (see Figure 5-4, B);
brief but frequent rest periods throughout the workday;
light exercise during breaks to keep the blood flowing
freely to all tissues; balancing repetitive motions of ADL
or sports that simulate job duties, with appropriate
periods of rest; and training the worker’s body to become
fit—like an athlete—through exercise, nutrition, and
rest to withstand the daily stress on the job.
coccygeal) of spinal nerves.35 The cervical spinal nerve,
or mixed spinal nerve, is formed by the convergence of
the dorsal and ventral spinal nerve roots close to the
intervertebral foramina (Figure 5-7).35 The ventral root
is composed primarily of efferent (80% motor, 20%
sensory) somatic fibers that carry motor impulses to the
voluntary muscles.35 These somatic fibers, or axons, orig-
inate from nerve cell bodies located in the ventral horn
of the spinal cord. The corresponding cervical interver-
tebral disk and uncovertebral joint are in close proxim-
ity to the ventral nerve root (Figure 5-8).35 The dorsal
nerve root is entirely sensory and conveys afferent
impulses back to the dorsal horn of the spinal cord from
somatic, visceral, and vascular sources.35 The cell bodies
of these afferent fibers, or axons, are located in the spinal

Neurologic Relationship
The shoulder is tied to the spine neurologically via
sensory, motor, and sympathetic relationships. Each of
these relationships will be evaluated in greater detail
throughout this section and the rest of the chapter.
The spinal cord is surrounded by meninges (dura
mater, arachnoid mater, and pia mater), which at the
level of the foramen magnum are directly continuous
with those covering the brain.35 The spinal cord is a seg-
mented structure, as indicated by the attachments of 31 Figure 5-7 Anatomy of the dorsal and ventral nerve
pairs (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 roots in a typical cross-section segment of the cervical spine.

Figure 5-8 Anatomy of the

pathway of the mixed spinal and the recur-
rent meningeal nerve in a typical cross-
section of the cervical spine.
144 SECTION II NEUROLOGIC CONSIDERATIONS
ganglia of the dorsal root.35 The dorsal root ganglia is
oval and usually located between the perforation in the
dura mater, by the dorsal root, and the intervertebral
foramina (see Figure 5-8).35 The first and second cervi-
cal ganglia, however, are on the vertebral arches of the
atlas and axis, respectively.35 The cervical facet joints are
in close proximity to the dorsal nerve roots (see Figure
5-7).
As the mixed spinal nerve emerges from the inter-
vertebral foramina it immediately diverges into several
nerve branches. The recurrent meningeal (sinuvertebral)
nerve divides off of the mixed spinal nerve just as it exits
the intervertebral foramina (see Figure 5-8).22,35-37 The
recurrent meningeal nerve then receives input from
the grey rami communicans.22,35-37 This nerve, now a
mixture of sensory and sympathetic nerves, returns back
through the intervertebral foramina to innervate the
dura mater, walls of blood vessels, periosteum, ligaments,
uncovertebral joints, and intervertebral disks in the ven-
trolateral region of the spinal canal.22,23,35-37 Occasionally,
branches of the recurrent meningeal nerve will innervate
the dorsal dura, periosteum, and ligaments.22,35-37
After leaving the intervertebral foramina, the mixed
spinal nerve divides into dorsal (posterior) and ventral
(anterior) rami (see Figure 5-8).22,35 Near its origin, each
ventral ramus receives a grey ramus communicans from
the corresponding sympathetic ganglion.22,35 The dorsal
ramus of the cervical spinal nerves divides, except the
first cervical, into medial and lateral branches to supply
the muscles and skin of the posterior regions of the
neck.22,35,36 The medial branch is also distributed to
the capsules of the cervical facet joints, where it relays
afferent input from fibers of type I, II, and III encapsu-
lated mechanoreceptors and the type IV unencapsulated
nociceptors back to the dorsal horn of the spinal
cord.23,36,38
The type I receptors are most abundant in the joint
capsules of the cervical facet joints, shoulder, and hip.39
The actual number of active type I receptors may decline
more rapidly in elderly patients or those who have suf-
fered repeated traumas because of the superficial loca-
tion of these mechanoreceptors within the joint capsule.
One study did show a higher density of type II versus
type I mechanoreceptors in the cervical spine.38 The
subjects (n = 3) were few, however, and they were either
deceased or had suffered traumatic cervical spine injuries
previous to the time of the study.38 Type I receptors fire
impulses for up to 1 minute (slowly adapting) after
stimulation and are activated by deformation in the
beginning or end range of tension for the capsule.23 The
type I receptors produce tonic reflexogenic effects on the
neck and limb muscles, postural (low threshold) and
kinesthetic sensation, and pain inhibition.23,38-40
The type II receptors, which are located deep in the
joint capsule, fire an impulse for one-half second (rapidly
adapting) after stimulation and are activated by defor-
mation in the beginning or midrange of tension for the
joint capsule.23 These receptors are most abundant in the
ankle and foot, wrist and hand, and temporomandibu-
lar joints.39 Type II receptors are responsible for dynamic
(phasic) reflexogenic effects on the muscles of the trunk
and limbs.23,38-40 They also provide information on joint
acceleration and deceleration (low threshold).39 Type II
mechanoreceptors may also be activated to inhibit pain.
Type III receptors are also dynamic mechanorecep-
tors. Within the facet joint capsules of the cervical spine,
these receptors are found at the junction between the
dense fibrous capsule and the loose areolar subsynovial
tissue.38 These mechanoreceptors may also be found in
ligaments and tendons.38,39 They have a high threshold
for activation and are very slow to adapt.38,39 The type
III mechanoreceptors have the lowest density in the
facet joint capsules of the cervical spine when compared
with types I and II.38
The type IV receptors are responsible for transmit-
ting impulses that eventually reach the higher centers of
the brain for perception as painful stimuli.39 These noci-
ceptors may be activated by trauma or chemical stimu-
lation (mediators of inflammation).23 In addition, the
three encapsulated mechanoreceptors (types I to III) can
produce a noxious stimulus in response to excessive joint
motion.39
The cervical ventral rami supply the anterior and
lateral portions of the neck.22,35 The third cervical ventral
ramus appears between the longus capitis and the
scalenus medius.22,35 The ventral rami of the fourth
through eighth cervical spinal nerves emerge between
the scalenus anterior and scalenus medius.22,35
The upper four cervical ventral rami form the cervi-
cal plexus. The lower four, including the first thoracic
ventral ramus, form the brachial plexus (see Plate 5-
4).22,41 The cervical plexus supplies some nuchal muscles,
the diaphragm, and areas of skin in the head, neck, and
chest.22,41 The formation of the brachial plexus allows for
rearrangements of the efferent and afferent somatic and
autonomic fibers so that they are redirected through the
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
various trunks, divisions, and cords into the most appro-
priate channels (terminal branches) for distribution
to the muscles, skin, vessels, and glands in the upper
limbs.22,41
The dorsal scapular nerve (C5) arises from the
uppermost root of the brachial plexus.22,41 It pierces the
scalenus medius muscle as it travels to supply the levator
scapulae and the rhomboid major and minor muscles
(see Plate 5-4).22,41 The suprascapular nerve (C5 and
C6) arises from the superior trunk of the brachial plexus
(see Plate 5-4).22,41 It supplies the supraspinatus and
infraspinatus muscles, glenohumeral and acromioclavic-
ular joints, and suprascapular vessels.22,41 The axillary
nerve (C5 and C6) originates from the posterior cord of
the brachial plexus (see Plate 5-4).22,41 It supplies the
glenohumeral joint and the deltoid and teres minor
muscles.22,41 The upper subscapular nerve (C5 and C6)
arises from the posterior cord and innervates the sub-
scapularis muscle (see Plate 5-4).2,22 The middle sub-
scapular nerve, or thoracodorsal nerve (C7 and C8),
arises from the posterior cord and innervates the latis-
simus dorsi muscle (see Plate 5-4).2,22 The lower
subscapular nerve (C5 and C6) also arises from the
posterior cord in proximity to the upper subscapular
and the thoracodorsal nerves. The former innervates
the subscapularis and teres major muscles (see Plate
5-4).2,22
Central Sensitization and
the Facilitated Segment
Central sensitization (central referring to the central
nervous system (CNS); sensitization referring to its
hypersensitivity and overreaction to incoming stimuli)
refers to the changes that occur in the nervous system
(forebrain, brain, sympathetic nervous system (SNS),
peripheral afferents, and dorsal horn of the spinal cord),
which result in chronic pain, hyperalgesia, and allodynia
long after tissue healing has occurred at the original
site of injury. Repeated stimulation, such as reaching
overhead for a patient with shoulder impingement of
peripheral primary afferents including the unmyelinated
C-fibers from Group IV and the thinly myelinated Ad-
fibers from Group III, leads to an increase in the hyper-
sensitivity of neurons in the dorsal horn of the spinal
cord.42 Receptors on postsynaptic neurons in the dorsal
horn of the spinal cord will undergo changes secondary
to this barrage of nociceptive afferent input. Presynap-
145
tic nociceptive afferent neurons have their terminals in
the dorsal horn, which release—on noxious stimula-
tion—excitatory amino acids (glutamate) and excitatory
neuropeptides (substance P and neurokinin A).43-45
Glutamate receptors on the postsynaptic neurons,
such as the AMPA (a-amino-3-hydroxy-5-methyl-4-
isoxazolepropionic acid), kainite ligand-gated ion chan-
nels, and NMDA (N-methyl-D-aspartate), react to
repeated glutamate stimulation by making the neuron
more sensitive to incoming glutamate, and therefore
more sensitive to incoming impulses from peripheral
afferent nociceptors.43-45 Morphologic changes, such
as an increase in the number of glutamate receptors on
the postsynaptic neuron, may lead to an irreversible
change in hypersensitivity.46 This central sensitization is
observed clinically as hyperalgesia (excessive pain from
a noxious stimulus) and as mechanical allodynia (pain
from a nonnoxious stimulus). The change in sensitivity
of the postsynaptic neuron in the dorsal horn is facili-
tated by a loss of supraspinal inhibition, part of which
originates in the forebrain.44,46
Forebrain activity, such as fear, anxiety, and depres-
sion, can amplify and prolong the pain experience
beyond the stages of tissue healing. Facilitory impulses
descending down to the dorsal horn will increase central
sensitization by lowering the threshold for activation of
the interneurons in the dorsal horn. Following a barrage
of nociceptive afferent input from the periphery (for
example, a shoulder injury), negative thoughts and emo-
tions from the forebrain will decrease the normal pain
inhibitory impulses that would otherwise descend down
to the dorsal horn. This decrease in inhibitory impulses
will increase the chances of forming a facilitated
segment. A facilitated segment, also referred to as
central sensitization, may also be defined as any segment
of the spinal cord that has a lower than normal thresh-
old for activation of the interneurons within the dorsal
horn (Figure 5-9).47 This segment of the spinal cord (for
example, C5) facilitates, through a lowered threshold of
activation for interneurons within the interneuron pool,
the ability of incoming afferent stimuli to reach the
critical threshold in order to elicit an efferent (motor)
response, resulting in muscle guarding, or to ascend to
the higher centers of the brain to be perceived as pain.
Depending on the stimulus they receive from the
forebrain, descending neural pain pathways from the
brain stem, specifically from the periaqueductal grey
(PAG) and the rostral ventromedial medulla (RVM),
146 SECTION II NEUROLOGIC CONSIDERATIONS

A B

Figure 5-9 A normal and a facilitated segment of the cervical spinal cord. A, A
normal segment with a low level of electrical activity and a high threshold for activation of
the interneurons. B, A facilitated segment with a high level of electrical activity and a low
threshold for activation of the interneurons.

can facilitate or inhibit the activity of the interneurons
within the spinal cord.48 These descending pathways are
intimately connected with the forebrain and are influ-
enced significantly by the activity and output coming
from the forebrain.42 Descending pathways from the
brain to the dorsal horn include both the ventrolateral
column and the lateral column of the PAG.48 Nerves
arising from the lateral column use noradrenaline as a
neurotransmitter and are described as noradrenergic.
This system of descending nerves controls the release of
morphine (analgesic) in response to a mechanical noci-
ceptive event. Nerves descending down through the ven-
trolateral column use serotonin as a neurotransmitter
and are therefore described as serotonergic. These nerves
control the release of morphine as a result of noxious-
thermal stimulation.48 The release of substance P by
presynaptic neurons in the dorsal horn, because of a
noxious mechanical stimulation, can be inhibited at the
spinal cord level by descending inhibitory impulses from
the PAG and the RVM.48
The modulation of pain by the forebrain is depend-
ent on a person’s state of attention, cognition, and
emotion. Chronic symptoms in the extremities may not
be from ongoing microtrauma and inflammation (for
example, the diagnosis of supraspinatus tendinitis), but
rather from the forebrain and dorsal horn mediated
central sensitization that results in the perception of
shoulder pain long after the tendon has healed. The
actual site of pain production shifts as the patient leaves
the acute stage of healing and inflammation, and most
of the primary healing is completed—from the periph-
ery (for example, the supraspinatus tendon) to the dorsal
horn (for example, the C5 segment of the spinal cord).
Pain continues to be perceived from the shoulder, but
the real source of the pain is now in the dorsal horn
because of changes in the glutamate receptors on the
postsynaptic neurons that effectively lower the thresh-
old of activation of the nerve impulses within the
interneuron pool. Now allodynia is pervasive. The
primary tissue in lesion is no longer the supraspinatus
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 147

tendon; now it is the hyperreactive, sensitized, spinal
cord interneurons in the dorsal horn with an extremely
low threshold for activation. The primary role of the
physical therapist is now as a desensitizer.42 The goal
is to try to desensitize the interneurons in the dorsal
horn directly, using manual therapy and exercise, and
indirectly by minimizing inappropriate input from the
periphery (for example, excessive shoulder impingement
motions and postures) and the forebrain (fear, anger,
anxiety, and depression).
Another way that a facilitated segment, or central
sensitization, can develop is through a loss of the almost
constant barrage of inhibitory impulses from type I and
type II mechanoreceptors.23 Because of their superficial
location, type I receptors within the facet joint capsules
are at a greater risk of being damaged. As a result of
spondylosis or trauma (for example, S/P MVA), there
will be a decline in the number of type I mechanore-
ceptors available to produce inhibitory impulses in the
dorsal horn.23 This may subsequently lead to a lowering
of the threshold for activation of the interneurons
within that segment of the spinal cord, producing a
facilitated segment or central sensitization. Corpuscular
mechanoreceptors in the skin and subcutaneous tissues
will also send inhibitory impulses to the spinal cord.23
The loss of these receptors, via scarring, burns, superfi-
cial wounds, or diseases, may lead to the lowering of the
threshold and subsequent formation of a facilitated
segment as well.23 In this way normally subliminal affer-
ent stimuli, ADL for example (Figure 5-10), may actu-
ally produce a motor or sympathetic efferent impulse, or
reach the higher centers of the brain and be perceived
as pain (shoulder), because the interneurons in that
segment of the spinal cord (C5) have been facilitated
(for example, chronic spondylosis and acute injury to the
C4-5 facet joint) due to the loss of Type I and possibly
Type II mechanoreceptors within the C4-5 facet joint
capsule.49
The segment of the spinal cord that is facilitated
acts as a neurologic magnifying glass. The facilitated

Figure 5-10 Electrical activity within the interneuron pool and the effect of activities
of daily living (ADL). On the bottom is a normal segment with a low level of electrical activ-
ity that increases with ADL, but does not reach the threshold. On the top is a facilitated
segment with a high level of electrical activity that easily reaches the threshold for activation
following normal ADL.
148 SECTION II NEUROLOGIC CONSIDERATIONS
segment focuses and exaggerates the effects of all incom-
ing afferent impulses upon the tissues innervated from
that segment.50 Even ordinary innocuous events and
ADL may become relatively demanding and stressful to
the neuromusculoskeletal system (see Figure 5-10).50
Role of the Sympathetic Nervous System
The sympathetic nervous system (SNS) can adjust cir-
culatory, metabolic, and visceral activity depending on
the postural and musculoskeletal demands.51 In order
for the SNS to perform this role, it must receive direct
(via segmental somatic afferents) and indirect (via higher
centers of the central nervous system) sensory input
from the musculoskeletal system.51 Sympathetic nervous
system hyperactivity has been associated with, and
segmentally related to, musculoskeletal trauma and
dysfunction.51 Long-term hyperactivity of a particular
sympathetic pathway can be deleterious to the associ-
ated tissue.51 Some of the consequences of prolonged
hyperactivity of the SNS are: (1) ischemia because of
vasoconstriction, and (2) the shortening of tendons,
muscle atrophy, and joint contractures.51
The cervical spine is capable of inducing real patho-
logic conditions (for example, adhesive capsulitis, ten-
dinitis, or bursitis) within the shoulder joint.18,36,40,49,52-56
Wiffen,57 in his review of adhesive capsulitis, suggests
that this chronic painful condition of the shoulder may
develop and/or be maintained by central sensitization in
the dorsal horn of the spinal cord and by an overactive
SNS. These shoulder pathologic conditions may be pre-
cipitated by vasoconstriction to the shoulder joint via
cervical sympathetic activity as a result of cervical nerve
root irritation.40,49,54 Sympathetic cell bodies are found
in spinal cord segments C4-8. The transmission of the
preganglionic fibers, in the ventral roots of C5-8, has
also been demonstrated.53,58 The lowest somatic seg-
mental supply to the upper extremity is at T3, with the
lowest sympathetic supply to the upper extremity as low
as T8.58
Synapses within the interneuron pool in the dorsal
horn, between somatic and sympathetic neurons, can
result in a sympathetically mediated vasoconstriction
message that targets the shoulder. (See Plate 13-2.)49
These impulses may produce inflammation, exudation,
fibrosis, adhesions, capsular thickening, degeneration,
and calcification within the rotator cuff and joint
capsule.40,49 Cervical nerve root irritation may also give
rise to complex regional pain syndrome type I (CRPS-
I), with the changes mentioned previously to the capsule
and tendons associated with the shoulder.40 A previous
asymptomatic event, such as active motion of the shoul-
der, may become symptomatic because of cervical spine–
initiated vasoconstriction of the tissues in and around
the shoulder. Another way that allodynia can develop in
the shoulder is by the formation of a facilitated segment
(C3, C4, C5, or C6) within the spinal cord. This may
occur because of a chronic barrage of afferent nocicep-
tive impulses; a loss of inhibitory impulses from type I
or type II mechanoreceptors; or a loss of supraspinal
inhibition from the forebrain.23,30,49 This results in a
lower threshold of activation of the interneurons respon-
sible for relaying nociceptive impulses to the higher
brain centers for the perception of pain.
Musculoskeletal Syndromes
Involving the Spine, Ribs,
and Shoulder
Omohyoid Syndrome
Neck, shoulder, and/or arm pain may be the primary
complaint of a patient with an omohyoid syndrome.59-63
This syndrome is characterized by the sudden onset of
a severe muscle spasm on one side of the neck.59-63 The
omohyoid muscle belly may contain myofascial trigger
points.63 The etiology is often a contraction combined
with a stretching of the omohyoid muscle.60 An example
would be a yawn combined with an attempt to swallow
as the head is bent to one side.59 Forceful motions, such
as vomiting, also may cause the omohyoid muscle to go
into spasm.63
Symptoms. Patients will report the sudden onset of
pain and muscle spasms, often during yawning, swal-
lowing, or vomiting.59-61 The symptoms are typically
aggravated by swallowing.59-62 Pain will be on one
side of the neck and may include the shoulder and
arm.59-63
Signs. The patients often have their head flexed
and bent ipsilaterally.59,60 There will be audible breath-
ing and an alteration in the quality of the voice, such
as slurred speech.60 Swallowing will be painful.59-62
Neck flexion will decrease the symptoms.60 Pain will
be reproduced with stretching (extension, side bending,
or rotation away) or palpation of the omohyoid
muscle.59-61
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
Levator Scapulae Syndrome
Another source of neck and shoulder pain is the levator
scapulae syndrome.64,65 This is proposed to be a bursitis
involving a bursa associated with the levator scapulae at
its attachment to the scapula.64 It is thought to occur
because of friction between the levator scapulae, the ser-
ratus anterior, and the scapula as the muscles pull in
opposite directions during repeated upper extremity
tasks with the arm elevated.64 A sustained head posture
in rotation during prolonged typing or telephone calls
may also precipitate a problem in the levator scapulae.65
Additional risk factors include vigorous tennis or
swimming.65
Symptoms. Patients will complain of pain in the
superior-medial angle of the scapula. There may be a
“heaviness” or “burning” sensation, which will radiate to
the neck or shoulder.64
Signs. There is full active and passive ROM at the
neck and shoulder. Symptoms are reproduced through
palpation or stretching of the levator scapulae muscle.
Results of thoracic outlet, impingement, and neurologic
testing are normal as are plain radiographs of the
shoulder.64
Droopy Shoulder Syndrome
The droopy shoulder syndrome, another source of neck
and shoulder pain, may be considered a brachial plexus
stretch injury. Chronic postural strain, drooping
shoulders, produces tension on the brachial plexus. This
syndrome is normally exclusive to women.66,67
Symptoms. The patient may complain of head,
neck, chest, and bilateral shoulder and arm pain. Patients
often report paresthesia in the upper extremities,
without objective numbness, weakness, or atrophy. The
patients may describe their symptoms as “tightness,”
“electrical,” “jabbing,” or “pulling.”66,67
Signs. Postural examination will show a swan neck
with low-set shoulders and horizontal clavicles. Symp-
toms are reproduced with palpation at the supraclavicu-
lar fossa or stretching of the brachial plexus (Upper
Limb Neurodynamic Testing). Passive scapular depres-
sion will increase the symptoms, whereas passive eleva-
tion will decrease the symptoms. There is no vascular
insufficiency, claudication, or Raynaud’s phenomenon.
149
Lateral radiographs of the cervical spine will allow visu-
alization of the second thoracic vertebra. Normally, a
lateral radiograph of the neck only allows visual inspec-
tion down to the sixth cervical vertebra because of inter-
ference by the shoulder. Electromyographic studies will
be within normal limits.66,67
Snapping Scapula Syndrome
The snapping scapula syndrome is a source of scapu-
lothoracic pain and dysfunction. Ten different muscles
have attachment sites on the scapula that control its
movement across eight ribs. Under normal circum-
stances, the scapula glides smoothly across the thorax,
without interruption or interference, with the help of
these 10 well-coordinated muscles. The scapula is
curved to match the contour of the thoracic wall.
Symptoms. The patient will complain of scapu-
lothoracic pain and report a grating or snapping sensa-
tion under the scapula during active movements of the
upper extremity.68,69 The complaints of pain are often
diffuse and nonspecific in a region surrounding the
scapula. The pain is thought to be because of tendinitis
of one or more of the scapula muscles and/or a scapu-
lothoracic bursitis.68-70 The snapping or grating noise is
thought to be from a combination of poorly controlled
scapula muscles, bony incongruity of the scapulothoracic
“joint,” and possibly the scapula riding over a fibrotic
scapulothoracic bursa.68-70
Signs. The patient will be able to voluntarily
produce an audible and palpable grating, crepitus, or
clunking noise with active movement of the scapula. The
onset is thought to be secondary to a variety of proposed
factors such as trauma; poor posture; poor scapulotho-
racic rhythm; a loss of muscle tone; atrophy of the ser-
ratus anterior and/or subscapularis muscles; an adherent
and fibrotic scapulothoracic bursa; or skeletal abnormal-
ities that may include an abnormal angulation of the
scapula or ribs, scapula exostoses and osteochondromas,
and a bony or fibrocartilaginous protrusion or incon-
gruity at the superior angle of the scapula.68-71 A careful
examination of the ribs (r/o subluxation), spine (scolio-
sis), and scapula (hypomobility versus hypermobility) is
indicated. This syndrome is more common in women.
Although research into the use of conventional com-
puted tomography (CT) scans in the diagnosis of snap-
ping scapula has been contradictory, there is evidence
150 SECTION II NEUROLOGIC CONSIDERATIONS

that three-dimensional CT scans are a valid tool in
recognizing bony incongruity of the scapula in persons
with this syndrome.71,72
Cervical Spine Tissues
Capable of Referring Pain
and Dysfunction to
the Shoulder
Disk
Cervical disk disease (internal disruption, degeneration,
herniation, or prolapse), without nerve root involve-
ment, can be a source of shoulder pain.52,53,73-79 The
recurrent meningeal nerve receives afferent impulses
from the posterior and posterior lateral regions of the
intervertebral disk and posterior longitudinal ligament
(see Figure 5-8). This nerve then joins the mixed spinal
nerve, sending sensory information into the dorsal horn
of the spinal cord.22,35,37 In this way, referred pain at the
shoulder may be experienced with disk abnormalities at
the same segmental levels that innervate the shoulder.
Degenerative disk disease can result in instability at
that segment, which may lead to injury of ligaments or
facet joint capsules.80 In the late stages of this disease,
osteophytes or a prolapsed disk can induce nerve root
irritation.80
Symptoms. Pain, usually a dull ache, can vary in
distribution from the occiput, mastoid, and temporo-
mandibular joint (TMJ) to the anterior chest, upper
back/scapula, and down to the elbow (Figure 5-11).78,79
Pain may be unilateral or bilateral. Grubb and associ-
ates78 reported that bilateral symptoms occur 33% to
50% of the time depending on the disk level. Pain nor-
mally will not travel below the elbow. Without nerve
root involvement there will be no complaints of numb-
ness, pins and needles sensation, or specific muscle
weakness. Pain is normally not referred to the biceps
brachii muscle or anterior portions of the upper arm.
Signs. Reproduction of symptoms is expected
during the following special tests: compression of the
cervical spine in neutral, flexed, and extended postures
(Figures 5-12 and 5-13); the segmental shear test
(Figure 5-14); coughing and/or sneezing; and Valsalva’s
test.81 The shear test may also demonstrate increased
shearing and hypermobility at the involved segment if
there is degenerative disk disease, minimal muscle
guarding, and the segment is not ankylosed. Often there
is no nerve root compression or irritation, in which case
the results of the nerve root examination (sensation,
strength, and DTR) and the nerve root special tests
(quadrant, doorbell sign, ULNT) will be normal. In
general, you may find that the symptoms are reproduced

C2-3 C3-4 C4-5 Figure 5-11 Referred pain patterns of specific

A B C cervical intervertebral disks following diskography. (Modi-
fied from Grubb S, Kelly CK: Cervical discography: clinical implica-
tions from 12 years of experience, Spine 25(11):1382, 2000.)

C5-6 C6-7 C7-T1

D E F
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 151

Nerve
Irritation or partial compression of an inflamed cervical
nerve root (dorsal root, ventral root, or the mixed spinal
nerve) by a intervertebral disk; osteophytes from a
facet or uncovertebral joint; or tumor or other space-
occupying lesion can be a source of neck, shoulder,
and arm pain (Figures 5-15 and 5-16).36,40,73,74,86-88 Com-
pression of an uninjured (without signs of inflammation)
spinal nerve root will normally not give rise to pain.
Paresthesia and complaints of itching, crawling, or
varying degrees of numbness will occur depending on
the degree of compression.87

Symptoms. Patients often describe the pain as

sharp, electrical, or “like a nerve is being pinched.” Pain
may start in the neck or shoulder and radiate as far as
Figure 5-12 Axial compression of the cervical spine the fingertips (see Figure 5-16). Pain may also be felt in
in neutral may produce pain from the intervertebral disk, ver- the posterior shoulder, scapula, or interscapular regions.
tebral body, uncovertebral joint, inflamed nerve root, or facet
The patient may complain of numbness, pins and
joint.
needles, or weakness down the arm. Symptoms may be
bilateral to the shoulder, but are usually unilateral with
with provocation of the cervical spine and not the shoul- respect to the upper extremities. Because nerve root irri-
der, although this may not always be the case. tations and compressions are often associated with disk
injury, the patient may also complain of discogenic
Physician-Ordered Tests. Plain radiographs, symptoms.
although helpful in examining the general morphology
of the cervical spine, are not diagnostic. They may
demonstrate decreased disk height or osteophytosis.
Signs. Patients often get relief of symptoms by
resting their involved hand on their heads.79,89,90 Repro-
Even in the presence of positive findings, the clinician
duction of symptoms is expected during the following
must realize that many asymptomatic people have
special tests: passive extension, ipsilateral bending, or
similar findings on plain film radiography. Myelography
ipsilateral rotation of the cervical spine; cervical quad-
can demonstrate spinal cord or nerve root compression,
rant test in extension (Figure 5-17)53,79,89,90; at least one
but it cannot tell if it is a disk, osteophyte, or tumor cre-
abnormal finding with neurologic testing of motor
ating the compression. A CT scan following a myelo-
(Figure 5-18), sensory, or deep tendon reflexes; cervical
gram will allow for the differential diagnosis of the tissue
compression in an extended posture; and doorbell sign36
responsible for compression of neurologic tissues, but
(palpation of the vertebral gutter outside the interverte-
it cannot indicate if a specific disk itself is sympto-
bral foramina). Axial compression in the neutral posture
matic.82,83 Magnetic resonance imaging (MRI) can iden-
of the cervical spine may be abnormal or normal, while
tify a degenerated, desiccated, or herniated/prolapsed
compression in a flexed posture will be normal (see
disk, but it cannot tell you if the disk is sympto-
Figure 5-13). Cervical axial distraction, or traction in a
matic.78,79,82-84 CT discography can clearly identify a
flexed posture, will often bring temporary relief of symp-
symptomatic disk and determine if internal disk dis-
toms. But symptoms can be aggravated if an inflamed
ruption is present.* This diagnostic procedure, though
and tethered nerve root is stretched over a bulging disk,
sometimes used to alleviate the patient’s symptoms, is
osteophyte, or other space-occupying lesion.79,86,89 If
usually used to provoke and reproduce pain.†
discogenic symptoms are present, then the results
*References 52, 73, 76, 78, 79, 84, 85. of tests for discogenic pain noted earlier will also be
†
References 52, 73, 76, 78, 79, 85. abnormal.
152 SECTION II NEUROLOGIC CONSIDERATIONS

A B

C D
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 153

Figure 5-13 Differential diagnosis using axial com-

pression testing of the cervical spine. A, Cervical spine in
neutral. B, Flexion. C, Extension. D, Extension with retrac-
tion to target the lower cervical and upper thoracic segments.
With the cervical spine in neutral, pain may be produced from
the intervertebral disk, uncovertebral joint, nerve root, facet
joint, or vertebral body. For disk-generated pain, symptoms
will be reproduced in all three positions (neutral, flexion, and
extension). For uncovertebral–joint generated pain, symptoms
will be preferentially reproduced in a position of slight flexion
combined with ipsilateral bending. For nerve root–generated
pain, symptoms will be reproduced in a position of extension.
In severe cases, neutral may also be symptomatic. If an unin-
jured nerve root is being compressed, then you can expect to
produce paresthesia into the upper extremity. If an inflamed Figure 5-14 Shear test of the cervical intervertebral
nerve root is being compressed, then you can expect a repro- disk. Test of the C5-6 segment, for example: Patient is posi-
duction of pain often radiating down below the elbow. Other tioned in side-lying position. The patient’s head rests on the
neurologic signs and special tests will also be positive. For facet clinician’s forearm with her forehead in contact with the clin-
joint–generated pain, sharp pain will be reproduced in a posi- ician’s biceps. The clinician’s right hand supports the upper
tion of extension only. In severe cases, the patient may report cervical spine and occiput. The cervical spine is flexed down
discomfort in the neutral position as well. Facet-generated through C4-5, but not C5-6. Keeping C4-5 and above in
symptoms do not include paresthesia or pain radiating down flexion, the clinician oscillates his right forearm and humerus
below the elbow. For vertebral body–generated pain, symptoms back and forth in an A/P shear motion as he palpates the
will be reproduced in all three positions, similar to discogenic amount of A/P shear at C5-6 with his left index finger.
pain. Vertebral body–generated pain may be preferentially
stimulated by lightly tapping the spinous process (where acces-
sible) with a reflex hammer or a tuning fork. A review of
imaging studies will also help to rule out bone as a source of
your patient’s symptoms.

Osteophytes from a cervical facet joint may hit the

mixed spinal nerve or the dorsal (sensory) root only. (See
Figures 5-7 and 5-15.) In the latter case, expect to see
sensory, but no motor, disturbances. If the ventral
(motor) root is spared, then expect the results of EMG
testing to be normal.91 If the nerve root irritation or
compression is secondary to an osteophyte on the facet
joint, then the patient may also demonstrate positive
signs of facet joint pain and/or crepitus because of
degeneration of the articular cartilage. A cervical herni-
ated disk (contained bulging disk or complete prolapse),
Figure 5-15 Degenerative joint disease and osteo-
or osteophytes from the uncovertebral joint (see Figure phytosis of the left cervical facet and uncovertebral joint.
5-15), may hit the mixed spinal nerve or the ventral root Notice the narrowing of the intervertebral foramen and the
alone (see Figure 5-7).91 In this case, expect motor, but bony encroachment towards the transverse foramen (vertebral
usually not sensory, signs and symptoms. (However, note artery). (From Tillmann B: Slides in human arthrology, Munich, 1985,
that the motor nerve root is composed of up to 20% JF Bergman Verlag.)
154 SECTION II NEUROLOGIC CONSIDERATIONS

Figure 5-16 Dermatomes C2 through T5. (From Bland JH: Rheumatologic Neurology. In Disorders of the cervical
spine: diagnosis and medical management, ed 2, Philadelphia, 1994, WB Saunders.)

sensory nerve fibers.) If nerve root irritation or com- C3 Nerve Root

pression is secondary to a disk problem, the patient may
• Weakness of cervical side bending, although
demonstrate signs for discogenic pain. If the nerve root
weakness may be difficult to detect
pathologic condition is caused by an osteophyte on the
• Weakness of the SCM, trapezius, and neck flexors
uncovertebral joint, then the patient may also display
may be noted
signs for this joint lesion. Signs of specific nerve root
• Decreased sensation in the C3 dermatome; however,
compression are noted below. Refer to Figure 5-16 (der-
patients rarely complain of numbness
matomes) and Figure 5-18 (myotomes) as needed.*
C4 Nerve Root
C1 Nerve Root
• Weakness of shoulder shrug, although weakness may
• Weakness of upper cervical extension
be difficult to detect
• Weakness of the SCM may be noted
• Weakness of the trapezius, neck flexors, rhomboids,
• Decreased sensation in the C1 dermatome
and rotator cuff may be noted
C2 Nerve Root • Decreased sensation in the C4 dermatome; however,
patients rarely complain of numbness
• Weakness of upper cervical flexion
• Weakness of the SCM and trapezius may be noted C5 Nerve Root
• Decreased sensation in the C2 dermatome
• Weakness of shoulder abduction and external
*References 55, 77, 79, 88, 90, 92-94. rotation
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
Figure 5-17 Cervical quadrant test in extension. The
cervical spine is passively rotated, bent backwards (ipsilateral
side bending), and extended. This position maximally com-
presses the intervertebral foramen, facet, intervertebral disk,
and vertebral body. The contralateral side will experience a
notable stretching strain to the soft tissues. Pain from the com-
pressed side may be produced from the intervertebral disk
(posterolateral compression), an inflamed spinal nerve root, the
facet joint, or the vertebral body. Holding the position for at
least 10 seconds will help you assess if the initial pain subsides
or if neurologic signs and symptoms begin to appear. A slight
overpressure may be given if no symptoms occur initially. This
position may also stress the vertebral artery. Note: To suffi-
ciently test the lower cervical/upper thoracic segments, espe-
cially for patients with a forward head posture, have them
perform cervical retraction before starting the test.
• Weakness of elbow flexion
• Decreased biceps and/or brachioradialis DTR
(inconsistent)
• Decreased sensation in the C5 dermatome
C6 Nerve Root
• Weakness of elbow and finger flexors
• Weakness of shoulder internal rotation
155
• Weakness of pronation and wrist extension
• Occasionally, weakness in shoulder abduction
• Decreased biceps and/or brachioradialis DTR
• Decreased sensation in the C6 dermatome
C7 Nerve Root
• Weakness of elbow extension and forearm
supination
• Weakness in wrist and finger flexion or extension
• Decreased triceps DTR
• Decreased sensation in the C7 dermatome
C8 Nerve Root
• Weakness in elbow and wrist extension
• Weakness in wrist flexion and intrinsic muscles of
the hand; loss of grip strength
• Decreased triceps DTR
• Decreased abductor digiti minimi DTR
• Decreased sensation in the C8 dermatome
• Mimics a brachial plexus injury, ulnar neuropathy,
and neurogenic thoracic outlet syndrome (TOS)
Note: Sensory changes and referred pain patterns are
variable among patients and may not correspond to exact
anatomic dermatomes.
Physician-Ordered Tests. Plain radiographs are
not diagnostic, but they may show foraminal stenosis
(oblique view) or osteophytes on the uncovertebral or
facet joints. MRI (74% to 88% accuracy), CT scan (72%
to 91% accuracy), myelography (67% to 92% accuracy),
and CT-myelography (75% to 96% accuracy) are diag-
nostic tests used to determine the cause of nerve root
irritation and compression.83 EMG and nerve conduc-
tion velocity (NCV) tests can provide information on
the extent of the nerve damage.85,89
Facet Joint
Irritation of a cervical facet (zygapophyseal) joint (C4-
5, C5-6, C6-7, C7-T1) can refer pain to regions in and
around the shoulder (Figures 5-19 and 5-20).75,95-100
Structures of the facet joint capable of provoking pain
include the joint capsule and the meniscoids within the
joint itself.39,101 It has been suggested that the articular
cartilage within the joint, normally considered to be
avascular and without nervous innervation, may acquire
nociceptive fibers if the tissue is undergoing “remodel-
ing” because of injury or disease of the cartilage.
 C1 C2 C3 C4 C5 C6 C7 C8 T1
Sternocleidomastoid-Trapezius
Rectus capitis posterior major
Rectus capitis posterior minor
Obliquus capitis superior
Obliquus capitis inferior
Geniohyoid
Thyrohyoid
Rectus capitis lateralis
Rectus capitis anterior
Stemohyoid
Stemothyroid
Omohyoid
Longus capitis
Semispinalis capitis
Levator scapulae
Longus colli
Anterior intertransversarii
Posterior intertransversarii
Diaphragm
Splenius capitis
Scalenus medius
Interspinales
Multifidus
Scalenus anterior
Semispinalis cervicis
Rhomboids-Major & Minor
Supraspinatus
Infraspinatus
Teres major
Deltoid
Teres minor
Subscapularis
Brachioradalis
 Biceps brachii
Coracobrachialis
Supinator
Pectoralis major (clavicular portion)
Scalenus posterior
Serratus anterior
Extensor carpi radialis longus
Flexor carpi radialis
Pronator teres
Pectoralis minor
Latissimus dorsi
Triceps brachii
Longissimus capitis-cervicis
Anconeus
Abductor pollicis longus
Extensor pollicis brevis
Extensor carpi radialis brevis
Extensor indicis proprius
Extensor carpi ulnaris
Extensor digitorum
Palmaris longus
Flexor carpi ulnaris
Extensor pollicis longus
Extensor digiti minimi
Pectoralis major (sternal portion)
Flexor digitorum superficialis
Iliocostalis cervicis
Flexor pollicis longus
Flexor pollicis brevus
Flexor digitorum profundus
Abductor pollicis
Flexor digiti minimi
Opponens pollicis
Pronator quadratus
Palmaris brevis
Abductor digiti minimi
Palmar and dorsal interossei
Lumbricals
Abductor pollicis brevis
Oppponens digiti minimi

Figure 5-18 Muscles of the cervical spine, shoulder, and upper extremity with their corresponding motor nerve innervation. (From Bland JH: Embryology: prac-
tical clinical implications and interpretation. In Disorders of the cervical spine: diagnosis and medical management, ed 2, Philadelphia, 1994, WB Saunders.)
158 SECTION II NEUROLOGIC CONSIDERATIONS
Research has documented that it is much more likely for
a patient to have a symptomatic cervical disk along with
a symptomatic facet joint, than it is to display either
pathologic condition independently.102
Symptoms. Pain is unilateral and may be felt in the
neck, top or posterior portions of the shoulder, scapula,
or interscapular region (see Figures 5-19 and 5-20).
Patients often report a sharp pain or pinch if they
quickly turn their head toward the painful side or look
up. Pain is generally not referred to the anterior shoul-
der, biceps brachii muscle, or below the elbow. There are
no complaints of numbness, pins and needles, or specific
weakness in the upper extremity.
Signs. Reproduction of symptoms is expected
during the following special tests: cervical quadrant test
in extension (see Figure 5-17); passive cervical spine
extension and often with ipsilateral passive side bending
or rotation; cervical spine compression test in extension
and occasionally in neutral (see Figure 5-13); and facet
joint tenderness to palpation. Segmental mobility exam-
ination is usually abnormal at the suspected level. Quite
Figure 5-19 Referred pain patterns from specific
cervical facet joints. (From Dwyer A, Aprill C, Bogduk N: Cervi-
cal zygapophyseal joint pain patterns: 1. A study in normal volunteers,
Spine 15:453, 1990.)
often you will find that the symptomatic facet joint is
part of a hypermobile segment. This segment, however,
may initially test as hypomobile because of an acute
entrapment of a meniscoid or from acute muscle guard-
ing. The results of neurologic examination are normal,
including nerve root compression and nerve tension
tests. Discogenic examination results are normal with
respect to Valsalva’s test and cervical compression in
flexion.
Physician-Ordered Tests. Plain radiographs,
although helpful in examining the general morphology
of the cervical spine, are not diagnostic. They may
demonstrate decreased disk height or osteophytosis of
the facets. Even in the presence of abnormal results, the
clinician must realize that many asymptomatic people
have similar findings on plain film radiography. MRI
and CT scans are not diagnostic for the source of pain,
but they may be helpful in terms of the general status of
the spine, revealing degenerative changes within the disk
or facet joints. Myelography is not useful in this case.
Facet joint injection blocks or anesthesia of the medial
branch of the dorsal ramus are the most accurate,
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 159

Figure 5-20 Referred pain patterns from specific lower cervical and upper thoracic facet joints. (From Fukui S, Ohseto K,
Shiotani M: Patterns of pain induced by distending the thoracic zygapophyseal joints, Regional Anesthesia 22(4):332, 1997.)

specific, and sensitive diagnostic examinations of the
facet joints.95,96,102
Injury to the cervical facet joints, regardless of direct
referral patterns, can lead to shoulder pain and dysfunc-
tion. Erl Pettman, a physical therapist and master clini-
cian, likes to use the following case example to illustrate
this point:103
A post-traumatic hypomobility of C3-C4 on the left
leads to a compensatory hypermobility of C3-C4 on the
right (a hypomobile C2-3 or C4-5 on the right may also
lead to a hypermobile C3-C4 on the right). This facil-
itated C-4 segment creates a hypertonus of the right
levator scapulae muscle because of the increased motor
output from the ventral horn. This increased activity in
the levator scapulae places the scapula in a position of
relative adduction. In this new position, the rotator cuff
muscles are forced to work more as stabilizers instead
of the superior-glenohumeral joint capsule. The inter-
scapular portion of the biceps tendon slackens and
buckles, predisposing it to impingement. During eleva-
tion the levator scapulae muscle, hypertonic because of
the C-4 facilitated segment, will limit the excursion of
the scapula during the first 150° of ROM; this will
require excessive motion from the glenohumeral joint,
which can lead to glenohumeral joint laxity, instability,
and possible labrum damage.
Other disorders within the cervical spine can also lead
to an intrinsic shoulder problem, such as adhesive cap-
sulitis, tendinitis, or bursitis.18,36,40,49,52-56 Muscle guard-
ing of the rotator cuff muscles, because of a lesion at the
160 SECTION II NEUROLOGIC CONSIDERATIONS
C5 or C6 segment of the spine, can lead to tendinitis.40
Adhesive capsulitis of the shoulder may be caused by
cervical disk disease or a C5 or C6 radiculopathy.40,54-56
One study reported that cervical spondylosis was found
in 40% of patients with adhesive capsulitis.74 When
examined by thermography, 80% of these patients
had hot spots on their cervical spine, with only 20% of
them demonstrating hot spots on their shoulder.74 Even
though a patient may have reproduction of symptoms
from a mechanical examination of the shoulder, it is
important to remember that a cervical disorder can lead
to a real shoulder dysfunction and the patient is then
likely to have dual pathologic conditions.18,36,49,52
Any tissue, from the skin and subcutaneous fat down
to the center of the bones, with sensory afferent nerves
feeding into the dorsal horn of the spinal cord between
the C3 and T3 segments, is capable of referring pain and
dysfunction to the shoulder.
Thoracic Spine Tissues
Capable of Referring Pain
and Dysfunction to
the Shoulder
Disk
The thoracic spine often gets the least respect in con-
trast to the cervical and lumbar spine. Primary sources
of pain and injury are less common in the thoracic spine.
This region typically gets less attention from clinicians
in terms of evaluation and treatment, except in the case
of postural analysis. Upper thoracic discogenic pain can
be referred to regions of the posterior thorax, which
can include the scapula—especially along the medial
border.104 Discogenic pain from as far down as T6-7 has
the ability to refer pain to the inferior angle of the
scapula. Disk injuries in the thoracic spine are much less
common than in the cervical or lumbar spine. Upper
thoracic disk injuries are often not diagnosed for many
months or years after the onset of symptoms because
most clinicians suspect that referred pain to the shoul-
der originates in the cervical spine. Subsequently, cervi-
cal spine imaging studies are ordered and may be
normal, in which case the pain is thought to be myofas-
cial. Or there may be subtle degenerative joint disease
(DJD) or subtle disk bulges that are blamed for the pain.
Thoracic disk injuries, bulges, and prolapses, can be dev-
astating because of the small diameter of the central
spinal canal in the thoracic region and the close prox-
imity of the spinal cord.
Lower thoracic disk ruptures have been associated
with shoulder pain and dysfunction.105 Wilke and asso-
ciates105 discuss a case in which a woman was treated for
chronic shoulder pain (diagnosed as supraspinatus cal-
cific tendinitis). There was no success after she received
16 cortisone injections, 30 visits with a physiotherapist,
and finally subacromial decompression and debridement
of the calcific deposit. The patient’s shoulder and
neurologic status got progressively worse after surgery.
A chronic, but recently exacerbated, T10-11 disk
prolapse was then discovered. The patient improved
rapidly after surgical decompression of the T10 disk pro-
lapse. The authors of the study are convinced that the
shoulder symptoms, if not a primary referral source
of the T10-11 disk condition, were a direct result of
changes in the dorsal horn of the thoracic spinal cord.
This led to a central sensitization that hindered the
rehabilitation of the shoulder symptoms.105 In other
words, the pathologic condition of the T10-11 disk was
putting a strain on the shoulder, which exacerbated the
symptoms from the shoulder and interfered biomechan-
ically, and probably neurophysiologically, with the reha-
bilitation of the shoulder.
Symptoms. Pain, usually a dull ache, that is referred
a short distance from the source to surrounding regions
of the thoracic spine and scapular region (T1-T6). Pain
may be referred to the chest. Nausea or sweating with
pain may be reported because of the connection between
the sinuvertebral nerves (innervating the annulus fibro-
sus) and the sympathetic ganglion. There are generally
no complaints of numbness, pins and needles sensation,
or specific muscle weakness. Pain is usually not referred
to the extremities nor to the anterior or apical portions
of the shoulder.
Signs. Reproduction of symptoms is expected
during the following special tests: compression of the
cervical and thoracic spine in neutral, flexed, and
extended postures; segmentally specific P/A glides in a
prone position (Figure 5-21); coughing and/or sneezing;
and Valsalva’s test.81 Neurologic indications are normal,
including nerve root compression and nerve tension
tests. In general, you may find that the symptoms are
reproduced with provocation of the thoracic spine and
not the shoulder. Central sensitization, however, can
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
Figure 5-21 Prone thoracic P/A glides. This tech-
nique, placing the pisiform of each hand on the transverse
processes of the target vertebra, can be used in several ways: as
a provocation to help rule out a symptomatic thoracic spine;
to assess general thoracic P/A mobility; as a mobilization
technique (utilizing a variety of speed and force techniques/
oscillations or stretch) to inhibit pain and increase segmental
mobility; and to deliver a high-velocity low-amplitude thrust
when appropriate.
produce the perception of pain during the examination
of a relatively normal shoulder. In addition, chronic tho-
racic disk disease can induce true intrinsic disorders of
the shoulder. In this example, the shoulder may respond
with pain immediately during provocational testing,
whereas the thoracic spine may only become sympto-
matic after prolonged activity.80
Physician-Ordered Tests. Plain radiographs,
though helpful in examining the general morphology of
the thoracic spine, are not diagnostic. They may demon-
strate decreased disk height or osteophytosis. Even in
the presence of abnormal findings, the clinician must
realize that many asymptomatic people have similar
findings on plain film radiography. Myelography can
161
demonstrate spinal cord or nerve root compression, but
it cannot indicate if it is a disk, osteophyte, or tumor
creating the compression. A CT scan following a mye-
logram will allow for the differential diagnosis of the
tissue responsible for compression of neurologic tissues,
but it cannot show if a specific disk is symptomatic.
Magnetic resonance imaging can identify a degenerated
or herniated/prolapsed disk, but it cannot show if the
disk is symptomatic. Discography within a specific
segment of the thoracic spine, however, can clearly iden-
tify a symptomatic disk.106
Nerve
First thoracic nerve root irritations and compressions
(for example, from a T1-T2 disk injury) can produce
neck, shoulder, and arm pain.94,107,108 Differential diag-
nosis of these symptoms must include cervical radicu-
lopathy (C8), TOS, ulnar neuropathy, and brachial
plexus injuries to name the most obvious neuromuscu-
loskeletal choices. Visceral pain to consider includes
the lung (Pancoast’s tumor) and the heart (myocardial
infarction).107 Radiculopathy of T1, therefore, can go
undiagnosed for many months because the symptoms
mimic other disorders and most imaging studies will
tend to focus on the cervical spine and miss the T1-2
segment. Nerve root injuries from T2 through T5 can
also refer pain to the posterior shoulder and scapula (see
Figure 5-16).109
Symptoms. Patients often describe the pain as
sharp, electrical, or “like a nerve is being pinched.” Pain
may start as a dull ache in the scapular region and
progress to sharp radicular pain and paresthesia down
the medial aspect of the arm, forearm, and hand (see
Figure 5-16).107,108 The patient may also complain of a
loss of grip strength. Because nerve root irritations
and compressions are often associated with disk
injuries, your patient may also complain of discogenic
symptoms.
Signs. Reproduction of symptoms is expected
during the following special tests: cervical quadrant test
in extension with retraction (see Figure 5-17)53,81,89,90;
passive extension, ipsilateral bending, or ipsilateral rota-
tion of the cervical-thoracic spine; compression in an
extended posture; T1 nerve root special test (Figure 5-
22); and at least one abnormal finding with neurologic
testing of motor (see Figure 5-18), sensory, or deep
162 SECTION II NEUROLOGIC CONSIDERATIONS

A B

Figure 5-22 T1 nerve stretch test. A, The patient, seated, is instructed to externally rotate
and abduct the involved extremity to 90° and flex the elbow to 90° as well. This position should be
relatively pain free without a reproduction of the patient’s primary complaints. B, The patient is then
instructed to maximally flex the elbow by placing the hand behind the neck. The test is positive if
the patient’s complaints of pain in the scapula and medially down the arm are reproduced. Pares-
thesia may also be exacerbated. This result of this test will also be abnormal in persons with ulnar
neuropathy.

tendon reflexes. Findings from axial compression in the
neutral posture of the cervical-thoracic spine may be
abnormal or normal, whereas results from compression
in a flexed posture will be normal (see Figure 5-13).
Cervical-thoracic axial distraction or traction in a flexed
posture will often bring temporary relief of symptoms,
but symptoms can be aggravated if an inflamed and teth-
ered nerve root is stretched over a bulging disk or osteo-
phyte.81,86,89 There may be loss of sensation in the T1
dermatome, loss of strength in the T1 myotome (grip),
and atrophy of the intrinsic muscles of the hand.94,107,108
Because of the connection between the T1 nerve root
and the sympathetic nervous system, Horner’s syndrome
may be present.108 The signs of Horner’s syndrome are
miosis (pupil contraction), ptosis (partial drooping of the
eyelid), enophthalmos (recession of the eyeball into the
orbit), and loss of sweating on the side of the face. The
standard upper extremity DTR examination will not
be affected. If discogenic symptoms are present, then the
test results for discogenic pain noted earlier will also be
abnormal.
Physician-Ordered Tests. Plain radiographs are
not diagnostic, and may be within normal limits
(WNL), but they can show the morphology of the spine
in terms of degenerative changes of the facets and ver-
tebral endplates, for example. MRI, CT scan, myelog-
raphy, and CT-myelography can be diagnostic for nerve
root irritation and compression. Examination using CT-
myelography will probably give the most accurate and
relevant information to help determine a rehabilitation
strategy, prognosis, and the need for a surgical consult.
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
Information on the extent of the nerve root damage is
best assessed by EMG and NCV studies.
Facet
Injuries to the upper thoracic facet joints (C7-T1 to
T5-6) can refer pain to the posterior regions of the
shoulder and scapula (Figure 5-23). (See also Figure 5-
20.)98,104,110,111 Menck and associates112 describe a patient
with complex regional pain syndrome type I (CRSP-I),
which progressed rapidly after receiving manipulation
(high velocity, short amplitude thrust) to the facet and
costotransverse joints from T3 to T5. In addition to the
sympathetic symptoms, the patient had shoulder and
upper extremity pain and dysfunction. Rapid improve-
ment in shoulder ROM and pain was noted following
the manipulations to the mid- and upper-thoracic seg-
ments.112 The authors theorized that the increased
ROM of the shoulder was because of a decrease in the
thoracic kyphosis.112
Figure 5-23 Referred pain patterns from specific
thoracic facet joints. (From Dreyfuss P, Tibiletti C, Dreyer SJ, et al:
Thoracic zygapophyseal pain: a review and description of an intraarticu-
lar block technique, Pain Dig 4:44, 1994.)
163
In addition to the thoracic spine referring pain
directly to the shoulder, injury and dysfunction in the
thoracic spine can lead to pain, injury, and dysfunction
in the shoulder. Full elevation of the arm is dependent
on elevation of the upper ribs, thoracic extension, tho-
racic side bending, and thoracic rotation. Restrictions in
any of these motions will put additional stress on the
shoulder, which may lead to repetitive strain injuries and
a limitation in shoulder ROM and function.
Symptoms. Pain is unilateral and may be felt in the
upper thoracic area and posterior portions of the shoul-
der, scapula, or interscapular region (see Figures 5-20
and 5-23). Patients may report a sharp pain or pinch if
they quickly extend or turn toward the painful side. Pain
is generally not referred to the anterior shoulder, biceps
brachii muscle, or down the arm. There are no com-
plaints of numbness, pins and needles, or specific weak-
ness in the upper extremity.
Signs. Reproduction of symptoms is expected
during the following special tests: thoracic quadrant test
in extension; passive thoracic spine extension and often
with ipsilateral passive bending or rotation; and the
seated thoracic spine compression test, in extension and
occasionally in neutral. Segment specific P/A glides in a
prone position (see Figure 5-21) may also elicit pain.
Segmental mobility examination is usually abnormal
at the suspected level. Quite often, you will find that
the symptomatic facet joint is part of a hypermobile
segment. This segment, however, may initially test hypo-
mobile because of an acute entrapment of a meniscoid
or from acute muscle guarding. Neurologic examination
results are normal, including nerve root compression and
nerve tension tests. Discogenic examination results are
normal with respect to Valsalva’s test and seated thoracic
compression in flexion.
Physician-Ordered Tests. Plain radiographs,
though helpful in examining the general morphology of
the thoracic spine, are not diagnostic. They may demon-
strate decreased disk height or osteophytosis of the
facets. Even in the presence of abnormal findings, the
clinician must realize that many asymptomatic people
have similar results on plain film radiography. MRI and
CT scans are not diagnostic for the source of pain, but
they may be helpful in terms of the general status of the
spine—revealing degenerative changes within the disk
164 SECTION II NEUROLOGIC CONSIDERATIONS
or facet joints. Myelography is not useful in this
instance. Facet joint injection blocks or anesthesia of the
medial branch of the dorsal ramus are the most accu-
rate, specific, and sensitive diagnostic examinations of
the facet joints.95,96,102
Any tissue, from the skin and subcutaneous fat down
to the center of the bones, with sensory afferent nerves
feeding into the dorsal horn of the spinal cord between
the C3 and T3 segments, is capable of referring pain and
dysfunction to the shoulder.
Rib Injuries that Refer Pain
and Dysfunction to
the Shoulder
The ribs and rib cage in general are often overlooked as
a source of pain and dysfunction related to the shoulder.
First rib injuries and diseases (for example, costotrans-
verse and costovertebral joint sprains, fractures, and
bony tumors) refer pain to the shoulder almost exclu-
sively.113-115 First rib disorders often go undiagnosed
for many months because evaluation of the painful
shoulder in the presence of a first rib injury can mimic
shoulder impingement or rotator cuff tendinitis.
Imaging studies are often directed to the cervical spine
and shoulder and therefore may not adequately visual-
ize first rib injuries. Besides the obvious problem of
delaying an accurate diagnosis and appropriate treat-
ment, fracture of the first rib can lead to devastating con-
sequences because of the proximity of the subclavian
artery, brachial plexus, and lung.
Injuries to the second or third rib at the costotrans-
verse joint may also refer pain to the shoulder.116 In these
cases, patients are often incorrectly diagnosed with a
rotator cuff tear, tendinitis, or impingement syndrome.
The impingement test is thought to give a false-positive
result secondary to the elevation and stress placed on the
upper ribs during the Neer or Hawkins procedure.116
The empty-can test (for supraspinatus tendinosis) may
also give a false-positive result because of referred pain
from the stress of the procedure on the upper ribs and
motor weakness as a result of reflex inhibition.116
Symptoms. Pain is the primary complaint and may
be perceived in the neck, chest, posterior shoulder,
scapula, or arm.113-115 The patient may report an episode
of sharp pain during a particular motion, usually a fast
motion such as during sports. If the rib injury is on the
left, the pain may mimic the symptoms of angina or a
myocardial infarction.113
Signs. There is usually full AROM of the shoulder
with pain at the end range.113-115 Full cervical AROM is
common. Tenderness may be noted in the thoracic inlet
on the first rib or deep in the axilla.1,113 Results of provo-
cational testing to the ribs (Figures 5-24 to 5-26) will
be abnormal. Various rotator cuff special tests (for
example, Hawkins, Neer, and empty-can) may produce
false-positive results because of the stress put on
the upper ribs, especially the first rib, during these
maneuvers.
Physician-Ordered Tests. Plain radiographs in an
A/P view of the cervical spine, chest, or shoulder are
usually sufficient to visualize the first three ribs. Unfor-
tunately, some clinicians fail to closely examine the
upper ribs on a cervical spine x-ray.113-115 On occasion it
may be necessary to obtain an oblique view of the shoul-
der or a supine chest x-ray. In cases of ambiguous or
subtle stress fractures, a bone scan may be necessary.
Any tissue, from the skin and subcutaneous fat down
to the center of the bones, with sensory afferent nerves
Figure 5-24 Mobility testing of the first rib. The
patient, in a supine hook-lying position, is relaxed with her
head and neck passively rotated and side bent to the affected
side in order to reduce the strain on the first rib from the
scalenus muscle group and surrounding fascia. The clinician,
using the lateral edge of the proximal phalanx of his index
finger, gently mobilizes the first rib in an inferior and medial
direction. This technique may be used in several ways: as a
provocation test for first rib injuries; to test mobility; and to
treat an elevated and/or restricted first rib.
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
Figure 5-25 Mobility testing of ribs R2-R6. The
patient, in a supine hook-lying position, is using her right hand
to cover her breast. The clinician, using the web space and the
lateral portion of his index finger of his left hand, gently sta-
bilizes the inferior rib (for example, R3). His right hand has a
firm hold of the proximal humerus that is passively guided into
flexion as his left hand assesses the mobility between R2 and
R3. This technique may be used in several ways: as a provoca-
tion test for rib injuries; to test mobility; and to treat restricted
mobility between the ribs. Note: Alternate techniques for ribs
R4-12 include mobility testing the lateral portion of the rib
cage in a side-lying position or the posterior portion of the rib
cage with the patient prone.
feeding into the dorsal horn of the spinal cord between
the C3 and T3 segments, is capable of referring pain and
dysfunction to the shoulder.
Lumbar Spine and Pelvic
Tissues Capable of Referring
Dysfunction to the Shoulder
The most direct link to the shoulder from the low back
is via the latissimus dorsi muscle. Injuries to the low back
may cause muscle guarding or adaptive shortening in
165
this muscle and subsequently make it harder for the
shoulder to achieve full elevation and full external rota-
tion, which causes stress to the tissues attempting to
elevate the shoulder. Low back injuries that substantially
alter spinal posture can adversely affect shoulder func-
tion as well. Christie and associates117 found that persons
with acute low back pain have a significant increase in
thoracic kyphosis, both in sitting and standing positions,
and demonstrate a forward head posture. The associa-
tion between posture and shoulder dysfunction was
made previously.
In erect standing, external loads applied to the spine
through the upper extremity and shoulder (for example,
resisted horizontal adduction of the shoulder) must be
counteracted by increased activity in muscles of the
lumbar spine (for example, multifidus and iliocostalis)
for the body to remain erect and in its usual posture.118
Movement of the shoulder in persons without low back
pain is preceded by contraction of the transversus ab-
dominis muscle.119 The transversus abdominis muscle is
the focus of recent research and exercise design in terms
of its role as an important stabilizer of the lumbar spine.
In persons with chronic low back pain, the transversus
abdominis contracts after the prime movers of the
shoulder contract.119 This indicates a decrease in motor
control for spinal stability in persons with chronic low
back pain. It also demonstrates the close relationship of
the lumbar spine and the shoulder. Altered motor
control and stability of the lumbar spine because of low
back pain can adversely influence the dynamic control
and coordination of the upper extremity and shoulder
since the latter depends on proximal stability for its
distal mobility. Therefore any tissue injury in the low
back that alters the posture, function, or stability of the
lumbar spine or pelvis can have an adverse effect on
shoulder function, eventually leading to an intrinsic
shoulder problem or injury.
Case Study
OVERVIEW
The purpose of our initial examination is to evaluate
the pain, the strain, and the brain. Our rehabilitation
program then focuses on treating the specific tissue pro-
ducing the pain, the various tissues producing a strain,
and the influence of the brain, using the acronym
WOMEN (wisdom, optimism, manual therapy, exercise,
and nutrition).
166 SECTION II NEUROLOGIC CONSIDERATIONS

A B

Figure 5-26 First rib special test: cervical rotation lateral flexion (CRLF) is a special test
to quickly assess if a patient may have an elevated first rib or other possible first rib injuries and dys-
functions. The patient, seated, is asked to actively rotate his or her neck as far as possible. Then,
holding that rotation, they actively laterally flex the neck as far as possible. The test result is abnor-
mal if there is a significant difference in the amount of lateral flexion from one side versus the other.
A, Testing R1 on the left: right rotation with left lateral flexion. B, Testing R1 on the right: left
rotation with right lateral flexion.

PAIN flexed, neutral, and extended posture; coughing and/or

Patients come to us because they are in pain. One of
our responsibilities is to determine the source of the
pain. This becomes a search for the primary “tissue in
lesion.” First, the therapist must determine the region
(for example, cervical spine versus shoulder) of the
painful tissue, then the specific tissue (for example, facet
joint versus intervertebral disk) in that region that is the
primary generator of the patient’s pain. Specific provo-
cational testing of all the tissues in a specific region
allows for a reasonable differentiation of the tissue, or
tissues, responsible for the pain. For example, a painful
cervical facet joint injury is provoked by different stimuli
(direct palpation and cervical axial compression in
extension only) versus a painful cervical disk injury (seg-
mental disk shear test; cervical axial compression in a
sneezing; and Valsalva’s test). Once we have found the
tissue in lesion (for example, left C5-6 facet joint
impingement), we can provide specific treatment to the
pain generator (the left C5-6 facet joint) to inhibit pain
and to provide the optimal stimulus for regeneration of
this tissue.
STRAIN
The next objective of the evaluation is to analyze all
the chronic postural and biomechanical strains that may
have caused the painful injury in the first place (pain of
gradual or insidious onset) and the strains that may be
perpetuating the pain after direct trauma (for example,
MVA). The following are examples of strains that can
produce or perpetuate pain: postural dysfunction;
poor spinal or extremity stability and motor control;
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
significant leg length differences; lower kinetic chain
dysfunction (hip, knee, foot, or ankle); adaptive short-
ening of musculotendinous tissue and fascia; and joint
hypomobilities or hypermobilities above and below the
pain generator.
The other strains to look for are co-morbid medical
diseases. Patients with systemic problems such as
rheumatoid arthritis, osteoporosis, diabetes, cardiovas-
cular disease, medication abuse, and poor diet or nutri-
tional habits (for example, high caffeine, tobacco, or
alcohol intake) can adversely affect the progress, prog-
nosis, and eventual outcome of their rehabilitation—
especially if these strains are not identified and addressed
during the time they are under our care. Patient abuse
of nonsteroidal antiinflammatory drugs (NSAIDs) over
a prolonged period also can be a strain. The prolonged
use of NSAIDs, usually as a “pain killer,” in patients who
do not have an inflammatory disease, such as rheuma-
toid arthritis, can have the following consequences: (1)
the direct interference with the regeneration of bone and
articular cartilage; (2) allow patients who would nor-
mally be limited by pain to overuse and overstress tissues
that have not yet fully regenerated; and (3) in some cases
death.120-125 As many as 16,500 people die each year in
the United States directly as a result of complications
from NSAID use.120
Once we have found the strains (thoracic kyphosis
with forward head associated with adaptive shortening
of the pectoralis minor, SCM, hip and knee flexors;
hypomobilities identified at C4-5 and C7-T4; hyper-
mobility at L4-5; chronic right ankle instability; osteo-
porosis; and a pack-a-day smoker for the past 20 years),
we can provide specific treatment to these dysfunctions
and decrease the adverse load on the primary tissue in
lesion (left C5-6 facet joint impingement). Some
patients have so many strains that it is not possible to
give specific individualized attention to every little
detail. In these cases, patient education and a compre-
hensive home instruction program can be extremely
helpful.
BRAIN
The final objective in the initial examination process
is to recognize how the patient’s brain (frontal lobe: fear,
anxiety, and depression versus motivation, determina-
tion, and optimism; and spinal cord: central sensitiza-
tion) is reacting to their injury or disease. Our treatment
plan for one patient with a left C5-6 facet joint impinge-
ment may be different versus another patient with the
167
same diagnosis, depending on the status of their “brain.”
Issues such as fear and anxiety, chronic pain, prolonged
medical leave from work, litigation, workers’ com-
pensation, signs of depression, low functional status,
poor support network, poor self-motivation, and high
dependence on others can dramatically alter both the
progress and prognosis of a patient if these issues are not
recognized and addressed.
One of the greatest things we can do for our chronic
pain patients is to remove their fear and anxiety. Many
of them will experience high levels of pain, stress, and
anxiety because they do not understand the source of
their pain, why they have hurt for so long, and what they
can do without risking reinjury. We can help remove an
enormous amount of fear and anxiety simply by educat-
ing them on their problem, their prognosis, and the
realistic likelihood of reinjury during work and ADL.
Explaining the differences between pain and injury, that
is “pain does not equal injury,” goes a long way in terms
of removing the activity and exercise avoidance issues
that many chronic pain patients exhibit because of their
fears and anxieties. This latter approach is much better
suited for the chronic pain patient rather than the
patient with an acute injury or acute surgical repair. The
patients that have an acute injury, have had recent
surgery, or have persistent pain from tissues that are
weak and not fully healed, should respect pain for safety
reasons. However, chronic pain patients who complain
long after their tissues have healed (those with central
sensitization), are the ones who truly need to understand
that reasonable activities that cause pain do not cause
injury. Our treatment approach involves providing
wisdom and optimism for the patient in hopes of alter-
ing their adverse or negative forebrain output. The goal
is to help the patient increase the pain inhibitory
impulses descending down from the forebrain, PAG,
and RVM to the spinal cord and into the dorsal horn to
raise the threshold for activation of the interneurons
responsible for nociceptive transmission.
Treatment may involve providing the patient with
options for counseling, support groups and relaxation, or
visualization techniques. Giving your patient relaxation
and breathing techniques or visual imaging exercises
can be very helpful. Patients can be taught to visualize
themselves moving their injured arm as freely as the
uninjured arm, or visualize themselves participating in
full duty work or their favorite sport. In cases of severe,
debilitating pain, have your patient visualize their pain
168 SECTION II NEUROLOGIC CONSIDERATIONS
as a red balloon that slowly shrinks in size as it changes
to blue. Staying upbeat and optimistic around the
patient and being a cheerleader can do wonders. Give
your patients a realistic prognosis for increasing their
function. Take the focus away from their pain and put it
on their functional abilities. “How are you functioning
today?” versus “How much pain do you have today?” Any
small doubts, hesitation, or negativity about recovery
that the clinician has can be multiplied and exaggerated
by the patient and used as a confirmation of their own
negative thoughts and fears about chronic pain and dis-
ability. The clinician should act and talk like an expert,
without being phony, to take advantage of the placebo
effect. If the patient perceives you as an expert, then
almost any treatment you do will help to some degree.
If the clinician acts unsure, not confident, and without
the appearance of expertise, then the patient may
loose faith in the treatment approach and even the
best manual therapy program may only be marginally
successful.
The other aspect of treatment to the “brain” involves
the spinal cord and the plastic changes that happen
within the dorsal horn in patients suffering from chronic
pain. Changes in the glutamate receptors on the postsy-
naptic neurons can lead to a facilitated segment that
now acts as the pain generator after the original primary
tissue in lesion—supraspinatus tendinosis—has healed.
Recognition of this source of chronic pain is the first
step. Treatment involves the wisdom and optimism
noted above along with manual therapy to segmentally
related tissues (for example, skin, fascia, muscle, and
joints) to provide inhibitory impulses (via type I, II and
III mechanoreceptors) into the dorsal horn to raise the
threshold for activation of the interneurons responsible
for nociceptive transmission. These soft tissue and joint
mobilizations of varying speeds and amplitudes, below
the threshold for activation of pain or muscle guarding,
have the potential to stimulate inhibitory interneurons
within the dorsal horn that will subsequently alter the
patient’s perception of the pain experience. The laying-
on of expert and caring hands to the patient can also
help calm the forebrain’s thoughts and perceptions and
help to increase the amount of inhibitory impulses
descending from the forebrain to the level of the spinal
cord.
PATIENT PRESENTATION
This case study was originally published in the
third edition of Physical Therapy of the Shoulder (edited
by Robert A. Donatelli); it is reprinted here with
minor modifications to enhance the learning experience
and to fit the format of the Guide to Physical Therapist
Practice.
DEMOGRAPHICS
Bewell is a 49-year-old right-handed white woman
and college graduate whose primary language is English.
Her health maintenance organization (HMO) covers
her medical and physical therapy care. Today, Nov. 13,
2000, is her first visit with us.
SOCIAL HISTORY
She lives with her husband and two teen-age daugh-
ters. She denies any cultural or religious beliefs that she
feels may affect her care with us. Bewell is a legal secre-
tary with a light physical demand level. Her job duties
include prolonged sitting; frequently speaking on the
phone (no head set); prolonged keyboard and mouse use
sitting at a computer; occasional reaching, lifting and
carrying up to 20 lbs; and infrequent lifting of up to
10 lbs overhead. She has been out of work since May 1,
2000.
LIVING ENVIRONMENT
Bewell lives in a two-story home with one step and
no railing leading to her front door. She denies the
existence of any substantial obstacles in and around her
home. She ascends and descends stairs with a railing
daily in her home and ambulates freely without the use
of assistive devices.
GENERAL HEALTH STATUS
She states that she is in good health and has had no
major life changes in the past year.
SOCIAL/HEALTH HABITS
Bewell drinks 3 to 4 cups of coffee a day, has smoked
half a pack of cigarettes a day for the past 25 years, and
has a couple of beers on the weekend. She does not sup-
plement her diet with vitamins, minerals, herbs, or other
health care products. Before surgery and the onset of her
symptoms, Bewell’s exercise routine included running,
the Stairmaster, step aerobics, and lifting free weights.
FAMILY HISTORY
Her father died of prostate cancer; her grandmother
died of a stroke; and she states that all the women in her
family seem to suffer from osteoarthritis.
MEDICAL/SURGICAL HISTORY
Bewell reports a history of allergies (cats), fractured
fibula (1980), borderline hypoglycemia, and a neck
injury at work in 1991 because of a tray table that hit
her on the head. She complained of neck and shoulder
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 169

pain for 1 year. She had an open-reduction-internal-

fixation surgery to her right fibula in 1980; a meniscec-
tomy of her right knee in 1981; and a caesarian section
in 1986. Concerning her left shoulder, Bewell reports
she had arthroscopic subacromial decompression surgery
in 1998 because of a work-related injury. She received a
total of at least 6 months of physical therapy (elsewhere)
before and after her surgery. Most of her symptoms
have been resolved. On May 5, 2000, she had another
surgery to her left shoulder in which the surgeon
performed a bursectomy, acromioplasty, and excision
of the distal clavicle. In the past year, she has complained
of occasional headaches, weight gain because of a
lack of exercise, difficulty sleeping, and pain at night
from her shoulder. She denies any current gynecological
difficulties, but notes she had endometriosis in 1992.
She also denied a history involving motor vehicle
accidents.
CURRENT CONDITION(S)/CHIEF COMPLAINT(S)
Bewell came to physical therapy (November 13,
2000) with a prescription for work hardening and the
following diagnosis: S/P left shoulder A-scope with
decompression. The patient reports that surgery (May 5,
2000) was performed because of chronic pain in her
shoulder. She denies experiencing any trauma to the
shoulder between her first and second surgery. Bewell
Figure 5-27 Pain diagram of a 49-year-old right-
handed woman following surgery for subacromial decompres-
states that her left shoulder pain gradually returned sion of her left shoulder.
approximately 6 months before her last surgeries. She
received 2 months of physical therapy (at another facil-
ity) following surgery, but her symptoms progressively
worsened. She then went for approximately 2 months
without therapy and her symptoms subsided. Three the pain.” She is under the care of her primary care
weeks ago, she started working out on her own by lifting physician for this problem.
weights up and over her head. Subsequently, she expe- FUNCTIONAL STATUS/ACTIVITY LEVEL
rienced a severe exacerbation of neck and left shoulder Before surgery and the onset of her symptoms, the
pain. patient’s exercise routine included running, the Stair-
Specifically, Bewell is complaining of periodic severe master, step aerobics, and lifting free weights. Bewell
(0/10 to 8/10) neck and left shoulder pain (Figure 5- scored 39 out of a possible maximum score of 100 on
27). She notes that there is a periodic “slipping out” of the Sharp Functional Activity Survey (Sharp FAS) for
her left shoulder. Bewell states that in certain positions the Neck & Shoulder region (© Sharp HealthCare
her shoulder will pop or click. She also reports a grind- 1998). Because of her use of medications to control her
ing sound in her neck if she looks up and over her pain, Bewell’s Sharp FAS score of 39 overstates her true
left shoulder. She denies headaches, dizziness, tinnitus, functional abilities. Therefore an asterisk is placed next
nausea, vision changes, swelling, radiation of pain down to her FAS score (39*). She reports moderate difficulty
the upper extremities, weakness, or paresthesia in her with most ADL with the exception of lifting and car-
upper extremities. Bewell reports that driving, talking on rying, which give her severe difficulties, and sports
the telephone, and sitting increase her symptoms. Her (surfing and basketball with her daughter) or athletic
symptoms decrease with rest. Her goal is to “get rid of activities (running, aerobics, weight lifting) that she
170 SECTION II NEUROLOGIC CONSIDERATIONS
cannot perform. She was placed on medical leave from
work 6 months ago.
MEDICATIONS
Bewell denies taking any prescription drugs other
than birth-control pills. She admits that she has been
taking Tylenol (acetaminophen = analgesic) and Advil
(ibuprofen = NSAID) almost daily since May.
OTHER CLINICAL TESTS
The only tests reported by Bewell in the past year
were a mammogram (results were normal), a blood test
(normal), and x-rays: chest (normal) and shoulder. (See
Imaging Studies.)
CARDIOVASCULAR/PULMONARY SYSTEM
Bewell has no symptoms related to her cardiopul-
monary system. She does have risk factors associated
with this system (decreased activity level, 13 pack-year
smoker, age, fear and frustration, and a family history of
stroke). However, results from recent blood tests and a
chest x-ray were normal. Therefore evaluation of this
system was deferred. Her cardiopulmonary system
would have been evaluated if our results from examina-
tion of her musculoskeletal system were abnormal.
Bewell’s cardiopulmonary system will be evaluated in
the future if her symptoms change.
INTEGUMENTARY SYSTEM
Bewell’s skin appears healthy, with a good continuity
of color and no substantial changes in temperature. Old
surgical scars are noted at her right ankle and her right
knee. Three small scars, well healed and almost white,
are also noted on the left shoulder—the result of two
previous arthroscopic surgeries.
COMMUNICATION, AFFECT, COGNITION,
AND LEARNING STYLE
There are no known learning barriers identified for
this patient. She reports that she learns best when given
a picture followed by a demonstration. Bewell did not
show any deficits with regard to her cognition, orienta-
tion, or ability to effectively communicate. She is frus-
trated with her poor recovery from surgery 6 months ago
and her inability to return to work. She is fearful of rein-
juring her shoulder by doing too much. Bewell does not
understand why she is still having shoulder pain and she
is upset because she cannot play basketball with her
daughter, who just made the local high school team. The
education needs identified for Bewell were: an explana-
tion of the source of her pain and what strains are
feeding into it; an understanding that at this stage pain
may not equal injury for her shoulder; nutritional and
diet advice; ergonomic instructions for sitting at her
computer at work; home care instructions; and home
exercises.
MUSCULOSKELETAL SYSTEM
Posture
In standing, she has a forward head posture with
rounded shoulders, protracted scapula, and a moderate
increase in her thoracic kyphosis. Notable items were a
slight increase in lumbar lordosis, mild right genu
valgum, right calcaneal valgus with excessive pronation,
and a moderate hallux valgus on the right.
Range of Motion
Cervical spine AROM:
There were moderate restrictions to cardinal move-
ments of extension, left side bending and left rotation.
Pain was reproduced during each of these motions. The
patient’s head deviated to the left during flexion and to
the right during extension. Repeated flexion, right side
bending, or right rotation failed to reproduce the
patient’s primary complaints of pain. Results from com-
bined motions of flexion, left side bending, left rotation;
flexion, right side bending, right rotation; and extension,
right side bending, right rotation were all normal. Pain
was reproduced with combined extension, left side
bending, left rotation.
Cervical spine PROM:
The same restrictions to movement were found as
with AROM. The same movement patterns that repro-
duced the patient’s pain above were also noted during
PROM testing.
Shoulder AROM:
Discomfort was reported with flexion and horizontal
adduction only. There were no limitations to motion.
Shoulder PROM:
Discomfort was reported in all directions except
internal rotation. There were no limitations to
motion.
Scapula and elbow ROM:
Results from testing were normal and non-
contributory.
Thoracic spine ROM:
Active and passive ROM testing failed to reproduce
the patient’s primary complaint of pain. Moderate
restrictions were noted with active and passive
extension.
Rib ROM:
Active and passive ROM testing failed to reproduce
the patient’s primary complaint of pain. Full expansion
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
of the rib cage during inhalation was inhibited by the
patient’s thoracic kyphosis.
Lumbar ROM:
Active ROM was WNL with a slight deviation, vari-
able from left to right on repeated examination, noted
during active extension. The patient reported pain, local-
ized to the upper lumbar spine, at the end ROM of
active extension.
Muscle Performance
Cervical spine resisted testing:
Each resisted direction (six) is isometrically tested
in three different muscle lengths: shortened, mid, and
lengthened. The purpose of the test is to differentiate
pain arising from contractile tissue (painful in all three
muscle lengths tested) versus noncontractile tissue (pain
may occur only in a position that allows the contracting
muscle to compress or stretch the truly injured tissue,
such as the cervical facet joint or, when testing the
shoulder, the supraspinatus tendon because of a position
of impingement). For example, if resisted left side
bending is abnormal in the shortened (cervical spine is
side bent left into a pain-free range), mid (cervical spine
is in neutral), and lengthened (cervical spine is side bent
right into a pain-free range) positions, then it is reason-
able to assume the pain is arising from the contractile
tissues of the left scaleni, left SCM, and/or left upper
trapezius muscle groups. If, however, resisted left side
bending is painful (on the left side) only in the short-
ened muscle length, then the pain is probably from com-
pression of a noncontractile tissue, such as the facet
joint, uncovertebral joint, intervertebral disk, or a spinal
nerve root.
For the aforementioned case study, pain was repro-
duced in the shortened range of resisted extension, left
side bending, and left rotation—tested separately. These
same symptoms were reproduced in the lengthened
range of resisted flexion, right side bending, and right
rotation—tested separately. All of these painful positions
are compressive to noncontractile tissues, such as the
facet joints on the left side of the cervical spine. Results
from resisted testing to the cervical spine were normal
when the facet joints on the left were not in a closed-
pack position.
Shoulder resisted testing:
Pain was reproduced during flexion and abduction
testing only with the muscle in the shortened position
(impingement posture). External rotation was only
painful when the muscle was in the lengthened range.
171
When pain was reported, it only occurred at the time
resistance was released—a sign of instability.
Scapula and elbow resisted testing:
Results from testing were normal and noncontributory.
Thoracic spine resisted testing:
There was no reproduction of the patient’s primary
complaint of pain.
Rib cage resisted testing:
There was no reproduction of the patient’s primary
complaint of pain.
Note: There was no pain-free weakness noted in the
muscles of the spine and upper extremities.
Sensory Integrity
This part of the examination was deferred to save
time during the evaluation and because the patient
denied having any neurologic symptoms.
Reflex Integrity
This part of the examination was deferred to save
time during the evaluation and because the patient
denied having any neurologic symptoms.
Pain
Palpation:
Pain and discomfort were reported with palpation of
the C5-6 facet joint on the left. Tenderness was noted
within the left supraspinatus and infraspinatus muscle
bellies, left upper trapezius, bilateral scalenus (left >
right), and bilateral SCM.
SPECIAL TESTS
Cervical Spine (Positive Tests)
Compression testing of the cervical spine in
extension—pain (see Figure 5-13).
Posterior and superior traction force on the neck (facet
distraction)—relief.
Left cervical quadrant test in extension—crepitus and
left local pain only (see Figure 5-17).
Shear test at C5-6, mild increase in shearing, no pain
(see Figure 5-14).
Cervical Spine (Negative Tests)
Compression tests with the cervical spine flexed and
with the cervical spine in its normal neutral
alignment
Coughing provocation test
Valsalva’s test
Right cervical quadrant test in extension
Right and left cervical quadrant test in flexion
Doorbell sign (palpating spinal nerve at the foraminal
gutter)
172 SECTION II NEUROLOGIC CONSIDERATIONS

Shoulder (Positive Tests) Sternoclavicular: Normal (grade 3) in all directions.

Sulcus sign—mild inferior capsular laxity; no pain Acromioclavicular: N/A (S/P excision of the distal
Anterior instability tests—all results indicated mild clavicle).
capsular laxity; no pain Scapulothoracic: Normal (grade 3) in all directions.
• 90°/90° anterior relocation test Thoracic spine: Slight hypomobility (grade 2) in all
• 90°/90° anterior fulcrum test directions except flexion from T1-4; slight hypomobil-
• Anterior drawer (90°) ity (grade 2) in extension from T4-9.
Shoulder (Negative Tests) Ribs: Slight hypomobility (grade 2) of the first rib
Distraction and compression of the glenohumeral on the left.
joint. Lumbar spine: Slight hypermobility (grade 4) at L1-
Hawkins’ impingement sign 2 in extension.
Empty-can NEUROMUSCULAR SYSTEM
Speed’s Bewell had no gross gait, locomotion, or balance dis-
AC joint compression orders. In general she had good motor function. Specif-
Crank test (labrum) ically, however, she had only fair motor control and
O’Brien test (SLAP) coordination of her scapula during elevation of her left
Apprehension sign arm.
Load and shift anteriorly (0°) IMAGING STUDIES
Load and shift posteriorly (0°) Plain Radiographs
Posterior instability tests Cervical:
Thoracic Spine (Positive Tests) 1998 ( June): Mild disk space narrowing at C5-6
Mobility and provocation testing using prone P/As— with minimal anterior endplate spurring and mild
limited mobility, no pain. (See Figure 5-21.) degenerative changes at the C5-6 facet joints bilaterally.
Thoracic Spine (Negative Tests) Ponticulus ponticus is again noted at C1. Other seg-
Thoracic quadrant tests in flexion and extension; ments are relatively WNL.
T1 nerve root tension test. (See Figure 5-22.) 1992 (February): WNL with incidental note of a
Ribs (Positive Test) ponticulus ponticus at C1.
Mobility and provocation testing of first rib—limited 2000 (March): Type II acromion with osteophyte
mobility on left, no pain. (See Figure 5-24.) formation at inferior acromioclavicular (AC) joint and
Cervical rotation lateral flexion “CRLF” test—limited moderate AC degenerative joint disease.
mobility on left, no pain. (See Figure 5-26.) Chest:
Ribs (Negative Tests) 2000 (February): WNL.
Deep inspiration and expiration (a measure of rib DIAGNOSIS
expansion and pain provocation) Musculoskeletal Pattern D: impaired joint mobility,
Lateral compression of mid and lower ribs (supine) motor function, muscle performance, and range of
Mobility and provocation testing of ribs R2-5 motion associated with connective tissue dysfunction;
anteriorly (see Figure 5-25). and Musculoskeletal Pattern B: impaired posture.
Mobility and provocation testing of ribs R6-12 This is a 49-year-old right-handed legal secretary
(prone) whose signs and symptoms suggest an irritable left C5-6
JOINT INTEGRITY AND MOBILITY facet joint impingement with mild anterior and inferior
Cervical spine: Slight hypomobility (grade 2) at C5- instability of her left glenohumeral joint. In addition, this
6 in flexion, right side bending, and right rotation; severe patient demonstrates poor posture; mobility dysfunc-
hypomobility (grade 1), with pain, at C5-6 in extension, tions in her thoracic and lumbar spine and first rib; and
left side bending, and left rotation. biomechanical dysfunctions in her right knee, foot, and
Shoulder: ankle. The patient appears to be an independent self-
Glenohumeral: Slight hypermobility (grade 4) in motivator in chronic pain, with some fear and anxiety
anterior and inferior glides; and slight hypomobility about her chronic pain and the fear of reinjury. She has a
(grade 2) in posterior glide. moderate intake of caffeine, tobacco, and Advil.
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
Pain. The primary pain generator for this patient
is her left C5-6 facet joint.
Strain. The strains that are exacerbating the pain
and dysfunction at C5-6 include poor posture, segmen-
tal hypomobilities in the thoracic spine, hypomobile first
rib, hypermobile glenohumeral joint, hypermobility in
the lumbar spine, mild genu valgum, and a notably
pronated foot. There is a nutritional strain via the exces-
sive intake of caffeine, tobacco, and Advil. There are no
strains identified as systemic diseases.
Brain. The patient has experienced approximately
12 months of chronic shoulder pain, 6 of those months
following surgery. Most of the primary tissue healing
in her shoulder should have occurred after 3 months.
She also has been suffering with persistent pain from an
untreated and undiagnosed cervical facet joint impinge-
ment. She has been out of work for 6 months and is
exhibiting signs of anger, frustration, fear of reinjury, and
possibly symptoms suggestive of mild depression. The
number of actively functioning type I mechanoreceptors
in the collagen tissues surrounding her neck may have
decreased because of her age and her history of neck
trauma 9 years ago. The assumption that this patient has
developed some degree of central sensitization can be
supported by the following: (1) we can expect a loss of
supraspinal inhibitory impulses from her forebrain
because of her visible anger, frustration, and fear, (2)
nociceptive impulses have been hitting her dorsal horn
at the same segment of the spinal cord for approximately
12 months, and (3) there may be a loss of inhibitory
impulses from her type I mechanoreceptors.
PROGNOSIS
Bewell has a very good prognosis for return to full
duty work and a return to full function with ADL; and
a good long-term prognosis for returning to surfing and
playing basketball with her daughter.
PLAN OF CARE
Anticipated Goals
1. Bewell’s goal: “Get rid of the pain.” Reduce her pain
experience to a minimal (3/10) level that is easily
tolerated and allows her to focus on other aspects of
her life.
2. Minimal misalignment of her sitting and standing
posture.
3. Minimize (3/10) her level of fear, frustration, and
anger.
173
4. Full cervical AROM.
5. Minimal loss of gross active thoracic spine extension.
6. Minimal (3/10) difficulty carrying up to 20 lbs, or
lifting up to 10 lbs overhead.
7. Return to meaningful employment.
8. Sharp FAS score of (80/100) without the use of med-
ications to control her pain.
9. Independent with her home care instructions and her
home exercises.
EXPECTED OUTCOMES
At the time of discharge, this patient is expected to
have minimal difficulty with most functional ADL, and
minimal difficulties returning to work and her previous
athletic activities. In addition, this patient will be
expected to take control and responsibility for her con-
tinued rehabilitation on her own with a clear under-
standing of the realistic risks of reinjury and a realistic
view of her prognosis.
INTERVENTIONS
Wisdom
The patient was educated on the anatomy and inter-
relationship of the spine and ribs to the shoulder. She
was informed that most of her pain was actually coming
from a joint in her neck and was referred towards her
shoulder. Further explanation helped the patient realize
that she could minimize discomfort to her neck and
shoulder by correcting her posture and avoiding pro-
longed or repeated positions of cervical extension.
Central sensitization was also explained to Bewell as a
phenomenon that she may be experiencing in which she
could be perceiving more frequent and more intense
pain than is necessary, that is, her nervous system may
be overreacting to some of her innocuous ADL. The
patient was also educated on all the strains feeding
into her neck problem. She was told that although her
primary pain generator was her neck, she did have some
mild anterior and inferior instability in her gleno-
humeral joint that necessitated rehabilitation. With
respect to her left shoulder, Bewell was advised to avoid
fast, ballistic movements; repetitive or sustained over-
head reaching; and motions that combined abduction
with external rotation. The patient was relieved to hear
she would not need another surgery, that the problem
was not serious, and that her prognosis for returning to
work was very good. The patient was given a home
instruction packet (HIP) for her neck and shoulder,
which detailed activity modification, home and office
ergonomics, sleeping and driving positions, pain
174 SECTION II NEUROLOGIC CONSIDERATIONS
management (hot and cold packs, light stretching,
postures of comfort, self/partner massage, and visual
imagery), nutritional advice, and a set of detailed home
exercises. Because Bewell was not taking any physician-
prescribed medications, the clinician took the opportu-
nity to discuss with her the rationale and side effects of
taking an over-the-counter NSAID for her condition.
She was encouraged to minimize her use of NSAIDs
and to review the section in her HIP that offers several
options for pain management. Because of the notable
pronation of her right foot and the biomechanical con-
sequences it may be causing up the kinetic chain, the
patient was referred to a colleague for evaluation and, if
necessary, casting for an orthotic.
Optimism
The clinician was upbeat during treatment sessions
and realistically optimistic about the patient’s prognosis.
Any level of improvement, related to functional im-
provements or musculoskeletal progress, was greeted
with great enthusiasm by the clinician. The therapist
had performed a very detailed evaluation that now
allowed every little detail of progress to be recognized.
The patient’s focus was taken away from pain and put
into function. Instead of “How are you feeling today?”
or “Where is the pain today?” or “How bad is the pain
today?” the clinician asked, “How are you functioning
today and what can you do now that you could not do
a week or two ago?” The idea here is to refocus atten-
tion on function, and away from the pain and injury.
Manual Therapy
Soft tissue mobilization (STM) was performed on
the muscles and fascia of the spine, rib cage, and
shoulder that were in guarding or demonstrating adap-
tive shortening. In this case, the targeted muscles were
the SCM, pectoralis minor, scalenus, trapezius, and
subscapularis. The STM was performed with varying
degrees of speed and force. In general, low velocity com-
bined with high force will give you the greatest gains in
ROM. Conversely, high speed combined with low force
can produce the greatest gains in pain reduction. This
latter approach involves rapid and repeated stimulation
of mechanoreceptors in the various connective tissues
(for example, skin, muscle, tendon, fascia, ligament, and
joint capsule) to provide a high intensity afferent stim-
ulus to the dorsal horn for inhibition. The ability to
provide inhibitory impulses, versus facilitatory, to the
dorsal horn depends on the clinician’s ability to avoid
overstimulating any hyperreactive or hyperirritable
(acute injury or inflammation, for example) tissues
during the performance of the STM. Techniques may
include STM without joint motion (effleurage, petris-
sage, tappotment, vibration, transverse friction, skin
rolling, and myofascial trigger point techniques), STM
with joint motion (PROM, shorten-anchor-stretch,
stripping, and tendon sheath gliding), passive pump
massage (Figure 5-28), active pump massage (Figure
5-28), and STM with a contract-relax or hold-relax
component.
Joint mobilization was performed on the C5-6
segment in order to inhibit pain, decrease muscle guard-
ing, and increase joint mobility. A stretch articulation,
usually held for at least 10 seconds, was used in the
direction of facet distraction (Figure 5-29). This stretch
of the facet joint collagen accomplishes several goals: (1)
stretching for at least 10 seconds will allow the collagen
to creep, thereby increasing mobility; (2) the stretch will
stimulate fibroblasts, which will in turn increase their
production of collagen fiber and GAG (glycosamino-
glycan). This increase in GAG production will lead to
an increase in elasticity and eventually mobility as well;
and (3) stretching the joint capsule in distraction (versus
a flexion or extension glide) will stimulate the greatest
number of mechanoreceptors (Type I is preferentially
activated by an end range stretch versus Type II) avail-
able to inhibit pain and muscle guarding. An alternate
technique is performed with the patient seated, using a
method that unilaterally distracts only the involved facet
joint (Figure 5-30). This last technique can also be used
for a short-amplitude, high-velocity thrust. A short-
amplitude, high-velocity thrust is particularly helpful in
patients with an acute meniscoid entrapment. Oscilla-
tory articulations, gliding the facet joint back and forth
at various speeds and amplitudes, were also part of our
patient’s treatment plan. Oscillations accomplish several
goals: (1) to help maintain newly gained ROM follow-
ing a stretch articulation, (2) to inhibit pain via prefer-
ential activation of type II mechanoreceptors (most
active in the beginning and mid range of capsular
tension and an important emphasis in patients who may
have lost some of their superficial Type II mechanore-
ceptors), and (3) to provide nutrition to the hyaline car-
tilage of the facet joint through repeated intermittent
compression-decompression and gliding motions. This
latter goal is achieved by decreasing the viscosity of the
synovial fluid, which allows for a greater absorption of
the synovial fluid (nutrients) into the articular cartilage.
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 175

A
B

Figure 5-28 Passive and active pump massage of the upper trapezius muscle. Passive pump massage: A, The clini-
cian uses his left hand, which has a firm grip just proximal to the patient’s elbow, to shorten the upper trapezius. His right
hand anchors a portion of the upper trapezius muscle belly. B, The clinician passively stretches the patient’s upper trapez-
ius muscle using his left hand to pull down on the humerus. The clinician progressively releases his right hand from the
muscle belly, as the muscle tenses under his hand because of the stretch into a lengthened ROM. Repeat rhythmically.
Active pump massage: B, The clinician uses his left hand, which has a firm grip just proximal to the patient’s elbow, to
lengthen the upper trapezius. His right hand anchors a portion of the upper trapezius muscle belly. A, The patient actively
contracts her upper trapezius muscle, actively elevating the scapula, as the clinician supports, but offers no resistance to her
elbow. The clinician progressively releases his right hand from the muscle belly, as the muscle bulges under his hand because
of the contraction into a shortened ROM. Repeat rhythmically. (From Yousef Ghandour’s private collection.)

A B

Figure 5-29 Bilateral distraction of the C5-6 facet joints. A, The clinician is stabilizing the laminae of C6 with
the fleshy pads of his thumb and index finger of his left hand and firmly grasping C5 with the thumb and index finger of
his right hand. The spine is “locked” in flexion from the occiput down through C4-5. B, The patient relaxes in a supine
hook-lying position with her head slightly off the edge of the table. Her head is held firmly between the clinician’s forearm
and the anterior portion of his shoulder. At this point, a distraction force is produced by the clinician depressing his shoul-
der girdle down and back, which also allows the patient’s occiput and C1-5 to move down and back—away from C6. With
the occiput through C4-5 “locked” in flexion, movement occurs only at the C5-6 segment and perpendicular to the plane
of the facet joints.
176 SECTION II NEUROLOGIC CONSIDERATIONS

A B

Figure 5-30 Unilateral distraction of the left C5-6 facet joint. A, The clinician “locks” the
occiput down through C4-5 in flexion and right side bending (the midcervical spine will naturally
rotate right). The patient’s forehead rests on the clinician’s left biceps. B, The ulnar side of the clin-
ician’s left hand grasps the posterior arch of C5. The clinician’s right thumb stabilizes the C6 segment
by applying pressure to the right side of the C6 spinous process. A glove is used to improve traction
and stabilization. Keeping the midcervical spine in flexion and right side bending/right rotation, the
clinician uses his left arm to rotate occiput through C5 to the left as a single fixed unit. Since C2-
3 through C4-5 is “locked” in flexion, right side bending, and right rotation, the mobilization force
into left rotation is focused at the C5-6 segment.

Joint mobilizations were also performed on the
strains identified for this patient. In particular, joint
mobilizations were directed at the left first rib (see
Figure 5-24), posterior glenohumeral joint (Figure 5-
31), and thoracic spine (Figure 5-32).
Exercise
Following the manual therapy at each visit, our
patient completed a series of therapeutic exercises
involving the principles of scientific therapeutic exercise
progressions (STEP), which originated from medical
exercise therapy (MET).126,127 Initially the patient was
instructed to exercise the joints for self-mobilization
and coordination at 40% to 50% of her one repetition
maximum (1 RM)—usually 40 to 50 repetitions per set.
The purpose here is to build on the mobility gained
during the manual therapy. The light resistance allows
for a greater number of repetitions without achieving
muscle fatigue. Her self-mobilization exercises included
supine cervical retraction, seated thoracic extension, and
thoracic rotation exercises using a wedge and a mobi-
lization bench (Figure 5-33). In addition, exercise to
vascularize the muscles and tissues that have been in
guarding, ischemic, and full of lactic acid and other
metabolic waste products is performed at 60% of 1
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 177

Figure 5-31 Bilateral distraction of the T3-4 facet joints. A, The patient is in a supine hook-lying posi-
tion with her hands behind her neck and her elbows together. The clinician wraps his right arm around her
elbows and grabs the posterior portion of her left shoulder with his right hand. The clinician “locks” C0-1 down
through T2-3 in flexion by depressing or elevating his shoulder girdle as needed. When the clinician depresses
his shoulder girdle against the patient’s elbows, he induces thoracic flexion. Conversely, when the clinician ele-
vates his shoulder girdle, he induces thoracic extension, B, The clinician makes a fist, or semifist, with his left
hand and places it under the patient to stabilize the T4 segment. The spinous process of T4 falls between the
clinician’s thenar eminence and the middle phalanx of his middle finger. The right transverse process of T4 is
stabilized by the thenar eminence of the clinician’s left hand, and the left transverse process of T4 is stabilized
by the middle phalanx of the same hand. A, Using his body weight and shoulder girdle, the clinician pushes
through the patient’s elbows, in the direction of her left humerus, posteriorly and superiorly. Since the occiput
through T2-3 is “locked” in flexion, the distraction force is focused at the T3-4 segment. A wedge may be sub-
stituted for the hand for stabilization. This technique can also be performed as a high-velocity short-amplitude
thrust.

RM—usually 25 to 30 repetitions per set (Figure 5-34).
The patient should experience substantial muscle fatigue
before reaching the 30th repetition. Rest for as long as
a minute between sets may be necessary in some cases
in order for the muscle to recover. The primary muscles
in guarding for this patient are the SCM, pectoralis
minor, trapezius, scalenus, and subscapularis. Develop-
ment of muscle coordination usually requires thousands
and thousands of repetitions. To achieve this level of
repetitions, six to eight different neck and shoulder exer-
cises are often required with three to five sets per exer-
cise. As weakness, muscle guarding, and joint limitations
subside, additional exercises may be added to the pro-
gression. Exercises in this stage of the rehabilitation
process have a strong emphasis on the coordinated
actions of the spine with the shoulder in functional
178 SECTION II NEUROLOGIC CONSIDERATIONS
Figure 5-32 Extension mobilization of the T3-4
facet joints. The patient is in a side-lying position with her
hands behind her neck and her elbows together. The clinician
wraps his right arm around her elbows and grabs the posterior
portion of her neck, on top of her hands, with his right hand.
The distal portion of the patient’s triceps is resting against the
clinician’s right biceps. His left hand is pinching, between his
thumb and index finger, and stabilizing the T4 segment. The
clinician gently shifts his weight to the right, pushing against
the patient’s arms and elevating them, to produce an extension
mobilization specific to T3-4.
movement patterns (Figure 5-35). In general, exercises
are progressed from supported to unsupported; non-
weight bearing/gravity eliminated to weight bearing/
against gravity; 40% to 50% 1 RM to 80% 1 RM; high
repetition (40-50) to low repetition (15-20); endurance
and coordination to power; slow speed to fast; and single
plane exercises to multiplane functional synergies.
Nutrition
Bewell was provided with extensive nutritional advice
and a few select high quality research studies to support
the advice given by her therapist. Specifically, Bewell was
instructed to avoid the following: (1) tobacco—besides
the well known increased risk for cardiovascular disease,
stroke, and lung cancer, smoking has also been associ-
ated with a loss of bone density, increased degenerative
disk disease, and increased musculoskeletal pain;129-133
(2) caffeinated drinks—such as coffee, tea, and soda—
the caffeine increases the urinary loss of calcium and
magnesium;134,135 and (3) sources of arachidonic acid—
precursor to prostaglandin E2, which stimulates the
inflammatory response, nociceptors, and hyperalge-
sia.136-139 Sources of arachidonic acid include red meats
(beef, pork, lamb, and organ meats), shellfish (lobster,
shrimp, and clams), and dairy fats (milk and cheese
products). For this chronic pain patient, there is no
reason for her to be taking NSAIDs, especially consid-
ering all the potential side effects, the risk factors, and
the interference with the regeneration process of her
tissues. If necessary, she can continue to take a safe anal-
gesic like Tylenol. Safer methods of pain control are cold
or hot packs, home STM/stretching, relaxation tech-
niques, visual imagery, or a home TENS unit.
She was then advised to supplement her diet with the
following: (1) glucosamine sulfate, chondroitin sulfate,
vitamin E, and vitamin C to slow down the process
of degenerative joint disease at C5-6 and elsewhere.
Patients with diabetes or shellfish allergies should
consult their physician before taking glucosamine
sulfate. Those on blood thinners should consult their
physician before taking chondroitin sulfate.140-152 (2)
Magnesium to support muscle performance, strength
training, and bone density;153-156 (3) microcrystalline
hydroxyapatite (a source of calcium), zinc, copper, man-
ganese, and vitamin D3 to minimize the possible adverse
effects on this 49-year-old woman’s bone density, sec-
ondary to the heavy tobacco and caffeine intake;157-161
(4) bioflavonoids, which have been shown to inhibit the
release of arachidonic acid, work as an antiinflammatory
agent, and decrease tissue degeneration;162-164 and (5)
omega-3 fatty acids (EPA = eicosapentaenoic acid and
DHA = docosahexaenoic acid), which have been shown
to inhibit the metabolism of arachidonic acid and
provide a mild long-term antiinflammatory effect.165,166
Sources of omega-3 fatty acids include cold-water fish
(Atlantic mackerel, Atlantic herring, blue fin tuna, and
salmon), nuts (butternuts and walnuts), and oils
(flaxseed, soybean, canola, fish oil, cod liver oil, and
walnut).
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER 179

Figure 5-33 Self-mobilization exercises for the thoracic spine. Combining coordination exercise of the
neck and shoulder with a mobilization technique to increase extension and left rotation of the upper thoracic
spine. The initial progression for our patient, with the mild anterior and inferior glenohumeral capsular laxity
and the left C5-6 facet joint impingement, was to have her perform straight extension with her hands behind
her neck and her elbows adducted. A, Progression of self-mobilization technique for the upper thoracic spine
incorporating a greater demand on the patient to be able to control the movement of both her neck and shoul-
der towards a ROM associated with pain and instability. B, A less specific thoracic mobilization with a greater
demand, the patient is holding a 2-lb weight, for coordinated motion of the neck and shoulder.

Figure 5-34 Exercising the internal rotators of the
shoulder while placing a demand on the spine to maintain
good postural alignment and stability.
Summary
Every patient who has a history of gradual onset shoul-
der pain, even occupational repetitive injuries, should
always receive a screening of the cervical and thoracic
spine and ribs to rule out referred symptoms. Even in
cases of irrefutable direct shoulder injury and pathologic
conditions, the spine and ribs need to be evaluated for
dysfunctional strains that can aggravate and perpetuate
shoulder pain and dysfunction. In the absence of an
identifiable cervical disorder, the patient may still benefit
from articulation to the joints of the cervical spine to
achieve pain and muscle guarding reduction in cases in
which shoulder mobilization is contraindicated, that is,
in acute injury, immediately post surgery, or in cases of
patient anxiety.
180 SECTION II NEUROLOGIC CONSIDERATIONS

A B

Figure 5-35 Examples of exercises integrating the coordinated

efforts of the spine with the shoulder. A, Upper trunk rotation and
scapula retraction with the pelvis and lower extremities stationary. B,
C Patient starts facing the pulley in a stooped posture with her spine in
flexion and left rotation, then moving into spine extension and right
rotation with accompanying shoulder flexion. C, The standing resisted
“swimmers” exercise is one of the most challenging for coordinating
movements of the spine and extremities.
CHAPTER 5 INTERRELATIONSHIP OF THE SPINE, RIB CAGE, AND SHOULDER
The spine, ribs, and shoulder are codependent, and
as such, inseparable. You cannot work solely on the
shoulder of a patient who complains of shoulder pain.
The joints and soft tissues of the spine and rib cage also
need manual therapy and exercise. Conversely, you
cannot simply treat the neck of a patient who complains
about his or her cervical spine. As noted in this chapter,
the spine and ribs need to be evaluated for referred pain
and strains. In addition, the contribution of the brain
(forebrain and spinal cord) cannot be ignored. Treat-
ment then is focused on rehabilitation for the pain,
strains, and brain utilizing techniques incorporated in
the acronym WOMEN (wisdom, optimism, manual
therapy, exercise, and nutrition).
ACKNOWLEDGMENTS
The authors would like to thank Yousef Ghandour,
AnneMarie Kaiser, Jim Rivard, Andrew Vertson, and
Nancy Zavala for their assistance in preparing the
figures in this chapter for publication.
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Neural Tissue Evaluation
and Treatment
U pper quarter pain includes pain perceived in
variable regions of the neck, upper back, upper
chest, suprascapular area towards the shoulder,
shoulder, and arm. Associated headache is a frequent
accompaniment. In the absence of any form of neuro-
logic deficit of the peripheral nervous system or in the
absence of definitive results from diagnostic tests such
as imagery techniques, diagnoses may ensue as a result
of individual clinician bias. Although diagnostic bias
with respect to upper quarter pain syndromes may result
from trends and areas of clinician specialty, it may fre-
quently relate to inadequate physical examination of the
neuromusculoskeletal system.
In this chapter an aspect of clinical practice and phys-
ical examination is presented that we have found
fundamental to the clinical reasoning process, or the
logic, necessary to evaluate upper quarter pain syn-
dromes. Presentation of the topic in this way should not
be construed as the author’s bias toward neural tissue
being a major origin of pain or the tissue of involvement
in most upper quarter pain syndromes. A detailed eval-
uation and assessment of the findings is required before
any clinical hypothesis or diagnosis regarding neural
tissue as a pain source can be made. Even then, an open
mind is essential, and continued critical assessment is
necessary.
In neuromuscular disorders, identification of the
source of pain is essential before administration of phys-
ical treatment or prescription of patient-generated treat-
ment programs. Among a range of physical evaluation
tests to assist in this task are neural tissue provocation
187
6
Robert L. Elvey
Toby Hall
tests. Tests used to diagnose upper quarter pain dis-
orders, originally described by Elvey in 1979,1,2 have
gained popularity in physical therapy literature in recent
years.3,4
This chapter deals with pain disorders unaccompa-
nied by neurologic deficit and without definitive inves-
tigative diagnostic results. This type of disorder of the
upper quarter is very common in physical therapy and
manual therapy practice. The most apt descriptive term
is cervicobrachial pain syndrome or cervicobrachial disorder.
The diagnostic term radiculopathy, although techni-
cally incorrect for the cervical spine, is frequently and
loosely used in referring to upper quarter pain disorders
when pain radiates as far as the forearm or hand.
Radiculopathy may therefore be considered an appro-
priate term for communication purposes within the
context of neuromusculosketal pain, but it may also be
considered incorrect in the absence of evidence of neu-
rologic deficit of the peripheral nervous system.
Incidence in the Community
When measured in terms of lost productivity, medical
treatment costs, and disability insurance claims, upper
quarter pain in the form of cervicobrachial pain syn-
drome and cervical radiculopathy represents a substan-
tial problem for society. In the United States there was
an increase of 45% in the rate of hospitalization for cer-
vical spine surgery between 1979 and 1990.5
Because of the lack of population-based studies, the
precise incidence of cervicobrachial pain is not known.6
188 SECTION II NEUROLOGIC CONSIDERATIONS
However, several investigators have addressed this
problem. Thirty-four percent of responders to a cross-
sectional questionnaire of Norwegian adults reported
“neck pain” in the previous year. Fourteen percent
reported neck pain that lasted more than 1 year.7
Lawrence,8 who surveyed 3950 persons in England,
found that 9% of men and 12% of women complained
of cervicobrachial pain. Furthermore, Hult9 showed that
the mean incidence of neck stiffness and arm pain in
Swedish working men aged 25 to 54 years was 51%.
The most incidences were between the ages of 45 and
49 years. An extensive epidemiologic survey of cervical
radiculopathy was carried out in Rochester, Minn.,
between 1976 and 1990.10 This survey of 70,000 people
uncovered 561 subjects, mostly male, with cervical
radiculopathy. Their ages ranged from 13 to 91, with a
mean age of 38 years for both men and women. The
average annual age-adjusted incidence rates per 100,000
were 83 for the total, 107 for men, and 64 for women.
The age-specific annual incidence rate per 100,000
population reached a peak of 203 for the age group
between 50 and 54 years.
The onset of cervicobrachial pain or radiculopathy
can either be traumatic or insidious. Frequently in an
older patient with preexisting cervical spondylosis, no
single traumatic event is recalled and the clinical picture
develops insidiously.11 In their review of cervical radicu-
lopathy, Ellenberg and associates12 reported that 80% to
100% of patients have arm pain, with or without motor
weakness or paresthesia, and generally without preced-
ing trauma or other determinable precipitating cause.
In summary, cervicobrachial pain and cervical radicu-
lopathy are relatively common. Recurrent episodes of
cervicobrachial pain and cervical radiculopathy increase
in incidence with age and there is usually no precipitat-
ing trauma. A frequently seen cause of these disorders is
motor vehicle accidents involving “whiplash” injuries of
the cervical spine.13
Upper Quarter Pain
In the evaluation of pain and the various types of “pain
patterns” that may accompany disorders of the upper
quarter, it is essential for the clinician to keep an open
mind with respect to any judgment of the tissue of origin
of pain. Although symptoms such as tingling, burning,
pins and needles, and numbness are generally accepted
as an indication of a pathologic condition affecting the
nerve root or peripheral nerve trunk, unaccompanied by
paresthesia, pain may be very difficult to analyze in
terms of tissue of origin. The pain may be of the fol-
lowing types:
1. Local pain, where it may be an indication of
pathologic conditions in somatic tissues
immediately underlying the cutaneous area of
perceived pain
2. Visceral referred pain, where a visceral disorder may
cause a perception of pain in cutaneous tissues
distant to the viscera involved
3. Somatic referred pain, giving rise to perceived pain
in cutaneous tissues distant to the somatic tissues
4. Radicular referred and neuropathic referred pain,
where it is again perceived in cutaneous tissues that
may be distant from pathologic neural tissues
5. Variable combinations of the preceding
Although detailed descriptions of nociception, the
physiology of pain, and the mechanisms of somatic,
visceral, and radicular referral of pain are beyond the
scope of this chapter, a brief outline will be given to help
gain an understanding of the topic.
Referred Pain
The phenomenon of referred pain is well recognized, but
not well understood. It is a frequent source of difficulty
in the identification of symptomatic vertebral segments
and soft tissues, and therefore in correctly localizing
treatment.14
The topography and nature of referred pain in any
one person is inadequate as a single factor in differen-
tial diagnosis of both the tissue involved and the seg-
mental level.15 Two types of referred pain are recognized:
somatic referred pain and radicular pain.
Somatic Referred Pain
Somatic referred pain is pain perceived in an area adja-
cent to—or at a distance from—its site of origin, but
usually within the same spinal segment.16 A number of
theoretical models have been put forward to explain
somatic referred pain.17 One theory, which is supported
by sound experimental evidence, is that the anatomic
substrate for somatic referred pain is the convergence
of afferent neurons from one body region onto central
nervous system neurons, which also receive afferents
from topographically separate body tissues.15 Figure
6-1 illustrates one of the physiologic mechanisms
thought to be responsible for somatic referred pain. In
this case, there is afferent input from an intervertebral
disc that is converging on the same neuron in the dorsal
CHAPTER 6 NEURAL TISSUE EVALUATION AND TREATMENT
Figure 6-1 A physiologic mechanism for somatic
referred pain.
horn as neurons from the skin in a topographically sep-
arate area.
Inman and Saunders18 put forward the concept of
myotomes and sclerotomes to explain segmentally
referred pain from deep structures, a concept similar to
that of the dermatomes for cutaneous sensation mapped
by Foerster.19 Dermatomic, sclerotomic, and myotomal
charts published in standard texts should not be taken
as patterns to which referred pain must invariably
conform. There is known to be wide variation between
individuals in the patterns of referred pain.20,21
There have been numerous studies of referred pain
patterns following noxious stimulation of different
tissues in the cervical spine. Landmarks in the study
of referred pain are the investigations by Kellgren,22
Cloward,23 and Inman and Saunders.18 Cloward23
studied pain referral patterns during cervical discogra-
phy. His findings prompted him to assert that pain radi-
ated almost exclusively into the dorsal aspect of the
upper trunk and arm. These findings have subsequently
not been supported.24 Recently pain patterns associated
with cervical zygapophyseal joint stimulation have been
investigated.25-27 The results have vindicated the use of
pain charts to accurately predict the segmental location
of the symptomatic joint(s) in patients with cervical
zygapophyseal joint pain.26
Radicular Pain
Radicular or projected pain is pain perceived to be trans-
mitted along the course of a nerve either with a
segmental nerve or a peripheral nerve distribution,
depending on the site of the lesion.16 Examples of pro-
jected pain with segmental distribution are the pain of
radiculopathy, caused by herpes zoster, or other diseases
189
involving the nerve trunk before it divides into its major
peripheral branches. Examples of projected pain with
peripheral distribution include trigeminal neuralgia,
brachial plexus neuralgia, and meralgia paresthetica.16
Two types of pain following peripheral nerve injury
(neuropathic pain) have been recognized: dysesthetic
pain and nerve trunk pain.28 Dysesthetic pain is pain
perceived in that part of the body served by the damaged
axons (Figure 6-2). This pain has features that are not
found in deep pain arising from either somatic or vis-
ceral tissues. These include abnormal or unfamiliar sen-
sations, frequently having a burning or electrical quality;
pain felt in the region of sensory deficit; pain with a
paroxysmal brief shooting or stabbing component; and
the presence of allodynia.17
Nerve trunk pain is pain that follows the course of the
nerve trunk. It is commonly described as deep and
aching, familiar “like a toothache,” and made worse with
movement, nerve stretch, or palpation.28
In an individual with a nerve injury, dysesthetic pain,
nerve trunk pain, or both may be present.28 For this
reason it can sometimes be difficult to distinguish, on
subjective grounds, between referred pain arising from
either somatic tissues or neural tissues.29 The pain and
paresthesia that occur in cervical radiculopathy are not
localized well anatomically because a number of roots
may cause a similar distribution of pain or even pares-
thesia. In a study of 841 subjects with cervical radicu-
lopathy, Henderson and associates30 found only 55% had
pain following a typical discrete dermatomic pattern.
The remainder had diffuse, nondermatomic distributed
pain. By contrast, Smyth and Wright31 stated that lower
limb radicular pain is felt along a narrow band “no more
than one and a half inches wide.”
Figure 6-2 Radicular pain.
190 SECTION II NEUROLOGIC CONSIDERATIONS
Evaluation
Combinations of local pain of somatic origin, somatic
referred pain, and radicular referred pain are commonly
encountered in disorders evaluated for physical therapy
intervention. Peripheral referred neuropathic pain is also
seen as a discrete symptom or in combination with other
patterns of pain.
To evaluate a disorder for effective manual therapy
management, the clinician must carry out a physical
examination without presuming the source of symptoms
and in a manner that results in a sufficient number of
signs correlating with and supporting each other in the
formulation of a clinical hypothesis or diagnosis.
In the evaluation of neural tissue for possible
involvement in a disorder, clinical experience indicates
that a number of very specific correlating signs must
be present before any suggestion that neural tissue is
involved can be made. This is necessary for accurate
treatment prescription when considering a manual
therapy approach. Physical treatment, in the form of
manual therapy, cannot be prescribed from imagery or
nerve conduction studies, although it may well be
strongly influenced and guided by such studies even to
the degree that the results of either may contraindicate
manual therapy.
The physical signs of neural tissue involvement
include the following:
Physical Signs of Neural Tissue Involvement
1. Active movement dysfunction
2. Passive movement dysfunction, which must
correlate specifically with 1
3. Adverse responses to neural tissue provocation
tests, which must relate specifically and
anatomically to 1 and 2
4. Hyperalgesic responses to palpation of specific
nerve trunks, which must relate specifically and
anatomically to 1 to 3
5. Hyperalgesic responses to palpation of cutaneous
tissues, which relate specifically and anatomically
to 4 and 6
6. Evidence in the physical examination of a local
area of abnormality, which would involve the
neural tissue showing the responses in 3 to 5
The physical therapist involved in treating disorders
of the upper quarter must also consider visceral referred
pain. Obviously medical referral of patients should over-
come this potential problem for the physical therapist.
However, not all visceral conditions are readily diag-
nosed during a routine medical or clinical evaluation.
Should a condition of viscera be accompanied by strong
shoulder pain and active shoulder movement restriction,
there may be some difficulty in making a clinical diag-
nosis involving viscera.
The liver, diaphragm, and heart are viscera requiring
particular consideration when the physical therapist sus-
pects the possibility of visceral referred pain. If any sus-
picion or doubt exists, medical opinion must be sought.
We have seen examples of this need twice in the past
year. The first example was a liver disorder in a middle-
aged woman who saw her doctor because of increasing
severity of pain in the right lower chest and upper right
abdominal quadrant, which she said radiated from the
middle of her back. She had pain on the right side of
the neck, right shoulder, and upper arm, and had diffi-
culty elevating her arm above the shoulder level. She was
very tender on palpation of the right upper abdominal
quadrant and the midthoracic spine. Her doctor referred
her for examination, including ultrasonography of the
liver and plain radiographs of the thoracic spine.
The ultrasonogram was reported as normal, and the
plain radiographs indicated mild degenerative changes
evident in the midthoracic levels. She was referred for
physical therapy for treatment, with the thought that her
chest pain was either somatic or radicular referred. We
were not happy with the situation and contacted the
referring doctor, who investigated the patient further.
The result culminated in a diagnosis of liver disease.
Of concern to us was the paucity of physical evalua-
tion findings to suggest a muscular or neuromuscu-
loskeletal disorder. In addition, we were concerned by
reproduction of right lower chest pain on palpation of
the anterior surface of the right scalenus anterior muscle,
which travels on the phrenic nerve. We were also con-
cerned about reproduction of shoulder pain on palpation
of the upper trunk of the brachial plexus in the right
posterior triangle of the neck and reproduction of both
shoulder and chest pain on provocation tests of the right
upper limb when involving the upper trunk. In addition,
although palpation of the right upper abdominal quad-
rant was extremely painful locally, it also caused pain to
be perceived in the right side of the neck.
CHAPTER 6 NEURAL TISSUE EVALUATION AND TREATMENT
In the absence of other physical findings—in partic-
ular any spinal dysfunction—and in keeping with the
severity of the pain, we postulated that a liver disorder
was indicated because of the resultant diaphragm irri-
tation, phrenic nerve sensitization, and subsequent
facilitation of the related cervical dorsal horn neurons
resulting in perceived shoulder and arm pain and sensi-
tization of the upper trunk of the right brachial plexus.
These findings excluded physical therapy as a treatment
option and a physician treated her.
A second example was a middle-aged man who had
received physical therapy, upon referral by his doctor, for
neck and bilateral shoulder pain. On this occasion, he
was not referred but had seen his doctor. He complained
of neck stiffness and a heavy feeling with some pain in
both upper arms, extending from his neck. Because of
his previous history of neck-related shoulder symptoms
he sought physical therapy. The symptoms were activity
related on all occasions.
As in the first example, physical evaluation did not
show any dysfunction of the neuromusculoskeletal
system that was in keeping with his complaint. He was
referred back to his doctor, who referred him for cardiac
stress testing. This revealed coronary artery insufficiency
and he underwent medical treatment.
Of note were the right upper limb symptoms, which
would relate again to spinal dorsal horn sensitization—
including a mechanism of contralateral sensitization
resulting in the bilateral referred pain of visceral origin.
These cases, together with three cases of thoracic
outlet area tumors also seen in our practice and referred
for treatment for “stiff painful shoulder” syndrome,
highlight the necessity of careful evaluation of indica-
tions resulting from accurate differential physical tests.
With respect to neural tissue involvement, the signs
were present earlier and will be discussed further.
It is necessary to consider the sensory innervation of
the connective tissues by the peripheral nervous system
and the relative dynamics of peripheral nerves to under-
stand the structured scheme of evaluation for the pres-
ence of specific signs. Nerves and nerve tissue, when
sensitized by pathologic events, can become a source
of pain because of an inherent sensory innervation.28
When diseased, nerve tissue may cause a projection
of pain to be perceived along the course of anatomically
related peripheral nerve trunks. The peripheral nerve
trunks in turn become sensitized and thus hyperalgesic.
The target cutaneous tissues of the affected neural
191
tissues become sensitized and tender.20 Herpes zoster
(shingles) and causalgia are good examples of the signs
attributed to pathologic neural tissue, nerve as a pain
source, and peripheral nerve trunks that can become
hyperalgesic.
Peripheral nerve trunks are dynamic relative to the
associated movement of anatomic surrounding tissue
and structures. This means that nerve trunks have to
adapt to positional changes of posture with movement
of both the trunk and limbs. In other words, they have
to be compliant with movement. Therefore nerve trunks
can be physically tested in a selective manner.
If nerve tissue becomes abnormal, and therefore
tender and hyperalgesic, the outcome would be pain
associated with any trunk or limb movement in which
the trunks of that nerve tissue had to adapt. The nerve
trunks would become noncompliant with movement
because of the pain. This noncompliance would be
demonstrated by limitation of movement, where the
limitation is because of muscle tone and activity in
groups of muscles antagonistic to the direction of move-
ment. In other words, the muscles would prevent pain
by halting movement. (See the section on electromyo-
graphy (EMG) responses later in this chapter.)
In more severe cases of pain with neural tissue origin,
the increased tone of muscles becomes widespread and
may involve muscles quite distant from the source of
pain. In addition, a type of dystonia may be present,
whereby an upper quarter pain syndrome of neural tissue
origin may appear as a “painful stiff shoulder” or “frozen
shoulder.” Hence the common clinical presence of
tumors in the thoracic outlet region (for example, a
Pancoast tumor), in which the tumor cells invade the
nerve trunks resulting in nerve trunk pain, is one of
“stiff painful shoulder” or “frozen shoulder.”
The signs associated with neural tissue abnormalities
listed above require very careful and precise evaluation,
an open mind as to the significance of each sign, and an
open mind with respect to the formulation of a clinical
hypothesis.
Active Movement Dysfunction
Previous studies1 have shown that a position of
shoulder girdle depression, shoulder abduction/lateral
rotation, elbow extension, and wrist/finger extension,
with the cervical spine in contralateral lateral flexion, has
the effect of placing the neural tissues of the brachial
plexus and related cervical neural tissues and peripheral
192 SECTION II NEUROLOGIC CONSIDERATIONS
nerve trunks in the upper limb in a maximum anatom-
ically lengthened state.
It has also been demonstrated that any movement of
the upper quarter to attain this position will influence
the same neural tissues to variable degrees. Neural
tissues as a structure slide within the anatomic sur-
rounding tissues, or the surrounding anatomic tissues
glide over the neural tissues, or both as in functional
movement. Hence in causalgia conditions, in which a
nerve is painful, a patient will display active movement
dysfunction. So will a patient with shingles when the
herpes zoster virus affects a dorsal root ganglion of the
brachial plexus. In the same manner, a patient with a
Pancoast tumor affecting the lower trunk of the brachial
plexus will have a “painful stiff shoulder.”
With applied anatomy, it becomes clearly evident
that different anatomic positions of the shoulder, elbow,
and wrist will influence the peripheral trunks of the
brachial plexus in different ways. The median nerve will
be in its most lengthened state in the position described
at the start of this section. The radial nerve will be in
its most lengthened position with abduction/medial
rotation of the shoulder, elbow extension, wrist/finger
flexion in the position of the shoulder girdle depression,
and cervical spine contralateral lateral flexion. The ulnar
nerve will be in its most lengthened position with
abduction/lateral rotation of the shoulder, elbow flexion,
wrist/finger extension, and again with the same common
position of the shoulder girdle and cervical spine.
If any neural tissue tract of the upper quarter becomes
involved in a painful disorder, various active movements
will be affected, depending on the involvement of the
particular tract. Obviously, active shoulder abduction,
with shoulder girdle depression and contralateral flexion
of the cervical spine, will affect all tracts of neural tissue
from C5 to T1.
In testing a disorder to determine the possibility of
neural tissue involvement, active shoulder abduction
should be used in or behind the coronal plane. If pain
is provoked, or if the range of movement is limited, the
clinician can differentiate between shoulder joint and
neural tissue abnormalities by gently resisting the
concurrent shoulder girdle elevation occurring with
active abduction and—at the same time—position the
patient’s head and neck in contralateral lateral flexion.
Should neural tissue be involved, the response to active
abduction would be a more painful and further limited
range of movement.
This is a basic approach to analysis of active move-
ment in the physical evaluation of neural tissue. With
some thought to applied anatomy, the clinician can eval-
uate active movements in different directions and in
various ways to support a clinical hypothesis formed at
this early stage of evaluation. For example, a disorder of
the C4, C5 motion segment may involve the C5 nerve
roots or spinal nerve. This may cause an observable dys-
function of shoulder abduction and movement of the
hand behind the back because of the increased tension
that these movements place on the suprascapular and
axillary nerve trunks. Contralateral lateral flexion of the
head and neck would increase the dysfunction.
Passive Movement Dysfunction
Neural tissue tracts must comply with passive movement
as they do with active movement. If there is a specific
painful active movement dysfunction because of a dis-
order involving neural tissues, passive movement in the
same directions must also be affected by pain and, as a
consequence, limitation of range.
As with active movement, the clinician works
through a differential evaluation process for a determi-
nation of possible neural tissue involvement in which
there is a painful limitation of range. Should passive
abduction be painfully limited in range, it would corre-
late with a painful active limitation of range. In addi-
tion, the pain would increase and the range decrease,
should passive shoulder abduction be performed with
the shoulder girdle fixed in depression or the head and
neck be positioned in contralateral lateral flexion.
This clinical approach applies to applicable passive
movements in different directions, which always corre-
late with active movement dysfunction. The quadrant
position of shoulder joint examination described by
Maitland32 is of particular interest in passive movement
evaluation. In the quadrant position, the humeral head
has an upward fulcrum effect on the overlying
neurovascular bundle in the region of the axilla
(Figure 6-3).1 Therefore it is conceivable to use this
not only as a test of the shoulder, but also of the com-
pliance of the neurovascular tissues and, in the context
of this chapter, the neural tissues of the brachial plexus
and its proximal and distal extensions. To do this, the
quadrant test is performed as described by Maitland,32
and with the shoulder girdle in elevation and depression,
and the head and neck in ipsilateral and contralateral
lateral flexion.
CHAPTER 6 NEURAL TISSUE EVALUATION AND TREATMENT 193

Figure 6-3 Cadaver study at autopsy demonstrating the fulcrum effect of the
humeral head on neural tissue at the level of the shoulder with abduction/lateral rota-
tion. This indicates how shoulder motion may be affected by sensitized neural tissue,
as may be the case in radiculopathy. L, Lateral cord of the brachial plexus. H, Head of
the humerus. M, Median nerve stretched over a finger.

These additional positions subtract or add distance
over which the neural tissues travel, thereby affording
the clinician the ability to differentiate the test responses
as to whether they may represent neural tissue or
shoulder joint signs.
Adverse Responses to Neural Tissue
Provocation Tests
Provocation tests are passive tests that are applied in a
manner of selectivity for the examination of compliance
of different neural tissues with functional positions. This
means that identifying a specific type of functional posi-
tion noncompliance enables the clinician to form a
hypothesis, not only on the possible involvement of
neural tissue in a disorder, but importantly also on the
possible site of involvement. Validity with respect to the
clinical implications of such tests as described by Elvey1,2
has been demonstrated by Selvaratnam and associates.4
Provocation tests can only be carried out within the
available range of passive movement, which is governed
by the severity of pain associated with the disorder.
These passive movements are those that would lengthen
the course over which the neural tissue extends to reach
its maximum length. In more severe painful conditions
involving neural tissue, it is obvious that passive
movements and positions, well short of their maximum
length, would result in a pain response sufficient to
cause limitation of range or the inability to gain a
functional position because of the pain and protective
muscle.
Therefore it is unrealistic to develop a standard form
of the provocation test technique. The clinician is
required to formulate test techniques according to the
maladies of each patient with unique symptoms and
signs.
There is a necessity for functional anatomic knowl-
edge, an appreciation of the effects of evoked pain
and associated muscle activity, and a methodological
approach taking into account these considerations in the
physical examination of neural tissues. However, to
introduce the physical examination of neural tissues by
provocation tests, a written formula is necessary as a
baseline starting point.
Test Technique from Distal to Proximal. Subject
is supine and clinician’s hands are positioned to control
194 SECTION II NEUROLOGIC CONSIDERATIONS
shoulder girdle elevation and elbow and wrist/finger
flexion/extension, and also to alter shoulder rotation,
head/neck lateral flexion, and forearm pronation/
supination.
1. Via median nerve. Shoulder abduction/lateral
rotation, forearm supinated, head/neck neutral,
shoulder girdle neutral; extend elbow. Increase
effects of the test with incremental wrist/finger
extension, shoulder girdle depression, and
head/neck contralateral lateral flexion.
2. Via radial nerve. Shoulder abduction/medial
rotation, forearm pronation, head/neck neutral,
shoulder girdle neutral; extend elbow. Increase
effect with incremental wrist/finger (including
thumb) flexion, shoulder girdle depression, and
head/neck contralateral lateral flexion.
3. Via ulnar nerve. Shoulder abduction/lateral rotation,
forearm pronation, head/neck neutral, shoulder
girdle depression (because of the different
inclination of the lower trunk of the brachial plexus
to the upper and middle trunks, which form the
major part of the median and radial nerves); elbow
flexion. Increase the effect with incremental
wrist/finger flexion and head/neck contralateral
lateral flexion.
Test Technique from Proximal to Distal. Subject
is supine and clinician’s hands are in a position to control
head/neck lateral flexion, shoulder girdle elevation and
depression, and shoulder abduction and rotation.
1. Via median nerve. Shoulder abduction lateral
rotation, with the arm comfortably in a position of
elbow extension, slight wrist extension (positions
naturally occurring as a result of the placement of
the arm), head/neck contralateral lateral flexion.
Increase the effect with shoulder girdle depression.
2. Via radial nerve. Shoulder abduction medial
rotation, with the arm in a position of elbow
extension; slight wrist flexion (positions naturally
occurring as a result of the placement of the arm);
head/neck contralateral lateral flexion. Increase the
effect with shoulder girdle depression.
3. Via ulnar nerve. Shoulder abduction lateral rotation,
elbow and wrist/finger extension, forearm
pronation, shoulder girdle depression, head/neck
contralateral lateral flexion. Increase the effect with
increased shoulder girdle depression. As the name
implies, with passive neural tissue provocation tests
a response is the clinician’s goal. This response
should be threefold in the presence of sensitization
in evaluating the neural tissue.
a. Clinician appreciation of an increase in muscle
tone in muscles that are in a position to prevent
further movement in the direction of the test
movement, that is, the antagonists to the
movement. This increase in tone should coincide
with the first experience of the onset of pain.
b. The identification of the increased muscle tone
amounts to a first limitation of range of the
passive test movement. This is not a lack of
range, as might be related to tethering or any
other form of physical prevention of movement,
but one directly related to an evoked pain
response and resultant muscle activity to prevent
further pain via the provoking movement.
c. Having produced an initial adverse response, the
test movement should be carefully taken further
into range to attempt to reproduce the reported
pain. Reproduction of symptoms is always a
requirement in manual therapy evaluation to
ensure that a condition is suited for a specific
physical treatment.
Hyperalgesic Responses to Nerve
Trunk Palpation
If neural tissue sensitized because of some form of
pathologic process responds with a painful reaction to a
stimulus applied through its length in a longitudinal
manner, such as with active or passive movement, it must
also follow that there would be a painful reaction or
response to a stimulus applied directly above or to the
nerve trunk. This stimulus in the physical evaluation is
a result of nerve trunk palpation, and the response when
adverse or abnormal is one of hyperalgesia.
Nerve trunks are selectively palpated. The nerve
trunks or neural tissues of the uninvolved upper quarter,
or the upper quarter of least severity, are palpated first
to allow the patient to make a comparison and for a
correct interpretation to be made of a perception of
hyperalgesia.
Nerve trunks are palpated through cutaneous, subcu-
taneous, and in some regions muscle tissues, gently and
precisely, gradually applying increasing pressure until
deemed sufficient to complete the examination. Palpa-
tion of neural tissue of the upper quarter is done in the
following way.
CHAPTER 6 NEURAL TISSUE EVALUATION AND TREATMENT
Nerve Trunk Palpation in Supine-lying Position
Palpate:
1. The trunks of the brachial plexus in the posterior
triangle of the neck. Selectively examine from the
cranial to caudal and from the lateral margins of
scalenus anterior and medius towards the midthird
of the clavicle and hence the first rib.
2. The neurovascular bundle of the brachial plexus as
it travels beneath the coracoid process.
3. The three major peripheral nerve trunks of the arm
at their commencement in the axilla, where they
may not be identifiable individually, but can
certainly be identified as nerve trunks.
4. The median nerve, in the lower third of the medial
upper arm, where it can be identified as a structure;
and anterior at the level of the wrist, where it
cannot be identified as a structure.
5. The radial nerve, in the posterolateral aspect of the
upper arm, where in some individuals it can be
identified as a structure. At the lower third of the
lateral aspect of the upper arm, where it crosses
into the anterior compartment. At the lateral aspect
of the forearm below the elbow, and on the
posterolateral region of the wrist. The nerve cannot
be identified as a structure at the latter sites.
6. The ulnar nerve, at the posteromedial aspect of the
elbow, where it is readily identifiable, and at the
anteromedial aspect of the wrist.
Nerve Trunk Palpation in Prone-lying Position
Palpate:
1. The suprascapular nerve, through the trapezius on
the superior border of the scapula, where it cannot
be identified as a structure.
2. The axillary nerve, through the posterior aspect of
the deltoid and on the upper lateral border of the
scapula as it enters teres minor. The nerve is
unidentifiable as a structure at either site.
3. The dorsal scapular nerve, through the rhomboids
and medial to the scapula, where it cannot be
identified.
Hyperalgesic Responses to Palpation of
Cutaneous Tissues
In disorders of pain involving neural tissue, it becomes
readily apparent that palpation of tissue in regions
anatomically related to the involved neural tissue will
show marked tenderness to the point of being hyperal-
195
gesic. These tender points will be predictably found in
areas that appear to be target tissues of the involved
nerve or its spinal anatomical segments of origin.
There is a suggestion that the tender points may
represent ectopic pacemaker sites,38 perhaps terminating
cutaneous or subcutaneous branches of the nerve in
question. The most common area found in disorders of
the upper quarter, such as cervicobrachial syndrome, is
medial to the medial border of the scapula.
Evaluation for Signs of a Local Area
of Disease
In pathologic conditions of nerve tissue, all of the
features discussed may readily be found or determined
during a physical evaluation. However, this does not
mean the condition is one suited to manual therapy
management. It is quite possible for a painful diabetic
neuropathy, a painful neuropathy caused by a tumor infil-
tration, or carpal tunnel syndrome to cause all of the fea-
tures discussed thus far, including limitation of active
and passive movement. Therefore the clinician must
determine a cause for the neural involvement.
As an example in the upper quarter, disk disease will
often result in radicular arm pain and a specific cervical
spine motion segment dysfunction. This would be man-
ifested by passive spinal segmental motion palpation for
aberrant movement, and by accessory spinal segmental
motion palpation where an association between an
abnormal pain response and aberrant motion can be
made. An example of this would be evident where a
radiculopathy of C6 resulted in all of the features dis-
cussed and there was a well-defined motion segment
dysfunction consisting of a painful restriction of passive
movement at the C5, C6 motion segment.
Emg Responses to
Non-Noxious Mechanical
Stimulation of Nerve Trunks
in Cervical Radiculopathy
The concept of neural tissue provocation testing1,2
has been investigated for clinical relevance,4 as have
the mechanisms of muscle responses in positive test
findings.33 EMG activity indicates a mechanosensitivity
of the peripheral nerve trunks that bear anatomic rela-
tionships to the anatomic levels of spinal radiculopathy.33
It also presents a logical reason for the clinical signs pre-
viously outlined before a clinical diagnosis can be made
196 SECTION II NEUROLOGIC CONSIDERATIONS
of cervicobrachial syndrome or radiculopathy. This indi-
cates a mechanosensitivity of the peripheral nerve trunks
that bears an anatomic relationship to the anatomic level
of spinal radiculopathy. It also presents a logical reason
for the clinical signs previously outlined that must be
present before a clinical diagnosis can be made of cervi-
cobrachial syndrome or radiculopathy.
Manual Therapy Treatment
of Neural Tissue
The treatment of neural tissue in manual therapy
involves passive movement techniques, in which the
anatomic tissues or structures surrounding the affected
neural tissue are gently mobilized with controlled and
gentle oscillatory movement. Treatment can be more
progressive through use of mobilizing techniques in a
similar manner, but involving movement of the sur-
rounding anatomic tissues or structures and the affected
neural tissue together in the oscillatory movement.34
Passive movement of the abnormal neural tissue
without movement of its surrounding anatomic tissues
should be avoided, and any stretching of affected neural
tissue is contraindicated.
With clinician experimentation in treatment of
neural tissue disorders, it becomes readily apparent that
the disorder may show exacerbation if the guidelines
outlined are not followed. Clinicians report that because
of frequent exacerbation of conditions, they tend to
avoid the use of such techniques. It becomes obvious
that the clinician in these circumstances is not prescrib-
ing treatment according to the physical signs demon-
strated on evaluation. The clinician is treating too
strongly, or commonly is mobilizing neural tissue
solely—rather than with the surrounding anatomic
tissues—and therefore producing a stretched effect. It
stands to reason that if neural tissue is sensitized, undue
stimulation of it will cause further sensitization and
exacerbate the condition. This is the fundamental reason
for the muscle activity that results from provoking
maneuvers to prevent further and undue stimulation of
already sensitized neural tissue. The clinician must be
guided at all times by an appreciation of protective
muscle activity.
In general manual therapy terms, treatment of neural
tissue is indicated when the physical evaluation demon-
strates that neural tissue is the origin of the subjective
complaint of pain; or in the more commonly seen con-
ditions, where it is the dominant tissue of origin.
To meet this requirement, it is essential that all the
signs previously listed are present in the physical evalu-
ation of the disorder. If they are not present, another
form of treatment—directed to tissue other than
neural—would have to be considered. In addition, these
signs must be dominant to signs of other tissue or struc-
ture involvement.
The authors have used passive movement techniques
in the treatment of neural tissue disorders for many
years, with excellent results, when a disorder has not
developed on a pathologic basis to a more severe neuro-
pathic type. This is particularly true where there are
central nervous system mechanisms of pain and sympa-
thetically maintained pain syndromes. Although to date,
support for such treatment outcome is anecdotal, early
results of a study presently being conducted give support
to this and are demonstrating the validation of treating
appropriate disorders involving neural tissue with
passive movement techniques.35
Two treatment techniques that have been found to be
the most useful with regard to treatment of the upper
quarter will be described: cervical lateral glide and
shoulder girdle oscillation.
Cervical Lateral Glide
Patient is supine, with the shoulder slightly abducted to
a few degrees of medial rotation and elbow flexion to
about 90° such that the hand rests on the chest or
abdomen. The clinician gently supports the shoulder on
the acromial region with one hand while comfortably
holding and supporting the head and neck. Technique:
Gentle controlled lateral glide to the contralateral side
in a slow oscillating manner up to a point in range where
the first resistance occurs in the form of antagonistic
muscle activity.
The first resistance represents the treatment barrier.
Should this barrier not be reached, change the patient’s
arm position. This would involve more abduction or
possibly extending the elbow while maintaining the
shoulder position. The arm must be fully supported on
the treatment couch at all times. In more acute condi-
tions, additional support should be given by using a
pillow.
The technique progresses on subsequent treatment
days, but only when indicated by a demonstrable
CHAPTER 6 NEURAL TISSUE EVALUATION AND TREATMENT
improvement. A demonstrable improvement can be
detected by performing the lateral glide with the
shoulder in gradually increased amounts of abduction.
The most obvious indicator of successful treatment
using this technique would be an improvement of active
shoulder abduction.
Shoulder Girdle Oscillation
Patient is prone with the forehead resting on the palm
of the hand of the uninvolved side. The involved arm is
supported in a comfortable position by the clinician
towards a position where the hand is behind the back.
The clinician places the other hand on the acromial area.
Technique: Gentle oscillation of the shoulder girdle in a
caudad cephalad direction. The range of oscillation is
governed by the onset of first resistance in the caudad
direction. This represents the treatment barrier and is
the commencement of increased muscle tone.
The technique progresses during subsequent treat-
ment sessions and when indicated by performing the
oscillation in gradually increased amounts with the hand
behind the back. The most obvious indicator of suc-
cessful treatment would be an improvement of active
hand-behind-the-back function.
The amount of time the techniques are performed
is variable, depending largely on the experience of the
clinician, but, as in any disorder, this also depending
on symptom severity and irritability. The composure of
the patient is a prime consideration with regard to the
amount of time devoted to a technique. Should the
patient begin to show signs of lack of total relaxation,
the technique should be temporarily ceased and
methods of soft tissue mobilization should be employed
until composure is regained.
With experience, a clinician will learn to use differ-
ent techniques. However, the two just described will
serve well when applied appropriately and correctly. In
general in conditions that are more acute, the anatomic
tissues surrounding the neural tissue should be mobi-
lized. In the less acute conditions, or where progression
is required, the neural tissue should be mobilized along
with the surrounding anatomic tissue.
As in so many disorders managed by manual therapy
techniques, it is necessary to consider treatment of
tissues affected secondarily and as a consequence of the
primary neural tissue abnormality. Treatment would
commonly be given for adaptive shortening that
197
inevitably follows neuropathy. This shortening mostly
involves muscles that have been facilitated and have
been involved in tonic reflex activity to prevent move-
ment that would cause pain. In addition, long-term lack
of movement affects articular and periarticular tissue
mobility, and therefore may require joint treatment. The
treatment for these associated dysfunctions must be
chosen at a time when the neural tissue signs are resolv-
ing, indicating reduced irritation of the peripheral nerve;
the treatment must be carried out without any distur-
bance caused by stretching of the neural tissue.
Commonly in upper quarter conditions involving
neural tissue, a time will come in the treatment program
to treat the scaleni and the shoulder abductors/medial
rotators for loss of extensibility and to facilitate the
shoulder abductors/lateral rotators. In addition, the cer-
vical spine and the shoulder joint may require mobiliz-
ing treatment. The extent of the treatment to other
tissues and structures is dependent on the chronicity of
the disorder and its severity.
Self-treatment and management are most important.
For neural tissue of the upper quarter, these can be per-
formed in a variety of ways. A relatively simple treat-
ment can be conducted by placing the hand of the
involved side in a comfortable position against a wall,
with a degree of elbow flexion. This is followed by very
gentle and controlled contralateral flexion. This should
not cause pain, but a pulling sensation in the shoulder
and upper arm region.
This movement is repeated three times daily. This
may appear unsubstantial, but it is essential to regard the
movement as self-treatment and not exercise. It becomes
evident that a condition can readily be exacerbated if this
technique is used as an exercise rather than a treatment.
A condition also can become acute if it has settled into
chronicity. Functional training in the form of exercise at
a time deemed appropriate by the clinician also becomes
essential to the self-management program.
Case Study
GENERAL DEMOGRAPHICS:
Mrs. F.O. is 53 years old, white, and English speak-
ing, complaining primarily about severe left shoulder
pain radiating down the arm to the hand and accom-
panied by a “pins and needles” sensation in the thumb
and index finger.
198 SECTION II NEUROLOGIC CONSIDERATIONS
SOCIAL HISTORY
Mrs. F.O. is married and has one grown son, who
lives in another state. She does not smoke or drink.
EMPLOYMENT AND ENVIRONMENT
She was employed in a nursing home in the early
months of 1991, but because of steady deterioration of
her symptoms, she was forced to cease work some
months after her accident in February, 1991.
GROWTH AND DEVELOPMENT
No abnormalities noted, and she is right-hand dom-
inant.
LIVING ENVIRONMENT
Mrs. F.O. lives in a one-story ranch home with her
husband.
FAMILY HISTORY
Mother and father both alive and in good health. No
siblings.
HISTORY OF CHIEF COMPLAINT
Mrs. F.O. was sitting in her stationary motor vehicle
when it was struck from behind in February 1991. She
sustained a “whiplash” injury to her neck. Her immedi-
ate complaint was one of neck pain on the left side
extending into her upper back. Bilateral upper arm pain
developed to the degree that her left arm pain radiated
to the hand, thumb, and index finger, and was accom-
panied by a sensation of “pins and needles.” Her symp-
toms slowly improved through 1993 and 1994, but
remained substantial. Right shoulder mobility was full
range, but mobility remained limited in her left shoul-
der and neck. All litigation was completed in 1994. In
early 1995, there was a gradual increase in pain for no
apparent reason, culminating in a severe exacerbation of
left upper quarter symptoms. Marked restriction of
shoulder mobility by pain once again mimicked a frozen
shoulder. In May 1995, Mrs. F.O. was referred to us by
a consulting physician, who specialized in assessment for
pain management, for evaluation and potential treat-
ment. The working diagnosis at the time was left C6
radiculopathy. The referring physician’s next option of
treatment was to be a C6 nerve root sleeve block.
PRIOR TREATMENT FOR THIS CONDITION
At the onset of symptoms in 1991, treatment and
management consisted of rest, medication, and physical
therapy for “frozen shoulder.”
OTHER TESTS AND MEASURES
Plain radiographs identified ossification of the ante-
rior longitudinal ligament at the C4 and C5 levels and
prominent ossification adjacent to the C6, B7 disk. A
computed tomography (CT) scan of the cervical spine
in March 1995 identified degenerative facet changes and
C5-, B6-level disk degeneration with anterior and pos-
terior osteophytic spurring.
HYPOTHESIS DIFFERENTIAL—PATHOLOGY/IMPAIRMENT
• Frozen shoulder—In 1991, active left shoulder
mobility become so painfully limited that she was
said to have developed a “frozen shoulder”
• Impingement syndrome because of bone spurring
• Cervical radiculopathy
CRANIAL AND PERIPHERAL NERVE INTEGRITY
Neural tissue provocation tests could only be carried
out in the 40° available range of shoulder abduction.
Consequently, there was a need to compensate for an
inability to reach a sufficient anatomic length of neural
tissue in test positions by making maximum use of
maximum shoulder girdle depression and contralateral
lateral flexion of the cervical spine (Figures 6-4 and
6-5). Although wrist extension in shoulder girdle
depression reproduced symptoms, the shoulder girdle
elevated wrist extension did not reproduce the shoulder
and arm pain.
Neural tissue provocation tests—via the median and
radian nerves—reproduced symptoms, but testing via
the ulnar nerve did not, thus indicating a spinal involve-
ment from C5 to C7. In testing from proximal to distal,
the shoulder could again only be positioned in a small
available range of abduction. The shoulder girdle there-
fore had to be fixed in caudad depression to compensate
for the lack of ability to be able to place the neural tissue
in a more lengthened position.
Palpation of particular peripheral nerve trunks of the
left upper quarter produced hyperalgesic responses.
These responses were not produced on palpation of all
peripheral nerve trunks. Hyperalgesic responses were
obtained in the left posterior triangle with respect to:
the upper trunks of the brachial plexus, immediately
inferior to the left coracoid process; the neurovascular
bundle; the axilla; and the neurovascular bundle and the
upper arm to the median and radial nerves. Palpation on
the suprascapular and axillary nerves also produced
hyperalgesic responses.
Palpation of cutaneous and subcutaneous tissues in
regions that had a neuroanatomic relationship to the
hyperalgesic upper trunk of the left brachial plexus also
indicated hyperalgesic responses. These areas were par-
ticularly evident medial to the medial border of the
scapula, the upper chest, the shoulder, and the upper
CHAPTER 6 NEURAL TISSUE EVALUATION AND TREATMENT 199

Figure 6-4 Mrs. F.O., demonstration of gross limitation of active range

shoulder motion because of sensitization of neural tissues.

Figure 6-5 Neural tissue provocation test. Wrist extension performed in

maximum available range of shoulder abduction, influencing the median nerve, brachial
plexus, and ultimately the cervical nerve roots. Note should be made of the small pillow
elevating the arm from the couch. At the time of initial evaluation, because of
shoulder and arm pain, the patient was unable to lie supine with the arm resting on the
couch by her side.
200 SECTION II NEUROLOGIC CONSIDERATIONS
arm. Responses of a similar nature were not found in
corresponding tissues on the right.
EMG RESPONSES
For the subject in this case history, EMG responses
to upper limb nerve trunk palpation were recorded using
the protocol described by Hall and Quintner.33 EMG
responses on the side of the arm being tested were
recorded from the ipsilateral biceps, triceps, deltoid, and
upper trapezius muscles. EMG activity in the four
muscles was simultaneously recorded during gentle deep
palpation on the anatomic site of the ipsilateral radial
and median nerve trunks in the upper arm, and of
the ulnar nerve trunk behind the medial epicondyle.
Recordings were also made during gentle palpation
of the skin and subcutaneous tissues overlying each
Figure 6-6 EMG responses in this subject with cer-
vical radiculopathy are similar to those reported by Hall and
Quintner33 in a similar case. They found painful responses to
gentle palpation on the radial and median nerve trunks in the
symptomatic arm of their patient, and recorded widespread
(multisegmental) EMG responses on palpation of these puta-
tively tender nerve trunks. Neither pain nor EMG responses
were noted during palpation of the skin and the subcutaneous
tissues overlying these nerve trunks, and of the adjacent muscle
bellies of biceps and triceps brachii.
presumed tender nerve trunk. They were also made in
the case of the median and radial nerve trunks during
palpation of the bellies of the adjacent biceps and triceps
brachii muscles.
When the radial and median nerve trunks were pal-
pated on the painful side, a burst of activity was recorded
in the sampled left biceps, triceps, and upper trapezius
muscles (Figure 6-6). The other stimuli, including pal-
pation of the ulnar nerve, had no effect upon EMG
activity and were not painful. On the opposite (asymp-
tomatic) side, there were no EMG responses to nerve
trunk palpation (Figure 6-7).
JOINT INTEGRITY AND MOBILITY
Motion palpation of the cervical spine indicated
restricted motion at C5, B6 and C6, B7. Accessory
motion palpation indicated a pain and stiffness rela-
tionship at the same levels. In spite of palpation of
the shoulder subcutaneous tissues producing painful
responses and active and passive motion being limited
in range, accessory movement of the articular surfaces
was freely available.
Figure 6-7 EMG activity of the right biceps, triceps,
deltoid, and upper trapezius muscles during palpation of the
radial, median, and ulnar nerves in the upper arm/elbow of the
asymptomatic side.
CHAPTER 6 NEURAL TISSUE EVALUATION AND TREATMENT
POSTURE
At initial evaluation, the left shoulder girdle was
elevated with the arm held in a protective position.
RANGE OF MOTION
Left shoulder function was recorded as 80° of flexion
and 40° of abduction (see Figure 6-4). Although cervi-
cal range of motion was limited in all directions, partic-
ular note was made of the greater limitation of right
lateral flexion than left lateral flexion. Of further inter-
est was that active shoulder mobility was more painful
and more limited in range when performed with head
and neck positions in contralateral lateral flexion. Passive
left shoulder mobility was limited in range by pain to
the same degree as active mobility. Retesting passive
mobility, with the head and neck positioned in con-
tralateral lateral flexion, demonstrated a further decrease
in range and increased pain.
PHYSICAL THERAPY CLINICAL IMPRESSION: PROGNOSIS
AND PLAN OF CARE
The physical findings and the EMG analysis corre-
lated accurately with the subjective complaint and sup-
ported a disorder categorization of cervicobrachial pain
syndrome, in which there was strong evidence of neural
tissue involvement and of being the major pain source.
A diagnosis of C6 radiculopathy was also loosely sup-
ported in view of the “pins and needles” sensation felt in
Figure 6-8 Neural tissue
treatment technique. The arm is in a
position to shorten the course over
which neural tissue travels in the upper
quarter. Note again the pillow under
the arm. The shoulder girdle is sup-
ported lightly by the therapist’s left
hand, while the right index finger is at
C5 with the head and neck fully sup-
ported. The technique is one of a
passive lateral glide to the right in an
oscillatory manner.
201
the thumb and index finger, and the CT results. Treat-
ment of choice, with respect to physical treatment, was
therefore using a technique that indirectly had a postu-
lated physiologic effect, and hence a therapeutic effect
on neural tissue.
INTERVENTIONS
Treatment commenced with therapist intervention
only. Severity of pain prevented any patient-generated
management at the time. Treatment consisted of gentle,
controlled oscillation of the neck from the midline
towards the right by performing a right lateral glide of
C5 on C6. The left arm was supported in the position
shown in Figure 6-8. Assessment of treatment was
carried out by reevaluation of active left shoulder mobil-
ity. Because of the severity of the condition, small frac-
tional improvements of range were deemed acceptable.
Treatment initially was carried out three times per week.
Mrs. F.O. was instructed to use a thin but firm pillow
under the axilla when sitting to support the shoulder
girdle in a degree of elevation. She was asked to refrain
from anything causing depression or caudad stress to the
shoulder girdle, and while walking, to place her hand in
the waistband of her clothing. These measures were
taken to shorten the course over which the brachial
plexus traveled and therefore to overcome the provoca-
tive effect of the drag on sensitized neural tissue by the
202 SECTION II NEUROLOGIC CONSIDERATIONS
weight of the shoulder girdle. Medications and medical
advice remained unchanged.
Mrs. F.O. was given a complete explanation of the
disorder, and it was noted that improvement would be
extremely slow and would take at least 2 months before
knowing the true value of the treatment approach. This
was also acceptable to her referring physician.
With some subjective improvement occurring after 2
weeks, and a knowledge that the disorder was stabiliz-
ing as judged by maintenance of improved function,
treatment was stepped up to involve techniques to facil-
itate the shoulder abductors and lateral rotators. The
function of these appeared inhibited, presumably as a
result of pain. The treatment also was stepped up to
inhibit the abnormally excessive influence of the adduc-
tors and medial rotators, which appeared facilitated pre-
sumably as a protective measure to prevent pain.
This was done in supine-lying position, with con-
trolled isometric hold-relax techniques supplemented
as time went on with proprioceptive neuromuscular
facilitation (PNF) patterning techniques stimulating the
abductors and lateral rotators. These techniques were
performed in painless positions.
Mrs. F.O. commenced her own treatment program
involving neural tissue after 4 weeks. This consisted of
the method described earlier. As the condition improved
and the symptoms became more stable, a program of left
shoulder abduction and lateral rotation was begun. This
involved sitting sideways at a table with the left arm
supported on a pillow to give 90° abduction. An active
abduction was then performed to take the weight off the
arm only, hold for 2 seconds, and then relax it back onto
the pillow. At the same time the shoulder girdle did not
elevate. This was repeated six times and was followed by
lifting the forearm from the pillow, without lifting the
elbow, as a maneuver of lateral rotation of the shoulder.
This was repeated six times with the same relaxation
between lifts. The aim of these techniques was to stim-
ulate the abductors and lateral rotators and to regain
normal muscle recruitment patterns of arm elevation.
Treatment was successful at the time of writing this
report. As treatment proceeded, the severity of pain were
reduced and the range of left shoulder mobility was
increased in unison. The improvement of both variables
was on the order of 50%, a level of improvement accept-
able to all parties concerned when considering the
history and severity of the disorder. The same medica-
tions were continued, but decreased in quantity. There
was no need to carry out a nerve root sleeve block.
Symptomatic deterioration was reported before the
treatment intervention.
It is anticipated Mrs. F.O. will continue to improve
and in time progress to an active functional training
program.
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1. Elvey RL: Brachial plexus tension tests and the pathoanatom-
ical origin of arm pain. In Idczak RM, editor: Proceedings:
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2. Elvey RL: The investigation of arm pain. In Grieve GP,
editor: Modern manual therapy, Edinburgh, 1986, Churchill
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3. Butler DS: Mobilisation of the nervous system, Melbourne,
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4. Selvaratnam PJ, Matyas TA, Glasgow EF: Noninvasive dis-
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5. Davis H: Increasing rate of cervical and lumbar spine surgery
in the United States 1979-1990, Spine 19:1117, 1994.
6. Loeser JD: Cervicobrachial neuralgia. In Bonica JJ, editor:
The management of pain, ed 2, Philadelphia, 1990, Lea &
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7. Bovim G, Schrader H, Sand T: Neck pain in the general
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8. Lawrence JS: Disc degeneration: Its frequency and relation-
ship to symptoms, Ann Rheum Dis 28:121, 1969.
9. Hult L: Frequency of symptoms for different age groups and
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10. Radhakrishnan K, Litch WJ, O’Fallon WM, et al: Epidemi-
ology of cervical radiculopathy: a population-based study
from Rochester, Minn., through 1990, Brain 117:325,
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11. Connell MD, Wiesel SW: Natural history and pathogenesis
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13. Spitzer WO, et al: Scientific monograph of the Quebec task
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15. Grieve GP: Referred pain and other clinical features. In
Boyling JD, Palstanga N, editors: Grieves modern manual
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pain. In Bonica JJ, editor: The management of pain, ed 2,
Philadelphia, 1990, Lea & Febiger.
17. Fields HL: Pain, New York, 1987, McGraw-Hill.
18. Inman VT, Saunders JB: Referred pain from skeletal struc-
tures, J Nerv Ment Dis 99:660, 1994.
19. Foerster O: The dermatomes in man, Brain 56:1, 1933.
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20. Elliot FA: Tender muscles in sciatica: EMG studies, Lancet
1:47, 1994.
21. Brodal A: Neurological anatomy in relation to clinical medicine,
ed 3, Oxford, 1981, Oxford University Press.
22. Kellgren JH: On the distribution of pain arising from deep
somatic structures with charts of segmental pain, Clin Science
4:35, 1939.
23. Cloward RB: Cervical diskography: a contribution to the eti-
ology and mechanism of neck, shoulder and arm pain, Ann
Surg 150:1053, 1959.
24. Klafta LA, Collis JS: The diagnostic inaccuracy of the pain
response in cervical discography, Clev Clin Quart 36:35, 1969.
25. Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint
pain patterns: 1. A study of normal volunteers, Spine 15:453,
1990.
26. Dwyer A, Aprill C, Bogduk N: Cervical zygapophyseal joint
pain patterns: 2. A clinical evaluation, Spine 15:458, 1990.
27. Dreyfuss P, Michaelson M, Fletcher D: Atlanto-occipital and
lateral atlanto-axial joint pain patterns, Spine 19:1125, 1993.
28. Asbury AK, Fields HL: Pain due to peripheral nerve damage:
an hypothesis, Neurology 34:1587, 1984.
29. Dalton PA, Jull GA: The distribution and characteristics of
neck-arm pain in patients with and without a neurological
deficit, Aust J Physiother 35:3, 1989.
30. Henderson CM, Hennessy R, Shuey H: Posterior lateral
foraminotomy for an exclusive operative technique for cervi-
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cases, J Neurosurg 13:504, 1983.
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31. Smyth MJ, Wright V: Sciatica and the intervertebral disc: An
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33. Hall TM, Quintner JL: Mechanically evoked electromyo-
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Auckland, 1995.
34. Elvey RL: Treatment of arm pain associated with abnormal
brachial plexus tension, Aust J Physiother 32:224, 1986.
35. Vicenzino B: An investigation of the effects of spinal manual
therapy on forequarter pressure and thermal pain thresholds
and sympathetic nervous system activity in asymptomatic
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37. Farmer JC, Wisneski RJ: Cervical spine nerve root compres-
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38. Devor M: Neuropathic pain and injured nerve: peripheral
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 7
Neurovascular
Consequences of
Cumulative Trauma
Disorders Affecting the
Thoracic Outlet: A
Patient-Centered
Treatment Approach
Peter I. Edgelow

N eurovascular compression syndromes of the

upper quarter involve a complex and bewil-
dering set of problems when seen as separate
diagnoses. Thoracic outlet syndrome (TOS) as a diag-
nostic entity is receiving increased attention; yet one
must not fall into the trap of ignoring other potential
anatomic sites of neurovascular entrapment. Therefore,
although issues will be presented that focus on the tho-
racic outlet and symptoms that can derive from this
region, one must consider the potential for multiple
entrapment sites.
In the past 12 years in an outpatient orthopedic
clinic, more than 1000 patients with the diagnosis of
TOS received physical therapy. These patients had
severe, chronic pain problems that failed all conservative
treatments and, in some instances, failed multiple
surgeries. These patients commonly exhibited signs and
symptoms in multiple areas. The patients all had 2 or
more years of symptoms before TOS was diagnosed. An
evaluative procedure and treatment protocol has been
the result of this clinical experience.
A clear understanding of the neural consequences of
cumulative trauma disorders (CTDs) affecting the tho-
racic outlet will help the practicing physical therapist
comprehend the etiology of these disorders. Also, as the
basis for evaluating and developing an effective plan of
care, it is necessary to think of CTDs as having multi-
ple causes rather than having a single cause.
The guiding principles for effective treatment of neu-
rovascular entrapment build on the fundamental idea
that neurovascular entrapments occur as a consequence
of trauma to the body affecting the nervous system

205
206 SECTION II NEUROLOGIC CONSIDERATIONS
and/or the vascular system. Such trauma may occur in
an individual with few or many preexisting risk factors.
Three concepts have been developed based on clini-
cal experience: common sense, findings from surgery,
and hypotheses derived from the basic sciences.
The first concept is patients must be in control of
their own care in order for treatment to be long lasting.
In the current medical climate, issues that cannot be
controlled by the patient include the interaction between
the health care practitioner, the patient’s employer, and
the patient’s insurance provider. Therefore, factors that
can be controlled—such as individual risk factors, health
habits, daily living demands, and belief systems—take
on an increasing importance in the treatment process.
The second concept is that neurovascular entrap-
ments are a problem of stenosis. Stenosis should not be
thought of as a rigid narrowing of an anatomic part, but
rather a series of events or circumstances, some of which
may result in an irreversible narrowing and others that
are reversible. For example, the stenosis caused by the
presence of a cervical rib or scalenus minimus may be
irreversible, but the stenosis due to postural changes or
paradoxical breathing patterns is reversible.
The third concept is that an understanding of fluid
dynamics must complement investigations of neural and
structural changes. This concept is based on research
concerning fluid dynamics in the carpal tunnel and
appears to be equally relevant for the thoracic outlet. As
structural and fluid changes cause restriction in the size
of the outlet, these changes could contribute to disrup-
tion of the pressure gradient and affect both the local
neural circulation and the venous and lymphatic return
from the whole upper extremity.
Relevant signs and symptoms will be introduced that
are important indicators leading to an understanding of
the pathology as well as treatment goals and objectives.
This information is essential when treating either a
single-tunnel thoracic outlet problem or a multiple-
tunnel problem when one of the tunnel problems is in
the anatomic region called the thoracic outlet.
Two case histories are presented to illustrate the use
of the knowledge presented in this chapter in evaluation
and treatment. The first case has early signs of a cumu-
lative trauma disorder and the second has a more severe
problem of longer duration. In the first case, it is my
contention that if adequately addressed at the time the
symptoms and signs first appear, problems can be pre-
vented from developing into the kind of unremitting
condition being discussed. The second case is an
example of a good outcome for a patient with more
severe, longstanding TOS.
Importance of Treating the
Whole Person
Patient empowerment is an essential ingredient in
treatment. It is based on the theory that the most
successful outcome involves engaging the whole person
in treatment. Although TOS is a physical problem, it
affects the whole person. Simplistically stated, the
impact is to change the person from being in control of
their life to being out of control. This feeling state of
being out of control negatively affects the body and
mind connection. Restoring the feeling of being in
control is one method to have a positive impact on this
connection.
To be empowered, patients must be ready to take
control of their own care. Once patients are committed
to this process, the physical therapist acts as a coach to
guide them through recovery while they learn to
monitor daily activities and the home treatment
program.
There are two key issues that facilitate the feeling of
being in control: understanding “the problem” and “the
solution to the problem.” Patients need to understand
why they have the problem and how their actions can
help resolve it. This requires the therapist to translate
the pathoanatomic knowledge inherent in the diagnosis
into a language that empowers the patient. This can be
done in a number of ways. One method is to relate a
simple story, using analogies and metaphors to guide
treatment rather than using medical terminology. The
problem with medical terminology is that it may have a
negative connotation based in the patient’s belief system.
It is this belief system that can increase or decrease the
patient’s feeling of control. For example, the belief that
nothing can be done to correct a problem will have a
negative impact on everything that is done to help.1,2 If
there was a quick fix to this issue then the therapist could
overpower this negative belief by fixing the problem.
However, it is my experience that there is no quick fix
for severe neurovascular entrapments.
Therefore patients must understand that treatment
requires substantial self-discipline to arrive at a satisfac-
tory outcome and a significant, sustained change. It
can take 3 months before enough stability and positive
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
results are obtained for the patient to feel in control. For
this reason, a negative belief system can sabotage initial
treatment efforts if not addressed. A discussion of the
work done by orthodontists can be a useful analogy to
illustrate the difference between a quick fix and signifi-
cant, sustained change. If you went to the orthodontist
with crooked teeth, and he said that he could fix them
immediately and took out a pair of pliers, one could
understand that you might look for another practitioner.
Common sense and experience have taught us there is
no quick fix for crooked teeth. Wearing braces for 2 years
to have a beautiful smile may not be the answer the
patient wants to hear, but experience indicates it is the
best available answer.
One of the negative feeling states surrounding this
diagnosis is significant frustration by the patient. Clin-
ical experience teaches that there are several methods
used to relieve this negative feeling state. The first
method is to deny the existence of the condition. This
may work in the short term, but in the long term the
problem gets worse. The second method is to use drugs.
Again, this is a short-term solution only. The third
method is to be told that you must accept the problem
and get on with your life without addressing the
problem. Patients find that this also fails, and the
problem gets worse. The fourth method, which is
the clinical solution in this treatment approach, is for
patients to be trained to become mindful so they can
effectively use the treatment techniques. This means
that patients must understand that symptoms are the
language of the body. Pain and muscle tension can be
thought of as words to listen and respond to.3-5
With repetitive strain disorders, initial symptom lan-
guage is felt as tension. If one reacts to this tension in
an appropriate manner, it goes away, and the problem
appears corrected in the short term. However, if one
doesn’t change the underlying reason for the tension,
then repetition over time leads to intermittent pain in
addition to tension. Again, if one reacts to these symp-
toms in an appropriate manner they will ease. Over time,
the intermittent symptoms become constant, but still
vary according to activity and rest. Eventually, if suc-
cessful corrective steps are not taken, the symptoms
become constant and severe, and do not respond to any
previously effective treatment. In this state, the pain is
no longer experienced as communication, but as a curse.
It is important for the patient to understand the risks
and rewards of paying close attention to symptoms and
207
not to succumb to hypervigilance, but not to deny the
problem either. To understand the problem and the solu-
tion, and to do what it takes for the rest of one’s life to
minimize the problem, is ultimately to be in control.
The common statement of “no pain, no gain” has no
place in the treatment of these patients. This is particu-
larly important with injuries to the nervous system and
the musculoskeletal system, because the body’s pain
response will be to protect the neurovascular structures.
This protective response has an adverse effect on healing
when overuse, overtreatment, or recurrent injury pro-
longs the muscle tension reaction. Current research in
neuroplasticity, learning, conditioned reflexes, and the
fight or flee response supports the importance of not
ignoring the pain.6-9
Anatomy
A review of the anatomy and potential risk factors will
focus on the thoracic outlet. This area is a source of
symptoms secondary to congenital factors and/or
trauma and is the primary region that exhibits dysfunc-
tion as a result of pathologic reflexes secondary to other
sites of entrapment. In the author’s clinical experience,
early evidence points to the fact that neglect in address-
ing dysfunction in the thoracic outlet may be a con-
tributor to the high incidence of failure in conservative
management of patients with CTDs of the upper
extremity.
The anatomy of the thoracic outlet might be consid-
ered as tunnels made up of bones and muscles. The
nerves and blood vessels may become compromised
within one or more of these tunnels (Figure 7-1). The
concept of tunnels is an essential perspective to under-
stand the problem associated with TOS and the
proposed solutions. Figure 7-2 shows a diagrammatic
representation of the major tunnels of the spine and
upper extremity, and Figure 7-3 shows an overlay of the
tunnels on the anatomy. The author has found these
diagrams to be of assistance in explaining the problem
to the patient.
The basic anatomic structures will briefly be dis-
cussed together with the potential risk factors within
these structures.
Bones
The bony tunnel comprises a floor consisting of the first
through fifth ribs; an anterior wall, which is formed by
208 SECTION II NEUROLOGIC CONSIDERATIONS

Subclavius Anterior scalene

& phrenic nerve
Brachial Plexus &
Axillary vessies Posterior scalene
Stellate
Pectoralis minor Middle scalene ganglion
C8 Vent
ramus
Rib # 1
T1 Vent
ramus

Figure 7-1 Anatomy of the thoracic outlet. The clavicular head of the sternocleidomastoid muscle has been removed
to view the anterior scalene muscle with the phrenic nerve crossing it. The C5, C6, C7, C8, T1 ventral roots of the plexus
are visible as they pass in front of the middle scalene muscle. (Courtesy Peter Edgelow.)

the clavicle; a posterior wall, which is formed by the
scapula; a medial wall, made up of the cervical vertebrae
and disks with the external opening of the intervertebral
foramina; and a lateral wall formed by the glenohumeral
joint (see Figure 7-1). Potential risk factors within these
structures are as follows:
1. Structures that can affect the distance the lower
roots of the brachial plexus must traverse to reach
the extremity; that is, the breadth of the first rib.
2. Structures that can affect the diameter of the
tunnel based on congenital issues, which might
include the size of the transverse process of C7, the
length of the clavicle, and the presence of a cervical
rib. Although present in 2.5% of the population, a
cervical rib occurs in 5% of TOS patients.3,10,11
3. Factors that can affect the diameter of the tunnel
based on trauma in the past or from the injury that
immediately preceded the onset of symptoms.
These include callus formation following fracture of
the clavicle or first rib; and degenerative
hypertrophy of an arthritic glenohumeral joint,
which can contribute to trauma of the
neurovascular bundle during arm movements.6,10,11
4. Functional changes, such as the mobility of the
sternoclavicular, acromioclavicular joints, and the
first rib, occur as a result of postural changes or
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET 209

Figure 7-2 Diagrammatic representation of tunnels within the upper quarter that may be compromised by
acquired, congenital, or postural stenotic lesions. 1, Vertebral canal; 2, intervertebral foramina; 3, scalenes; 4, infra-
clavicular; 5, pectoralis minor; 6, cubital tunnel; 7, carpal tunnel; and 8, canal of Guyon. (Courtesy Peter Edgelow.)

dysfunctional breathing patterns. These changes
affect the course of the lower roots of the plexus by
increasing the distance traveled to pass from the
intervertebral foramen of T1 up and over the first
rib to then join C8 and pass into the arm. The
relationship of the clavicle can affect the costo-
clavicular space and therefore the potential for
changing the vascular flow through that space.
Muscles
The muscular components separate this bony tunnel
into two additional “soft-tissue” tunnels. A medial
210 SECTION II NEUROLOGIC CONSIDERATIONS

5 4 3

7 8

Figure 7-3 This overlay of the tunnels upon the anatomy emphasizes 1, the close proximity of the intervertebral foram-
ina; 2, the space between the anterior and middle scalene; 3, the course of the subclavian vein passing over the first rib and
beneath the clavicle between the muscular attachments of the anterior scalene (posteriorly) and the subclavius (anteriorly);
4, the space posterior to pectoralis minor; 5, distally, the cubital tunnel at the elbow; 6, the two tunnels at the wrist; 7, the
carpal tunnel; and 8, canal of Guyon. (Courtesy Peter Edgelow.)

tunnel is formed by the anterior and middle scalenes
as they pass from their origins to their insertions.
The scalenus anticus arises from the anterior knob
of the transverse process of C3 through C6 cervical
vertebrae to insert in a common tendon on the anterior-
superior surface of the first rib. The scalenus medius
arises from the posterior knob of the transverse process
of the same vertebrae and inserts onto the posterior-
superior surface of the first rib. The pectoralis minor
muscle forms a lateral muscular tunnel as it passes
from its origin on the third, fourth, and fifth ribs to
the coracoid process of the scapula (see Figure 7-1).
The anterior bony wall of the tunnel is further reinforced
by the presence of a muscular component (subclavius),
which passes from its point of origin along the
lateral one third of the undersurface of the clavicle to
its insertion at the medial superior surface of the first
rib.
Potential risk factors within these structures are as
follows:
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
1. Narrowing of the scalene triangle and pectoralis
minor contractile tunnels as a result of abnormal
breathing and overused accessory breathing
muscles, in conditions such as asthma or chronic
obstructive pulmonary disease (COPD).
Paradoxical breathing patterns, in which the
scalenes and pectorals are used as the initiators of
each breath—rather than assisting the diaphragm
and lower intercostals during a deep inspiration—
could be considered as a reason why the scalenes
alter their physiology (see No. 3).
2. Anatomic variations of the anterior and middle
scalene muscles, such as unusual proximity, wide
distal attachments of the first rib, distal
interdigitations, and the presence of a scalene
minimus muscle.11,12 Fibrous bands that attach
lower cervical transverse processes or a cervical rib
to the first rib are present in half of the normal
population although fewer than 1% are afflicted by
TOS. So these are not considered primary risk
factors, but can certainly provide a predisposition
for development of symptoms.11
3. Shortening in the muscular elements secondary to
poor posture and/or traumatic scarring from scalene
muscle trauma with resulting inflammation,
fibrosis, and contracture has been verified by
histological studies.13 The scalene muscles of
patients with traumatic TOS have shown consistent
abnormalities in fiber type, size distribution, and
amount of connective tissue. Normal scalene muscle
fibers are composed of 50% of type I fibers and
50% of type II fibers. Type I fibers contract and
relax slowly, develop tension over a narrow range,
and are very resistant to fatigue, making these fibers
specialized for the long-term contraction necessary
in the maintenance of posture. Type II fibers are
characterized by rapid contraction and relaxation,
develop a wide range of tensions, and often fatigue
quite rapidly. They are suited for high-intensity,
short-duration muscular activity.14 The TOS
samples showed a predominance of type I (slow)
fibers over type II (quick) fibers. TOS samples
averaged 77% type I to 23% type II. These studies
also showed a significant increase in connective
tissue. The average amount of connective tissue in a
healthy muscle is 14.5%. The average amount in
scalene samples from surgery was 36.6%. This
suggests that fibrosis of the scalene muscles
211
secondary to trauma, such as whiplash, may be an
important contributor to the cause of TOS.13
4. Posttraumatic scarring along the deep cervical fascia
could be another source of dysfunction. The deep
cervical fascia is continuous with the axillary
sheath, which encases the neurovascular bundle.15
Scarring in one area could lead to decreased
mobility throughout the length of the tissue.
Nerves
The brachial plexus comprises the C5 through T1 nerve
roots with a contribution from C4 and T2. However, it
is the ventral rami of C8 and T1, as they anastomose to
form the lower trunk of the brachial plexus, that is of
particular importance with TOS, because it is their
relationship with the floor of the tunnel (first rib) and
fibrous bands that places them in jeopardy. The sympa-
thetic supply to the upper extremity comes from the stel-
late ganglion, which lies on the neck of the first rib (see
Figure 7-1). Potential risk factors within these structures
are as follows:
1. The possibility of an abnormally large contribution
of T2 fibers to the T1 root, termed a postfixed
plexus. The effect on available neural mobility is to
cause the exiting T1 root to be more caudal,
resulting in a longer course to get over the first rib
and into the arm.
2. Any change in mobility of the plexus as a whole or
a segment of the plexus because of scarring of the
extraneural elements secondary to trauma. Such
change places the affected segment at risk if more
mobility is required. In other words, a slumped
posture increases the length of the dura mater in a
caudal direction, thus increasing the distance the
C8-T1 roots have to traverse to get into the
arm.16,17
Blood Vessels
The subclavian vessels enter and exit the chest in this
region, together with the nerves. The subclavian artery
courses through the scalene triangle, which is formed by
the anterior and middle scalene muscles and the first rib.
The subclavian veins, also in a muscular tunnel, have the
anterior scalene as the posterior border and the subclav-
ius muscle as the anterior border. Distal to the first rib,
the subclavian vessels are renamed the axillary artery and
vein. Normally there is “harmonious coexistence” among
these structures.10 However, if the delicate balance is
212 SECTION II NEUROLOGIC CONSIDERATIONS
disturbed, the osseous or fibromuscular components can
cause compression on the neurovascular structures—
creating neurogenic or vascular symptoms (see Figure
7-1).10,18-20
Potential Risk Factors. Clinical experience
demonstrates that 100% of these patients breathe with
the accessory breathing muscles (pectoralis minor and
scalenes). Therefore the muscular tunnel becomes
narrow between the middle and anterior scalene, which
houses the artery, and the muscular tunnel between the
anterior scalene and subclavius, which houses the vein.
Because the heart pumps blood through the artery into
the arm, it is less affected by this narrowed tunnel than
the venous return. In the case of the venous return, the
pump is large muscle activity of the arm. This patient
population is using fine motor activity of the hands and
forearms. Consequently, the muscular pump is less effec-
tive and leads to the risk factor of intermittent increase
in fluid in the arm, which manifests itself as swelling in
the hand.
It must be remembered that while 100% of the fluid
that enters the arm does so via the artery, the fluid that
exits the arm does so both via the vein and the lymphatic
system.21
Other Issues in
Understanding the
Pathophysiology of
Cumulative Trauma Disorders
As can be seen, the thoracic outlet tunnel diameters can
be narrowed by a combination of bony, soft tissue, neu-
rologic, and traumatic abnormalities. In addition, dys-
functional reflexes; fluid system dynamics; and postural,
ergonomic, and gender factors can further affect the
scalene/first rib triangle and interfere with the course
of the neurovascular structures, causing vascular
compression.
Dysfunctional Reflexes That Can Affect
Tunnel Diameter
There are three reflexes that can affect the diameter of
the thoracic outlet and the blood flow to and from the
upper extremity. In severe neurovascular entrapments,
these reflexes are all pathologic and may worsen if the
reflex activity does not become normal.
A paradoxical breathing pattern is the most common
and frequently overlooked dysfunctional reflex. This
common dysfunctional pattern (sympathetic) is the ten-
dency to breathe with the upper thorax, with an absence
of abdominal movement. This could be viewed as a
protective response adversely affecting breathing (for
example, gasping and breath holding).22,23 This protec-
tive response acts to elevate the first rib, thereby nar-
rowing the tunnel. Changing the breathing pattern to
relaxed, diaphragmatic breathing (parasympathetic)
would assist in opening the tunnel and releasing the
resulting muscle tension. The normal breathing reflex is
to breathe in the quiet mode with the diaphragm and
only use the scalene muscles as accessory muscles of
breathing when the inspiration deepens. In paradoxical
breathing, the scalenes are used even when breathing
quietly. The resulting change in the normal reflex pattern
of breathing becomes conditioned into a “new normal”
or pathologic breathing. In treatment, it is essential to
decondition this conditioned reflex, because it perpetu-
ates a vicious cycle of pain, spasm, and congestion.
In patients with paradoxical breathing, the involved
scalene begins to contract with the initiation of inspira-
tion and contracts through the full inspiratory phase.
This pattern of contraction can be palpated, and note
should be made of the difference in size, time of con-
traction, and sensitivity to pressure as compared with the
uninvolved side. As the first rib elevates, because of the
abnormal breathing pattern, it approaches the clavicle
and affects the available space for the subclavian vein.
Further clinical observation with these patients
indicates increased tone in the muscles of the upper
quarter and a decrease in hand temperature and blood
flow. This clinical observation, and its relevance to the
perpetuation of the problem, has led to a hypothesis to
try to explain this phenomenon and how to restore
homeostasis.
The somatic nervous system has a normal protective
reflex, which is called the flexion withdrawal reflex.
Under normal circumstances, when the extremity
experiences a noxious stimulus—such as touching a hot
stove—the reflex pulls the extremity away from the
stimulus towards the center of the body. Following this
reflex, relaxed, repeated movements of the extremity will
result in a relaxation response of the muscles that pro-
duced the flexion withdrawal.
The autonomic nervous system also has a normal
protective response: vasoconstriction. If there is a trau-
matic event such as a cut, the autonomic nervous system
stimulates a vasoconstriction. This results in a decrease
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
in blood flow and allows time for the blood to clot.
Following clotting, there is a reflex vasodilatation, which
then increases blood flow to promote more rapid
healing. Relaxed, repeated movements of the injured
part can stimulate this vasodilatation response. The
effect of the relaxed, repeated movements is experienced
as a warming of the extremity.
These reflexes become dysfunctional in patients with
cumulative trauma disorders. The somatic nervous
system’s flexion withdrawal reflex becomes hyperactive,
so that relaxed, repeated movements of the extremity
cause an increase in muscle tension of the flexor muscles
rather than a softening or release of tension. The auto-
nomic system in the dysfunctional state results in a
decrease, rather than an increase, in blood flow with
relaxed, repeated movements. The breathing reflex in the
dysfunctional state is paradoxical. These reflexes—
flexion withdrawal, vasoconstriction, and paradoxical
breathing—become conditioned by repeated noxious
stimuli to respond with persistent cooling, increased
muscle tension in the extremity, and increased tension
in the scalenes, subclavius, and pectoralis minor. An
important component in treatment is to decondition
these abnormal reflexes by training the patient to
perform relaxed, repeated movements in a range
that does not elicit the tension/cooling response, but
does elicit the relaxation/warming response while main-
taining relaxed scalenes during quiet diaphragmatic
breathing.
Fluid Dynamics, Tissue Repair, and Centrally
Mediated Pain
The traditional paradigm in considering the typical
musculoskeletal consequences of an injury is to see the
Table 7-1
FLUID SYSTEMS WITHIN THE UPPER QUARTER
Circulatory System Structures Supplied
Arteries and veins Muscles, ligaments, bone
Lymph Fascia
Synovial fluid Joints
Cerebrospinal fluid Dura, meninges, nerve roots
Intervertebral disk fluid Disk
Intraneuronal transport system Nerve
213
consequences as both neural/pain responses and bio-
mechanical responses. In the common injury, the pain
consequences are driven by the nociceptors in the region
of the injury. The biomechanical consequences are seen
as a loss of flexibility, coordination, endurance, and
strength. This paradigm then directs treatment for
typical musculoskeletal injury to relieving nociceptive
pain and restoring losses in flexibility, coordination,
endurance, and strength. This paradigm needs to be
expanded to include both circulation or fluid systems,
and centrally mediated pain.
There are six separate fluid systems within the upper
quarter. These fluid systems must be working at their
best to maximize healing from trauma to this area. Table
7-1 briefly summarizes these systems, the structures they
supply, and the pumps that maximize the flow necessary
for adequate repair and health. Because the key ingredi-
ents for adequate circulation of all of the systems involve
both movement and diaphragmatic breathing, both the
problem and the solution become obvious.
An additional issue is pressure and its effect on circu-
lation. The blood supply within a peripheral nerve relies
on a pressure gradient system for adequate nutrition. In
research on pressure gradients within the carpal tunnel,
the pressure in the nutrient arteriole was found to be
more than the pressure in the capillary, which was more
than the pressure in the nerve fascicle. The pressure in
the nerve fascicle was more than the pressure in the vein,
which was more than the pressure in the tunnel (Figure
7-4). Imbalance in the pressure gradient because of an
increase in the tunnel pressure caused the venule to col-
lapse, creating venous stasis and hypoxia. If nothing was
done to reverse this problem then the hypoxia continued,
leading to edema, which ultimately led to fibroblastic
Pump
Heart
Movement
Movement
Breathing
Walking
Movement
214 SECTION II NEUROLOGIC CONSIDERATIONS
A varying structure throughout the body.16 This is impor-
B is high, and the pollution content is low. Should there
C arm through the arterial system. The majority of the
Figure 7-4 Representation of the pressure gradients
in the carpal tunnel and the stages that follow alteration of the
pressure gradients. For simplicity, one nerve fiber in a fascicle
is represented. A, Normal tunnel pressure gradient: artery >
capillary > nerve > venule > tunnel. B, Hypoxic and edema-
tous tunnel and nerve: increased tunnel pressure > venule =
collapse = venous stasis and hypoxia. C, Neural and tunnel
fibroblastic response: further increase in tunnel pressure and
hypoxia, scar tissue. A, Arteriole; C, capillary; N, nerve; T,
tunnel; V, venule. (Adapted from the work of Sunderland, 1976;
Courtesy Peter Edgelow.)
activity and scar formation within the nerve fascicle.16,24
From this evolved a hypothesis that initial trauma around
the nerve could lead to extraneural scarring.This scarring
would not necessarily affect the intraneural function of
the nerve. Once the pressure gradient changes lead to
intraneural fibrosis, then permanent neural change
would occur.16 This hypothesis, if true, emphasizes the
importance of early treatment to reduce swelling and the
risk of permanent neural change.
Although the pressure gradient research has been
described for the median nerve in the carpal tunnel, the
model could be generalized to the entire nervous system
because it is continually housed within tunnels of
tant in the thoracic outlet because, as previously men-
tioned, structural and dynamic changes cause restriction
in the size of the outlet, which could contribute to dis-
rupting the pressure gradient and affect the neural cir-
culation. A useful analogy to describe this situation is a
river flowing into a lake and a river flowing out of the
lake, in which the inflow equals the outflow. In this state,
the volume of the lake is constant, the oxygen content
be an obstruction affecting the outflow, then the volume
of the lake would increase, the oxygen content would
decrease, and the pollution would increase. This condi-
tion would be called a swamp (Figure 7-5).25 Because
the blood flow to and from the upper extremity passes
through the tunnel of the thoracic outlet, the concept of
narrowing of the tunnel can be a mechanical explana-
tion for the circulation problem.
As previously mentioned, 100% of the fluid enters the
fluid exits the arm via the venous system and a small
percentage exits the arm via the lymphatic system.21 The
heart is the pump that moves fluid through the thoracic
outlet between the anterior and middle scalene muscles.
Large muscle movement of the arm is the pump that
moves blood back through the thoracic outlet between
the anterior scalene and subclavius muscles. If one
assumes that the protective response affects the diame-
ter of both tunnels equally, then venous flow will be
more impeded than arterial flow. Lymphatic drainage
from the lower body, left arm, and left side of the head
empties into the lymphatic channels in the left thoracic
outlet. Lymphatic drainage from the right arm and right
side of the head empties into the lymphatic channels in
the right thoracic outlet. It is not clear if this anatomic
difference is a risk factor in thoracic outlet syndrome,
but clinical experience demonstrates that patients who
have surgical decompression on the left thoracic outlet
often have more lymphatic complications than patients
who have surgical decompression on the right thoracic
outlet.26,27
A further issue following injury involves the repair
process itself. For normal repair and restoration of full
function, micro stresses are required to stimulate matu-
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET 215

Figure 7-5 An analogy of a healthy lake to describe to the patient the possible sce-
nario of venous stasis leading to congestion (swamp) within the tunnel(s), and hence the need
to decongest the tunnel (drain the swamp) before proceeding to other treatments. (Courtesy Peter
Edgelow.)

ration of the scar. In the inflammatory stage of repair,
C-fibers invade the site of injury to provide neuropep-
tides that guide the healing process.10 While repair pro-
gresses, these C-fibers gradually withdraw from the area,
thus allowing increasing stresses to be applied with
decreasing pain. This ability to stress the healing tissue
is a necessity for adequate remodeling and maximum
recovery.
Histological studies of scar removed from around the
nerve roots within the thoracic outlet indicate the pres-
ence of C-fibers, signaling that the repair process is in a
less than mature stage and that stretching of the scar
would be painful.10,26 That these histological studies
were performed on patients months or years after the
initial trauma is further indication that inadequate
circulation and/or inadequate stress could be factors
indicating the need for surgery. This supports clinical
experience emphasizing that adequate circulation to the
thoracic outlet and the application of micro forces over
time are important contributions to full recovery.
To understand the significance of chronic pain, and
how this pain changes the physiology of the patient’s
nervous system, one needs to look at recent research on
neuroplasticity and chronic pain.
Animal research has demonstrated that neuroplastic
changes induced by peripheral deafferentation also occur
216 SECTION II NEUROLOGIC CONSIDERATIONS
in subcortical structures, such as the dorsal horn, the
nucleus cuneatus, and the somatosensory thalamus.
Reorganization in the thalamus, or even at multiple
levels of the somatosensory system, has also been
recently reported in human patients with chronic, severe
deafferentation.28,29
Studies of amputee patients with phantom limb pain
show that the amount of cortical reorganization is pos-
itively correlated with the magnitude of pain experi-
enced by the subjects.30 Suppression of the phantom
pain with regional anesthesia results in a reduction of
cortical reorganization.31
Additional research on unconscious fear condition-
ing, and its effect on human physiology, further sub-
stantiates the impact of emotions on the autonomic
nervous system—particularly on vascular flow to the
extremities.6
Occupational and Activities of Daily
Living Issues
Certain occupations that involve constant turning or
sustained peering with the eyes (keyboard jobs), repeti-
tive use of arms (assembly line work), lifting or holding
the arms above the shoulders (painters, electricians), and
working with vibrating tools seem to predispose people
to develop symptoms.10 Studies have compared occupa-
tions of heavy industry work (packers and assembly
workers), office work, and cash register work for inci-
dence of TOS symptoms. One study found that the
awkward work posture and continuous muscle tension
of cash register work produced the highest percentage
of TOS symptoms (32% of cash register workers).14
Some of these symptoms may be because of postural
stresses, such as carrying heavy packs or weights by those
unaccustomed to heavy work, or by debilitation and poor
posture.10,32-34 Recent clinical experience has shown that
musicians are another occupational group in which there
is a significant incidence of CTDs because of periods of
intense, sustained, and highly repetitive physical activity
involving high cognitive demand.35
Another possible risk factor related to the thoracic
outlet is the narrowing of the costoclavicular space by a
hypomobile, elevated first rib.34 It is suggested that
patients with emphysema are predisposed to TOS
because the first rib is chronically elevated.18 Also, a high
thoracic lordosis lifts the upper ribs towards the clavi-
cle, which approximates these structures and causes
impingement of the neurovascular contents.36 It is
important to remember that anything affecting the
circulation through the thoracic outlet could then
compromise the nutrition of the nerve at a distal site.
Sleeping postures are also a risk factor, and patients
who sleep on their side may awaken with their arm
having fallen asleep. The arm may even momentarily
become flail and require some passive movements with
the aid of the uninvolved arm to help restore circulation
and mobility.
An important fact to appreciate is that the nervous
system is a continuous tissue tract. While the effect of
specific trauma and age affects the mobility of the
nervous system, certain postures that place the nervous
system in its lengthened range can be potentially injuri-
ous or irritating, particularly if they are sustained. For
example, many seated office workers commonly sit in
a slumped position. Sitting slumped, with the
coccyx/sacrum in a flexed position and a loss of lumbar
lordosis when accompanied by a thoracic kyphosis,
causes the spinal cord/dura mater caudal to the
cervico/thoracic junction to approach its end range of
motion.16 Add to this the use of the arms in an extended
position, such as working with a mouse on the computer,
and you stress the lower roots of the brachial plexus. The
functional position of holding a phone to the ear would
further stress the lower roots of the plexus. This analy-
sis is based on the pioneering work of Bob Elvey on the
brachial plexus provocation test.37 This knowledge is
important in analyzing the stresses of activities of daily
living (ADL) and in examination and treatment, as is
mentioned later in this chapter.
Gender Issues
It is not known why the incidence of TOS in women is
twice that of men. It is speculated that the increased
incidence may be because of less developed muscles,
more horizontal clavicles, or a greater tendency for
drooping shoulders. Or it may be because of more preva-
lent congenital anomalies in the thoracic outlet in
women.38
It has been suggested that a narrowed thoracic outlet
may be caused by the lower position of the female
sternum, which decreases the angle between the scalene
muscles.39 Another factor is the biomechanical conse-
quences of having breasts. Perhaps instead of drooping
shoulder girdles, the problem is chronically contracted
pectoral muscles or undue tightness of the scalene
muscle group.15 In women, another issue may be the
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
menstrual cycle and the monthly impact of the hor-
mones on the circulation.40 Another factor has to do
with power in the workplace. Although progress has
been made in this area, women often have less control
over their work environments than men. When they are
in jobs more likely to lead to TOS, they often have less
authority to limit these stresses.40
Differential Diagnosis
Neurogenic thoracic outlet patients are remarkable for
lack of objective evidence of neurologic injury or posi-
tive radiologic findings. It is the subtle soft tissue signs
of neural irritability, vascular abnormalities, changes in
breathing patterns, changes in first rib and thoracic
mobility, and the quality of muscle contraction that con-
tribute to the diagnosis.
A complete clinical evaluation should always consider
conditions that may simulate or coexist with TOS.
These include cervical disk disease or cervical spondy-
losis, angina pectoris, spinal cord neoplasm, Pancoast
tumor, multiple sclerosis, carpal tunnel syndrome, ulnar
nerve compression at the elbow/wrist, orthopedic prob-
lems of the shoulder and spine, and inflammatory
conditions of the joints and soft tissues.11,41
In addition, T4 syndrome includes symptoms of dull
pain, aching, and discomfort or paresthesia in the arm
that do not follow any dermatomal pattern and often
manifests in a vague feeling of tightness or pressure in
the posterior midthoracic region. The signs on palpation
of the T4 syndrome are located between T3 and T6 as
differentiated from the supraclavicular tenderness
associated with TOS.15
Many patients have issues involving more than one
“tunnel” (called multiple crush). Sorting out the contri-
bution of each is challenging. A major contribution to
the clarification of cervical tunnel involvement comes
from the work of Dr. Herman Kabat.42 He devised a
simple clinical test to evaluate the quality of muscle con-
traction in three distal arm muscles innervated by the
C8/T1 nerve roots. These muscles are adductor pollicis,
flexor pollicis brevis, and flexor carpi ulnaris. A positive
Kabat sign implicates C8/T1 roots as a potential source
of irritation. This sign is defined as weakness in adduc-
tor pollicis, flexor pollicis brevis, and/or flexor carpi
ulnaris that is reversed by 30 seconds of what Kabat
called self-cervical traction. (See Treatment later in this
chapter.) Clinical observation of patients with bilateral
217
arm pain indicates that sometimes the cervical motor
root problem is in one arm while the TOS problem is
in the other.
Another challenging diagnostic problem concerns
carpal tunnel syndrome (CTS). True CTS involves the
median nerve only and is often associated with Tinel’s
sign and/or Phalen’s test.10 CTS is associated with
TOS in 21% to 30% of TOS cases. Ulnar nerve com-
pression at the elbow is associated with TOS in 6% to
10% of cases.43,44 The double crush syndrome indicates
the existence of more than one area of nerve compres-
sion in an extremity.45 The presence of a proximal lesion
does seem to make the distal nerve more vulnerable to
compression.46
It is believed that in some cases there can be a mul-
tiple crush syndrome involving any combination of cer-
vical spinal nerves, trunks and cords of the brachial
plexus, ulnar nerve compression at the elbow/wrist, and
median nerve compression at the carpal tunnel.43 The
author’s experience is that the lower extremity neural
tension signs, such as straight leg raising (SLR) and
dural mobility, can also be affected in severe cases of
TOS.
Examination Findings
Subjective Symptoms
Symptom Patterns for Patients With TOS. Com-
plaints may include paresthesia (numbness and tin-
gling), pain (aching or sharp), and sensory and motor
loss. Aching pain is noted as the most common
symptom.38,41 Pain is frequently felt in the lateral aspect
of the neck, supraclavicular area, shoulder area, axilla,
medial arm, medial forearm, frequently in the hypo-
thenar area, and fourth and fifth digits. The pain may
radiate to the chest wall.15,47,48
Arterial obstruction produces coolness, cold sensitiv-
ity, numbness in the hand, and exertional fatigue.
Venous/lymphatic obstruction may cause cyanotic dis-
coloration, arm edema, finger stiffness, and a feeling of
heaviness.19,38,49,50 Venous symptoms are more common
than arterial ones. Peripheral embolization can cause
gangrene of fingertips and is an arterial complication of
TOS.10,51
Initial symptoms may be proximal (cervical) and
progress distally (hand) or begin distally and progress
proximally. Symptoms often begin in one arm and
progress to include both arms.
218 SECTION II NEUROLOGIC CONSIDERATIONS
Functional Profile for Patients With TOS. Symp-
toms are aggravated by dependency of the arm and any
use of the arm in lifting, pushing, pulling, reaching over
the head, or repetitive activity such as writing, data entry,
or playing a musical instrument. Fine coordination may
be affected, with patients complaining of symptoms with
sustained upper extremity activity—such as combing
hair, reaching, carrying a heavy bag, and holding a news-
paper, telephone, or steering wheel. Pain is often worse
after—rather than during—use, and is referred to as
latency. This latent pain is a characteristic of neuropathic
pain. The pain may be particularly disturbing at night49
and symptoms can be bilateral or unilateral.10
Symptoms are eased by avoiding aggravating activity
and through support of the involved extremity, such as
wearing a sling, keeping the hand in a pocket, or resting
it on a fanny pack.
History for Patients With TOS. In the patients
with TOS seen by the author, there was a high incidence
of trauma. The trauma could either be sudden or pro-
gressive. The most common sudden traumatic event was
a motor vehicle accident. The most common progressive
trauma was injury from repetitive use of the hands under
high cognitive demand10,52 because of poor workstation
design or poor hand/arm/neck use. Particular stress was
placed on the neck and eyes caused by peering at the
computer screen.53
There may be a past history of trauma to the head,
neck, or upper extremity that was subsequently
resolved—leaving the patient apparently asymptomatic
or with minor residuals that did not compromise normal
function. If this trauma affected the diameter of the
canal(s) or the flexibility of the nervous system as it tra-
versed the canal(s), or caused trauma to the vascular
system, then the trauma may have contributed to the
onset of symptoms by establishing risk factors in the
form of scarring.
Tests and Measures for Patients With TOS
Specific diagnosis of TOS can be made by radiograph
and computed tomography (CT) scans. Radiologic
studies can identify any bony abnormalities, degenera-
tive changes, Pancoast tumors, or other pulmonary dis-
eases.11 Previous history of clavicular fracture picked up
on radiography is important, because it can predispose
an individual to embolization of the subclavian artery.47
CT and magnetic resonance imaging (MRI) are often
necessary to rule out frank cervical disk disease, spinal
stenosis, and fibrous bands.10 Recent introduction of
MRI neurograms offers a method to identify soft tissue
and vascular anomalies that may contribute to the
condition.54,55
An important finding, whose significance is often not
appreciated, is the presence of an elongated transverse
process of C7 seen on the anterior/posterior view of
plain x-rays. It is the experience of the vascular surgeons
at the University of California-San Francisco that the
presence of an elongated transverse process is a marker
for other anomalies within the thoracic outlet, such as
soft tissue changes within the scalene triangle and
fibrous bands.26,27 One can hypothesize that the con-
genital anomalies at the C7/T1 junction are analogous
to the more widely accepted congenital anomalies at
L5/S1, and that the likelihood of soft tissue anomalies
in the presence of an identified bony anomaly is more
likely.
Diagnosis of vascular TOS is made by duplex
scanning (ultrasound combined with Doppler velocity
waveforms), angiography, or venography.10,56,57 The in-
fraclavicular area should be auscultated for the presence
of a bruit with the arm in various positions.38,39,51 A bruit
indicates an arterial lumen narrowing.10
Electrodiagnostic tests include electromyography
(EMG), late F-wave responses, nerve conduction veloc-
ities (NCV), and somatosensory evoked potentials
(SSEP). Positive electrodiagnostic studies can indicate
chronic, severe lower trunk brachial plexopathy. Such
tests may indicate an abnormality in nerve function, but
do not give the specific cause of the abnormality. Low-
amplitude ulnar sensory responses are the most widely
accepted of these studies, but there is disagreement over
the reliability of the results. There is a wide range of
conduction times found in asymptomatic individuals,
which may be the result of inaccurate placement of the
proximal electrode at Erb’s point.10,15,43,57,58 Many TOS
patients have normal electrodiagnostic studies. This may
be the result of the intermittent nature of the symptoms,
which are dependent on certain positions. Instead of
testing these patients in the anatomic position, they
should be tested in the symptom-provoking position.59
Most agree that these studies are helpful in ruling out
carpal tunnel syndrome and ulnar nerve entrapment at
the elbow.10,19,43,57
Some practitioners have used thermography as an aid
in diagnosis of TOS.60 Thermography indicates either
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
an increase or a decrease in heat emission secondary to
change in blood flow. These alterations in heat emission
can be measured by thermography and could be because
of venous occlusion or a decreased flow, as in arterial
compression or nerve fiber irritation from neurogenic
compression. Because pathologic conditions such as cer-
vical radiculopathy, ulnar nerve injury, and reflex sym-
pathetic dystrophy can produce similar patterns, the lack
of specificity can make interpretation of thermography
difficult.57
A study was conducted in which 123 patients under-
going thoracic outlet decompression were monitored
during surgery with continuous emission infrared pho-
tography. In all cases there was a temperature differen-
tial with cooling in the ulnar border of the hand. During
surgery, as neurolysis was being performed at both upper
and lower roots of the plexus, depending on the site of
adhesions, there was an immediate and appropriate
increase in hand temperature in 89% of the cases.61
A scalene muscle block is another technique used as
a diagnostic aid. Relief of symptoms after the muscle
block, by injecting lidocaine into the muscle belly, can
implicate the anterior scalene muscle as the source of
pathologic abnormality. Improvement after the block
correlates with good response to surgery.10
Objective Examination by Physical Therapist
for Patients With TOS
The objective examination is limited in the traditional
scope and range of motion examined because of respect
for the neuropathic irritability of the condition. Active
movements of the cervical spine are examined to the
point of onset or increase of symptoms only. When
examining the brachial plexus provocation test, it is
essential to examine to the initial barrier or point at
which involuntary muscle guarding/tension comes into
play. This is before the range in which the symptoms of
pain, numbness, or tingling are elicited. If this precau-
tion is not adhered to, the risk of a latent exacerbation
of symptoms is heightened. It is the irritability of the
nervous system that is at the physiological core of the
problem. Because all movements of the spine and
extremities have a biomechanical effect on the nervous
system, all movements need to be examined to the initial
point of muscle tension only.
Observation. Typical postural deviations to look
for in these patients involve protective positioning of the
219
upper quarter to reduce stress on the neural and vascu-
lar structures. This can manifest in subtle protraction
and elevation of the shoulder girdle. In more extreme
cases, the patient may hold the upper extremity in a
fully flexed posture much like the posture seen in
hemiplegia.
In more severe involvement, the protected posture
may be absent. Postural deviations, such as a thoracic
kyphosis, may be seen as aggravating the neural struc-
tures with forward head posture and/or a lowered shoul-
der girdle on the more painful side. The presence of a
winged scapula on the more painful side, indicating
weakness of serratus anterior, is a sign of possible long
thoracic nerve involvement. Other signs to look for
include soft tissue fullness in the supraclavicular area and
transient discoloration and/or swelling of the hands.
Active and Passive Movements Used to
Evaluate Sensitivity of the Nervous System
Active Movements. The nervous system is exam-
ined both actively and passively. Active examination
involves movements of the neck and upper extremities.
These movements are evaluated to the initial barrier or
point of tension. This area of tension is assessed to
determine if it is characteristic of a sensitized nervous
system or sensitized muscles, joints, ligaments, or
tendons. Based on the author’s clinical experience, when
the point of initial tension falls within the first 50% of
normal full range of motion, then it is presumed to be
within the range where the flexion withdrawal reflex
is elicited as a protective response for a sensitized
nervous system. Secondly, the more distal the site of
tension, the more likely the tension is because of neural
sensitivity.
The cervical movements examined are flexion, exten-
sion, and bilateral rotation. The shoulder movements
examined are flexion with full elbow extension and
flexion with full elbow flexion. (Table 7-2 illustrates
the typical patterns of restriction, symptoms produced,
and the presumed neural tissue responsible for the
restriction.)
Passive Movements. Passive examination involves
movements of the brachial plexus and sciatic plexus to
the initial point of tension. The brachial plexus exami-
nation is confined to the brachial plexus provocation test
(BPPT), biased toward the median nerve. This test can
differentiate between an upper-root sensitivity versus
220 SECTION II NEUROLOGIC CONSIDERATIONS

Table 7-2

ACTIVE AND PASSIVE MOVEMENTS TO EVALUATE SENSITIVITY OF THE NERVOUS SYSTEM WITH SYMPTOMS PRODUCED AT
POINT OF TENSION AND PRESUMED NEURAL STRUCTURES

Presumed Sensitized Neural Structure

Symptoms Produced at (when Range of Motion (ROM) is in
Movement Examined Point of Tension First 50 Percent of Active ROM)

Cervical flexion Pull at cervical/thoracic junction Dura

Cervical extension
Right cervical rotation
Left cervical rotation
Right shoulder flexion w/elbow
extension
Left shoulder flexion w/elbow
extension
Right shoulder flexion w/elbow
flexion
Left shoulder flexion
w/elbow flexion
Pull in anterior/cervical region
Pull in left supraclavicular
region or left extremity
Symptoms into right upper
extremity
Pull in right supraclavicular
region or right extremity
Symptoms into left upper
extremity
Pull in neck or right upper
extremity in dermatomal
distribution (median nerve)
Pull in neck or right upper
extremity in dermatomal
distribution (ulnar nerve)
Pull in neck or left upper
extremity in dermatomal
distribution (median nerve)
Pull in neck or left upper
extremity in dermatomal
distribution (ulnar nerve)
Pull in neck or right upper
extremity in dermatomal
distribution (median nerve)
Pull in neck or right upper
extremity in dermatomal
distribution (ulnar nerve)
Pull in neck or left upper
extremity in dermatomal
distribution (median nerve)
Pull in neck or left upper
extremity in dermatomal
distribution (ulnar nerve)
Roots of the brachial plexus, either
intraforaminal or extraforaminal
Roots of the left brachial plexus
(extraforaminal)
Roots of the right brachial plexus
(intraforaminal)
Roots of the right brachial plexus
(extraforaminal)
Roots of the left brachial plexus
(intraforaminal)
Roots of the right brachial plexus, C5 through
C7 or median nerve
Roots of the brachial plexus, C7 through T1 or
ulnar nerve
Roots of the left brachial plexus, C5 through
C7 or median nerve
Roots of the left brachial plexus, C7 through
T1 or ulnar nerve
Roots of the right brachial plexus, C5 through
C7 or median nerve
Roots of the right brachial plexus, C7 through
T1 or ulnar nerve
Roots of the left brachial plexus, C5 through
C7 or median nerve
Roots of the left brachial plexus, C7 through
T1 or ulnar nerve
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
lower-root sensitivity based on the pattern of symptom
production, that is, tension produced in the dermatomal
distribution of the median nerve incriminating the C5
through C7 roots, or the peripheral median nerve.
Tension produced in the dermatomal distribution of the
ulnar nerve incriminates the C8 through T1 roots, or the
peripheral ulnar nerve. This test is discussed in detail in
Chapter 6 and so only a brief description will be given
here.
There are four tests designed to measure the extensi-
bility and sensitivity of the neural structures of the upper
limb. Each one biases a different aspect of the cervical
roots, trunks, and peripheral nerves. With TOS, com-
pression of the neural structures provides a site of tensile
stress concentration and limits the normal mobility and
extensibility necessary to accommodate to the stresses of
neck and arm movement. The resulting abnormal
amount of tension will produce a positive BPPT.62
The first of these tests, BPPT 1, is a general test of
the brachial plexus with a bias towards the median nerve
and nerve root levels C5, C6. BPPT 2 has two varia-
tions that more selectively bias the median and radial
nerves and the C5, C6, and C7 nerve roots. BPPT 3 is
biased for the ulnar nerve and nerve root levels C8-T1.16
(See Chapter 6 for a description of these tests.) In the
author’s experience the BPPT 1 and 2 are positive and
symptomatic in all patients. As previously mentioned, an
identifying characteristic of these patients is the irri-
tability of the neural structures. Therefore, when pas-
sively examining the nervous system, one must examine
it to the point of muscle tension (the point at which the
pathologic flexion withdrawal reflex is elicited). Toex-
amine the patient in the range in which symptoms, such
as numbness, tingling, or pain, are produced is to over
examine them. Once this has been done, it is too late to
back up. There will most commonly be a latent flare,
which may take hours or days to subside.
Other Tests to Examine Neurologic Sensitivity.
The Tinel’s sign is used to evaluate the sensitivity of the
nervous system to tapping. Tapping is done at the
brachial plexus, ulnar nerve at the elbow, ulnar nerve at
the wrist, and median nerve at the wrist. The expected
positive finding is one of numbness, tingling, and pain
along the distribution of the nerve or nerves being
tapped distal to the site of the tap. In some cases,
the tap will cause symptoms proximal to the site of
the tap.10,39,43,49
221
Palpation. In patients with neurogenic TOS there
is pain with direct pressure over the scalene muscles, the
pectoralis minor muscle distal to its origin on the cora-
coid process, and the subclavius muscle that can be pal-
pated under the inferior border of the clavicle.
Strength Testing
Muscle weakness, if present, is mild and involves most
commonly the thenar, hypothenar, and interosseous
muscles innervated by the ulnar nerve. The traditional
grip and pinch tests are within normal limits. To iden-
tify weakness, it is necessary to examine the Kabat sign.
Kabat Sign. In more than 25 years of clinical expe-
rience treating patients with neck and arm pain, Kabat—
the father of proprioceptive neuromuscular facilitation
(PNF)—developed a unique method of evaluating neu-
romotor control in the muscles of the hand/wrist.
Kabat’s clinical experience led him to observe a consis-
tent weakness in the ulnar-innervated muscles of the
thumb and wrist in patients with neck and arm pain. He
tested the strength of adductor pollicis, flexor pollicis
brevis, and flexor carpi ulnaris in the shortened range of
those muscles and found that in 80% of these patients
there was weakness unilaterally in response to an iso-
metric contraction.
Kabat’s test minimized the activity of the median
innervated muscles (opponents, long flexor of the
thumb, and lumbricals) by measuring isometric contrac-
tion of flexor brevis/adductor pollicis while the distal
interphalangeal (DIP) joint is held in maximum exten-
sion, with the thumb in the plane of the palm and the
fingers hyperextended. The author’s clinical experience
with more 500 patients has verified the presence of
this weakness in this patient population when tested
appropriately.
Kabat further contributed to an understanding of the
significance of this weakness by having patients perform
an isometric contraction of longus colli (ICLC) for 30
seconds using the fist under the chin (Figure 7-6). The
effect of this 30-second isometric contraction was deter-
mined by immediately reevaluating the identified thumb
weakness. Kabat found this identified weakness to be
partially or completely reversed. The author has identi-
fied this finding as a positive Kabat sign to give credit
to the originator.
Initial testing is performed manually and then quan-
tified using a device termed a ThumbometerR developed
222 SECTION II NEUROLOGIC CONSIDERATIONS
Figure 7-6 Dr. Kabat’s method of performing an iso-
metric contraction of longus colli as a method of reversing
identified weakness in adductor pollicis or flexor pollicis brevis
(deep head). The traction force is sustained for 15 to 30
seconds and then released slowly. Retesting of the weak
muscles should demonstrate immediate increase in motor
power.42 (From Kabat H: Low back and leg pain from herniated cer-
vical disc, St Louis, 1980, Warren H. Green; Courtesy Peter Edgelow.)
by the author (Figure 7-7). Kabat further qualified the
significance of the weakness by sequentially applying
minimal stresses to the neck in eight directions. These
directions consist of a tap to the patient atop the head
(superior); a push against the chest (anterior); a push
against the right and left arms (lateral); a push down on
the right and left shoulders (superior border of shoulder
girdle); and a push against the right foot and left foot
(inferior).
Following each stress, the hand is retested for
strength. If the patient has a positive Kabat sign, then
one—and only one—direction of stress will bring back
the weakness. Once the weakness returns, an ICLC is
performed to ensure that the weakness is again reversed
before testing other directions.42
The most common direction of stress that reproduces
the weakness is superior stress through the top of the
head. In the Edgelow protocol, this reversible weakness
is called a positive Kabat sign. This sign identifies a
Figure 7-7 The Thumbometer is constructed using a
half ounce eye drop–like bottle connected by a piece of green
Theratubing to the sphygmomanometer from a standard
manual blood pressure cuff.
functional instability in the region of the cervical
thoracic junction.
Patients with a positive Kabat sign can be further dif-
ferentiated into those with structural instability with a
fully erect posture versus a fully flexed posture. These
patients have a comfortable midrange neck posture,
which is in some degree of forward head posture. In this
neutral position, the thumb is strong. In the fully erect
posture, or full-neck flexion posture, weakness returns.
Breathing Pattern. One hundred percent of these
patients have an abnormal breathing pattern, which is
evident during quiet inspiration. The normal pattern—
called “diaphragmatic” during quiet inspiration—should
begin with the diaphragm and progress to the inter-
costals with a relaxed expansion of the abdomen and
without sternal/chest elevation, indicating parasympa-
thetic control. In contrast, in the abnormal breathing
pattern present in these patients, movement is in the
chest rather than the abdomen with inspiration coinci-
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
dent to contraction of the accessory breathing muscles
(scalenes and pectoralis minor).
To test for this abnormal pattern, the scalenes are pal-
pated lateral to the sternocleidomastoid and superior to
the clavicle (see Figure 7-1). Patients are then asked to
take a relaxed inhalation. If contraction of the scalene
occurs and the chest elevates, this is incorrect and
brought to their attention and they are instructed to
breathe in with the “belly only” and to not elevate the
chest. If they cannot do this, their breathing pattern is
paradoxical, and abnormal.22
More Traditional Objective Tests for Thoracic
Outlet Syndrome. The standard clinical tests to
implicate particular areas that could be responsible for
causing compression to the neurovascular structures are
sometimes open to interpretation. Among the more
common diagnostic tests are the following:
1. Adson’s test. This has been used to implicate the
anterior scalene muscle’s role in obliterating the
pulse when the muscle is put on stretch.10
2. The exaggerated military position. This purports to
test the costoclavicular component of the thoracic
outlet by lowering the clavicle onto the first rib,
causing compression there.10
3. Hyperabduction of the arms (arms overhead with
elbows flexed, as assumed in sleep). This produces a
pulley effect of the neurovascular structures under
the pectoralis minor tendon and coracoid process,
causing compromise at that site. This position can
also narrow the costoclavicular space. Both pulse
obliteration and typical symptom reproduction are
considered positive for these tests.20,39
4. The abduction external rotation test (AER),
commonly called the hands-up test. This has the
reputation of being the most reliable of the TOS
tests. This postural maneuver involves shoulder
abduction and external rotation to 90°, producing a
scissorslike compression of the neurovascular
structures by the clavicle on the first rib. It can be
considered positive by reproduction of the patient’s
symptoms or by pulse change.10, 11,38 Positive
response for pulse obliteration is only 5% to 10% in
normal studies.12
5. An additional claudication test is added to the
AER position, during which a patient opens and
closes the hands for up to 3 minutes. This is called
the elevated arm stress test (EAST). This test will
223
evaluate all three types of TOS because of
compression by the position and the added stress of
exercise.11
The problem with these traditional tests is that when
pulse obliteration is used as the critical sign, the tests
have shown too many false-positive results to be reliable,
because some asymptomatic individuals have pulse
changes with the maneuvers.12 Reproduction of the
patient’s symptoms using these test positions is a more
reliable sign of thoracic outlet syndrome.39 The hyper-
abduction and costoclavicular maneuvers are positive if
there is simultaneously an obliteration of the arm pulses
and reproduction of neurologic symptoms.
Each of these standard TOS tests has components of
the BPPT within them. Depression of the shoulder
girdle, or the exaggerated military position, causes a
“drag on the nerve roots.”12 Abduction and external rota-
tion of the arm, or the AER test, places a traction force
on the brachial plexus and is further exaggerated by the
hyperabduction maneuver.18 Adson’s test involves lateral
flexion of the head to the contralateral side. Compared
with the BPPT, these tests involve only partial tension
of the neuromeningeal system. However, progressively
adding tension up to the limit of the neuromeningeal
system may be required with more mild cases. This may
explain why many times the results of these classic tests
are negative, and why performing the BPPT is a better
test of the limit to which the compromised system can
be taken. No single test of the more traditional tests is
specific enough to eliminate other potential sources of
pathology.
Reflex Testing. Standard tendon tap reflex testing
usually elicits a response that remains symmetrical bilat-
erally or hyperactive. It is this author’s contention that
the more subtle signs of abnormal reflex activity are
found in the hyperactive flexion withdrawal, as outlined
previously, and asymmetric finger temperature. The
abnormal flexion withdrawal reflex is a sign of height-
ened somatic nervous system activity, while the asym-
metrical temperature is presumed to be a sign of
abnormal autonomic nervous system control.
Temperature Testing. The temperature of the
second and fifth digits of both hands is evaluated using
an indoor/outdoor thermometer. Four thermometers are
used to measure the temperature of each digit simulta-
neously. The indoor temperature of each thermometer is
224 SECTION II NEUROLOGIC CONSIDERATIONS
recorded to get a baseline before taping the tip of the
outdoor lead to the fingers. The outdoor temperatures
are recorded after 2 minutes.
The expected normal temperature is symmetrical
hand-to-hand and finger-to-finger. In the author’s expe-
rience, when temperatures are in the 90° range they are
within normal limits. Temperatures in the low 70° range
could be abnormal. This author considers it to be abnor-
mal if the temperature is not increased by diaphragmatic
breathing with spinal motion or by aerobic walking on
the treadmill. Asymmetry between fingers occurs most
commonly with a colder fifth digit compared with the
second digit. This difference in temperature is correlated
with the area of symptoms. Because the fifth digit
receives its sensory innervation from the ulnar nerve and
the second digit from the median nerve, one can expect
an ulnar distribution of pain to correspond with a colder
ulnar digit.
Sensory Testing. Traditional sensory tests of light
touch and pinprick are often normal. Hypesthesia may
occur in the C8-T1 dermatomes.39
Nancy Byl’s work on focal hand dystonia indicates
the need for additional sensory tests. These tests include
localization, graphesthesia, and stereognosis. Dysfunc-
tions revealed by these tests can be present in the more
severe forms of neck and arm pain.63,64
Vestibular Testing. Testing for vestibular control
can be done with a traditional balance evaluation, such
as a two-leg balance with eyes open and then with eyes
closed.65
Treatment
The Edgelow Protocol
The Edgelow Protocol trains patients to develop phys-
ical control of their condition under the guidance of a
physical therapist. The components of the program are
illustrated in Figure 7-8. The patient is at the top of the
figure to emphasize that this is a patient-centered
program.
The next part is the evaluation phase to emphasize
that this treatment protocol is designed for injuries of
the neck and upper quarter with neurovascular, sensory
motor, and whole body consequences that overshadow
the musculoskeletal consequences. The evaluation phase
has previously been described under the “Objective
Patient
Edgelow protocol
Evaluation
Neuro- Sensory
vascular
Core
motor
component component
Whole
body
component
Figure 7-8 The Edgelow Protocol.
Examination” Section. In this phase, the patient is
trained to monitor specific physical signs and to deter-
mine the effect of the selected exercises on these signs.
The selected exercises (core of the treatment) are
directed to reversing the neurovascular, sensory motor,
and whole body effects of the injury.
Patient-Guided Treatment
Core exercises have been developed to assist the patient
to achieve a change in physical signs without increasing
pain.
The goals of the core exercises are to:
1. Restore symmetry in thumb strength if the physical
examination demonstrates reversible weakness
(positive Kabat sign)
2. Increase tension-free range of motion of the upper
extremities
3. Increase hand temperature
4. Improve diaphragmatic breathing control
5. Increase spinal mobility with an emphasis on
extension
6. Improve aerobic condition through a graded
walking program
7. Establish symmetry in selected muscles
8. Establish greater vestibular control
These goals must be achieved without increasing pain
that the patient perceives as harmful. From a clinical
perspective, pain is perceived as harmful if one of two
responses occurs: either a tension response, which results
in muscle activity when relaxation is the expected result;
or a cooling response in the involved extremity when a
warming response is the expected result.
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
The protocol requires patients to draw upon their
physical, emotional, and intellectual resources to treat
the condition.
Physical Components Associated With TOS
1. A change in the normal breathing pattern from
belly (diaphragmatic) breathing to sternal (scalene)
breathing.
2. An increased sensitivity of the nervous system, so
that moving the arm(s) causes pain, along with an
increase in tension of the muscles and coldness in
the hand(s)—not the normal response of relaxation
of the muscles and warming of the hand(s).
3. In some cases there is weakness of the ulnar-
innervated muscles of the thumb and wrist in one
hand. This weakness is reversed by gentle pressure
under the chin to promote an isometric contraction
of longus colli muscle (positive Kabat sign).
Elements of an Effective Treatment Program
1. Restore the normal relaxed diaphragmatic breathing
in all functional positions.
2. Restore the normal sensitivity of the nervous
system so that relaxed movements of the arms
increase blood flow and relieve tension.
3. Restore strength and endurance to the weak thumb,
longus colli, lower fibers of trapezius, serratus
anterior, and abdominal muscles—particularly
transversus and oblique.
A home program has been developed that is sepa-
rated into a core program and a series of progressions.
Not all patients will be able or need to progress through
all parts of the program, but the whole program will
encompass the essential parts.
Components of the Core Program
1. The “thinking” position as a method of activating
longus colli during activities of daily living
2. Diaphragmatic breathing with spinal motion to
restore pain-free movement of the spine
3. Cardiovascular conditioning
4. Specific strengthening of longus colli and
abdominal muscles using the methods developed by
Gwen Jull66
Core Outcomes
1. The patient will be able to perform the “thinking”
position for 30 seconds without increasing pain or
225
symptoms while maintaining equal strength in the
thumbs (see Figure 7-6).
2. The patient will be able to perform diaphragmatic
breathing with spinal motion and use assistive
devices without increasing pain or symptoms while
increasing tension-free range of motion of the
BPPT.
3. The patient will be able to walk 3 to 4 miles per
day without increasing pain or symptoms to achieve
normal cardiovascular conditioning.
4. The patient will be able to self-assess hand
strength, neural sensitivity, hand temperature, and
cardiovascular conditioning to track his or her
progress.
5. The patient will modify ADL at home and at work
to minimize mechanical stress on the neck and
arms.
Core Treatment Methods
Action of “Thinking” Position for Reversible
Weakness of the Hand. If there is reversible weakness
in the thumb, indicated by a positive Kabat sign, then
perform the “thinking” position for 15 to 30 seconds
every 60 minutes and practice good body mechanics in
ADL to reduce stress on the spine. There is a maximum
reduction of stress done for 24 hours to manage a flare
and a minimum reduction of stress to maintain the gains
made in hand strength.67 Maximum reduction of stress
involves eliminating all but essential sitting for 24 hours.
When doing essential sitting, such as sitting on the
toilet, the “thinking” position should be assumed to
reduce stress on the spine.
It is important to use the Thumbometer self-testing
device described in Figure 7-7 to quantify the strength
of the hand. This device has been developed by the
author to quantify the strength of adductor pollicis flexor
pollicis brevis (see Figure 7-7). Patients are taught to use
this device to measure their own hand strength before
and after the “thinking” position to ensure that they get
a strengthening response. Once the hands are equally
strong, the patient measures the hand strength on a daily
basis to ensure that the recovered strength is maintained
over time.
How to Perform the “Thinking” Position Exercise
(see Figure 7-6)
• Patients are instructed to stand with the back
against the wall so that the buttocks and mid back
226 SECTION II NEUROLOGIC CONSIDERATIONS
are resting on the wall. The head and neck are held
in a comfortable position. (In this patient
population, this position is commonly a forward
head posture.)
• Patients are instructed to nod the chin down as if to
rest it on the hand, using the stronger hand.
• They should gently engage the deep neck flexors by
pressing against the chin with the fist of the
stronger hand. They should hold this position for 15
to 30 seconds, then slowly release. The neck should
feel slightly elongated and it should feel as if they
have reduced the stress of gravity. (The gentle
pressure should cause no pain in the neck or arm.
The pressure can be measured by placing the
Thumbometer between the chin and the fist, and
the pressure must be limited to no more than 40
mmg.) Pressure on the temporomandibular joint is
reduced by holding the tongue on the roof of the
mouth behind the front teeth.
Relaxed Diaphragmatic Breathing With Spinal
Motion. The breathing exercises should be done for a
minimum of four times a day. The goal is to be able to
do the breathing for 20 minutes each time without
increasing pain. Initially the patient may only be able to
do parts of the full breathing program because some
parts may cause pain. As patients progress and the
pathologic condition improves, they should be able to do
more until the goal of the full breathing program has
been reached.
How to Perform the Diaphragmatic Breathing
Exercise: Part One (Figure 7-9)
• Instruct patients to lie on their back on the floor
without a pillow with knees bent. (Note: If they
have to use a pillow because of neck pain then they
should do so. Over time, the goal will be to slowly
reduce the thickness of the pillow until they can
perform the exercise without a pillow.)
• Instruct patients to support the involved extremity
in the position of maximal comfort. The position of
comfort will be found by placing the nervous system
in its most tension-free anatomic position. Usually a
wedge pillow to support the shoulder, with the
elbow flexed, will relieve tension in the neck and be
most comfortable.
• Patients should breathe in (inhale) through the nose
and fill the lower lungs with air. This causes the
abdomen to rise like a balloon filling up with air.
• Patients then breathe out (exhale) through pursed
lips, as if playing the flute. Exhaling should be
accomplished by tightening the abdominal muscles,
which has the effect of lowering the rib cage.
• Patients are instructed to continue this rhythm of
breathing, in through the nose and out through the
mouth, making sure that the only motion that
Figure 7-9 Diaphragmatic breathing
exercise—Part One (Courtesy Peter Edgelow.)
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
occurs is in the stomach. This is diaphragmatic
breathing.
The patient then adds the following gentle and
relaxed movements of the spine while keeping their neck
and legs relaxed:
• Patients are instructed to slowly arch the low back as
they inhale, shortening the spine and causing the
chin to nod down.
• Patients next slowly flatten the low back as they
tighten the abdominal muscles and exhale,
lengthening the spine and causing the chin to nod
back up.
This gentle motion of the head and neck should
occur naturally. There should be no active movement of
the neck. The neck muscles should remain relaxed.
How to Perform the Diaphragmatic Breathing
Exercise: Part Two (Figure 7-10)
• Patients are instructed to breathe exactly as they did
in Part One, except now the legs are straight. It is
important that the patients’ legs remain totally
relaxed while they are performing the breathing
exercises.
• Patients then slowly arch the low back as they
inhale.
• Then they slowly flatten the low back as they exhale
through pursed lips. Remember, the legs should
remain totally relaxed, and the exercise must not
increase pain.
Figure 7-10 Diaphragmatic
breathing exercise—Part Two (Courtesy
Peter Edgelow.)
227
If patients have problems keeping their back flat as
they blow out with the legs straight, then they may not
be ready for this and may progress to the exercises in
Part Five. The therapist will guide this decision.
How to Perform the Diaphragmatic Breathing
Exercise: Part Three (Figure 7-11)
• Patients are instructed to breathe exactly as they did
in Part Two, except as they relax the abdomen to
arch the back and inhale, they should relax the legs
and let them flop out.
• After patients have flattened the back while
exhaling, they should actively turn the legs in so the
knees and toes are pointing inward. This sequence is
repeated, with the legs turning in at the end of the
exhalation as the back is flat, and flopping out as
patients arch the back and inhale. Patients must be
able to maintain a flat low back as they turn their
legs inwards.
How to Perform the Diaphragmatic Breathing
Exercise: Part Four (Figure 7-12)
Patients are instructed to breathe as described in Part
One, but they must add the rib mobilizer (“ball on a
stick”).
• Patients place the ball against the base of the neck,
where the neck and shoulders meet. The end of
the stick should be resting against the wall behind
the patient and the ball should be resting on the
floor.
228 SECTION II NEUROLOGIC CONSIDERATIONS
Figure 7-12 Diaphragmatic breathing exercise—Part
Four. A rubber ball at the end of a wooden dowel is used to
assist in depressing the first rib as the patient flattens the spine
in conjunction with exhalation. (Courtesy Peter Edgelow.)
Figure 7-11 Diaphragmatic
breathing exercise—Part Three (Courtesy
Peter Edgelow.)
• The ball assists with the depression of the first rib.
As patients inhale, they move away from the ball; as
they exhale, they move into the ball.
How to Perform the Diaphragmatic Breathing
Exercise: Part Five (Figure 7-13, A-D)
• Patients are instructed to breathe as described in
Part One while resting the pelvis on an air bag.
• Patients progress with the exercise as they are able to
tolerate it while breathing with the air bag
positioned as follows:
• Beneath the pelvis (see Figure 7-13, A), the low
back (see Fig 7-13, B) the mid back (see Figure 7-
13, C), and the upper back (see Figure 7-13, D).
It is important that patients experience no increase in
pain or symptoms while doing the breathing with the
bag in each position. The position of the air bag, the
amount of air in the bag, and the amount of spinal
motion will affect how the patient feels in each position.
This exercise offers patients the opportunity to become
mindful in focusing on their ability to do the exercise
without pain. If performed absentmindedly or by rote,
patients will miss the essential benefit of the exercise.
“Snow Angel” Self-Assessment. Patients self
assess the effect of the breathing exercises on mobility
of the brachial plexus by abducting their arms with
elbows fully extended and hands and forearms supinated
(as if they were making a snow angel). They assess the
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET 229

Figure 7-13 Diaphragmatic breathing exercise—Part Five A, B, C, D. An air bag is partially inflated and used as a
fulcrum to gently increase spinal extension. The air bag used in this exercise is made by Sealed Air Corp. and is called a Rapid
FillTM packaging bag. Dimensions are 14 by 18 inches. (Courtesy Peter Edgelow.)

tension-free range of motion before doing the breathing
exercises. After the breathing exercises, they reassess the
tension-free range of motion. The range of motion
should increase if the exercise has been effective.
Cardiovascular Conditioning With Aerobic
Walking
An aerobic walk is an essential part of the road to well-
ness. Patients should:
• Begin with walking within their recommended
training zone67 or to the point of symptom increase
for a maximum of 20 minutes.
• Walk three to four times a day. They may need to
walk with the most painful arm supported by a
fanny pack, brace, or the hand in a pocket.
• Measure the pulse prewalk and postwalk until they
have achieved normal cardiac conditioning for their
age.67
• Have a warm-up period for a maximum of 21/2
minutes for the best changes in cardiovascular
conditioning, followed by maintaining the training
zone heart rate for at least 15 minutes, and ending
with a “cool-down” period for a minimum of 21/2
minutes.
230 SECTION II NEUROLOGIC CONSIDERATIONS
Selected Activities to Progress the Core Program
What follows is a sequence of activities used once the
patient has achieved the primary goals of the core
program. (These are presented in the order most com-
monly used but may vary according to the patient’s
response.)
• Diaphragmatic breathing while sitting
• Vestibular/balance retraining
• Progression of spinal extension/rib cage range of
motion
1. Restore pain-free movements of neck and arms
2. Retrain the sensory system of the hand using the
methods developed by Nancy Byl63,64
Devices that can be used may include a 6-inch by 3-
foot EthofoamTM roller, a ball on a stick rib mobilizer, a
3- by 18-inch EthofoamTM roller, and a gymnastic ball.
It is vitally important to begin with the core and to
progress only after patients have achieved the core objec-
tives and can maintain them as they progress through
the full program.
Influencing Factors
There are many outcomes that influence a treatment
program for patients with TOS. They can reflect the
education and experience of the therapists; the risks and
benefits as viewed by the patients; and the cost and ben-
efits as determined by insurers and employers; to
mention a few of the influencing factors. With acknowl-
edgment of these factors as ongoing parameters, the
general goals of the treatment program are to teach the
patient to control the problem and prevent recurrence
by taking control of selected and individualized thera-
peutic procedures. This is achieved through training and
monitoring of the physical problems; the emotional
response to the disabling and painful problem; and an
intellectual understanding of the issues related to causes,
methods for prevention and curing the disorder, and the
personal role in each. It is the basic premise of this
approach that the patient learns through the ability
to feel the change that occurs while performing the
exercises to both understand the problem and be guided
by the change in relevant symptoms towards the
solution.
Prevention
The patient is trained to prevent recurrence by using the
following routine every hour as they work:
1. Relieve pressure on the neck by sitting erect and
applying self-traction using the “thinking” position
for 15 to 30 seconds.
2. Relieve pressure on the scalenes and first rib
through quiet diaphragmatic inhalation and active
exhalation for 15 to 30 seconds to “blow” away the
tension in the neck and shoulders.
3. Relieve pressure on the eyes by closing them for 15
to 30 seconds and then looking at a distant object
to change perspective.
The preceding three activities can be called “quick fixes.”
4. Be in control of the body. No one else can see what
the patient feels, no one else can say, “It is time to
take your break.”
Ergonomic redesign is only one part of safe job con-
ditions. The other part is to know how to safely do
required tasks, knowing when to stop and take a break.
The visualization of “The Thinker,” pose (see Figure
7-6) serves to remind the patient to perform those
learned actions associated with the Edgelow Protocol.
“The Thinker” can be considered a metaphor, empha-
sizing to the patient the need to think about prevention.
Conclusion
There is much more that needs to be discovered to
explain the pathologic condition behind TOS. Until
more knowledge is available this approach presents one
method of treatment. Whatever treatment methods are
used, they must be integrative, considering all body
functions: musculoskeletal, neurovascular, and car-
diopulmonary. Two case studies are presented to illus-
trate the use of this protocol: one acute condition, with
an 8-year follow-up, and one chronic condition.
Case Study 1
HISTORY
A 25-year-old, right-handed billing clerk developed
right wrist pain on Oct. 26, 1995, while doing computer
entry. Over the next 2 days the symptoms spread from
the wrist up the forearm to the elbow and down into the
hand. Despite rest for 2 days the pain remained constant
and did not subside.
RISK FACTORS
The patient had been working overtime 6 days a
week, packing records in preparation for a move. Her
normal work commute was 45 minutes twice a day. She
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET 231

worked out at the gym for the prior 6 weeks, lifting
weights up to 60 lb. She had had two automobile acci-
dents, one in 1989 and one in 1991. She reported no
prior arm symptoms, but occasional neck pain that
responded to massage, self-mobilization, and rest. She
has had mild asthma since age 16. She wears glasses and
experiences eye fatigue from “peering at the computer
screen.” She gets aerobic exercise by using roller blades
for fun. Six weeks prior to the onset of symptoms, she
fell on outstretched hands and sprained her left wrist,
but was okay within 2 days.
PAIN PATTERN (BY REPORT)
The patient denied having headaches or any symp-
toms in the left upper extremity, low back or legs.
FUNCTIONAL PROFILE
1. Symptoms were aggravated during repeated data
entry with slight slowness in finger dexterity noted
when switching from 10-key entry to keyboard and
vice versa for the first few seconds. “The hand feels
as if it doesn’t want to work.”
2. Lifting weights at the gym or boxes at work increases
her neck pain.
3. Driving to and from work is uncomfortable in the
neck and shoulder blade and she feels tight in the
right supraclavicular region.
OBJECTIVE FINDINGS

Area of Symptoms Pain Characteristics

(Greatest Intensity & Visual Analogue
to Least Intensity) Scale
POSTURE
1. Right dorsal wrist Constant pain (7/10, 50% of
time at worst; 3/10 25% of Factor Observed Findings
time at best)
Cervical thoracic Forward head w/apparent
2. Right forearm/elbow Intermittent pain (6/10 at
alignment “step off ” at C7/T1
worst)
Shoulder girdle alignment Within normal limits
3. Right thumb, right Intermittent pain
Lumbar spine Within normal limits
thenar eminence,
Height and weight 5 ft 9 in, 150 pounds
and right fifth digit
Hands No discoloration or swelling
4. Right upper arm Intermittent soreness
5. Right neck Constant tenderness to
palpation

ACTIVE MOVEMENTS (TESTED TO INITIAL POINT OF TENSION ONLY )

Symptoms Produced at Point of

Movement Examined Range of Motion Tension

Cervical flexion 40° (80° = WNL) Pulls cervical spine right > left
Cervical extension WNL (60° = WNL) Pulls anterior/cervical spine
Right cervical rotation WNL (90° = WNL) Pulls left supraclavicular region
Left cervical rotation 80° (90° = WNL) Pulls right cervical spine; pain in left
upper trapezius
Right shoulder flexion w/elbow 135° (180° = WNL) Pulling whole arm to thumb
extension
Left shoulder flexion w/elbow 110° (180° = WNL) Pulling whole arm to thumb
extension
Right shoulder flexion w/elbow 180° (180° = WNL) No symptoms
flexion
Left shoulder flexion w/elbow flexion 135° (180° = WNL) Pulling into the upper arm

WNL, Within normal limits.

232 SECTION II NEUROLOGIC CONSIDERATIONS

PASSIVE NEURAL TESTING

Right brachial plexus Pull into right thumb

provocation test 80° abduction, 45°
external rotation, 120° elbow
extension with scapular depression
Left brachial plexus provocation test 60° abduction, 30° external rotation, Pull left lateral arm
150° elbow extension with
scapular depression
Right sciatic plexus provocation 60° Pull in hamstring
test—straight leg raise (SLR)
Left sciatic plexus provocation test (SLR) 60° Pull in hamstring
Right brachial plexus Tinel’s test NA WNL
Left brachial plexus Tinel’s test NA WNL
Right ulnar nerve at the elbow Tinel’s test NA WNL
Left ulnar nerve at the elbow Tinel’s test NA WNL
Right ulnar nerve at the wrist Tinel’s test NA WNL
Left ulnar nerve at the wrist Tinel’s test NA WNL
Right median nerve at the wrist Tinel’s test NA WNL
Left median nerve at the wrist Tinel’s test NA WNL

WNL, Within normal limits.

BREATHING PATTERN 2. Findings suggestive of plexus irritability bilaterally,

The pattern was paradoxical, with early scalene con-
traction on quiet inspiration on right side more than the
left.
PALPATION
Scalene sensitive to palpation, right side more than
left.
STRENGTH
Flexor carpi ulnaris/adductor pollicis/flexor pollicis
brevis: right 4/5, left 5/5
POSITIVE KABAT SIGN WITH DIRECTION OF SENSITIZATION
NECK COMPRESSION
As previously mentioned, a positive Kabat sign is
present when the identified weakness in the listed
muscles is reversed following 30 seconds of isometric
contraction of the longus colli. Weakness returned fol-
lowing minimal compression of the neck and was again
reversed following 30 seconds of “The Thinker” pose.
(See Figure 7-6.)
Thoracic spine, cervical spine, and rib cage: postural
dysfunction noted in flexion with bilateral elevated first
ribs.
ASSESSMENT
1. C8 motor root irritability on the right
right side greater than left, with elevated first rib on
the right and left and paradoxical breathing pattern
3. Postural factors influencing the problem
4. Cervical and upper thoracic dysfunction in flexion
TREATMENT PLAN
1. Instruct in “what is wrong” and use home kit for
treating upper quarter neurovascular entrapments
2. Progress through the home program approach to deal
with dysfunctions beginning with strengthening the
longus colli muscle and progressing through the
diaphragmatic breathing, spinal and rib mobilization
3. Restoration of the relaxation and warming response
during repeated movements of the upper extremity
4. Train in protective body mechanics to minimize
stress from work
5. Initial modification of work schedule; no overtime;
no lifting; awareness of posture; no sitting with legs
crossed; feet flat on floor; posture instruction
RESULTS AND DISCUSSION
This case history was chosen to illustrate that find-
ings present in severe cases of neurovascular entrapment
are evident early in the history. The problem is that if
they are not looked for they will often be missed. If
CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
addressed early, they disappear rapidly, and one has a
clear picture of the relevance of these findings. When
the patient can also see the relationship between the
findings and their ability to change those findings, this
reinforces the issues they need to address to get well and
stay well. There is much yet to learn with these prob-
lems. For example:
1. Was this an example of a progression of a problem
that clearly involved the cervical spine following the
auto accidents, but now was involving other tunnels
as well?
2. The initial treatment involved isometric longus colli
strengthening (see Figure 7-6) and breathing. The
result in 24 hours was to abolish the right wrist pain,
but now she complains of left wrist pain because of
using the left wrist and hand for “The Thinker” pose.
Examination of the left wrist revealed slight carpal
dysfunction secondary to the recent rollerblade fall
on the wrists. Self-mobilization of the left wrist
cleared that complaint in 24 hours and it did not
return.
3. Progression of treatment using the foam rollers and
self-mobilization of the neural tissue cleared all
symptoms.
PAIN PATTERN (BY REPORT)
Area of Symptoms (Greatest Intensity to
Least Intensity)
1. Left II/III fingers
2. Right IV/V fingers
3. Right trapezius
4. Right rib cage
5. Anterior neck, cervical thoracic junction, right neck,
and skull
FUNCTIONAL PROFILE
(Established by response to the DASH
questionnaire68)
Her score was 75 (normal is 27).
PRIOR TREATMENTS
Alexander technique for 8 to 9 months
Physical Therapy/Hand Therapy—8 months,
approximately 40 visits that included:
233
4. In the past 8 years, this patient has remained at her
job. Periodic symptoms of neck pain, numbness, tin-
gling, or pain in the hands have been resolved by
resuming the home exercise program.
Case Study 2
HISTORY
A 28-year-old, right-handed marketing representa-
tive had symptoms develop 21/2 years ago while working.
Initial symptoms were numbness in right IV/V fingers,
and within a year her left I, II, and III fingers also
became numb. She managed her symptoms with
common sense, but as they got worse she sought medical
advice. She was referred for hand therapy. She reports
her course has been up and down, with less nerve
pain at the fingers. But at her worst, she continues
to have numbness and/or tingling. At worst, she esti-
mates her pain as 5 out of 10 on a pain scale of 1-10.
She works full-time with typing limited to 11/2 hours
with a break.
Pain characteristics & Visual Analogue Scale
Intermittent numbness and tingling (2-3/10, 40% of time)
Intermittent numbness and tingling (1-2/10, 40% of time)
Constant tightness/pain (4-5/10)
Intermittent tightness/pain
Intermittent pain
• Stretching of the arms
• Strengthening of the arms with gymnastic ball
exercises
• Electrical stimulation
• Spinal mobilization
• Soft tissue massage
Chiropractic—two to three visits
234 SECTION II NEUROLOGIC CONSIDERATIONS

OBJECTIVE FINDINGS

POSTURE

Factor Observed Findings

Cervical thoracic alignment 2 inch forward head measured occiput to the wall
Shoulder girdle alignment Within normal limits
Lumbar spine Within normal limits
Height and weight 5 ft 5 in, 117 lb
Hands No discoloration or no swelling

ACTIVE MOVEMENTS (TESTED TO INITIAL POINT OF TENSION ONLY )

Movement Examined Range of Motion Symptoms Produced at Point of Tension

Cervical flexion 20° (80° = WNL) Pull in cervical/thoracic junction

Cervical extension WNL (60° = WNL) Tension C/T junction
Right cervical rotation 45° (90° = WNL) Pull left supraclavicular region
Left cervical rotation 45° (90° = WNL) Pull right supraclavicular region
Right shoulder flexion w/elbow extension 110° (180° = WNL) Pull in right fifth digit
Left shoulder flexion w/elbow extension 90° (180° = WNL) Pull left third digit
Right shoulder flexion w/elbow flexion 135° (180° = WNL) Pull third and fourth digits
Left shoulder flexion w/elbow flexion 135° (180° = WNL) Pull left thumb

WNL, Within normal limits.

PASSIVE NEURAL TESTING

Area Tested Range of Motion Symptom Produced

Right brachial plexus provocation test 95° shoulder abduction and 180° Tingling in right fourth and fifth digits
elbow extension with scapula in
neutral
Left brachial plexus provocation test 80° shoulder abduction and 180° Tingling into thumb and middle finger
elbow extension with scapula in
neutral
Right sciatic plexus provocation 85° hip flexion with knee extension Pull hamstrings and foot
test—straight leg raise (SLR)
Left sciatic plexus provocation test (SLR) 70° hip flexion with knee extension Pull hamstrings
Right brachial plexus Tinel’s test NA WNL
Left brachial plexus Tinel’s test NA WNL
Right ulnar nerve at the elbow Tinel’s test NA WNL
Left ulnar nerve at the elbow Tinel’s test NA WNL
Right ulnar nerve at the wrist Tinel’s test NA WNL
Left ulnar nerve at the wrist Tinel’s test NA WNL
Right median nerve at the wrist Tinel’s test NA WNL
Left median nerve at the wrist Tinel’s test NA WNL

WNL, Within normal limits.

CHAPTER 7 CUMULATIVE TRAUMA DISORDERS AFFECTING THE THORACIC OUTLET
BREATHING PATTERN
The pattern was paradoxical, with early scalene con-
traction on quiet inspiration on the left side more than
the right.
PALPATION
Scalene, subclavius, and pectoralis minor displayed
tenderness to palpation on the left. Only the scalene was
tender to palpation on the right.
STRENGTH
Flexor carpi ulnaris/adductor pollicis/flexor pollicis
brevis: right side 5/5, left side 4/5
POSITIVE KABAT SIGN22 WITH DIRECTION OF
SENSITIZATION NECK COMPRESSION
As previously mentioned, a positive Kabat sign is
present when the identified weakness in the listed
muscles is reversed following 30 seconds of isometric
contraction of the longus colli. Weakness returned fol-
lowing minimal compression of the neck and was
reversed following 30 seconds of “The Thinker” pose
(see Figure 7-6).
Hand temperature: second and fifth digits within 1°
of each other. Right and left hand temperatures were in
the low 70° range.
Thoracic spine, cervical spine, and rib cage: Postural
dysfunction noted in flexion with elevated first rib bilateral.
ASSESSMENT
1. C8 motor root irritability on the left
2. Findings suggestive of plexus irritability bilaterally,
left side greater than right, with elevated first rib on
the right and left and paradoxical breathing pattern
3. Postural factors influencing the problem
4. Hand temperature in the low 70° range
5. Cervical and upper thoracic dysfunction in flexion
TREATMENT PLAN
1. Instruct in “what is wrong” and use home kit for
treating upper quarter neurovascular entrapments
2. Progress through the home program approach to deal
with the dysfunctions beginning with strengthening
the longus colli muscle and progressing through the
diaphragmatic breathing, spinal and rib mobilization
3. Restoration of the relaxation and warming response
during repeated movements of the upper extremity
4. Train in protective body mechanics to minimize
stress from work and home
5. Posture instruction
The patient received the requested therapy one time
a week for 12 weeks plus 4 additional visits and the fol-
lowing report indicates the results.
235
PROGRESS REPORT/DISCHARGE SUMMARY
The patient has received 16 treatments in the past 11
months. At this stage, she has achieved the following
goals:
Pain
There has been a significant decrease in pain associ-
ated with the exercises. She estimates 70%. She feels in
control of her symptoms and while she can aggravate the
symptoms if she goes beyond her functional limits, she
is able to reduce the pain to a “best” level by doing her
home exercises.
Functional Limitations
Functional changes measured by comparing initial
questionnaire answers to present ones.
Disability of the Shoulder, Arm and Hand (DASH)68
Score was 75 and is now 59 (normal = 27).
OBJECTIVE CHANGES
• Hand strength is now equal bilaterally. (It was weak
left adductor pollicis/flexor brevis.) She has main-
tained this strength consistently since her eighth visit,
which was 8 months ago.
• Hand temperature can now be increased to the mid-
80s with a) walking at 3.9 mph for 20 minutes, and b)
Diaphragmatic breathing with spinal motion for 10
minutes.
• She is no longer limited in brachial plexus mobility
testing without scapular depression. The left now
equals 155° shoulder abduction/elbow full extension
with pull in pectoralis minor. Right now equals 155°
shoulder abduction/elbow full extension/wrist and
fingers neutral with pull in pectoralis minor. On initial
visit, the left equaled 80° with pull in fingers. The right
was equal to 95° with pull in fingers. (Normal range =
155°-180°)
• She demonstrated good diaphragmatic control in
lying and sitting positions, with activity including
hand use at the computer.
HOME EXERCISE PROGRAM
She initiated and met the following goals:
• Diaphragmatic breathing in supine with spinal
motion, including spinal mobilization with the air
pillow, was initiated on her first visit. and She met the
goal of demonstrated mastery by her fifth visit.
• Diaphragmatic breathing while sitting on the green
ball demonstrated mastery of this exercise without
pain during exercise.
• The “thinking” position: Demonstrated mastery of
cervical spine stability during all exercises without
236 SECTION II NEUROLOGIC CONSIDERATIONS
cueing (uses both “thinking” position and good body
mechanics).
• Vestibular balance: Demonstrated mastery of balance
during all exercises, including walking on an unstable
platform, such as a treadmill.
• Longus colli/lower fibers of trapezius/serratus ante-
rior/abdominal muscles: Demonstrates symmetry,
endurance, and control during exercises.
• She walks 3.9 mph for 20 minutes without increasing
pain.
• 6-inch foam roller: Demonstrated mastery of this
exercise without pain during the exercise. Demon-
strates measurable increase in brachial plexus mobility
and a decrease in sensitivity following the exercise.
• Rib mobilizer: Demonstrated mastery of this exercise
without pain during the exercise.
• 3-inch foam roll: Demonstrated mastery of this exer-
cise without pain during the exercise.
• Green ball/supine: Demonstrated mastery of this
exercise without pain during the exercise.
• She demonstrated commitment to self-management.
TREATMENT PLAN
• Has met all the goals of the Edgelow Protocol with
progressions
• Has completed biofeedback directed towards im-
proving hand function at the computer and with
writing
• Has initiated graded swimming program and can now
do 20 laps with either legs or arms or both
RESULTS AND DISCUSSION
This case was selected to illustrate the following:
1. The importance of empowering the patient in her
own care.
2. Despite a 21/2 year history and the failure of 8
months of Alexander treatment, 40 visits of hand
therapy and physical therapy including electrical
stimulation, stretching exercises, strengthening
exercise, massage, and 2-3 chiropractic treatments,
she benefited from only 16 visits totally devoted to
instruction in self-management techniques.
3. There was a subjective change of 70% decrease in
symptoms with a sustained change if she kept
doing the exercises daily.
4. She could reduce the pain from overuse with the
home exercises.
5. Objective changes: Warm hands; equal strength in
flexor pollicis brevis, adductor pollicis, and flexor
carpi ulnaris.
6. Increased range of motion of brachial plexus with
reduced sensitivity.
7. Because of her ability to control the pain she has
been able to increase the function of her arms using
swimming as the exercise.
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Evaluation and Treatment
of Brachial Plexus Lesions
T he Guide to Physical Therapist Practice (Guide;
2001) contains the preferred practice patterns
of impaired joint mobility, motor function,
muscle performance, range of motion, and reflex
integrity associated with spinal disorders and impaired
peripheral nerve integrity and muscle performance asso-
ciated with peripheral nerve injury to include persons
with injuries to their brachial plexuses.1 Predicted
impairments and functional losses related to these prac-
tice patterns include, but are not limited to: difficulty
with manipulation skills, decreased muscle strength,
impaired proprioception, impaired sensory integrity,
abnormal neural tension signs, loss of motion, and pos-
tural changes. Consequently, physical and occupational
therapists evaluate and identify the primary impairments
and conditions contributing to injury to restore function.
The brachial plexus supplies both motor and sensory
innervations to the upper extremities and the related
shoulder girdle structures. Lesions to the brachial plexus
compromise the neurologic integrity, and hence the
function, of the shoulder and related upper extremities.
Evaluation of shoulder dysfunction should include an
assessment of the integrity and functional status of
the brachial plexus. But the complex structure of the
brachial plexus requires a thorough understanding of the
multiple innervation patterns to the various muscles. In
addition, for proper and effective clinical management
of the brachial plexus, the clinician should understand
the mechanisms of injuries, the pathophysiologic
239
8
Bruce H. Greenfield
Dorie B. Syen
changes of nerve fibers and nerve roots, and the poten-
tial for recovery.
Therefore this chapter provides a review of the
anatomy of the brachial plexus, classification of brachial
plexus injuries, common musculoskeletal injuries that
result in injuries to the brachial plexus, and descriptions
of pathomechanical and pathologic changes to the
specific nerve fibers and nerve roots. In addition, this
chapter reviews an evaluation of the nature and extent
of impairments and functional losses resulting from
brachial plexus lesions. Clinical case studies offer a com-
bined physical and occupational therapy management of
a person with a brachial plexus injury. The cases incor-
porate the patient management schemes of the relevant
preferred practice patterns in the Guide.
Anatomy of the
Brachial Plexus
This review of the anatomy of the brachial plexus
describes the gross anatomy of the plexus and its rela-
tionship to surrounding structures, and the microscopic
anatomy of the nerve and nerve trunks.
Superficial Anatomy
The brachial plexus, shown in Figure 8-1, is composed
of the anterior primary divisions of spinal segments C5,
C6, C7, C8, and T1. The components of the brachial
plexus include the following:
240 SECTION II NEUROLOGIC CONSIDERATIONS
Figure 8-1 Segmental motor innervation of the muscles of the shoulder. (From
Hollinshead W: Functional anatomy of the limbs and back, ed 4, Philadelphia, 1976, WB Saunders.)
1. Undivided anterior primary rami
2. Trunks—upper, middle, lower
3. Divisions of the trunks—anterior and posterior
4. Cords—lateral, posterior, and medial
5. Branches—peripheral nerves derived from the cords
Figure 8-2 shows the segmental motor innervation of
the brachial plexus to the muscles of the shoulder. The
fourth cervical nerve usually gives a branch to the fifth
cervical, and the first thoracic nerve frequently receives
one from the second thoracic nerve. When the branch
from C4 is large, the branch from T2 is often absent and
the branch from T1 is reduced in size. This constitutes
the pre-fixed type of plexus. Conversely, when the
branch from C4 is small or absent, the contribution of
C5 is reduced in size and that of T1 is larger. The branch
from T2 is always present. This arrangement constitutes
the post-fixed type of plexus.
The following is the typical arrangement of the
brachial plexus. The fifth and sixth cervical nerves unite
at the lateral border of the scalenus medius muscles to
form the upper trunk of the plexus. The eighth cervical
nerve and first thoracic nerve unite behind the scalenus
anterior to form the lower trunk of the plexus, while the
seventh cervical nerve constitutes the middle trunk.
These three trunks travel downward and laterally and
just above or behind the clavicle, with each splitting into
an anterior and a posterior division. The anterior divi-
sions of the upper and middle trunks combine to form
a cord, which is situated on the lateral side of the axil-
lary artery and is called the lateral cord. The anterior
division of the lower trunk passes downward, first
behind and then on the medial side of the axillary artery,
and forms the medial cord. This cord frequently receives
fibers from the seventh cervical nerve. The posterior
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
Figure 8-2 Additional segmental motor innervation of the muscles of the shoulder.
divisions of all three trunks join to form the posterior
cord, which is situated at first above and then behind the
axillary artery.2
The brachial plexus contains autonomic sympathetic
nerve fibers consisting mostly of postganglionic fibers
derived from the sympathetic ganglionated chain.
The primary ramus T1 contains the only preganglionic
fibers in the brachial plexus.2 The sympathetic supply
to the eye travels through the T1 nerve root. Horner’s
syndrome results from a traction injury with avulsion to
that root. Constriction of the pupil and ptosis of the
eyelid on the involved side characterize Horner’s
syndrome.3
Anatomic Relationships
to the Brachial Plexus
To effectively isolate a plexus lesion, especially in the
presence of open trauma, the clinician must identify the
plexus and its relationship to the anatomic structures.
For example, knowledge of the portion of plexus that lies
between the clavicle and the first rib, in the presence
of clavicular fracture, can help the clinician isolate
the affected nerve and predict the affected muscles.
241
Topographic relationships of the plexus are delineated
in Gray’s Anatomy.2
The posterior triangle, which is the angle between
the clavicle and the lower posterior border of the ster-
nocleidomastoid muscle, contains the brachial plexus.
The plexus in this area is covered by skin, platysma, and
deep fascia. The plexus emerges between the scalenus
anterior and scalenus medius muscles, passes behind the
anterior convexity of the medial two-thirds of the clav-
icle, and lies on the first digitation of the serratus ante-
rior and subscapularis muscles. In the axilla, the lateral
and posterior cords of the plexus are on the lateral side
of the axillary artery and the medial cord is behind the
axillary artery. The cords surround the middle part of the
axillary artery on three sides: the medial cord lying on
the medial side, the posterior cord behind, and the
lateral cord on the lateral side of the axillary artery. In
the lower part of the axilla, the cord splits into the nerves
for the upper limb.
Anatomy of the Nerve Trunks
The nerve trunks and branches contain parallel bundles
(fasciculi) of nerve fibers comprising the efferent and
242 SECTION II NEUROLOGIC CONSIDERATIONS

afferent axons and their Schwann cells, which in some

cases contain myelin sheaths.2 Fasciculi within each
nerve trunk contain a few to many hundreds of nerve
fibers. Figure 8-3 shows the architecture of the nerve
trunk. A dense irregular connective tissue sheath, the
epineurium, surrounds the whole trunk, and a similar
but less fibrous perineurium surrounds the fasciculi
within each nerve trunk. A loose, delicate connective
tissue network—the endoneurium—penetrates the
spaces between nerve fibers. These connective tissue
sheaths serve as planes of access for the vasculature of
peripheral nerves and as protective cushions for the
nerve fibers.

Features of Nerve Trunks Providing Protection

from Physical Deformation. Several factors protect
the brachial plexus and nerve trunks from both traction
and deformation injuries. First, with two notable excep-
tions—the ulnar nerve at the elbow and the sciatic nerve
at the hip—the nerve trunks cross the flexor aspect of
joints. Because extension is more limited in range than
flexion, the nerves are subjected to less tension during
limb movements.
Second, as shown in Figure 8-4, the nerve trunks
run an undulating course in its bed, the fasciculi run
an undulating course in the epineurium, and the nerve
fibers run an undulating course inside the fasciculi. This
means that the length of nerve fibers between any two
fixed points on the limb is considerably greater than the
distance between those points.
Third, a large number of elastic fibers within the peri-
neurium impart a degree of elasticity in the nerve trunk
in response to tensile forces. Fourth, the nerve trunk
contains a large amount of epineurial connective tissue,
which separates the fasciculi. According to Sunderland,4
values of epineurial connective tissue of various periph-
eral nerves range in the body from 30% to 75% of the
cross-sectional area of the total number of nerve fibers
contained in each nerve trunk. Therefore the epineurium
provides a loose matrix for its fasciculi and cushions the
nerve fibers against deforming forces.
Figure 8-3 Structural features of peripheral nerve
fibers and a nerve trunk (cut away) showing a large number of
Features of the Nerve Roots Providing Protection fasciculi, which each contain a large number of nerve fibers.
from Injury. The nerve roots at the intervertebral (From Williams PL, Warwick R: Gray’s anatomy, ed 36, Edinburgh,
foramen possess several mechanisms that protect them 1980, Churchill Livingstone.)
from traction injury.4 Normal cervical spine, shoulder
girdle, and shoulder motions place repetitive strains on the
nerve roots forming the brachial plexus. Overstretching of
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
Figure 8-4 Example of the undulating structure of the
funiculi, which contains nerve fibers of a nerve trunk to the
point of failure. (From Sunderland S: Traumatized nerves, roots and
ganglia: musculoskeletal factors and neuropathological consequences. In Korr
IM, editor: The neurobiologic mechanisms in manipulative therapy,
New York, 1978, Plenum.)
nerve roots by transmitted forces generated in this manner
is normally prevented by the following factors.
First, the dura mater is adherent to, and part of, the
nerve complex at the level of the intervertebral foramen.
So when traction pulls the entire system outward, a dural
funnel is drawn laterally into the foramen. The dura
mater, being cone shaped at the junction of the inter-
vertebral foramen, plugs the foramen in such a way as
to guard against further displacement of the nerve
(Figure 8-5). Second, the fourth, fifth, sixth, and seventh
cervical nerve roots are securely attached to the verte-
bral column. Each nerve root, on leaving the foramen,
is lodged into the gutter of the corresponding transverse
process, bound securely by reflections of the prevertebral
fascia and by slips from the dura mater attachment to
the transverse processes. (See Figure 8-5.) Sunderland
suggests that the significance of these attachments
reduces the relative susceptibility to avulsion injury of
the several nerve roots contributing to the brachial
plexus. Traction injuries, which do not avulse nerve
roots, more commonly involve the spinal nerves where
these attachments exist. However, the incidence of avul-
243
Figure 8-5 Displacement of the nerve complex later-
ally through the foramen is resisted by plugging the funnel-
shaped dura mater and the dural attachment to the transverse
process. (From Sunderland S: Traumatized nerves, roots and ganglia:
musculoskeletal factors and neuropathological consequences. In Korr IM,
editor: The neurobiologic mechanisms in manipulative therapy, New
York, 1978, Plenum.)
sion injuries is much higher in the case of the nerve
roots, which do not have soft tissue attachments to the
transverse processes.
Classification of Brachial
Plexus Injuries
Box 8-1 indicates numerous types of classifications of
brachial plexus injuries. The majority of brachial plexus
lesions result from either direct or indirect trauma, as if
struck by an instrument, or a traction lesion to the cer-
vical spine or upper extremity.5-13 Lesions are pregan-
glionic or postganglionic. Preganglionic avulsion injuries
indicate that the nerve root has been torn from the
spinal cord and preclude the possibility of recovery. Post-
ganglionic lesions may be either in continuity (root and
sheath intact) or ruptured (root intact and nerve sheath
ruptured).6 Spontaneous recoveries may occur with the
first injury. But without surgical repair of the rupture, no
recovery will occur in the second lesion.
Finally, the postganglionic avulsions are supraclavic-
ular, which involves the trunks and divisions of the
plexus, or infraclavicular, which involves the cords and
branches.6 In a series of 420 brachial plexus cases involv-
ing operations, Alnot6 reports that 75% were supraclav-
icular lesions and 25% were infraclavicular lesions.
Supraclavicular Lesion
Isolated supraclavicular lesions affect the upper, middle,
or lower trunks of the brachial plexus. However, Alnot
244 SECTION II NEUROLOGIC CONSIDERATIONS

BOX 8-1 reports that 15% of the supraclavicular lesions are double
level—affecting two trunks—or combined supraclavicu-
lar and infraclavicular lesions. These lesions occur when
Etiologic Classification of Brachial Plexus Injuries
the arm is forced violently into abduction and the middle
as Related to the Shoulder and Cervical Spine
part of the plexus is blocked temporarily in the coracoid
region. Terminal branches tear and concomitant supra-
Traumatic clavicular lesions occur when the head is jerked violently
Open injuries to the opposite side. Entrapment may occur lower down
Fractures in the plexus in the musculocutaneous nerve, which is
Closed injuries tightly attached near the origin of the coracobrachialis
Fractures muscle. It also may occur in the axillary nerve in the
Obstetric
quadrilateral space behind the shoulder and/or the
Postnatal exogenous
Sports injuries (e.g., “burner” syndrome, shoulder suprascapular nerve in the suprascapular notch.6-7
dislocations)
Upper Trunk Lesion
Compression
Exogenous (sometimes isolated branches) Erbs palsy or Duchenne-Erb paralysis involves the C5
Anatomic predisposition (sometimes isolated and C6 roots of the brachial plexus.8 Palsy of C5 and
branches) C6 affects the strength of deltoid, biceps, brachialis,
Genetically determined (sometimes isolated infraspinatus, supraspinatus, and serratus anterior
branches) muscles. Also involved are the rhomboids, levator scapu-
Posture (muscle imbalances/spasms) lae, and supinator muscles. Therefore this injury causes
Tumors severe restriction of movement at the shoulder and
Primary tumors of brachial plexus
elbow joints. The patient is unable to abduct or exter-
Secondary involvement of plexus by tumors of
surrounding tissues nally rotate the shoulder. The patient cannot supinate
Vascular the forearm because of weakness of the supinator
Local vascular processes or lesions muscle. Sensory involvement is usually confined along
Participation in generalized vasculopathies the deltoid muscle and the distribution of the musculo-
(e.g., polyarteritis nodosa and lupus cutaneous nerve. According to Comtet and associates,8
erythematosus) partial or total spontaneous recovery of traumatic
Physical factors Duchenne-Erb paralysis is a frequent occurrence. The
Radiotherapy delay between the injury and reinnervation of the cor-
Electric shock responding muscle varies from 3 to 24 months. There-
Infectious, inflammatory, and toxic processes fore the patient should undergo long-term rehabilitation
Involvement of local sepsis
with periods of reevaluations.
Viral or infectious
Cryptogenic (neuralgic amyotrophy) Middle Trunk Lesion
Parainfectious
Related to serum therapy The middle trunk receives innervation from the C7
Genetic predisposition nerve root and extends distally to form a major portion
Cryptogenic of the posterior cord.8 The middle trunk offers a major
neural contribution to the radial nerve. Therefore a
Modified from Mumenthaler M, Narakas A, Gilliat RW: Brachial lesion affecting the middle trunk of the brachial plexus
plexus disorders, In Dyck PJ, Thomas PK, Lambert EH, et al, editors: weakens the extensor muscles of the arm and forearm,
Peripheral neuropathy, Philadelphia, 1984, WB Saunders.
excluding the brachioradialis, which receives primary
innervation from the C6 nerve root. Sensory deficit
occurs along the radial distribution of the posterior arm
and forearm and along the dorsal radial aspect of the
hand. Brunelli and Brunelli8 report that 11% of a total
series of brachial plexus injuries are isolated lesions to
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
the middle trunk. Trauma to the shoulder in an antero-
posterior location produces middle trunk lesions.
Lower Trunk Lesion
The lower trunk of the brachial plexus receives innerva-
tion from nerve roots C7 and T1. Therefore Dejerine
Klumpke paralysis or injury to the lower trunk affects
motor control in the fingers and wrist. Whether the
plexus is prefixed or postfixed determines the extent of
disability. The intrinsic muscles of the hand are only
slightly affected in a lesion involving a prefixed plexus,
whereas paralysis of the flexors of the hand and forearm
occurs in a lesion to a postfixed plexus.10 Sensory deficit
occurs along the ulnar border of the arm, forearm, and
hand. As indicated previously, Horner’s syndrome occurs
with injury to the sympathetic fibers contained within
the anterior primary ramus.3
Infraclavicular Lesion
Infraclavicular lesions include injuries to the cords or
the individual peripheral nerves of the brachial plexus.
In Alnot’s group of 105 patients with infraclavicular
brachial plexus injuries, 90% of the cases were young
people (15 to 30 years of age) who had been in a car or
motorcycle accident.6 The causes of the injuries include:
(1) anteromedial shoulder dislocation, which causes
most of the isolated lesions of the axillary nerve and the
posterior cord; (2) violent downward and backward
movement of the shoulder, which causes stretching of
the plexus; and (3) complex trauma with multiple frac-
tures of the clavicle, scapula, or upper extremity of the
humerus, which causes diffuse lesions affecting multiple
cords and terminal branches.
Lateral Cord Lesion
Alnot5 rarely finds injury to the lateral cord. Injuries to
the musculocutaneous nerve and the lateral head of the
median nerve result in a motor deficit consisting of palsy
in elbow flexion and a deficit of muscle pronators in the
forearm, wrist, and finger flexors. A proximal lesion
injures the lateral pectoral nerve, resulting in partial or
total palsy of the upper portion of the pectoralis major
muscle. Sensory deficit occurs at the forearm and at the
thumb level.
Medial Cord Lesion
Isolated injuries to the medial cord are rare. Instead,
upper medio-ulnar injury results in palsy, which is total
245
in the distribution of the ulnar nerve and only partial
in the distribution of the median nerve. Motor deficits
occur in the flexor pollicis longus muscle and the flexor
digitorum profundus muscle of the index finger. Partial
palsy of the lower portion of the pectoralis muscle results
in injury to the medial pectoral nerve.6
Posterior Cord Lesion
A posterior cord lesion involves the areas of distribution
of the radial, axillary, subscapular, and thoracodorsal
nerves. The lesion results in weakness of the extensors
in the arm, with impairment of medial rotation and
elevation of the arm at the shoulder.
Peripheral Nerve Lesion
Common peripheral nerve or branch injuries include,
but are not limited to, lesions of the long thoracic nerve,
axillary nerve, dorsal scapular nerve, and suprascapular
nerve. Chapter 4 reviews injuries to the dorsal scapular
and suprascapular nerves.
Long Thoracic Nerve Lesion
The long thoracic nerve originates from the anterior
primary rami of C5, C6, and C7 nerve roots after these
nerves emerge from their respective intervertebral
foramina. The nerve reaches the serratus anterior muscle
by traversing the neck behind the brachial plexus cords,
entering the medial aspect of the axilla, and continuing
downward along the lateral wall of the thorax.2
Although isolated injuries to the long thoracic nerve are
rare, traumatic wounds or traction injuries to the neck
that result in isolated weakness of the serratus anterior
muscle with winging of the medial border of the scapula
are presumptive evidence of a long thoracic nerve
lesion.3 Normal shoulder abduction and flexion result
from a synchronized pattern of movements between
scapular rotation and humeral bone elevation. Variations
in the scapulohumeral rhythm in the literature have been
reported.14-17 For every 15° of abduction of the arm, 10°
occurs at the glenohumeral joint and 5° occurs from
the rotation of the scapula along the posterior thoracic
wall.14 The rotation of the scapula results from a force
couple mechanism combining the upward pull of the
upper trapezius muscle, the downward pull of the lower
trapezius muscle, and the outward pull of the serratus
anterior muscle.17 Therefore palsy of the serratus ante-
rior muscle in the presence of a long thoracic nerve
injury, during abduction or flexion of the arm, results in
246 SECTION II NEUROLOGIC CONSIDERATIONS

partial loss of scapular rotation. The ability of the upper a traction apparatus with a neutral axis at the C7 verte-
and lower trapezius muscles to temporarily compensate bra when the arm is at the horizontal position.
for the inability of the serratus anterior muscle to exter- Specifically, he compares the brachial plexus in
nally rotate the scapula allows for nearly full range (180°) Figure 8-6 to a single cord with five separate points of
flexion and abduction of the arm.18 However, these attachment firmly snubbed at the transverse processes.
muscles quickly fatigue after four or five repetitions, According to Stevens, a traction apparatus must have a
resulting in notable loss of full active shoulder flexion neutral axis and a line of resistance. When the force of
and abduction range of motion. traction falls through this neutral center of axis at the
C7 vertebra, the traction is equally borne by all parts of
Axillary Nerve Lesion the apparatus as represented by nerve roots C5 through
The axillary nerve originates from spinal segments C5 T1. A slight deviation from this neutral axis creates an
and C6, travels to the distal aspect of the posterior cord unequal pull to one side or the other of the apparatus.
of the brachial plexus, and advances laterally through the That is, if the line of traction falls outside the neutral
axilla.2 The nerve bends around the posterior aspect of axis of C7, the entire force is transmitted from the
the surgical neck of the humerus to innervate the deltoid neutral axis and all tension is released on the cords on
muscle and the overlying skin, and the teres minor the other side. Therefore, if tension is imparted to an
muscle. arm elevated above the horizontal, stress is increased to
Anteromedial shoulder dislocation is the most fre- the lower roots of the brachial plexus. Conversely, if
quent cause of isolated axillary nerve lesions.5,7 In 80% tension is imparted to an arm depressed below the hor-
of cases, anteromedial dislocation results in a neu- izontal, stress is increased to the upper roots of the
rapraxia of the axillary nerve, with total recovery in 4 to brachial plexus (see Figure 8-6).19 Therefore the relative
6 months.6 position of the shoulder and neck at the time of injury
Complete lesion to the axillary nerve results in loss
of active shoulder abduction. Sensory changes include
an area of anesthesia along the deltoid muscle. However,
some patients may have active shoulder abduction and
external rotation in the presence of a total axillary nerve
lesion. Residual shoulder abduction results from the
actions of the supraspinatus and infraspinatus muscles,
and the biceps muscle. The stabilization of the humeral
head by the supraspinatus muscle combined with the
action of the long head of the biceps muscle allows, in
some cases, full overhead abduction. Specifically, by
externally rotating the arm, the patient places the long
head of the biceps muscle in the line of abduction pull.
However, the strength of abduction under these condi-
tions is poor, and loss of muscle power occurs quickly
with repetitive movements.

Pathomechanics of Traumatic
Injuries to the Nerves
According to Stevens,19 traction or tensile strains
produce the majority of traumatic injuries to the brachial
plexus. The brachial plexus stretches between two firm
points of attachment: the transverse processes proxi- Figure 8-6 Traction apparatus representing brachial
mally and the clavipectoral fascia junction distally in the plexus. (From Stevens JH: Brachial plexus paralysis. In Codman EA,
upper axilla. Stevens compares the cords of the plexus to editor: The Shoulder, Melbourne, Krieger Publishing.)
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
dictates the area and extent of the injury to the brachial
plexus.
In addition to the position of the shoulder and neck,
that magnitude of force affects the nature of a brachial
plexus injury. Spinner and associates20 report a substan-
tial correlation between the experimental test weight
imparted to restrained limbs in rats and the number of
avulsed nerve roots. A lower force produces a higher per-
centage of avulsions at C6, while a higher force produces
a higher number of avulsions at C7 and C8.
Musculoskeletal Injuries
As previously mentioned, a majority of brachial plexus
injuries result from trauma and occur as a complication
of musculoskeletal injuries. Examples of these injuries
include the so-called burner syndrome, shoulder dislo-
cations, fractures, and obstetric injuries.
Burner Syndrome
The burner or stinger syndrome is one of the most
common type of sports injuries that occur to the upper
trunk of the brachial plexus.7,11-13 This injury may occur
secondarily to traction in the brachial plexus when an
athlete sustains a lateral flexion injury to the neck.
Specifically, the syndrome results from an abrupt change
in the neck and shoulder angle—as experienced by foot-
ball players making a tackle—with depression of the
shoulder and rotation of the neck to the contralateral
shoulder.7,11,12 Markey and associates11 report a mecha-
nism of injury in the area of Erbs point when a shoul-
der pad compresses into the fixed brachial plexus and the
superior medial scapula. Regardless of the mechanism of
injury, at the time of injury the athlete relates a stinging
or burning pain, radiating from the shoulder into the
arm.11,12 Severe cases of injury may result in cervical root
avulsion.
Most burner injuries are self-limiting and resolve
within minutes of insult. Potential problems include
persistent neck tenderness and upper extremity weak-
ness. If these problems persist, electromyography should
be performed at 3 to 4 weeks to test for serious nerve
damage.10-12
Dislocations
Injuries to the brachial plexus can occur because of
shoulder dislocation. The incidence of secondary
brachial plexus injury after shoulder dislocation ranges
247
from 2% to 35%, according to most literature. Guven
and associates21 report the unhappy triad at the shoul-
der of concomitant shoulder dislocation, rotator cuff
tear, and brachial plexus injury. Axillary nerve injury
sometimes occurs with acute anterior dislocation of the
humeral head. Wang and associates22 describe a case
with concomitant mixed brachial plexus injury in the
presence of inferior dislocation of the glenohumeral
joint. Travlos and colleagues23 classify brachial plexus
lesions because of shoulder dislocation into diffuse in-
fraclavicular, posterior cord, lateral cord, and medial cord
injuries. The type of injury partly depends on the mech-
anism of injury and the direction of dislocation of the
humeral head.
Fractures
Brachial plexus injuries occur with traumatic injuries
associated with fractures in the shoulder girdle and
humerus bones. Della Santa and colleagues24 report 16
cases of costoclavicular syndrome related to compression
of the subclavian artery and brachial plexus because of
callus and scar formation as a result of fractures of the
clavicle. Stromquist and associates25 report three cases of
injury to the axillary artery and brachial plexus that com-
plicate a displaced proximal fracture of the humerus.
Blom and Dahlback26 report on 2 cases in a group of 31
cases regarding proximal humeral fractures with brachial
plexus injuries. Silliman and Dean7 report that an asso-
ciated complication of scapular fractures around the
scapular spine is a suprascapular nerve injury.
Obstetric Lesions
Ouwerkerk and associates report that obstetric brachial
plexus lesions (OBPL) occur in 0.5 to 3 out of every
1000 live births.27 Most infants (75% to 90%) recover
spontaneously within weeks or a few months, but 20%
have incomplete recoveries. Risk factors include large
heavy babies, shoulder dystocia, instrument delivery,
abnormal presentation, prematurity, and asphyxia. Dys-
tocia refers to difficult births, so that shoulder dystocia
refers to abnormality of an infant’s shoulder because of
a difficult birth.
The most common mechanism is a stretch injury to
the brachial plexus in cephalic presentations resulting in
extreme lateral flexion and traction on the head. Lesions
may produce either partial or full paralysis of the limb
depending on the level and extent of nerve root injury.
Injuries may also occur that include hematomas to the
248 SECTION II NEUROLOGIC CONSIDERATIONS
sternocleidomastoid muscle; fracture of the clavicle,
humerus, or ribs; lesions of the phrenic, facial, or
hypoglossal nerves; and lesions of the spinal cord.
Physical therapy should begin within three weeks.
The goal is to prevent contracture and joint deformities.
The physical therapist instructs parents to perform
gentle but frequent exercises to maintain full motion
of the involved shoulder, elbow, wrist, and fingers. If
spontaneous recovery does not occur within 2 months,
the authors recommend referral to a specialized center.
Failure to recover muscle function and evidence of severe
Horner’s syndrome after 3 months indicates likely
avulsion of nerve roots. Diagnostic confirmation occurs
using magnetic resonance imaging (MRI), myelo–
computed tomography, and neurophysiologic studies.
The authors recommend surgical treatment for patients
with nerve root avulsion.
Pathophysiology of Injury
The extent of injury to the nerve trunk, ranging from a
nondegenerative neurapraxia to a severance of the nerve
or plexus (neurotmesis), dictates the course of treatment,
(surgical versus nonsurgical), the prognosis, and relative
time frames for full recovery.
Sunderland28 describes five major degrees of injuries:
1. First-degree nerve injury. This injury is character-
ized by interruption of conduction at the site of the
injury with preservation of the anatomic continuity
of all components comprising the nerve trunk,
including the axon. Clinical features include
temporary loss of motor function in the affected
muscles, but the presence of electric potential is
retained because of axonal continuity. Cutaneous
sensory loss may occur but will recover in advance
of motor function. Most patients recover
spontaneously within 6 weeks after injury.
2. Second-degree nerve injury. In this injury, the axon is
severed and fails to survive below the level of injury
and, for a variable but short distance, the axon
degenerates proximal to the point of the lesion.
However, the endoneurium is preserved within the
endoneurial tube. Histologic changes to the nerve
include breakdown of the myelin sheath, Schwann
cell degeneration, and phagocytic activity with
eventual fibrosis. Clinical features include
temporary complete loss of motor, sensory, and
sympathetic functions in the autonomous
distribution of the injured nerve. Several months
pass before recovery begins, with proximal
reinnervation occurring before distal reinnervation
to the involved muscles.
3. Third-degree nerve injury. This condition is
characterized by axonal disintegration; Wallerian
degeneration, both distal and proximal to the site
of the lesion; and disorganization of the internal
structure of the endoneurial fasciculi. The general
fascicular pattern of the nerve trunk is retained
with minimal damage to both the perineurium and
epineurium. Because the endoneurial tube is
destroyed, intrafascicular fibrosis may obviate axonal
regeneration. Many axons fail to reach their original
or functionally related endoneurial tubes and are
instead misdirected into foreign endoneurial tubes.
Motor, sensory, and sympathetic functions of the
related nerves are lost. The recovery is long, up to
2 to 3 years, with a chance of notable residual
dysfunction.
4. Fourth-degree nerve injury. This type of injury is
similar to third-degree nerve injury, but the
perineurium is disrupted. Therefore the chance for
a residual dysfunction because of fibrosis and
mixing of regenerating fibers at the site of injury,
which may distort the normal pattern of
innervation, is high.
5. Fifth-degree nerve injury. In this injury, the entire
nerve trunk is severed, which results in the
complete loss of function to the affected structures.
Obviously, without surgical grafting, recovery
potential is negligible.
Patient Management
The five elements of patient management in the Guide
are examination (history, systems review, and tests and
measures), evaluation, diagnosis, prognosis (including
patient care and expected number of visits), and in-
terventions (including anticipated goals and expected
outcomes).
The clinician evaluates the nature and extent of the
brachial plexus lesion to develop an appropriate and
effective intervention using a thorough and systematic
examination. Most brachial plexus lesions slowly
improve over a long period of time, so that the clinician
must maintain and update accurate records concerning
the progress of the patient. The clinician should use a
chart like that shown in Figure 8-7 for recording results
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
Figure 8-7 Chart for recording results
of physical examination for brachial plexus
injury. (From Leffert RD: Clinical diagnosis, testing,
and electromyographic study in brachial plexus traction
injuries, Clin Orthop Rel Res 237:24, 1988.)
of the physical examination. Patient management is a
conjoint effort by a physical and an occupational thera-
pist that specializes in the treatment of hand and upper
extremity injuries. Knowledge of hand management and
rehabilitation is particularly important in lower trunk
injuries to the brachial plexus. Additionally, in the pres-
ence of fourth- and fifth-degree nerve injuries to the
brachial plexus, occupational therapy offers strategies for
splinting and equipment modification or assurance to
assist permanently dysfunctional individuals.
History
Mechanisms of Injury
Because most brachial plexus injuries result from
trauma, a thorough history should include questions
concerning the nature and mechanisms of injury.
249
According to Stevens,19 the different varieties of stress,
and the relative position of the arm and head at the time
of the stress, make tremendous differences in the kinds
of lesions suffered, in the location of the lesion, and in
prognosis. The magnitude of forces, that is, high-speed
versus slow-speed injuries, is important to ascertain.
According to Frampton,5 high-speed, large-impact
accidents are commonly associated with preganglionic
plexus injuries, while slow-speed, small-impact acci-
dents are commonly associated with postganglionic
injuries. An example of high-velocity injury is a fall
from a speeding motorcycle, while an example of low-
velocity injury is a fall down a stairway.
Pain
The clinician should document the area and nature of
pain. Pain, described as a constant burning, crushing
250 SECTION II NEUROLOGIC CONSIDERATIONS
pain with sudden shooting paroxysms, is central in
nature. This pain occurs as a result of deafferentation of
the spinal cord at the damaged root level, leading to
undampened excitation of the cells in the dorsal horn of
the spinal cord. The confused barrage of abnormal
firings is received and interpreted centrally as pain and
is eventually felt in the dermatomes of the avulsed nerve
root.29 In a group of 188 patients with posttraumatic
brachial plexus lesions, Bruxelle and associates29 report
that 91% experience pain for at least 3 years after their
injury. Pain may also result from secondary injuries to
bones or related soft tissues. The clinician should note
and document the report of any anesthesia or paresthe-
sia, including the presence of Horner’s syndrome. Ques-
tions concerning the course of events since injury or a
change in the severity of the symptoms establish an indi-
cation of an improving or worsening lesion. A condition
that is resolving spontaneously may indicate first- or
second-degree nerve injuries, whereas a condition that
has not changed across the course of 6 weeks may indi-
cate at least a third-degree nerve injury, according to
Sunderland’s classification. The clinician should record
the patient’s occupation, handedness, and previous state
of health to assist in establishing feasible goals for return
to the patient’s premorbid activity level.
Tests and Measures
The components of the physical examination include:
(1) posture; (2) passive range of motion of the cervical
spine, shoulder, and upper extremity; (3) motor strength;
(4) sensation; (5) palpation; and (6) special tests. The
occupational therapy evaluation includes assessment of
(1) edema; (2) coordination; (3) activities of daily living;
and (4) vocational and avocational pursuits. The physi-
cal evaluation should be repeated frequently during the
process of rehabilitation to carefully assess subtle signs
of nerve reinnervation.
Posture
The clinician observes the patient from the front, side,
and behind. From behind, the clinician looks for muscle
atrophy and “winging” of the scapula. Winging of the
scapula signifies weakness of the serratus anterior
muscle, which may indicate a lesion of the long thoracic
nerve. Suprascapular nerve entrapment results in ipsi-
lateral atrophy of the supraspinatus or infraspinatus
muscles. Atrophy of the deltoid muscle, in addition to
the supraspinatus and infraspinatus muscles, indicates an
upper trunk plexus lesion, such as Duchenne-Erb paral-
ysis of the C5 and C6 nerve trunks. Isolated atrophy of
the deltoid muscle indicates an isolated axillary nerve
lesion. From the side, the clinician looks for a forward
head posture including an accentuated upper thoracic
spine kyphosis, protraction and elevation of the scapu-
lae, an increase cervical spine inclination, and backward
bending at the atlanto-occipital junction. The forward
head posture results in muscle imbalances that can
further result in entrapment of various nerves of the
brachial plexus in the area of the thoracic outlet.30
Chapter 7 reviews thoracic outlet syndrome. From the
front, the clinician should observe the attitude or posi-
tion of the upper extremity and hand. Duchenne-Erb
paralysis results in an arm position of adduction and
internal rotation. Injury to the lower trunk of the
brachial plexus results in pronation of the forearm with
flexion at the wrist and metacarpophalangeal and prox-
imal interphalangeal joints.7 External deformities along
the clavicle may indicate a fracture. Both nonunions and
malunions of the clavicle can result in substantial com-
pression of the brachial plexus. The clinician inspects the
supraclavicular fossa for the presence of swelling or
ecchymosis in those patients with recent injury and for
nodularity and induration in the brachial plexus if the
injury is old.5
Passive Range of Motion
A standard goniometer is used to evaluate the passive
range of motion of all joints of the shoulder girdle and
upper limb. Deficits of joint motion from immobility
result in contracture of the joint capsule, adhesions in
the joints, and shortening of both muscle and tendons
above the affected joints. The classic studies of Akeson
and colleagues31 demonstrate the deleterious effects of 9
weeks of immobilization on periarticular structures,
including the loss of water and glycosaminoglycan
(GAG), randomization and abnormal cross-linking of
newly synthesized collagen, and infiltration in the joint
spaces of fatty fibrous materials.
Motor Strength
Several manuals are available that review proper isola-
tion, stabilization, and grading procedures for manual
muscle testing.32,33 Most grading systems grade muscle
from 0 to 5, with 0 being a flaccid muscle and 5 repre-
senting normal muscle strength.33 The clinician should
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
complete an upper extremity test to establish a database
for measuring improvement. Therefore the clinician
performs repeated tests. A thorough manual muscle
test assists the clinician in pinpointing the site and ex-
tent of the plexus lesion. Isolating and grading involved
muscles establish an appropriate strengthening program.
Isokinetic testing can also assist clinicians in measuring
muscle strength deficits, usually for peak torque, power,
and work, compared with the uninvolved upper extrem-
ity. Refer to Chapter 16 for a review of isokinetic testing
protocols in the shoulder.
Sensation
Examination of sensory loss assists in the diagnosis
of the level and extent of the plexus lesion. Total
avulsion of the plexus results in total anesthesia of the
related areas. However, in a mixed lesion—and when
recovery is occurring—the sensory pattern may vary in
the arm. The sensory evaluation may include deep
pressure, light touch, temperature, stereognosis, and
two-point discrimination, depending on the patient’s
status.5 Figure 8-7 shows the sensory changes along
dermatomes.
Coordination
Loss of sensation and muscle control in the presence of
a brachial plexus injury results in a loss of gross and fine
motor coordination in the affected upper extremity.
There are numerous tests on the market designed to
assess an individual’s coordination. Each requires
varying amounts of fine and/or gross motor coordina-
tion. The Purdue pegboard test (Lafayette Instructional
Co., Lafayette, IN), for example, assists the clinician in
assessing the patient’s manual dexterity. The clinician
instructs patients to place pegs with both the right and
left hands, singularly and in tandem, and to perform a
specific assembly task using pins, collars, and washers.
These tests are timed and compared with normative
values.34 The clinician determines the most appropriate
tests based on the patient’s level of functioning.
Vascular
Disruption of the subclavian or axillary arteries occurs
in the presence of severe brachial plexus injuries, partic-
ularly with associated fractures of the clavicle. Addi-
tionally, all patients who have had a substantial nerve
injury will have evidence of vasomotor changes.3 The
clinician inspects for dusky, cool skin indicating venous
251
insufficiency and assesses the brachial and radial
pulses.
Edema
The clinician looks for edema, which can cause in the
joints. Volumetric is an established and accurate method
to measure upper extremity edema. The clinician sub-
merges the patient’s hand in a lucite container (Vol-
umeter, Volumeters Unlimited, Idyllwild, Calif.), and
measures the amount of water displaced using a 500-ml
graduated cylinder. Both extremities should be measured
and the results recorded. Circumferential measurements
of the hand and forearm are another method of meas-
uring edema. This technique, however, is best suited for
individual digit swelling or in open wounds, the latter of
which may preclude the patient getting the extremity
wet. Manual palpation is also used to measure edema.
The severity of the edema is usually rated from 1 to 3,
with 1 being minimal edema and 3 being severe or
pitting edema.
Palpation
Manual palpation examines the patient for the presence
of myofascial trigger points about the affected shoulder
girdle and upper extremity musculature. Trigger points
result from tight and contracted muscles or from par-
tially denervated muscles that exhibit poor muscle
control and altered movement patterns. Active trigger
points refer pain into the affected upper extremity and
the shoulder girdle, neck, and head.35,36
Special Tests
The presence of Tinel’s sign, revealed by tapping over
the brachial plexus above the clavicle, can be quite useful
in distinguishing ruptures from a lesion in continuity.3,5
A distal Tinel’s sign indicates a lesion in continuity with
intact axonal connections within the nerve trunk. This
may correspond to a first-degree nerve injury or a regen-
erating second- or third-degree nerve injury. Conversely,
the presence of a localized tenderness, revealed by
tapping above the clavicle, indicates a possible neuroma
resulting from disruption of part of the plexus. This type
of injury would correspond to a fourth- or fifth-degree
nerve injury.
Activities of Daily Living
The clinician questions the patient regarding all aspects
of self-care to identify those specific tasks the patient is
252 SECTION II NEUROLOGIC CONSIDERATIONS
not able to perform because of the extent of the brachial
plexus injury. Such areas include feeding, bathing, groom-
ing, and dressing. Based on the specific limitations of the
patient, the occupational therapist determines whether
to provide the patient with specific adaptive equipment
or to instruct the patient in one-handed techniques.
Assessment for Splinting
In the case of a complete brachial plexus injury, the
occupational therapist fits the patient with a flail arm
splint, which allows him or her to use the extremity at
home and at work. The occupational therapist fits the
splint early to prevent the patient from relying on one-
handed methods as a means of performing specific activ-
ities.5 In the case of a C5-7 injury, the patient might
require a long-wrist and finger-extension assist splint
(Figure 8-8). The occupational therapist may fit the
patient with a resting-hand splint (Figure 8-9) to wear
at night to help maintain the wrist and fingers in a
balanced position.
Figure 8-8 A long metacar-
pophalangeal extension splint used with a
patient who has weak wrist extension and
trace finger extension.
Figure 8-9 A resting hand splint
used following a brachial plexus lesion to
prevent overstretching of weak and finger
extensor muscles by maintaining the wrist
in approximately 20° of dorsiflexion.
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
Vocational
The occupational therapist obtains a detailed job
description to assess the patient’s potential to return to
work. In addition, the patient may undergo a functional
capacity examination later in the rehabilitation process
to assess his or her physical demand level.
Avocational
Because the brachial plexus–injured patient is unable to
work, avocational pursuits are often an important source
of much needed diversion. The occupational therapist
questions the patient closely as to premorbid hobbies or
potential areas of interest. The occupational therapist
develops activities of interest that encourage use of the
affected extremity.
Laboratory Evaluations of
Brachial Plexus Lesions
Laboratory evaluation involves electrodiagnostic testing,
myelography, and radiographic assessment. These eval-
uations help the clinician diagnose the area and extent
of the lesion and provide baseline measurements to help
evaluate progress.
Radiographic Assessment
Every patient who has sustained a notable injury to the
brachial plexus should have a complete radiographic
series done on the cervical spine and involved shoulder
girdle, including the clavicle.3 The physician rules out
fractures of the clavicle with callus, which can impinge
on the nerve trunks along the costoclavicular juncture,
or fractures of the cervical transverse processes, which
can indicate a root avulsion.3,5
MRI detects injuries to the brachial plexus. Bilbey
and associates37 report on 64 consecutive patients with
suspected brachial plexus abnormalities of diverse causes
diagnosed using MRI. MRI is 63% sensitive, 100% spe-
cific, and 73% accurate in demonstrating the abnormal-
ity in a diverse patient population with multiple
etiologies of brachial plexus injuries.
Myelography
Myelography indicates the condition of the nerve roots
involving traction injuries to the brachial plexus.
According to Leffert,3 root avulsion can occur in the
presence of a normal myelogram. However, Yeoman38
253
indicates the efficacy of myelography as a valuable
adjunct to the diagnosis of brachial plexus root lesions.
Electromyography
Because the loss of axonal continuity results in pre-
dictable, time-related electric charges, knowledge and
assessment of these electric charges provide clinicians
with information concerning muscle denervation and
reinnervation.3
For example, while normally innervated muscle
exhibits no spontaneous electrical activity at rest with
needle electrodes, denervated muscle produces readily
recognizable small potentials (fibrillation) or large
potentials (sharp waves), which are the hallmarks of
denervation. These electrical discharges usually appear
3 weeks following injury to the plexus and signal the
onset of Wallerian degeneration of a specific nerve. The
clinician localizes the lesion by sampling muscles in-
nervated by different nerves and root levels.
The clinician should also perform an electromyo-
graphic evaluation of the posterior cervical musculature
when a root avulsion is suspected in a patient who has
sustained a traction injury of the brachial plexus. The
posterior cervical muscles are segmentally innervated
by the posterior primary rami of the spinal nerves that
provide the anterior primary rami to form the plexus.
Denervation of the deep posterior cervical muscles is
highly correlated with root avulsion. Conversely, if the
electromyogram is positive for the muscles innervated by
the anterior primary rami, but not for the posterior cer-
vical muscles, the clinician should suspect that whatever
possible damage exists is infraganglionic in nature.39
Nerve Conduction Studies
Nerve conduction velocity tests help distinguish muscu-
lar weakness in the affected upper extremity from cervi-
cal intervertebral disk protrusion, anterior horn cell
disease, or a brachial plexus lesion. Because anterior horn
cell diseases and intervertebral disk protrusions do not
influence nerve conduction latency, the clinician can be
certain that a proximal nerve conduction delay is a result
of a brachial plexus lesion.40
Another type of electrodiagnostic testing is the F
response, an outgrowth of the measurement of velocity
of conduction. This is a late reaction that potentially
results from the backfiring of antidromically activated
anterior horn cells. Electrical stimulation of motor
254 SECTION II NEUROLOGIC CONSIDERATIONS
points assesses the strength-duration curves of the
affected muscles.41 A denervated or partially denervated
muscle requires more time and current than a normally
innervated muscle. Serial strength-duration testing,
therefore, allows the clinician to assess neuromuscular
recovery.41
Rehabilitation Prognosis
and Intervention
The clinician approaches rehabilitation for brachial
plexus lesions by maintaining or improving soft tissue
mobility, muscle strength and function within the
constraint of the nerve injury, and function. Because
regeneration is excruciatingly slow, rehabilitation in
severe cases is a long-term process—taking as long as
3 years. Therefore patient and family education and
home exercise programs are integral components of
treatment.
The clinician should understand soft tissue healing
after surgical grafting in the presence of fourth- and
fifth-degree nerve injuries. The relatively high chance
of residual upper extremity dysfunction in some cases
necessitates vocational and avocational retraining, and
occupational therapy intervention for assistance-
providing devices and splints.
According to Framptom,5 rehabilitation falls into
three stages: (1) the early stage, consisting of diagnosis,
neurovascular repair, and education regarding passive
movement and self-care of the affected extremity; (2)
the middle stage, when recovery is occurring and inten-
sive reeducation may be indicated; and (3) the late stage,
when no future recovery is expected and assessment for
reconstructive surgery can take place. The clinician bases
the time frames and extent of each phase on the extent
of the lesion and on the individual’s own motivation and
recuperative capabilities.
Case Study 1
This case study presents a typical brachial plexus injury
affecting the shoulder and upper extremity function.
The evaluation presents the initial findings. The goals
and phases of intervention combine a physical and occu-
pational therapy approach with rationales.
HISTORY
A 25-year-old, right-handed man is in a motor
vehicle accident and suffers a traction lesion to his
brachial plexus. Electrodiagnostic testing indicates an
infraganglionic lesion to his left brachial plexus at
Erbs joint, which is the portion of the brachial
plexus where C5 and C6 unite to join the upper trunk.
Radiologic studies indicate no fractures at the cervical
spine or clavicle. The physician refers the patient to
physical and occupational therapy 4 weeks after the
initial injury.
The patient reports numbness and tingling along the
lateral aspect of his left shoulder, in the area of the
deltoid muscle, and weakness in his left shoulder, elbow,
wrist, and hand. He reports intermittent pain in his left
shoulder and neck made worse with attempted elevation
of his left arm. He reports less numbness and greater
strength in his left arm since the initial injury.
VOCATION
The patient works as a carpenter.
POSTURAL/VISUAL INSPECTION
The clinician observes atrophy in the deltoid,
supraspinatus, and infraspinatus muscles on the left
compared with the right side. The patient holds his left
arm in internal rotation along his lateral trunk, with his
forearm pronated and his wrist and fingers in slight
flexion.
PASSIVE RANGE OF MOTION
Elevation in the plane of the scapula measures 120°,
external rotation in adduction measures 30°, external
rotation in 45° abduction measures 60°, and external
rotation in 90° abduction measures 70°. His elbow,
forearm, wrist, and hand passive range of motion are
within normal limits.
ACTIVE RANGE OF MOTION
Elevation in the plane of the scapula measures 60°,
external rotation in adduction from full internal rotation
measures 20°, elbow flexion measures 30°, and supina-
tion measures 50°. The patient has full pronation, and
wrist and finger flexion and extension.
MOTOR STRENGTH
Motor strength is as follows:
Grade 0 = no contraction
Grade 1 = trace
Grade 2 = poor
Grade 3 = fair
Grade 4 = good
Grade 5 = normal
The clinician classifies the patient’s muscle strength
as follows: deltoid = 2, supraspinatus = 3, infraspinatus =
3, teres minor = 2, biceps brachii = 2, brachialis = 2,
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
serratus anterior = 5, subscapularis = 3, extensor carpi
radialis longus and brevis = 3, and supinator = 3. His
grip strength is 88 lbs on the right and 10 lbs on the left.
SENSATION
The lateral aspect of the left shoulder, in the area of
the deltoid muscle, and along the radial side of the
forearm shows impaired sensation to light touch and to
sharp/dull objects.
COORDINATION
The clinician assesses coordination using the Purdue
pegboard as follows: right hand, 14; left hand, 2; both
hands, 4; assembly task, 6.
EDEMA
The patient has 2+ edema along the dorsum of the
left fingers at the proximal interphalangeal joints and
metacarpal joints, and along the dorsum of the left hand.
His volumetric measurements are 482 cc on the right
and 525 cc on the left.
PALPATION
The clinician palpates trigger points in muscle bellies
of the left upper trapezius, left rhomboid, and left sub-
scapularis muscles.
ACTIVITIES OF DAILY LIVING (ADL)
Feeding—unable to cut his food.
Bathing—unable to wash his right shoulder and upper
arm.
Grooming—unable to apply deodorant to his right
underarm.
Dressing—unable to tie shoes, button shirt, zip pants
or jacket, or buckle belt.
ASSESSMENT
This is a patient with a traction injury to the upper
trunk of the brachial plexus involving nerve trunks C5
and C6. Because his affected muscles are spontaneously
improving since the initial injury, the extent of the injury
is between a first- and second-degree injury.28 In addi-
tion, the patient has impairments and functional losses
associated with the preferred practice pattern: impaired
peripheral nerve integrity and muscle performance associated
with peripheral nerve injury. For example, he has diffi-
culty with manipulation skills, decreased muscle
strength, impaired nerve integrity, impaired propriocep-
tion, and impaired sensory integrity. In this case, the
patient has impaired passive range of motion. One can
expect combined resolution of nerve function with full
return of function of the left upper extremity.
Passive range of motion in the affected shoulder
results from soft tissue changes described by Akeson and
255
colleagues,31 Tabary and associates,42 and Cooper,43 who
report on the effects of immobilization on the periartic-
ular capsule, tendon, and muscle, respectively. The loss
of motor control results in altered scapulohumeral
rhythm. The rotator cuff muscles, particularly the
supraspinatus, infraspinatus, and teres minor muscles,
are unable to adequately control gliding of the humeral
head during elevation of the shoulder. The resultant
weakness, even in the presence of a weak deltoid muscle,
results in impingement of the suprahumeral soft tissues
underneath the unyielding coracoacromial ligament.
Chronic impingement results in inflammation and
degeneration of the rotator cuff tendons.
Compensation for the scapula muscles in elevating
the arm in the presence of weakness of the rotator cuff
and deltoid muscles results in irritation and trigger
points in both the left upper trapezius and left rhom-
boid muscles. The shoulder and arm position in inter-
nal rotation and along the lateral trunk wall, which
maintains the subscapularis muscle in a shortened
position, produces a trigger point in the subscapularis
muscle. The contracted subscapularis muscle results in
the greater limitation of passive external rotation with
the arm adducted along the lateral trunk wall as opposed
to external rotation with the arm abducted to 45° or 90°
(Donatelli R: personal communication, 1996).
The weakness in the left upper extremity and hand
results in a loss of normal muscle-pumping activity to
remove interstitial fluid. In addition, the patient tends
to keep his arm down at his side. These two factors result
in increased edema in the left upper extremity, especially
the left fingers and hand, compared with the right. The
weakness in the left upper extremity and the patient’s
decreased manual dexterity interferes with some self-
care activities. Fortunately, the patient is right-handed,
which will expedite his return to employment as a
carpenter.
PROGNOSIS
Based on this preferred practice pattern, the progno-
sis for recovery ranges from 4 to 8 months. The expected
number of visits over that time period may range from
12 to 56. The Guide indicates that 80% of patients clas-
sified using this pattern will achieve the anticipated
goals.
INTERVENTION
Early Stage
First Goal
The first goal is to reduce pain.
256 SECTION II NEUROLOGIC CONSIDERATIONS
Intervention
The clinician applies heat, low-voltage surge stimu-
lation, and spray and stretch (see Chapter 16) to the
active trigger points in the left upper trapezius and left
rhomboid muscles. The clinician then applies transcuta-
neous neuromuscular stimulation, using a high-rate,
low-intensity conventional setting with dual channels
and four electrodes around the left shoulder. The patient
wears the transcutaneous neuromuscular stimulation 8
hours per day.
Rationale
According to Travell and Simons, myofascial trigger
points in the shoulder girdle muscles refer pain into the
left shoulder and arm in a consistent pattern.35 There-
fore the patient’s pain reduces as trigger point tender-
ness subsides in the left upper trapezius and left
rhomboid muscles. The conventional transcutaneous
neuromuscular stimulation setting stimulates large A-
beta sensory fibers that modulate impulses from the
small A-delta and C-fibers in the dorsal horn of the
spinal cord.44,45 Irritation of nociceptor endings in
the connective tissue sheaths surrounding the nerve
fibers and trunks, because of the traction injury, produces
pain impulses along the A-delta and C-fibers.45
Second Goal
The second goal is to restore full passive range of
motion and soft tissue mobility.
Intervention
In this patient, the clinician applies low-voltage surge
stimulation followed by spray and stretch techniques to
the active trigger points in the muscle belly of the sub-
scapularis. This treatment follows Maitland’s grades III
and IV mobilization of the various joints in the left
upper extremity.46
The clinician instructs the patient in at home range
of motion exercises so he can preserve the range of
motion for those joints in which there is no, or only
limited, active range of motion. The exercises also pre-
serve the range of motion for uninvolved joints so they
do not become restricted as a result of disuse. The
patient’s family should be familiar with the exercise
program so they can encourage the patient to follow
through and become active participants in the patient’s
rehabilitation.
Rationale
A contracted subscapularis muscle results in the
painful limitation of external rotation with the shoulder
adducted along the lateral trunk. Therefore spray and
stretch, followed by distraction of the medial scapula
border, elongates the subscapularis muscle and improves
external rotation with the shoulder in the adducted posi-
tion. Manual techniques at the shoulder mobilize the
inferior and anterior capsules to promote abduction and
external rotation movements, respectively. The scientific
literature indicates no optimum time frames for apply-
ing grade IV manual stretching to the periarticular
capsule. Clinically, we use three sets of 1-minute grade
IV oscillations for the restricted tissue preceded by heat
and followed by ice.
Third Goal
The third goal is to prevent neural dissociation to the
reinnervating muscles.
Intervention
The clinician applies high-frequency, low-voltage
muscle stimulation with a pulse duration of 30 ms, with
a duty cycle of 10 seconds on and 20 seconds off, for a
period of 30 minutes to the partially denervated muscle.
The patient uses a home muscle stimulator three to four
times daily.
Rationale
According to strength-duration studies, muscle stim-
ulation to a partially denervated muscle requires a higher
current and longer pulse duration than does stimulation
to a normally innervated muscle.38 In addition to main-
taining reinnervating muscle tissue viability, electrically
induced muscle contractions facilitate normal circula-
tion, decrease edema, and present potential nutritional
or tropic skin changes.47,48
Fourth Goal
The fourth goal is to reduce edema.
Intervention
The clinician elevates the patient’s hand above his
heart and performs a retrograde massage.49 In addition,
the clinician provides the patient and his wife with
written instructions regarding elevation of the arm, ret-
rograde massage, and fist pumping to activate muscle-
pumping action in the hand and forearm.
Coban (3 M Medical-Surgical, St Paul, Minn.) is a
gentle elastic wrap used for edema control. The clinician
wraps the Coban diagonally from the fingertips proxi-
mally overlapping approximately one-half inch. Coban
is reusable (thus reducing costs), may be worn for pro-
longed periods, and allows full range of motion.50
Rationale
Retrograde massage, in a gravity-assisted position,
facilitates the reabsorption of interstitial fluids into the
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
lymphatic system. Fist pumping, resulting in alternate
contraction and relaxation of the musculature in the
hand and forearm, promotes the return of venous blood
to the heart.
Fifth Goal
The fifth goal is to increase the patient’s ADL
independence.
Intervention
Adaptive equipment increases the patient’s inde-
pendent self-care. For example, a rocker knife helps him
cut his meat and a buttonhook helps him button his
shirt. The clinician instructs him in a one-handed
method to tie his shoelaces.
Sixth Goal
The sixth goal is to increase his emotional support.
Intervention
A patient’s emotional state affects his or her per-
formance in therapy. Consequently, the clinician helps
the patient through the initial stages of denial, anger,
and depression associated with a severe brachial plexus
injury and the related disabilities. The clinician should
be an active listener and recognize the normal process
of emotional recovery in patients with severe disability.
Fear is a major component and compounds a patient’s
anxiety. Patient education about the nature and extent
of the injury, the course of recovery, the course of
therapy, and the prognosis for recovery can reduce his
anxiety. Because family relationships may be strained
after serious injury, the patient’s family members may
need as much support as the patient and will also benefit
from the education process.
MIDDLE STAGE
First Goal
The first goal in the middle stage is to retrain rein-
nervating muscles.
Intervention
Three weeks after the initial evaluation the clinician
began manual proprioceptive neuromuscular facilitation
techniques emphasizing diagonal patterns, with the
patient supine, followed by isotonic strengthening using
adjustable cuff weights. Initial isotonic strengthening
emphasizes external rotation movement patterns at
the shoulder, flexion and extension movements at
the elbow, and pronation and supination at the forearm.
As strength improves, the patient progresses to isoki-
netic strengthening at slow speeds of approximately
60°, emphasizing rotational movement patterns in the
shoulder. The patient progresses to isokinetic diagonal
257
movement patterns in the supine position when isoki-
netic testing indicates a difference of left to right shoul-
der external rotation peak torque and power within 20%.
Vibration and tapping while the patient is exercising
or performing functional activities facilitate purposeful
movement.51 Biofeedback and neuromuscular electrical
stimulation help to retrain weak muscles.
Rationale
Manual proprioceptive neuromuscular facilitation
diagonals allow the clinician to assess early subtle
strength changes across treatments. Early isotonic
strengthening builds up the shoulder rotator cuff
muscles, specifically the supraspinatus, infraspinatus,
and teres minor muscles. The restoration of rotator
cuff muscle strength reestablishes the normal balance
between these muscles and the upward pull of the
deltoid muscle.52 Isokinetic strengthening offers the
advantage of accommodating resistance to maximally
load a contracting muscle throughout the range of
motion.53 The patient exercises at slower speeds, so that
he or she can consistently catch and maintain the speed
of the dynamometer. External rotational strengthening
restores the dynamic glide of the humeral head along
the glenoid fossa by reestablishing strength in the
supraspinatus, infraspinatus, and teres minor muscles.
Isokinetic testing every 2 to 3 weeks assesses peak torque
and power values of the involved, compared with the
uninvolved, upper extremity. Isokinetic diagonal
strengthening patterns eliminate the effect of the
muscles working directly against gravity. Diagonal
patterns are eventually performed with the patient
sitting or standing after bilateral strength deficits
between the left and right shoulder rotators are within
20%. Although not scientifically substantiated, we have
observed that when bilateral shoulder rotational strength
deficits are greater than 20%, impingement and pain
occur in the suprahumeral soft tissues during active
shoulder elevation.
Occupational Therapy
In occupational therapy, the patient works on table-
top activities with his left upper extremity supported.
The activities strengthen his elbow, forearm, and wrist
musculature. For example, he transfers pegs from one
bucket placed in front of him to a bucket placed to his
far left. This activity requires active elbow flexion and
extension in a gravity-eliminated position. As his
shoulder strength improves, he performs this same
activity unsupported. Additionally he stacks cones,
258 SECTION II NEUROLOGIC CONSIDERATIONS
which requires active shoulder abduction against gravity.
He uses light weights to strengthen wrist flexion and
extension, supination, and pronation. Elastic rubber
tubing, such as Theraband (Hygenic, Akron, Ohio),
improves elbow and wrist strength at home. He uses
therapeutic putty for hand-strengthening exercises.
Second Goal
The second goal is to continue mobilization of the
restricted joints.
Intervention
Low-load prolonged stretching using surgical tubing
stretches the restricted periarticular capsules, especially
the anterior aspect of the glenohumeral capsule, to
promote external rotation. The patient’s shoulder is in
45° of abduction and his elbow is in 90° of flexion. Sur-
gical tubing attached to his wrist provides a 30-minute,
low-load stretch into external rotation.
Rationale
Using rat tail tendons, Lehman and associates54
showed that the optimum method to stretch pericapsu-
lar tissue is to use a low-load-prolonged stretch. Accord-
ing to Lehman and colleagues, the prolonged stretching
allows the viscoelastic material in the capsular tissue,
including the water and GAG, to creep or to elongate
with the tissue.
Third Goal
If necessary, continue the third goal for edema
control.
Fourth Goal
The fourth goal is to reevaluate the use of assistance-
providing devices and to modify the use of these devices.
Fifth Goal
The fifth goal is to increase coordination.
Intervention
As the patient’s motor performance improves, coor-
dination activities become an integral part of his treat-
ment program. Initially, the activities focus on such gross
motor skills as placing large pegs into a bucket while
being timed, and later placing pegs into a pegboard. As
he continues to improve, the activities require more
fine motor skills, such as manipulating nuts and bolts
(graded from large to small), practicing on an ADL
board, turning coins, and so forth. The clinician times
all the activities to record progress. Trombly and Scott55
indicate that activities should be graded along a contin-
uum from gross to fine and that as the patient’s coordi-
nation improves, the activities should require faster
speeds and more accuracy.
LATE STAGE
First Goal
The first goal in the late stage is to optimize muscle
strengthening within the constraints of reinnervation.
Intervention
Isokinetic strengthening continues to all major
affected muscle groups in the left upper extremity,
including rotational and diagonal strengthening at the
shoulder. The clinician adds fast-speed training, at 180°,
when bilateral slow-speed deficits, at 60°, are within
20%. The patient performs an aggressive home strength-
ening program using adjustable cuff weights and func-
tional training, including lifting, carrying various size
weights, hammering, and sawing activities.
Rationale
Strengthening continues to provide gains, with
periodic isokinetic strength retests. Fast-speed training
improves muscle endurance. The reason fast-speed
training begins when slow-speed bilateral deficits are
within 20% is because the patient cannot consistently
catch and maintain the faster speeds of the dynamome-
ter. Functional training for this particular patient simu-
lates the working conditions and motor requirements of
carpentry.
Second Goal
The second goal is optimizing joint and soft tissue
mobility.
Third Goal
The third goal is to help the patient return to work.
Intervention
At 1-year post injury, a job analysis identifies those
tasks the patient needs to perform to be able to safely
and accurately do his job. At that time, the patient starts
on woodworking projects that require minimal fine
motor tasks such as sanding or staining. At 15 months,
he progresses to working on more intricate projects, and
at 18 months, he returns to work.
Case Study 2
The second case study shows a pattern of injury that
occurs to the lower portion of the brachial plexus. Initial
findings in the evaluation should be compared and con-
trasted with the findings in Case Study 1. The preferred
practice pattern with the prognosis, goals, interventions,
and principles of treatment are similar to Case Study 1.
CHAPTER 8 EVALUATION AND TREATMENT OF BRACHIAL PLEXUS LESIONS
HISTORY
A 42-year-old male construction worker working on
a scaffold slips and grabs a railing with his right hand.
The result is a forceful upward pull of the arm. This
injury occurred approximately 7 weeks ago. The patient
reports numbness and tingling along the ulnar border of
his right arm and radiating into the fourth and fifth
fingers. He reports occasional burning pain along the
same distribution and along the lower portion of his
right neck. He reports weakness in his right grip. He
also has slight drooping of his right eyelid. A neurolo-
gist performed an EMG last week indicating increased
insertional activity within the medial finger, wrist
flexors, and intrinsic hand muscles. The neurologist’s
diagnosis is a second-degree/third-degree lower trunk
brachial plexus injury. The neurologist prescribes non-
steroidal antiinflammatory medication and refers the
patient to physical and occupational therapy.
VOCATION
The patient is a construction worker and is right-
hand dominant.
POSTURAL/VISUAL INSPECTION
The intrinsic muscles of the right hand are mildly
atrophic. The clinician observes a claw hand deformity
with hyperextension of the fourth and fifth digits at the
metatarsal-phalangeal joints and flexion of the inter-
phalangeal joints.
ACTIVE AND PASSIVE RANGE OF MOTION
Mild to moderate restriction in flexion of fourth and
fifth metatarsal-phalangeal joints and extension of
fourth and fifth interphalangeal joints.
MOTOR STRENGTH
The clinician grades the patient’s muscles as follows:
flexor carpi ulnaris = 3+, medial half of flexor digitorum
profundus = 3, opponens digiti minimi = 3, abductor
digiti minimi = 3, flexor digiti minimi brevis = 3,
interossei muscles = 3, medial lumbricales (fourth and
fifth digits) = 3, flexor pollicis brevis = 3+, and adductor
pollicis brevis = 3.
SENSATION
The clinician’s sensory tests indicate impaired light
touch and sharp/dull sensation along the ulnar side of
the arm, forearm, and hand. Special tests: Froment’s
paper sign is equivocal. The patient grasps a piece of
paper between the thumb and index finger. With full
paralysis of the adductor pollicis brevis, the thumb
flexes. However, only slight flexion occurs when the cli-
nician pulls the paper away.
259
EDEMA
1+ edema is seen along the dorsum of the right hand.
The hand is slightly cool to palpation, with no trophic
changes. The Purdue pegboard indicates coordination
deficits in the right hand. ADL assessment indicates
difficulties in self-care similar to those outlined in Case
Study 1.
ASSESSMENT
The pathomechanics of injury involve an upward
traction injury of the right limb that affects the lower
portion of the brachial plexus. Lower plexus injuries
affect nerve roots C8 and T1. Ptosis of the right eyelid
indicates a potential sympathetic component (Horner’s
syndrome) and the physical/occupational therapist
should monitor the condition carefully for sympathetic
dystrophy in the right hand. Fibrillation potentials with
EMG examination, combined with clinical testing that
produced a minimum strength grade of 3 in all affected
muscle groups, indicate a probable partial denervation
of muscles affected by C8 and T1 nerve roots. The
diagnosis is a second-degree (rule out third-degree)
axonotmesis with Wallerian degeneration of some
muscle fibers, but probable preservation of the
endoneurial tube. Spontaneous recovery will occur in
case of axonotmesis, but axonal outgrowth takes a long
time in these cases (at least 1 year) because of the limited
growth rate and the long distance to their target muscles.
A comprehensive program of both physical and occupa-
tional therapy is a phased approach outlined in the initial
case. As with all lower trunk brachial plexus injuries, a
certified hand therapist designs a comprehensive hand
therapy program. Periodic electromyographic evalua-
tions check for reinnervation characterized by polypha-
sic action potentials. After 1 year, a lack of recovery
results in surgical exploration.
Summary
The case studies illustrate the problem-solving approach
to patient treatment. The clinician prioritizes signs and
symptoms in order of their functional significance. The
clinician establishes appropriate goals within the con-
straints of nerve reinnervation and uses the preferred
practice patterns to predict the impairments and func-
tional losses, and to determine the prognosis. The pre-
ferred practice patterns provide only guidelines to
intervention, so the clinician should use his or her
260 SECTION II NEUROLOGIC CONSIDERATIONS
clinical judgment with knowledge of evidence-based
outcomes to individualize each program. The patient
progresses through each phase based on the clinician’s
continued reevaluation of signs and symptoms, and dis-
charge takes place when clinical tests and evaluation
indicate no further improvement in the patient’s motor
capabilities. The clinician discharges the patient on a
home program, and he or she periodically reevaluates the
patient for improvement. Signs of motor reinnervation
results in resumed intervention.
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32. Highet WB: Grading of motor and sensory recovery in nerve
injuries. In Seddon HJ, editor: Peripheral nerve injuries,
Medical Research Council Report Series T2 282. London,
1954, Her Majesty’s Stationery Office.
33. Daniels L, Worthingham C: Muscle testing: techniques of
manual examination, ed 4, Philadelphia, 1980, WB
Saunders.
34. Hamm NH, Curtis D: Normative data for the Purdue
pegboard on a sample of adult candidates for vocational
rehabilitation, Percept Mot Skills 50:309, 1980.
35. Travell JG, Simons DG: Myofascial pain and dysfunction: the
trigger point manual, Baltimore, 1984, Williams & Wilkins.
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ders of the brachial plexus, J Magn Reson Imaging 4:13, 1994.
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tion lesion of the brachial plexus, Proc R Soc Med 51:365,
1958.
41. Scott PM: Clayton’s electrotherapy and actinotherapy, ed 7,
London, 1975, Balliere Tindall.
42. Tabary JC, Tardieu C, Tardieu G, et al: Experimental rapid
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Manual on management of specific hand problems, Pittsburgh,
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4, Philadelphia, 1976, WB Saunders.

The Shoulder
in Hemiplegia
H emiplegia, or paralysis affecting one side of the
body, is a common consequence of neurologic
disorders such as stroke, tumor, and brain
injury. In these disorders, damage to the sensory and
motor areas of the cerebral cortex and brain stem leads
to primary impairments, such as loss of central force
production (central weakness), diminished neuromuscu-
lar control, altered sensation, and abnormal muscle tone.
These primary impairments affect the muscles of the
shoulder and distal arm, and the postural muscles con-
trolling alignment of the spine and rib cage. However,
secondary impairments—such as muscle and soft tissue
restriction, shoulder pain, and glenohumeral joint sub-
luxation—are also frequently associated with hemiple-
gia. These secondary impairments develop over time and
are influenced both by the initial neuromuscular impair-
ments and by other intrinsic and extrinsic factors includ-
ing the effects of rehabilitative therapy.1 Primary and
secondary impairments have direct effects on both
movement and function.
This chapter reviews common primary neuromuscu-
lar and secondary musculoskeletal shoulder impairments
associated with hemiplegia and presents a framework for
examination and clinical intervention.
Neuromuscular Impairments
The primary impairments of central weakness (loss of
central commands for force production), muscle activa-
tion deficits, sensory deficits, and changes in muscle tone
result in a loss of functional movement patterns in the
263
9
Susan Ryerson
Kathryn Levit
arm.2 The loss of functional arm movement patterns
occurs in conjunction with similar primary impairments
in the trunk and leg, which add to the complexity of
evaluation and intervention planning. Weakness, loss of
control, sensory, and tonal changes can occur through-
out the arm in a balanced pattern or, depending on the
site of the lesion, be greater at the shoulder than the
lower arm, or vice versa. While neuromuscular impair-
ments occur because of central nervous system damage
or pathology, the status of these impairments may
change through the process of recovery and through
interactions with other systems of the body and the
environment.
Central Weakness: Loss of Force Production
Central muscle weakness is thought to be the major
impairment interfering with effective movement per-
formance.3 This loss of force production occurs because
of an interruption of the pyramidal tract.4 In the early
phase of recovery, many patients are unable to maintain
an upright position in sitting or standing, and have no
ability to move the affected arm. Over time, the ability
to produce force increases in some of the individual
muscles of the affected arm. In some individuals, this
return is balanced over the entire arm. In others, the
recovery is imbalanced across agonist/antagonist groups
or between proximal and distal segments. Common pat-
terns of early motor return in the shoulder include the
ability to elevate the scapula and to adduct or abduct
the humerus with internal rotation. Motor return in the
muscles that control scapular upward rotation and
264 SECTION II NEUROLOGIC CONSIDERATIONS
Figure 9-1 Left hemiplegia. Loss of force production
in the trunk and left shoulder girdle results in excessive upper
trunk flexion and scapular abduction.
glenohumeral joint external rotation occurs less fre-
quently, resulting in limitations in active range of motion
in forward flexion and horizontal abduction.
There is a growing body of evidence supporting a link
between movements of the trunk and the limbs.5,6 (In
addition, see Chapter 5.) The importance of this link for
normal functioning can be seen in trunk and scapu-
lar/humeral patterns in people with a hemiplegia where
weakness in the musculature of the trunk and shoulder
girdle affects control of trunk posture and stability in
antigravity positions. In cases of severe stroke, central
weakness affecting both the musculature of the trunk
and shoulder girdle typically results in excessive forward
flexion of the thoracic spine or lateral trunk flexion.
Excessive upper trunk forward flexion is accompanied
by scapular abduction and humeral internal rotation.
Similarly, a lateral spinal curve is accompanied by atyp-
ical scapular rotations (Figure 9-1). The combined
effects of gravity and this pattern of central weakness
have not been established. But clinical experience
supports the assumption that, in the acute phase of
recovery, atypical upper quadrant posture is a result of
severe loss of force production and the effects of the
force of gravity on the unsupported body structure.
These changes in the resting position of upper trunk and
scapula interfere with normal movements of the shoul-
der girdle. When these patterns remain unchanged,
they lead to glenohumeral joint subluxations and other
musculoskeletal changes. These problems are discussed
later in the chapter.
Because loss of force production leads to movement
deficits, therapeutic interventions designed to increase
movement control should include techniques for
increasing force production in muscles that demonstrate
central weakness and techniques for increasing func-
tional use of motor return. When force production is
insufficient to allow independent movement, therapists
begin with guided or active-assisted movements. They
then proceed to assisted movements with selected
objects (to replace the therapist’s assistance) and gradu-
ally increase the demand of the task to increase muscle-
firing endurance. For example, therapists may use
bilateral activities to increase force production and
practice antigravity movement. They add weight and/or
resistance to the task as strength and endurance
increase. Since many patients with hemiplegia lack suf-
ficient trunk control to exercise safely in sitting and
standing positions, arm exercises may initially be per-
formed supine—where the spine is supported and the
ability of the arm to produce force is isolated from
demands on the trunk. A person’s ability to move the
arm against gravity in a sitting position depends on the
integration of trunk and scapular movement in addition
to the ability to link force production of the upper
and lower arm.6,7 Arm movements while standing are
influenced not only by trunk position, but also by move-
ment and control patterns of the leg.8
Muscle Activation Deficits
In addition to central weakness, neurologic lesions are
often associated with changes in muscle activation.
These deficits affect the coordination of muscle syner-
gies and interfere with the performance of functional
movements. Muscle activation deficits lead to move-
ment disorders such as inappropriate initiation patterns,
altered sequences of muscle firing, excessive force pro-
duction, and difficulties with cessation of force patterns.
While muscle activation deficits are usually attributed to
changes in motor control,9,10 they may also occur because
of changes in alignment and soft tissue restriction when
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA
these secondary impairments block normal biomechan-
ical mobility. Since this impairment generally develops
as the person attempts active movement, they may also
develop because of learning, practice, or therapy that
reinforces atypical movement. Once acquired, atypical
patterns of muscle activation are difficult to remedy even
when underlying muscle strength is adequate to allow
the production of more efficient movement sequences.
Two basic patterns of muscle activation deficits are
most common following neurologic lesions: problems
with timing and sequencing of muscle synergies, and
problems with force regulation and the turning on
and off of muscle contraction. Problems with the timing
and sequencing of muscle synergies are present when the
patient actively uses an atypical pattern of movement
sequences to move the arm. For example, when attempt-
ing to pick up a cup from a table, atypical reach is
produced when the movement is initiated proximally
with shoulder elevation and abduction/internal rotation
instead of distally with wrist and finger extension and
increased elbow extension. Inappropriate sequencing
often occurs when stronger muscles are substituted for
weaker muscles. For example, shoulder elevation and
elbow flexion may be used to lift the hand to the mouth
when wrist and forearm control does not allow a more
appropriate distal pattern. When stronger proximal
patterns are substituted for weaker distal actions during
movement initiation, the resulting movements are inef-
ficient and do not appropriately position the hand for
function (Figure 9-2). The importance of retraining
distal initiation and sequencing in conjunction with arm
reach patterns is discussed later in this chapter.
Problems with force regulation and the turning on
and off of muscle firing produce a different movement
disorder. Excessive force production, or co-contraction,
occurs when the person activates too many muscles
during movement performance so that both the correct
muscles and additional inappropriate muscles are
working simultaneously. For example, people with
hemiplegia often forcefully co-contract shoulder and
elbow muscles, especially the biceps and upper trapez-
ius, during attempts at lifting the involved arm—pro-
ducing a stiff, flexed extremity. Knutsson hypothesized
that this excessive force production may be caused by
misdirected descending commands, whereas Katz has
suggested it may be an adaptation to poor strength and
a sensation of “heaviness.”11,12 In many cases, this exces-
sive muscle activation is abnormally prolonged so that
265
Figure 9-2 Person attempting to reach the left arm
forward is an example of proximal initiation, excessive co-
contraction, and an inability to sequence forward reach.
the arm is maintained in a fixed position instead of being
returned to a position of rest. Problems with the regu-
lation of muscle force and timing of muscle onset and
termination are an important cause of the slow and
effortful movement associated with neurologic lesions
and may contribute to excessive arm posturing and soft
tissue contracture.13 For this reason, interventions
focused on movement production should monitor the
force of muscle contraction, appropriate turning on and
off of muscles, and initiation and timing of muscle
contraction.
Altered Sensation
Sensory deficits include both changes in sensory aware-
ness and difficulties processing sensory information.
These problems are associated with damage to the
somatosensory and association areas of the cortex.
Sensory deficits may range from complete sensory
hemiplegia, where no sensory information from the
hemiplegic arm can be recognized, to mild deficits
affecting one group of sensory receptors. Individuals
with mild sensory involvement may show deficits in
light touch, while more severe deficits may involve
touch, deep pressure, and proprioception. These deficits
may involve the whole arm or just the distal portions.
Frequently, sensory loss is accompanied by central weak-
ness. Individuals who experience improved muscle
266 SECTION II NEUROLOGIC CONSIDERATIONS
control may also report increased sensory awareness fol-
lowing the same general distribution. Sensory deficits
may also affect muscle history and muscle memory or
the knowledge of feeling and executing movement.
Altered sensation influences the control of movement
in several ways. People with decreased sensation are less
aware of asymmetries in body posture and make fewer
attempts to move spontaneously or to use their involved
arm for function or weight support.14 This suggests that
sensory impairments may contribute to the problems
of “learned disuse” and neglect associated with the
hemiplegic arm.14-16 Loss of muscle memory and muscle
history may lead to the problems of movement initia-
tion and sequencing, thus contributing to atypical
patterns of movement. Afferent information is also
important for both feed forward and feedback systems
that contribute to relearning.17 This means that it will
be more difficult for individuals with sensory impair-
ments to monitor arm movement and position without
use of vision, and to use sensory feedback during move-
ment as a source of performance knowledge.
Recent research supports the belief that recovery of
cortical function is manifested by reorganization in
response to afferent input.18 This suggests that the
sensory experiences associated with therapeutic inter-
vention are important for motor recovery. Therapeutic
interventions that encourage active movement and func-
tional performance will provide sensory information
about how arm movements are initiated and sequenced,
and how movement relates to goal achievement.
Therapists should monitor the quality of movements
during these activities and provide verbal feedback about
the quality of movement performance to help the patient
use sensory feedback as a source of learning and self-
correction. When patients are unable to move inde-
pendently, therapists may use guided or assisted
movements to replicate functional performance and to
train appropriate patterns of initiation, sequencing, and
cessation. These assisted movements provide a sensory
memory for movement, which can be used as an
internal model of motor performance.
Spasticity and Hypertonicity
Increase in tone, spasticity, or hypertonicity is a fourth
category of neuromuscular impairment affecting the
shoulder and arm. The relevance of spasticity to therapy
interventions has changed in the past decade. Bobath
and Bobath identified spasticity as the major problem
interfering with movement and function in individuals
with central nervous system abnormalities and recom-
mended interventions to inhibit spasticity.19 Although
this perspective had an impact on therapy practice
for many years, recent perspectives have changed on
spasticity and hypertonicity. Spasticity—defined as an
increased response to stretch—is no longer believed to
be the major cause underlying motor dysfunction, but
rather only one of multiple impairments contributing
to loss of movement control.20-22 Today, the nature of
spasticity, its underlying mechanisms, and its relevance
to rehabilitation practice are being widely investigated
and debated.3,23,24 At the same time, the increasing
popularity of medical interventions for spasticity (for
example, botulotoxin injections) suggests its treatment
remains a priority within the medical community.
We believe that one source of confusion about the
clinical importance of increased tone relates to the
various ways that the term is used by physical therapists
and other medical professionals. To identify the aspects
of spasticity that are most relevant for intervention, we
propose to separate spasticity—measured at rest—from
the hypertonicity seen during attempts at active move-
ment in people with central nervous system abnormali-
ties. Lance defined spasticity as a reflex hyperactivity
occurring at rest or in passive conditions and character-
ized by velocity dependent stretch reflexes, an increase
in deep tendon reflexes, and clonus.25 Research has
demonstrated there is little or no relationship between
this reflexive type of spasticity and functional move-
ment.26-30 Because of its central origins, this type of
increased tone may also not respond to traditional phys-
ical therapy interventions. However, from clinical expe-
rience, we believe the hypertonicity present during active
attempts at movement is a combination of primary—
neural and secondary—nonneural impairments. Because
this type of hypertonicity occurs during active move-
ments and affects motor performance, the underlying
causal mechanism is an appropriate target for inter-
vention. There are at least three major categories of
hypertonicity:
1. Intermittent hypertonicity. Intermittent
hypertonicity is present when the muscle tone in
the arm fluctuates according to activity, body
posture, and balance demands. This type of increase
in tone is a result of the loss of central force
production in the musculature controlling trunk
and extremity linked patterns. Intermittent
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA
hypertonicity in the arm occurs when muscles in
the hemiplegic arm are activated in response to
postural stability and/or loss of balance. The
hypertonicity is intermittent because when trunk
control for the desired task is sufficient, the arm
does not posture. However, when trunk control is
insufficient for task performance or when balance is
precarious, the arm postures as the person attempts
to perform the skill. Hypertonicity and flexor
posturing of the arm may increase dramatically
during ambulation or during activities of daily
living that challenge available motor control in
the trunk and leg. This arm posturing can be
interpreted as a compensation, or active contraction
to assist or reinforce trunk stability. This assistive
response of the extremity diminishes or stops
completely when stability is restored and the person
returns to a quiet resting position. Because
intermittent hypertonicity occurs because of
insufficient postural stability, intervention
techniques that lengthen arm muscles or prevent
atypical arm patterns may maintain muscle length,
but will not decrease arm posturing. Arm posturing
will decrease when the postural instability
underlying the posturing is addressed. Thus
interventions to decrease arm posturing must
be designed to improve alignment and control in
the trunk and lower extremity.
2. Hypertonicity during voluntary movement. This
second category of hypertonicity comes from
deficits in muscle activation and from central
weakness affecting the muscles of the arm. It occurs
during active attempts to move the arm or use the
arm for function. Individuals with central loss of
force production or deficits affecting muscle
activation have difficulty controlling the initiation
and sequencing of muscle firing or patterns of force
gradation. When muscles are recruited in atypical
sequences or with excessive force, the result is a
“stereotypic” pattern, which therapists often
describe as “spastic” or “synergistic.” For example,
patients with diminished force production in the
lower arm and hand may use available shoulder
elevators and elbow flexors to position the hand,
producing a movement pattern that is often
described as flexor synergy. Since the arm pattern is
active, but reflects altered control, the change in
muscle tone that occurs is a result of active
267
recruitment, not abnormal reflex activity. For this
reason, intervention programs for patients with
hypertonicity during active movement should not
aim at inhibition of the flexor spasticity because
this will prevent all arm movement. A more
appropriate strategy would be to retrain arm
movement with proper initiation, sequencing, and
appropriate grading of force as muscle tone will
decrease when muscles are activated in more
normal patterns.
3. Positional (passive) hypertonicity. The third major
category of hypertonicity is increased muscle
tension resulting from mechanical changes in
muscle length related to changes in joint alignment.
Positional hypertonicity is most common in the
biceps brachii and the other two joint muscles of
the arm. Muscle tension in two joint muscles is
increased when changes in orthopedic alignment
from neurologic weakness or from persistent muscle
activation alter the length-tension relationship of
the muscle. Over time, the positional shortening
results in a “passive stiffness” of the muscle. This
type of hypertonicity comes from nonneural
elements and may result in changes in the physical
properties of muscle and soft tissue. Nonneural
elements of muscle and soft tissue are affected by
chronic positioning, the influence of the force of
gravity on weak body segments, and compensatory
training patterns.20,22,31 Because positional
hypertonicity is a result of altered joint alignment
and altered length-tension relationships, this type
of hypertonicity responds to intervention
techniques that gradually lengthen soft tissue,
realign joints, and focus on reestablishing
trunk/girdle muscle activity. Techniques that realign
joints and restore normal resting lengths of two
joint muscles may result in quick and dramatic
temporary reductions in hypertonicity if the
malpositioning is not chronic. In cases of chronic
malpositioning, positional hypertonicity is often
accompanied by soft tissue restrictions so that
reestablishing normal joint and muscle positions
may not produce an instantaneous tonal response.
Musculoskeletal Impairments
The following section contains a description of the most
common musculoskeletal problems of the hemiplegic
268 SECTION II NEUROLOGIC CONSIDERATIONS
shoulder and arm. These secondary impairments
develop after the initial brain damage and are not
directly caused by the neurologic lesion. This means that
musculoskeletal problems may be prevented or mini-
mized by effective treatment early in the recovery
process. If present, these problems have a substantial
impact on movement and function.
Soft Tissue Tightness and Contracture
Muscle and tissue tightness and contracture are
extremely common after central nervous system lesions.
Clinical experience demonstrates that patients begin to
experience soft tissue limitations in the affected arm
within weeks of their stroke. Recent research suggests
that soft tissue restrictions are characterized by changes
in the muscular cross bridge connections and sarco-
meres, and in the composition of tendon and connective
tissue.2 These mechanical changes contribute to the
background “stiffness” and resistance to passive motion
that is common after neurologic damage. They also
interfere with active motor control and functional use of
the arm by limiting available range of motion and
normal joint mechanics. In the hemiplegic arm, muscle
and soft tissue tightness may limit scapular rotation,
humeral external rotation, and the ability to disassociate
the scapula from the humerus—leading to atypical
patterns of arm movement and contributing to the
development of shoulder pain. These changes in the
extensibility of muscles and tissues may also be respon-
sible for the typical flexor posturing of the hemiplegic
arm, the third form of hypertonicity (see the previous
section).2
Soft tissue tightness and contracture develop for
several different reasons. Patients whose primary prob-
lems are weakness and loss of movement control develop
tightness in muscles and tissue, which are maintained in
shortened positions by abnormal positioning. These soft
tissue changes are related primarily to disuse and immo-
bility. In upright positions, the weak extremity hangs by
the side of the body. The dangling position of the arm
places a stretch on the muscles over the top of the shoul-
der, while shortening the muscles connecting the arm to
the rib cage. This leads to overstretching of the deltoid
and rotator cuff muscles, and predictable patterns
of tightness in the pectorals, latissimus, and lower
trapezius muscles. Tightness in these muscle groups
has a notable effect on passive and active arm motion
because it restricts the available external rotation of the
glenohumeral joint, horizontal abduction of the
humerus, and upward rotation of the scapula.
Soft tissue shortening and contracture also develop
in patients who have abnormal patterns of muscle acti-
vation and spasticity. In these patients, the soft tissue
restrictions are caused by active muscle contraction.
Patients with unbalanced motor return in the arm typ-
ically use scapula elevators, pectorals, and biceps muscles
to move the arm. These muscles also may be inappro-
priately activated during ambulation or while perform-
ing functional activities that challenge trunk stability.
Persistent activation of these muscles and the absence of
activity in reciprocal muscles result in changes in the
resting length and passive mobility in activated muscle
groups, as these muscles are maintained in shortened
lengths. These changes limit available mobility in scapu-
lar rotation and depression, humeral horizontal abduc-
tion and external rotation, and elbow extension. Similar
patterns of muscle tightness occur in patients with
strong spasticity and co-contraction in the flexor
muscles of the hemiplegic arm.
Subluxation
Shoulder subluxation, or partial separation of the
humerus from the glenoid fossa, occurs when any of the
factors contributing to glenohumeral joint stability are
disrupted. The subluxation is precipitated by a change
in the resting position of the scapula on the rib cage.
Under normal conditions, glenohumeral joint stability is
maintained by the position of the scapula and the
integrity of the soft tissue connecting the bony struc-
tures.32,33 The scapula rests on the thorax at an angle of
30° from the frontal plane.34 In this position, the artic-
ular surface of the fossa is retroverted relative to the head
of the humerus, so that the labrum of the glenoid fossa
provides inferior support to the humeral head. Joint sta-
bility is further reinforced by the shoulder capsule and
ligaments, and by the muscles connecting the trunk
and the bony structures of the shoulder girdle. These
structures are called upon to support the joint during
movement and dislocating forces that threaten joint
integrity. Thus the integrity of the shoulder joint depends
primarily on the biomechanical relationships between
soft tissue and bone rather than muscle activity.35
Both neuromuscular and musculoskeletal factors may
contribute to the development of subluxation by chang-
ing the biomechanics of the shoulder joint. Loss of
scapular stability occurs in all but the most minor
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA
strokes, and is influenced by factors such as the weight
of the flaccid arm, the development of postural asym-
metry, and the influences of motor recovery and treat-
ment. The orientation of the glenoid fossa and the
position of the humerus in the fossa are also affected
when these factors cause a change in the resting posi-
tion of the scapula. These changes set the stage for the
development of subluxation. Since subluxation results in
permanent changes in joint position and joint mobility,
it will have lasting effects on the mechanics of shoulder
movement and muscle function. A treatment program
that focuses on control of the shoulder girdle most easily
prevents subluxation. In all patients at risk of subluxa-
tion development, treatment goals must include restor-
ing normal resting alignment of the scapula, preserving
scapular mobility in all planes of motion, and retaining
motor control of the muscles that move the shoulder and
arm.
Several different types of subluxation occur fre-
quently after stroke and neurologic damage. Inferior sub-
luxations develop in the acute phase of recovery and are
associated with muscle weakness and poor trunk control.
Anterior, posterior, and superior subluxations are related to
hypertonicity and unbalanced atypical patterns of
muscle activation (Figure 9-3). These types of subluxa-
tion may be seen with acute head injury when severe
spasticity is present in the upper extremity. After stroke,
these patterns are less common in the early phase, but
develop in tandem with motor recovery and increases in
hypertonicity in the hemiplegic arm. The common types
of shoulder subluxation are discussed separately in the
sections below.
Inferior Subluxation. Inferior subluxation, where
the humeral head is positioned below the glenoid fossa,
is the most common and best described type of sublux-
ation associated with hemiplegia. Inferior subluxations
develop when muscle weakness leads to changes in the
position of the scapula on the thorax. They usually
become evident in the first weeks after stroke when
muscle weakness may be present in the entire hemiplegic
side of the body. Weakness profoundly affects the
patient’s ability to actively position the spine and rib
cage, scapula, and arm, particularly in upright postures
where the influences of gravity are most notable. People
with hemiplegia who have poor trunk control typically
avoid putting weight on the hemiplegic leg and have dif-
ficulty maintaining the trunk in an erect and symmetri-
269
cal position while sitting or standing.36 Typically, they sit
and stand with the trunk on the hemiplegic side in a
position of lateral flexion or forward flexion relative to
the other side, with resultant changes in the position of
the scapula and arm on the hemiplegic side. In addition,
the weight of the paretic arm exerts a downward force
on the upper trunk and the scapula. The combination of
an asymmetrical trunk position and a heavy arm places
the hemiplegic scapula in a position of downward rota-
tion. When the scapula is rotated downward, the slope
of the glenoid fossa becomes less oblique. This change
disrupts the passive locking mechanism of the shoulder
as the labrum and inferior portion of the fossa can no
longer provide inferior support.32,35 The weight of the
dependent humerus places a stretch on the nonelastic
shoulder capsule, causing it to become taut. Initially,
intrinsic tension in the shoulder capsule, the liga-
ments connecting the humerus to the capsule, and the
shoulder musculature may be adequate to maintain the
humerus in the glenoid. However, unless the arm is
mechanically supported, the weight of the flaccid arm
continues to exert traction on these tissues whenever the
patient assumes an upright position and the arm hangs
by the side of the body. Over time, the superior portion
of the capsule becomes permanently lax, and the muscles
connecting the humerus to the scapula lengthen. As
these tissues stretch, the humerus gradually slips below
the level of glenoid.
Inferior subluxations are clearly defined by a visible
gap between the acromial process and the superior
tuberosities of the humerus (Figure 9-4, A, B). Palpation
reveals that the bicipital tuberosity is also medial to the
acromion, indicating that inferior subluxation occurs
with internal rotation. Since it is scapular downward
rotation that sets up inferior subluxation, the scapulae of
patients with inferior subluxation are all initially rotated
downward. In acute hemiplegia, the scapula will often
be rotated downward and depressed relative to the posi-
tion of the opposite scapula, with winging of the infe-
rior angle. However, it is important to recognize that the
true position of the scapula may be masked by the posi-
tion of the upper trunk and rib cage. The position of the
scapula may also shift during recovery, if muscles con-
necting the scapula and trunk are recruited to stabilize
the scapula and arm. For this reason, it is not uncommon
to find inferior subluxations of the humerus with scapu-
lae that appear more elevated or adducted than down-
wardly rotated. In these cases, correcting the position of
270 SECTION II NEUROLOGIC CONSIDERATIONS

A B

C D

Figure 9-3 A, Normal glenohumeral alignment. B, Inferior glenohumeral joint subluxation. C, Anterior gleno-
humeral joint subluxation. D, Superior glenohumeral joint subluxation.

the trunk so that the two sides of the body are sym-
metrical will reveal the true position of the hemiplegic
scapula (Figure 9-5).
Anterior/Posterior Subluxations. In anterior and
posterior subluxations, the humeral head is displaced
inferiorly and laterally in the sagittal plane. In anterior
subluxation, it rests below and forward of the glenoid
fossa, resulting in apparent shortening of the clavicle.
Conversely, with posterior subluxation the humeral head
is positioned below and behind the socket. Anterior and
posterior subluxations are associated with unbalanced
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA 271

A B

Figure 9-4 A, Patient with a right inferior subluxation. B, The therapist’s right hand palpates the acromion while her
left hand marks the bicipital tuberosity and the lateral aspect of the humeral head.

muscle activation and spasticity, and are influenced by
both preferred trunk posture and available motor pat-
terns in the shoulder and arm. Most frequently, anterior
and posterior subluxations develop later in the recovery
phase, and in shoulders in which the shoulder has
already developed an inferior subluxation. While the
exact mechanism contributing to this progression is
unknown, it appears likely that the humerus is displaced
in an anterior or posterior position by atypical patterns
of shoulder muscle activation. With inferior subluxa-
tions, the humerus is not seated in the glenoid fossa and
the capsule is loose and nonrestrictive. This hyper-
mobility allows the humerus to be displaced further by
muscle firing or poor handling techniques.
In anterior subluxations, the proximal humerus is
very prominent below and in front of the acromion,
while the distal end of the humerus lies behind the
shoulder. This results in hyperextension with internal
rotation at the shoulder joint, and flexion of the elbow
(Figure 9-6). Generally, the scapula is elevated and tilted
forward on the rib cage. In our practice, patients with
anterior subluxation have moderate to severe hyper-
tonicity in the flexors of the elbow. This apparent spas-
ticity may be largely mechanical, as the anterior position
of the proximal humerus causes increased tension in the
long head of the biceps at the front of the shoulder,
leading to elbow flexion and forearm supination. Poste-
rior subluxations are observed less frequently and are
accompanied by shoulder joint flexion, adduction, and
internal rotation. With posterior subluxations, the supe-
rior aspect of the proximal humerus may be palpated
below and behind the superior angle of the scapula. This
272 SECTION II NEUROLOGIC CONSIDERATIONS

A B

Figure 9-5 Patient with a right hemiplegia. The contour of the right shoulder is lower than the left because of the altered
position of the upper trunk and rib cage.

position changes the resting length of the origins of
the triceps. For this reason, the elbow joint is fre-
quently locked in an extended position with a posterior
subluxation.
Superior Subluxation. In superior subluxations,
the humeral head is tightly lodged in the fossa under the
acromial arch. This position, where the space between
the humerus and the top of the shoulder joint is reduced,
closely resembles the pattern that is found with ortho-
pedic impingement syndrome (see Chapter 10). Supe-
rior subluxations are associated with unbalanced muscle
firing and co-contraction in the muscles connecting the
scapula and humerus. In our practice, patients with this
pattern of shoulder abnormality have scapulae that are
positioned in elevation and abduction. The shoulder
joint is generally internally rotated, with humeral hori-
zontal abduction, so that the elbow joint lies directly
below the shoulder in the frontal plane but is abducted
away from the rib cage. No separation of the humerus
from the fossa is evident and all movements of the
humerus result in immediate changes in scapular move-
ment. Although the mechanism leading to superior sub-
luxation after stroke is unknown, it is clearly associated
with abnormal patterns of muscle firing. Many patients
with this pattern of subluxation have strong activation
of deltoid and biceps muscles, and poor activation of
rotator cuff muscles.
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA
Figure 9-6 Patient with a left hemiplegia and an
anterior shoulder subluxation.
Pain
Shoulder pain is a major problem in hemiplegia.
It is estimated that up to 70% of all stroke patients
experience shoulder pain during their rehabilitation.37
Shoulder pain is a common reason for referral to
physical therapy in both early and long-term phases of
recovery as pain has major effects on both arm function
and quality of life. Although some sources describe a
typical pain in a hemiplegic shoulder, the pain may occur
for many reasons.32 At least four categories of shoulder
pain are common: joint pain, muscle pain, pain from
altered sensitivity, and pain associated with shoulder-
hand syndrome. Because each of these pain categories
has its own description, cause, and treatment, therapists
treating patients with neurologic lesions need to care-
fully assess each case before beginning treatment. The
major features of the four common types of shoulder
pain are discussed later.
273
Joint Pain. Joint pain occurs when a joint is moved
with improper biomechanics. In hemiplegia, shoulder
joint pain occurs during arm movement when the
humerus is not correctly aligned in the fossa or when
shoulder movements take place without normal scapulo-
humeral rhythm. Shoulder joint pain is described as
sharp or stabbing in nature. The pain is directly localized
to the shoulder joint. Patients with this type of pain point
to a specific place in the front of the joint when asked
where they feel the pain. Because normal shoulder align-
ment and rhythm are critical to pain-free motion at
about 90° of humeral elevation, when the scapula must
rotate to keep the humerus in the glenoid, shoulder pain
is induced most frequently with active or passive humeral
movements at or above 90° of flexion or horizontal
abduction.33 Joint pain is common in patients with
inferior subluxation because movement of the humerus
is not accompanied by rotation of the scapula. If the posi-
tion of the scapula and humerus is not corrected before
initiating shoulder elevation, the movement of the
humerus will pinch the capsule against the acromion as
the arm moves into flexion or abduction. Joint pain is also
associated with soft tissue tightness in the muscles con-
necting the scapula to the rib cage. Tightness in the
upper and/or lower trapezius and the latissimus prevents
the scapula from rotating upward, causing pain in the
joint when the humerus approximates the acromion.
Because joint pain occurs because of poor joint
mechanics, shoulder joint pain is relieved when the
humerus is moved back below 90° of elevation where
movement of the humerus may occur independently of
scapular rotation. If the pain is caused by shoulder sub-
luxation, pain-free elevation above 90° may be restored
by reducing the subluxation and stabilizing the humerus
in a position of external rotation while moving the arm
into elevation. Similarly, if the pain is related to loss of
scapular rotation, treatment to restore normal scapular
glides and lengthen tight muscles connecting trunk,
scapula, and humerus may be necessary to allow the
scapula to upwardly rotate with the movements of the
humerus. These precautions are important to ensure that
the shoulder joint can be moved passively and actively
without pain. If the therapist continues to ask for arm
movement without changing joint mechanics, the joint
will be traumatized and may become chronically painful.
Muscle Pain. Muscle pain occurs when tight tissue
is lengthened too quickly, with too much force, or with
274 SECTION II NEUROLOGIC CONSIDERATIONS
poor alignment. In hemiplegia, the most common
cause of muscle pain is the use of aggressive stretching
techniques in treatment. Muscle pain is also frequently
induced during passive range of motion and during
weight-bearing activities designed to inhibit spasticity.
Muscle pain occurs in muscles that have shortened or
developed contractures. As our discussion above makes
clear, muscle shortening is common in patients whose
primary problems are weakness and loss of movement,
and in patients with hypertonicity, co-contraction, and
unbalanced firing. With all these problems, the hemi-
plegic arm is passively positioned for long periods of
time and active or passive movement seldom lengthens
muscles held in shortened ranges.
Muscle pain is perceived as a stretching or pulling
sensation that is located along the muscle or muscles
being lengthened. Patients with hemiplegia will rub the
muscle belly or across multiple tight muscles when asked
where they experience the pain. Muscle pain is relieved
immediately if the tension across the tight tissue is
removed or decreased a few degrees. However, if the
painful stretch is maintained for longer periods, the pain
may continue upon completion of the treatment. If this
situation is repeated multiple times, muscle pain may
progress to tendonitis. Tendonitis pain is described as
sharp and achy, and is localized to a specific point on the
tendon attaching muscle to bone. In the hemiplegic arm,
two types of tendonitis are most common. Bicipital
groove tendonitis is localized to the front of the
shoulder and long head of the biceps, with pain occa-
sionally referred down the muscle belly. Biceps insertion
tendonitis is associated with pain in the forearm at
the biceps insertion. This type of pain may be referred
down the volar aspect of the forearm.
When elongating tight muscles and soft tissue is
a treatment goal, the muscle should be gradually
lengthened, and the stretch maintained for short
periods only to allow the tissue time to accommodate
to the new length. Stretching of multiple tight arm
muscles (for example, pectorals with biceps and forearm
pronator) simultaneously should be avoided because
it exacerbates the stretch on connective tissue and
fascia. Sore muscles and tendonitis are important
treatment problems because the treatment is often rest
and immobilization. This forced break from treatment
will slow down progress in restoring movement and
function.
Pain from Altered Sensitivity. Pain that results
from altered sensitivity to sensory information is most
common during the early stage of recovery. It usually
occurs in patients with dense hemiplegia and severe
sensory loss. This pain is described as both diffuse and
aching, and is often poorly localized to the area of the
shoulder. It typically occurs during the middle of a treat-
ment session that has included tactile, kinesthetic, and
proprioceptive stimuli. Whereas the actual cause of this
pain is unknown, one explanation may be that high
levels of sensory input during treatment may exceed the
ability of the central nervous system (CNS) to process
this type of information. Because patients with dense
hemiplegia are unable to move their arms, most of the
time they experience minimal sensory input from the
involved extremity. When treatment of the arm involves
movement, multiple sensory modalities are activated at
the same time, and at levels far above the normal level
of sensory activity. These unfamiliar levels of sensation
may be perceived as painful.
When episodes of pain from altered sensitivity occur
during treatment, treatment should stop for that session.
During subsequent treatments, the therapist should
carefully grade the type and amount of sensory input to
ensure that the patient’s sensory tolerance is not
exceeded. As the patient’s tolerance for sensory infor-
mation increases, treatment activities can be expanded
to incorporate more variability in sensory experience. It
is important to continue to treat the arm in a pain-free
fashion, as these patients may proceed to shoulder-hand
syndrome if treatment is stopped completely.
Shoulder Pain
Type Nature Location
Joint Sharp and stabbing Localized to the
joint—top or
front of joint
Muscle Stretching or pulling Muscle belly
Tendon Achy or sharp On tendon or
referred
Altered Diffuse Poorly localized
sensitivity
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA
Shoulder-Hand Syndrome. In hemiplegia,
patients who have either joint pain, muscle pain, or pain
from altered sensitivity may progress to chronic pain
conditions that resemble orthopedic shoulder-hand syn-
dromes. Generally, this progression occurs when the
therapeutic intervention fails to appropriately address
and eliminate existing pain. It is also more common in
patients with edematous hands. Shoulder-hand syn-
drome is a serious complication that is difficult to
remedy. For this reason, extreme care should be taken to
avoid causing pain during treatment and to eliminate
existing pain. Range of motion or stretching exercises
that are likely sources of pain should be carefully pre-
scribed and monitored as these may be sources of pain
if performed incorrectly or too aggressively. Similarly,
the elimination of hand edema should be a treatment
priority in all treatment settings. If these precautions
are followed, shoulder-hand syndrome should occur
relatively infrequently.
The stages of shoulder-hand syndrome in hemiple-
gia are similar to those described in orthopedic settings.
In hemiplegia, shoulder-hand syndrome begins with
diffuse aching and throbbing in the shoulder, arm, and
hand. The hand is swollen, warm to the touch, and
tender. Initially, the pain is present during active
and passive movements of the arm. It is described as
sharp and localized to the joint. During this stage, the
pain is usually decreased when the arm is supported,
although throbbing and aching in the arm and hand
are often present at night.
However, if passive motion is forced on the shoulder
or swollen wrist and hand, the joints become sharply
painful at rest and patients avoid moving or touching
their arm and hand. During this second stage, active and
passive range of motion (ROM) of the shoulder girdle,
wrist, and hand is painful. Many patients show trophic
skin changes, and stiff swollen hands. If unchecked, the
syndrome culminates with loss of bone, severe soft tissue
deformity, and joint contracture.38
Examination
Examination of the shoulder and arm in people with
hemiplegia includes objective measures of functional
performance and impairments, and the subjective
measure of descriptions of movement control. Objective
measures of functional performance and measures of
275
impairments in the shoulder and arm are important to
establish baseline data. We have selected measures of
functional performance commonly found in research
studies to allow therapists to begin collecting clinical
data that they can compare with, or relate to, experi-
mental data. The measures of primary impairments of
loss of force production and deficits of control are
extremely limited. The lack of reliable and valid meas-
ures of primary impairments makes it difficult to docu-
ment clinical improvement. However, improvement in
the primary impairments usually results in improved
functional performance, either in quantity of tasks
performed or in speed. In addition to these objective
measures, the therapist uses descriptions of movement
patterns—with and without manual assistance—to
assess the relative significance of primary and secondary
impairments that contribute to loss of functional
performance.
Objective Measures of
Functional Performance
Objective measures of functional performance for the
arm include the Wolf Motor Function Test, the Frenchay
Arm Test, and the Action Research Arm Test.
The Wolf Motor Function Test was developed in
conjunction with constraint-induced treatment research
protocols. It is a timed measure of arm movement in
both single and complex patterns and assesses functional
abilities. Interrater reliability and construct, and crite-
rion validity have been established for the test.39
The Frenchay Arm Test has five skilled-hand tasks,
which are performed in sitting. It was designed for
research studies and has good validity and reliability.40
The Action Research Arm Test measures four compo-
nents: grasp, grip, pinch, and gross arm movements. The
original test has been shortened to a 10-minute version,
which has good reliability and validity.41,42
Objective Measures of Primary Impairments
Force Production. Objective measures of move-
ment impairments are limited. Traditional manual muscle
testing (measured on a scale up to 5 by the Medical
Research Council) for strength is more subjective than
objective in nature and has not been used in patients
with central lesions because of problems of reliability
and validity.
276 SECTION II NEUROLOGIC CONSIDERATIONS
The Motor Assessment Scale (MAS) was developed by
Shepherd and Carr and includes items for upper arm
function, hand movements, and advanced hand activi-
ties.43 The upper arm function and hand movement
section of the MAS measures force production with a
0-1 score, whereas the advanced hand activities section
tests functional ability. The MAS is valid and has high
reliability.44
The arm portion of the Fugl-Meyer Assessment Scale
provides another measure of active arm and hand move-
ment. It is derived from the Brunnstrom method of
treatment and has moderate interrater reliability.45
Muscle Activation Deficits. At the present time,
there are no objective tests to measure initiation, timing,
and sequencing of functional movements.
Spasticity. Spasticity, defined as a stretch reflex, is
measured by the modified Ashworth Scale.46 However,
there are no objective measures for the following types
of hypertonicity that accompany active, voluntary move-
ment: increases in tone from changes in the mechanical
properties of muscle, from loss of trunk-extremity linked
control, or from changes in firing patterns.
Subjective Examination of Movement Control
In addition to standardized testing of functional
abilities and impairments, the therapist must perform a
subjective examination of basic movement components.
For the shoulder complex, this evaluation must include
the upper trunk and the arm.
Active Movement: Force Production and Control.
During functional movement, the shoulder complex
moves on a normally aligned spine and rib cage, and
motions of the arm and trunk are coordinated in linked
patterns for basic skills and postural control. Altered
trunk movement control and alignment influence arm
function by changing glenohumeral joint alignment and
altering the basis of stability for the arm. In the early
phase of recovery, with a severe inability to produce
force, the involved side of the trunk moves into a posi-
tion of thoracic flexion with a lateral curvature—thus
placing the scapula in abduction and downward rotation.
Lateral trunk flexion with the concavity on the affected
side will result in scapular downward rotation. Lateral
trunk flexion with the convexity on the affected side
leads to scapular elevation. When assessing weakness
and control of active arm movement patterns, the
Figure 9-7 The therapist assesses weakness and
control patterns in the shoulder and arm with the patient lying
in a supine position to support the trunk.
therapist should analyze and document the patient’s
patterns of posture and movement abilities in both
the trunk and arm by position (supine, side lying, sitting,
and standing) (Figure 9-7). Active movement control in
the arm is evaluated in individual muscles and in move-
ment sequences in increasingly complex patterns.
Assisted Movement. Following the evaluation of
active movement, therapists use their hands to gain
additional information about the relationship between
impairments of the trunk and shoulder, and between
primary and secondary impairments. The use of manual
assistance during this part of the evaluation has specific
aims. Handling is used to limit degrees of freedom of
one or more joints to assess force production or the
relationship between intralimb segments; to correct
alignment as an assessment of muscle tightness or joint
stiffness; to assist the movement of a weak muscle
through greater range to determine degrees of firing;
and to block an inappropriate movement to assess the
performance of a weaker group of muscles.
Secondary Impairments and Their Relationship
to Functional Movement. Evaluation of secondary
impairments of muscle shortening, subluxation, and
pain has been presented earlier in the chapter.
Clinical Decision Making
Clinical decision making is a problem-solving process of
gathering and analyzing examination information from
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA
the previously described functional and impairment cat-
egories; organizing and reflecting on this information to
develop hypotheses for causal relationships between
impairments and functional tasks; for interrelationships
between the trunk and shoulder; and to prioritize goals
for therapeutic intervention.
Intervention
Treatment of the shoulder and arm in patients after a
stroke is one of the most important components of
rehabilitation. Statistics indicate that while only 20% of
individuals have difficulty walking following a stroke,
33% to 60% have difficulty with arm use.40 The loss of
arm movements not only results in an inability to use
the hemiparetic arm, but also notably affects the ability
to perform bilateral arm tasks—our most common func-
tional pattern.
In the past decade, intervention protocols for the
hemiplegic shoulder and arm have undergone two
notable shifts. Evidence that altered central force pro-
duction and muscle activation deficits, and not spasticity,
are the major problems interfering with functional
movement has encouraged therapists to move from an
emphasis on inhibition of spasticity to a focus on
increasing central force production and control.2,47 The
strong association between the shoulder and the hand
during reach and object manipulation, in addition to
evidence that the hand initiates reaching movements,
has resulted in a second shift in intervention emphasis.
Therapists no longer need to wait for proximal return at
the shoulder before focusing on distal control, but can
combine appropriate distal and proximal considerations
for selected tasks.48 In early rehabilitation, intervention
focuses on activation of movement patterns in the
affected upper trunk and arm; reeducating initiation,
timing, and sequencing patterns; preventing the devel-
opment of secondary impairments; and teaching the
person to integrate the arm into daily tasks to avoid
learned nonuse. In the later stages of rehabilitation,
shoulder-arm treatment may have to initially address the
secondary impairments of muscle shortening and/or
joint malalignment and reeducating active functional
use.
While the arm can move in a multitude of patterns,
there are basic critical movement patterns that are the
building blocks for all patterns. An impairment-based
reeducation intervention strategy proceeds from the
277
belief that intensive practice of these basic patterns fol-
lowed by guidance for selection of task practice will
allow patients to regain functional abilities. These essen-
tial basic patterns include trunk-girdle linked patterns,
which allow functional movement, such as rolling, side
lying to sitting, sitting, standing; and intralimb segmen-
tal movements, which allow extremity movement in
space and in weight bearing. For effective reeducation of
impairments or task performance, the therapist allows
the patient to initiate the selected pattern and moves
from judicious use of manual techniques through a
progression of guided movement, assisted movement,
objected assisted practice, and, finally, independent prac-
tice. Therapists use their hands as guides to provide a
model for movement, to correct alignment, to assist
weak muscles through a pattern or to limit the degrees
of freedom of the arm, to change the dynamics of the
task, or to facilitate confidence (Figure 9-8).36,49
Interventions for Increasing Force
Production and Control
Intervention strategies for reeducation parallel normal
patterns of shoulder/arm use, such as movements in
space and weight-bearing movements. Movements in
space can be divided into three categories: simple reach-
ing movements, complex arm movements requiring
combinations of elbow and forearm patterns, and refined
movements requiring hand dexterity or finely tuned
adjustments in postural control.36 Weight bearing on the
arm is used to support body weight during transitional
periods of functional movements such as rolling, moving
from supine to sitting, using arms to assist sitting to
standing, or stabilizing objects against a work surface.36
This form of weight bearing requires active participa-
tion from trunk and girdle musculature, and adaptive
and responsive activity from the upper and lower arm.
Functional patterns of weight bearing include bearing
weight on the forearm and on the hand.
Movements in Space. Simple arm movements
include reach patterns that have minimal movement
changes at the elbow, forearm, or wrist. These patterns
require that the hand direct the task—distal initiation—
while the shoulder pattern provides appropriate move-
ment for stability or to assist hand placement. These
simple movements provide therapists with a means of
retraining scapulohumeral rhythm without competing
demands from the elbow, forearm, and wrist. Examples
278 SECTION II NEUROLOGIC CONSIDERATIONS

A B

Figure 9-8 Reeducation of movement. A, Patient with a right hemiplegia trying to reach forward and down to grasp
the object. B, The therapist uses guided movements to help the patient to learn a kinesthetic model of sequencing and distal
initiation. Continued

in sitting include patterns of reaching down to the floor,
leaning forward to a table, sideways, or backwards
(Figure 9-9). Therapists can keep the movement within
arm’s length initially to decrease the postural control
demands of the trunk.
Following the steps of reeducation, therapists ask the
patient to initiate the pattern while they provide manual
assistance, if necessary, for the purpose of guidance to
provide a model for the movement or to assist weak
muscles. Objects can be substituted for manual assis-
tance when the patient requires less assistance. Objects
that are rigid, such as a cane, provide more assistance to
the injured arm. Objects that are more flexible, such as
a towel roll or a plastic bin, demand more participation
from shoulder muscles (Figure 9-10). One of the easiest
reach patterns in sitting for a person in the early stage
of recovery is a downward reach pattern, because gravity
assists the movement. As shoulder force production
increases, the difficulty of the task can be increased with
movements above 60°, which necessitates control of
scapulohumeral rhythm. Patients can also practice
simple arm movements in supine and standing positions.
Complex arm movements include changing move-
ments of the elbow and forearm. These movements
require not only force production, but also sequencing
of intrasegmental joints. In sitting, when the hand is
moved to the mouth, the shoulder adjusts and adapts
and provides stability for the active biceps while the
forearm and elbow position change. During complex
arm movements the elbow pattern is used to change the
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA 279

Figure 9-8, cont’d. C, The therapist uses guided movements to help the patient to learn a kinesthetic model of
sequencing and distal initiation. D, Object-assisted practice. E, Independent object practice.

hand position; move it up, down, close to or away from
the body. The combination of practicing simple and
complex movements helps the patient learn appropriate
initiation instead of the prevalent clinical pattern of
using shoulder elevation to try to position the hand for
function. The highest level of movement in space
requires refined distal movements of the forearm, wrist,
and hand. Efficient shoulder and elbow movements,
which continue throughout the task, follow these
motions, allowing the hand to be specifically positioned
for the desired task (Figure 9-11).
Movements in Weight Bearing. Weight bearing
movements on the arm in a sitting or standing position
are used in intervention programs to activate force pro-
duction in the trunk and scapula, to reeducate patterns
of scapulohumeral rhythm, to maintain range of motion
in the arm, or to increase force production within the
arm. An active-arm, weight-bearing program stresses
active, self-initiated patterns in the trunk that are linked
with scapulohumeral movements (Figure 9-12, A-C). In
addition to assisting with reeducation of linked patterns
of force production, movements in forearm or extended-
arm weight bearing are used to reeducate timing and
sequencing of muscle activity. The use of arm weight-
bearing techniques varies according to the amount of
movement recovery in the trunk and arm. In the early
stage, when there is little trunk or arm movement, the
patient places both arms on the table to provide upper
body symmetry and to support the arm against the pull
of gravity while he actively initiates lower body anterior,
posterior, or lateral movement patterns. The position of
sitting with arm support provides a practice that links
trunk movements with shoulder movements.
280 SECTION II NEUROLOGIC CONSIDERATIONS

A B

Figure 9-9 A, Patient with right hemiplegia lifting an arm forward in a pattern of shoulder elevation, humeral internal
rotation, and abduction with elbow flexion. B, Practicing simple, arm-trunk linked movement with a cane, which allows self-
initiated assisted practice with the demands of the task and with the cane limiting shoulder internal rotation and abduction.

For example, as the patient initiates a lower body
posterior weight shift, the spine flexes and the scapula
abducts. As the body moves away from the arm, the arm
moves into increased shoulder flexion and elbow exten-
sion. Conversely, as the patient initiates a lower body
anterior weight shift, the upper body follows the forward
movement of the pelvis and trunk, and the scapula
adducts to neutral. As the body moves closer to the table,
the arm moves into less shoulder flexion and the elbow
flexion increases (Figure 9-13, A,B).
As trunk control increases, the demands of the tech-
nique are increased to activate arm muscles. The patient
is helped to learn how to depress the arm into a surface
for the purpose of using the arm to assist in stabilizing
objects, such as books or papers. As control increases,
patients can use this technique to increase force pro-
duction by using the arm to push against the table and
actively assist the trunk movements. As control increases
further, the patient can produce increased force by using
the arm to help push up from the arm of a chair from a
sitting position to standing.
Additional Interventions. Researchers are pre-
sently conducting multicenter studies to investigate the
efficacy of a technique that restrains the use of the unaf-
fected arm to force the affected arm to function. This
technique is based on the belief that treatment must be
intensive (up to 7 hr/day of supervised therapy and use
of the restraint during waking hours 4 hr/day for 14
days) and that people with stroke “learn” not to use their
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA 281

A B

Figure 9-10 A, Grasping cane with wrist extension. B, Practicing active shoulder flexion and elbow extension with
forward reach. Continued

affected arm. From our clinical experience, we believe
the learned nonuse may stem from emphasis in the
past on “inhibition” of spasticity—with little or no focus
on self-initiated active arm movements, the difficulty of
attempting to use the arm in the presence of sensory
deficits, and the tendency for patients to “wait” for
movement return to occur. The “forced-use” protocol has
high recovery inclusion criteria. The individual with a
stroke must be able to move their shoulder and elbow
and, more relevantly, must have 20° of wrist extension
and 10° of finger extension. The wrist and finger move-
ment criteria exclude most of the stroke survivors who
cannot use their arm. Preliminary results imply that it
may not be the sling or glove that makes the regimen
effective, but the intensity of treatment.16 Van der Lee
reported that traditional therapy in the control group
was as effective as constraint therapy in increasing func-
tional arm use in chronic stroke patients except for the
subgroup with sensory loss.14 The important message for
therapists from this new research is that the arm has
great potential for functional recovery and we must
guard against “learned nonuse.”
Functional Electrical Stimulation
Therapists have used functional electrical stimulation
with persons poststroke to promote muscle strength and
to decrease shoulder subluxation, spasticity, and pain. It
has also been used to minimize the secondary problems
of muscle atrophy and shortening that occurs because of
nonuse. While functional electrical stimulation (FES)
282 SECTION II NEUROLOGIC CONSIDERATIONS
C Electromyographic biofeedback is thought to improve
Figure 9-10, cont’d. C, Practicing active shoul-
der flexion and elbow extension with lateral reach.
is shown to increase force production in muscles after
treatment, there is little evidence that results can be sus-
tained and there is no evidence linking improvement in
force production at either the wrist and hand, or the
shoulder, to increased functional performance.50,51
Chantraine, in a large, random-controlled trial,
reported that FES provided a significant increase in pain
relief, subluxation reduction, and motor function at 6
months. The treatment effect gradually lessened at 12
and 24 months.52 Linn used FES to prevent subluxation
and found that while the treatment group displayed less
shoulder subluxation, there was no significant difference
between groups upon follow-up.53 Faghri found that
although the experimental group displayed increased
arm function and electromyogram (EMG) activity in
the deltoid muscle, the differences were not significant
upon follow-up.51 The lack of sustained results upon
follow-up is reflective of the differences in use of modal-
ity, length of treatment time, and length of time until
follow-up.
Newer uses of FES include low intensity stimulation,
with voluntary motor activity54 and surface FES systems
that are embedded in a mesh glove or in a polypropy-
lene wrist splint (HandMaster).55,56 These external
systems are used as adjuncts to conventional therapy and
allow grasp and release. There is no evidence yet of their
long-term effectiveness in people with hemiplegia.
Electromyographic Biofeedback
force production and muscle sequencing by providing
the patient with information about subthreshold muscle
activity that is present but insufficient to produce joint
movement.57 EMG biofeedback is used to help the
patient learn to turn a muscle on or off and to increase
motor unit firing through visual and auditory feedback.
Therapists often use EMG biofeedback initially to acti-
vate basic movement patterns and gradually introduce
functional practice patterns.
Interventions for
Musculoskeletal Impairments
Subluxation. If subluxation is present, interven-
tion must be preceded by careful examination and
manual reduction of the subluxation. Therapists then
begin the process of reeducating control in the trunk and
shoulder girdle to help maintain glenohumeral joint
integrity. Proper support of the shoulder girdle during
walking or prolonged periods of sitting is important in
the early phase of recovery to prevent or minimize
stretch on the joint capsule.
Proper examination of subluxation includes a
description of:
1. The exact position of the scapula, humeral head,
rib cage, and spine
2. Thoracic mobility and glenohumeral range of
motion
3. Degree and location of force production and
movement control
4. Presence and pattern of posturing at rest and
during movement
This examination will indicate the cause of the sub-
luxation, and appropriate intervention can then begin.
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA 283

A B

Figure 9-11 A and B, Active assistive movement of the right arm using the left arm as a guide.
Continued

A summary of the intervention therapy includes the
following:
1. Manual assistance to align and support the scapula
on the thorax and to help keep the humerus in the
glenoid fossa during self-initiated, trunk-arm linked
movements both in weight bearing and nonweight
bearing
2. Increased movement control in shoulder girdle
muscle groups
3. Lengthening of shortened muscles around the
shoulder girdle
4. Maintenance of pain-free ROM with careful
attention to scapulohumeral rhythm
5. Prevention of stretching of the shoulder capsule
through appropriate support
Proper support can be achieved through the use of
lapboards, tables, armrest, or pillows when sitting;
self-assisted motion during functional activities; and
weight-bearing support on the forearm or hand.
Shoulder Subluxation Supports. The shoulder
should be supported in the early stage of recovery to
prevent stretching of the capsule and/or to eliminate
pain. In the 1950s and 1960s, orthopedic slings were
given to patients with hemiplegia (Figure 9-14, A).
These slings held the humerus against the body in inter-
nal rotation and kept the elbow in flexion. The arm was
immobilized and the patient was unable to see the arm
or try to use the arm even for support. In the 1970s and
1980s, alternative slings were produced, including the
284 SECTION II NEUROLOGIC CONSIDERATIONS

C D

Figure 9-11, cont’d. C, The therapist limits degrees of freedom of the shoulder in preparation for active, self-
initiated movement of the elbow, wrist, and hand. D, The patient practices bilateral distal movements with a towel.

Rolyan hemi-arm sling,* the shoulder saddle sling,† and
variations on the axillary support‡ as described by
Bobath.19
*Rolyan hemi-arm sling (Sammons Preston Rolyan; Bolingbrook,
Ill.) This sling has a humeral cuff and a figure-eight suspension.
It provides moderate support to the humerus and allows variations
in elbow position. The arm is free to be moved and used for
support (see Figure 9-14, B).
†
Shoulder saddle sling (Sammons Preston Rolyan; Bolingbrook,
Ill.): This sling has a forearm cuff and a shoulder saddle suspen-
sion. It provides maximal support to the entire arm and prevents
the arm from “banging” around during functional or sports activ-
ities. This sling is excellent for the weak limb with pain. It allows
moderate humeral and elbow movement (see Figure 9-14, C).
‡
Axillary support: This support elevates the scapula and provides
minimal inferior support for the humerus. It should not be used
in patients with an elevated scapula. It has been criticized for
placing pressure on the brachial plexus when inappropriately
donned (see Figure 9-14, D).
Because no device is available that upwardly rotates
the scapula, no shoulder support will correct gleno-
humeral joint subluxation. Shoulder supports will help
support and/or maintain positioning on the rib cage
once the correction has been made. Shoulder supports
also prevent the weak arm from banging against the
body during functional activities, decreasing shoulder
joint pain and minimizing bruising. They also help to
relieve downward traction of the shoulder capsule caused
by the weight of the arm.
Therapy clinics should have different types of
shoulder supports available and should evaluate which
support provides the best protection for each patient.
Pain. The causes and intervention of shoulder
pain were described in detail earlier in the chapter. To
summarize, interventions for the painful shoulder and
arm should include:
 Figure 9-12 Weight-bearing positions for the upper extremity.
A, Left hemiplegia: rolling onto affected side. B, Left hemiplegia: moving onto
affected forearm. C, Left hemiplegia: supporting forearm on table.

Figure 9-13 A, As the patient initiates a lower body posterior weight shift, the spine flexes and the scapula abducts. As
the body moves away from the arm, the arm moves into increased shoulder flexion and elbow extension. B, The patient initiates
a lower body anterior weight shift, the upper body follows the forward movement of the pelvis and trunk, and the scapula adducts
to neutral. As the body moves closer to the table, the arm moves into less shoulder flexion and the elbow flexion increases.
286 SECTION II NEUROLOGIC CONSIDERATIONS

A C

B D

Figure 9-14 A, Orthopedic sling. B, Rolyan hemi-arm sling. C, Shoulder saddle sling. D, Axillary support.

1. Immediate cessation of any movement or activity
that causes or increases pain, including exercise
routines
2. Reduction or elimination of edema
3. Reestablishment of appropriate alignment of the
shoulder girdle/upper trunk complex either
through manual assistance from the therapist or
through self-initiated movements in weight
bearing or with assistance from carefully selected
objects
4. Reeducation of inactive muscle groups
5. A graded program of functional arm usage
Loss of range of motion. Loss of ROM at the
shoulder can lead to decreased arm mobility, decreased
arm function, and impaired balance in people with
CHAPTER 9 THE SHOULDER IN HEMIPLEGIA
hemiplegia. Although classic stretching procedures
(nonweight bearing) are often used to lengthen short-
ened shoulder muscles, self-initiated active patterns of
functional stretching through weight bearing are often
more effective. Persistent muscle activity, or hypertonic-
ity, may block active movements from occurring. The
inhibition of this muscle activity does not increase
in functional movement. However, the presence and
distribution of hypertonicity need to be considered
during an assessment of active movement control
because it may be an indicator of the person’s ability to
control the trunk and leg in transitional movements
and it may be an indicator of movement control. If
ignored, it may result in persistent patterns of soft tissue
tightness.
Summary
This chapter has reviewed the primary and secondary
impairments that interfere with functional shoulder and
arm movement in people with hemiplegia from stroke,
tumor, or brain injury. Atypical movement patterns arise
from an interaction of loss of central force production,
altered motor control, impaired sensation, and tonal
changes. The common secondary impairments of
shoulder subluxation and pain, and their relationship to
these atypical movements, were highlighted. Interven-
tion strategies must be based on an understanding of the
relationships between neuromuscular and musculoskele-
tal impairments and on the connection between impair-
ments and functional movement. The success of
intervention programs is dependent upon the clinician’s
systematic examination and problem solving skills. This
is especially true for intervention strategies to restore
functional movement in the arm in people with
hemiplegia.
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 10
Impingement Syndrome
and Impingement-Related
Instability
Bruce H. Greenfield
Robert A. Donatelli
Lori Thein Brody

I mpingement syndrome historically has been con-

sidered to be a continuum of a single pathologic
condition involving the subacromial soft tissue.1 As
our understanding of this complex problem has devel-
oped, the simple continuum model has become less
will facilitate an understanding of the factors that result
in abnormalities.

effective in guiding appropriate treatment. The purpose
of this chapter is to provide the reader with more precise
classifications of impingement syndrome and the
impingement stability complex to provide more efficient
and effective treatment procedures that address the
primary abnormality.
Compressive Cuff Disease
Impingement syndrome, or compressive cuff disease,
was originally described by Neer1 as mechanical
impingement of the supraspinatus and the long head of
the biceps tendon underneath the acromial arch.1,2 The
primary pathologic condition involves a bursal surface
lesion. The condition is often classified as primary
impingement syndrome—in contrast to secondary
impingement, which involves primary instability and is
discussed later. Because primary impingement involves
a spectrum of lesions of tissue in the suprahumeral space,
a working knowledge of its structural interrelationships
Suprahumeral Space
The suprahumeral space, also known as the subacromial
space or supraspinatus outlet, is formed by the superior
aspect of the humeral head below and the inferior
surface of the acromion, the acromioclavicular joint,
and the coracoacromial ligament above (Figure 10-1).
Within the subacromial space are the rotator cuff
tendons (supraspinatus, infraspinatus, and teres minor),
the long head of the biceps, and the subacromial-
subdeltoid bursa. The subacromial distance is quite
small, and has been measured on radiographs and used
as an indicator for proximal or superior humeral sub-
luxation because of rotator cuff abnormality. The dis-
tance was found to be between 9 and 10 mm in 175
asymptomatic shoulders. A distance of less than 6 mm
was considered indicative of rotator cuff disease.4,5
Coracohumeral Space
A second space for potential primary impingement has
been identified by Patte6 as the so-called coracohumeral
compartment. The coracohumeral space is the space

291
292 SECTION III SPECIAL CONSIDERATIONS
between the tuberosity and the lesser tubercle of the
humerus. Within the confines of this space are situated
the subscapularis bursa, subscapularis tendon, and sub-
coracoid bursa. In the resting position with the arm
in medial rotation, the distance between the tip of the
coracoid and the most prominent part of the lesser
tuberosity has been measured at approximately 8.7 mm
in healthy shoulders and 6.8 mm in the presence of sub-
coracoid impingement.7 A decrease in the size of the
subcoracoid space, caused by a fracture trauma to the
tip of the coracoid process, has been implicated in pri-
mary subcoracoid impingement.6 The clinician should
be aware of this diagnosis as a potential differential of
primary impingement, and in those patients who have
not responded to conservative treatment, particularly
after acromioplasty.
Because of the narrow confines of the subacromial
space, a small margin of error exists to allow for normal
excursion of the suprahumeral tissue to pass safely
under the acromial process. Several factors have
been implicated in abnormal narrowing of the sub-
acromial space and the resulting primary impingement
syndrome.8-15
A
CAL
GT
B
Factors Related
to Pathological Condition
For purposes of description, factors related to this
pathologic condition can be divided into intrinsic and
extrinsic factors. Intrinsic factors directly involve the
subacromial space and include changes in vascularity of
the rotator cuff, degeneration, and anatomic or bony
anomalies. Extrinsic factors include muscle imbalances
and motor control problems of the rotator cuff and
parascapular muscles; functional arc of movement;
postural changes; and precipitating factors, including
training errors and occupational or environmental
hazards.15-23 Because several of these problems can co-
exist with primary impingement, isolating a specific
factor as a cause is difficult. More likely, the cause of
primary impingement has multiple factors. All factors
may be important, and the key factor in any case
depends on the individual circumstances.
Extrinsic Factors
According to Neer,1 the anteroinferior one third of the
acromion is thought to be the causative factor in
mechanical wear of the rotator cuff through a process
C Figure 10-1 The subacromial
space. A, Acromion; GT, greater
tuberosity; CAL, coracoacromial
ligament. B, (Long head) biceps.
C, Coracoid process.
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY 293

called impingement. Neer believes that the supraspina-
tus and long head of the biceps are subjected to repeated
compression when the arm is raised in forward flexion.
Neer called this the functional arc of elevation of the arm
(Figure 10-2). Arthrokinematic movement dictates that
forward flexion of the humerus results in concomitant
internal rotation of the humeral head.24 The result is
that the suprahumeral tissue is effectively driven directly
under the anteroinferior one third of the acromion. The
coracoacromial ligament and acromioclavicular joint can
also be involved in impingement during this functional
movement. The Neer impingement test involves forced
forward flexion with internal rotation of the humerus to
simulate movement in the functional arc and to provoke
pain in symptomatic individuals (Figure 10-3). By
focusing on the anterior acromion as the source of
)
ne
pla
lar
pu
ca
” (s
on
impingement rather than the entire acromion, Neer
helped target the technique and approach to acromial
decompression to the area of the anteroinferior
acromion, thus avoiding excision of the lateral acromion
and significant deltoid muscle morbidity. The overall
result after acromial decompression or anterior acromio-
plasty is an accelerated and aggressive rehabilitation
program.
Scapula and Glenohumeral Muscle Imbalances.
Control of the scapula and humerus is primarily dictated
by a series of muscle force couples.25 A force couple is two
forces of equal magnitude, but in opposite direction, that
produce rotation on a body.26 The scapula force couple
is formed by the upper fibers of the trapezius muscle,
the levator scapulae muscle, and the upper fibers of the

30° – 40°
ati
lev
“Flexion” (sagittal plane)

“E

“Abduction” (coronal plane)

A B
Figure 10-2 Functional arc. A, The functional arc of elevation occurs from the sagittal to the plane of the
scapula. B, Superior view of anterior acromion. Elevation in the functional arc internally rotates the humerus under the
anteroinferior one third of the acromion.
294 SECTION III SPECIAL CONSIDERATIONS
Figure 10-3 Neer’s impingement test. Forceful ele-
vation of the humerus with internal rotation results in
impingement of the rotator cuff tendons and long head of
the biceps underneath the anteroinferior acromion. A
positive result is provocation of subacromial pain.
serratus anterior muscle. The lower portion of the force
couple is formed by the lower fibers of the trapezius
muscle and the lower fibers of the serratus anterior
muscle.3 Simultaneous contraction of these muscles pro-
duces a smooth rhythmic motion to rotate and protract
the scapula along the posterior thorax during elevation
of the arm. The scapula functions to provide a stable base
of support for the rotating humerus to allow the humeral
head to maintain its normal pathway or rotation along
the glenoid.27 Parascapular weakness of the serratus
anterior and the trapezius muscles can limit the upward
rotation of the scapula, resulting in an unstable base of
support for the humerus, and may result in inefficient
action of the rotator cuff muscles. In addition, the
acromion may not sufficiently elevate to provide ade-
quate clearance of the greater tuberosity of the humerus.
Furthermore, weakness of the scapular retractors may
cause increased protraction of the scapula, narrowing the
space under the acromion and facilitating an impinge-
ment of suprahumeral structures.
The coordinated action of the scapula muscles is
therefore believed by most clinicians to be indispen-
sable to overall normal shoulder function, and current
treatment programs are designed to restore normal
parascapular muscle control. However, objective data in
assessing changes in parascapular muscle control and
position are limited at best, and in some cases equivo-
cal.16,20,21 The best known test, developed by Kibler, is
known as the lateral scapula slide test, and measures the
ability of the scapular stabilizers to control the medial
border of the scapula during three positions of the
limb.20 Kibler found an increase of 1 cm or more in two
of the three positions correlated with shoulder impinge-
ment and instability in baseball players.
Glenohumeral Joint: Primary Instability. Budoff
and associates28 describe the etiology of impingement as
a primary instability and with secondary impingement.
The sequence of events that cause the instability is
described as glenohumeral muscle imbalances. The
supraspinatus is a small and relatively weak muscle in a
key position and is susceptible to overuse injury. When
repetitive eccentric overload occurs to the rotator cuff
muscles, weakness of the musculotendinous unit results
in damage to the tendon. Weak, fatigued, or injured
rotator cuff muscles, infraspinatus, teres minor, sub-
scapularis, are unable to oppose the superior pull of the
deltoid muscle.
The inferior- and horizontal-directed rotator cuff
muscle force vectors maintain the humeral head within
the shallow glenoid, thereby resisting the upward shear
of the deltoid generated during active elevation of the
arm.25 The result is that the rotator cuff muscles in effect
“steer” the humeral head along the glenoid during move-
ment of the humerus.29 The combination of the result-
ant contractions of the rotator cuff muscles and the
deltoid produces the glenohumeral joint force couple
(Figure 10-4). With an intact and normally functioning
rotator cuff muscle group, the center of the humeral
head is restrained in a very small arc of motion (within
3 mm) along the glenoid fossa. Poppen and Walker24 and
Weiner and MacNab5 found that in the presence of
rotator cuff disease, the arc of motion of the humeral
head increases to 6 mm or greater. The loss of the rotator
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY
RESULTANT
Infraspinatus
Figure 10-4 Glenohumeral force couple.
and teres minor
The resultant force of the rotator cuff muscles
results in compression and inferior glide of the
humeral head during elevation of the arm.
cuff force couple results in the superior migration of the
humeral head, which causes the greater tuberosity and
the rotator cuff to come in contact with the undersur-
face of the acromion and the coracoacromial ligament.
The repetitive contact against the acromion results in
reactive and degenerative osseous changes, such as
osteophytic spurring to the undersurface of the
acromion and/or traction spurs, which may form at the
anterior medial corner of the acromion. The traction
spur may easily be mistaken for an abnormal acromial
hook, or type III acromion.28 Therefore the superior
migration of the humerus can result in repetitive
impingement of the suprahumeral soft tissue. The result
is an inflammatory cascade and rotator cuff disease.
Anterior and Posterior Glenoid Impingement. Jobe30
describes the pathomechanics of posterior-superior
labrum impingement. Overhead-throwing athletes are
susceptible to forces that may result in impingement of
the head of the humerus against the posterior superior
labrum. During throwing, the glenohumeral joint is
between 60° and 90° of abduction, maximal external
rotation, and horizontal extension. The head of the
humerus is angulated in a posterior-superior direction
relative to the glenoid. In addition, the greater tuberos-
295
Supraspinatus
Del
is
toid
ular
scap
Sub
ity moves posteriorly, secondary to external rotation of
the humeral head. Angulation of the humeral head on
the glenoid is limited by the inferior glenohumeral lig-
ament and the subscapularis. The cause of impingement
occurs from hyperangulation of the humeral head to the
glenoid secondary to lack of resistance from a poorly
conditioned and fatigued subscapularis muscle. The sub-
scapularis is unable to control the excessive external
rotation and extension angulation of the humeral head.
Angulation, as opposed to translation, places an uneven
stretch to the capsule. The failure of the capsule results
from overstretching and instability of the anterior
capsule causing subluxations. The deep surface of the
supraspinatus is impinged between the humeral head
and the posterior-superior labrum.
Gerber and associates31 describe impingement of the
deep surface of the subscapularis tendon and the cora-
cohumeral ligaments (reflection pulley) on the anterior-
superior glenoid rim. With increasing internal rotation,
the lesser tuberosity and biceps tendon are brought close
to the anterior superior glenoid rim. Between 100° and
90° of shoulder flexion and full internal rotation, the
subscapularis, the biceps tendon, the superior and
middle glenohumeral ligaments are impinging on the
anterior glenoid labrum and rim. Patients involved in
296 SECTION III SPECIAL CONSIDERATIONS
overhead movements, which are typical of racquet sports
and overhead-throwing athletes, are more susceptible to
anterior-superior glenoid rim impingement. Eccentric
overload of the glenohumeral external rotator is
common in overhead-throwing athletes. Poorly condi-
tioned and fatigued infraspinatus and teres minor
muscles result in excessive internal rotation of the
humerus. In the final phase of pitching, the shoulder is
in flexion and internal rotation. Excessive internal rota-
tion of the humerus in the flexed position between 100°
and 90° could result in impingement of the above soft
tissue structures upon the anterior-superior glenoid rim.
Postural Changes. Changes in posture in the upper
quarter or quadrant of the body have been implicated as
a predisposing factor in primary impingement syn-
drome.15,17,19 A common postural change associated with
shoulder problems is the forward head and rounded
shoulder posture.17,19 Components of this posture
include an increased thoracic kyphosis, protracted and
downwardly rotated scapulae, internal rotation of the
glenohumeral joints, increased anterior cervical spine
inclination, and backward bending at the atlanto-
occipital joint. Kendall and associates,18 Kendall and
McCreary,19 and Janda17 indicated sequelae that accom-
pany this posture that result in muscle imbalances, which
putatively alter the force couple mechanisms about the
shoulder with potential pathomechanical changes. Bio-
chemical and clinical studies by Diveta and associates,21
Culham and Peat,32 Greenfield and colleagues,16
Griegel-Morris and associates,15 and Kibler20 have
evaluated postural variables in shoulder patients and
found mixed results in correlating postural changes with
muscle imbalances and shoulder dysfunction. Differ-
ences in methodologies and different operational defini-
tions of postural variables may account for the equivocal
results correlating posture with injury. Continued exam-
ination of posture and function is important to deter-
mine the relevance of posture in the overall evaluation
and treatment of shoulder dysfunction.
Precipitating Factors. Precipitating factors to injury
are any activities that involve repetitive use of the arm,
usually overhead or above shoulder level, that result in
subacromial impingement.22,23 The baseball pitcher who
pitches a nine inning game early in the season, the
retiree who decides to spend the weekend painting her
house, and the stock clerk who works two 12-hour shifts
to stock inventory are examples of individuals with
precipitating factors that result in overuse of the shoul-
der. A caveat to practicing clinicians is to identify these
factors early and to modify activities appropriate to the
stage of the pathologic condition of impingement and
degree of clinical reactivity.
Intrinsic Factors
The primary intrinsic factors can be divided into vascu-
lar, degenerative, and anatomic. The original significance
of rotator cuff tendon vascularity was described by
Codman.12 Codman referred to a critical zone in which
a rupture occurred in the supraspinatus. This zone was
located approximately 1 cm medial to the insertion of
the tendon. Moseley and Goldie33 noted that the anas-
tomosis of the osseous and tendinous vessels in the
supraspinatus occurred at this site. Rothman and Parke10
believed that this location was relatively avascular, a con-
dition intensified by aging. Microinjection studies of
normal shoulders in cadavers have shown an area of
decreased vascularity within the tendinous portion of the
supraspinatus tendon. Rathbun and Macnab9 noted that
the critical zone of the rotator cuff had an adequate
blood supply when the vessels were injected with the
arm in the abducted position, but this area was hypo-
vascular when the injection was given with the arm in
the adducted position. The authors propose a hypothe-
sis of transient hypovascularity in the critical zone as a
result of vessels being “wrung out” when the arm was in
the adducted position. The authors indicated that most
degenerative rotator cuff tears occur within this zone,
suggesting that hypovascularity of the supraspinatus
tendon may play a role in the pathogenesis of rotator
cuff tears. Lohr and Uhthoff 34 found that the area of
hypovascularity in the critical zone was more pro-
nounced along the articular than the bursal surface of
the supraspinatus tendon and within the site of early
degeneration. Others have disputed the hypovascularity
findings.35,36 A laser Doppler study of the rotator cuff
vasculature showed substantial blood flow in the region
of the critical zone, and increased blood flow at the
margins of rotator cuff tears.36 Although there is not
yet any definitive scientific evidence of a direct cause
and effect relationship, the finding seems to indicate a
vascular predisposition to the pathogenesis of rotator
cuff disease and impingement.
Degeneration. Evidence indicates a natural age-
related degeneration of the rotator cuff tendons.
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY 297

Codman12 noted that rotator cuff tendon rupture in
older patients normally occurred bilaterally and in the
presence of preexisting tendon degeneration. Uhthoff
and associates13 and Ozaki and colleagues14 found inser-
tional tendinopathy or preexisting tendon degeneration
in human specimens. These changes included histologic
changes in the arrangement of tendon fibers, fiber dis-
ruption at their insertion site, and microcysts and
osteopenia along the insertion site. These changes found
along the articular side (humeral side) were not usually
associated with changes in the acromial process.
Anatomic Anomalies. Morrison and Bigliani8
studied the shape of the anteroinferior acromion in
anatomic specimens and in patients. The authors
identified three types of acromions: type I (flat), type II
(curved), and type III (hooked) (Figure 10-5). In their
anatomic specimen studies, 70% of rotator cuff tears
were associated with type II or III acromions. None
had type I acromions. Although no causal relationship
between the shape of the acromion and rotator cuff tears
or impingement can be concluded, the clinical findings
support Neer’s theory of impingement occurring prima-
rily along the anteroinferior acromion.
Stages of Pathology
and Principles of Treatment
Program design for conservative management of
primary impingement syndrome is predicated on a

A B C
Figure 10-5 Three types of acromions. A, Type I, flat. B, Type II, curved. C, Type III, hooked.
298 SECTION III SPECIAL CONSIDERATIONS

problem-solving approach. This approach necessitates a
thorough evaluation to clarify the nature and extent of
the pathologic condition, the stage of reactivity, under-
lying dysfunction—including extrinsic problems to for-
mulate a physical therapy diagnosis—and other factors
that may affect treatment planning and outcome (for
example, age of the patient, motivation, and underlying
disease). Classifying the pathologic condition based on
the progression described by Neer can be correlated with
clinical signs and symptoms and can provide a basic
framework for preliminary treatment planning and pro-
gression. All program designs should be divided into
treatment phases that include specific goals and criteria
for progression, and continual reevaluation of both
subjective and objective findings. Table 10-1 presents a
summary of the stages of pathologic conditions
described by Neer. The stages are presented separately,
but represent a continuum of abnormality that in some
cases will overlap in a particular patient.
Stage I Impingement
Stage I of impingement is characterized by edema and
hemorrhage (inflammation) of the rotator cuff and
suprahumeral tissue. The patient is usually less than 25
years of age, and normally there is a precipitating factor
of overuse of the shoulder. The clinical symptoms
include pain along the anterior and lateral aspect of the
shoulder, which when acute or reactive will extend below
the elbow. The pain is usually described as a deep, dull
ache, with sharp subacromial pain during elevation of
the limb. The patient has full active and passive range
of motion (ROM), a painful arc (pain between 60° to
90° and 120° of elevation of the limb), and an abnormal
impingement sign. Muscle strength is usually normal for
the abductors and external rotators of the glenohumeral
joint, but can be painful and weak in an acute state.
Palpation elicits subacromial tenderness usually along
the greater tubercle and bicipital groove. Muscle spasms
are often present along the ipsilateral upper trapezius,
levator scapulae, and subscapularis muscles.
Principles of Treatment. Principles of treatment for
stage I are based on the stage of clinical reactivity and
associated dysfunction. For an acute presentation, goals
of treatment are to reduce and eliminate inflammation,
increase the patient’s awareness of impingement syn-
drome, improve proximal (parascapular) muscle control,
and prevent muscle atrophy or weakness because of
disuse at the glenohumeral joint. The patient should be
instructed to rest from activity, but not function, and to
perform all activities in front of the shoulder and below
shoulder level. Forceful active elevation above shoulder
level can produce a painful arc and impingement and
perpetuate the inflammatory response. The patient

Table 10-1

NEER STAGES OF IMPINGEMENT

Stages Clinical Presentation Treatment Principles

Stage I Subacromial pain/tenderness Reduce and eliminate inflammation

Age: Less than 25 years
Pathologic condition: Edema and
hemorrhage
Stage II
Age: 25 to 40 years
Pathologic condition: Tendinitis/
bursitis and fibrosis
Stage III
Age: over 40 years
Pathologic condition: Bone spurs
and tendon disruption
Painful/arc Patient education
Positive impingement/Neer’s test Restore proximal control (parascapular
Strong and painful for resisted muscular control)
abduction and external rotation
Add: Capsular pattern of limitation Reestablish glenohumeral capsular
at glenohumeral joint mobility
Add: Weakness abduction and Based on size of tear
external rotation, “squaring” of
acromion
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY 299

would do well to take an oral antiinflammatory medi- Stage II Impingement

cine (nonsteroidal), in conjunction with antiinflamma- Stage II impingement is characterized by fibrosis of the
tory modalities including ice, interferential stimulation, glenohumeral capsule and subacromial bursa and ten-
or pulsed or low-intensity ultrasound.37 Soft tissue dinitis of the involved tendons. The condition is nor-
work and stretching should be used to alleviate muscle mally seen in patients between 20 and 40 years old. The
spasms. Exercise, including manual resistance, can be clinical presentation can be similar to that of stage I,
used early to facilitate scapular parascapular muscle except that the patient has loss of active and passive
control without further aggravation of the suprahumeral ROM because of the capsular fibrosis. The loss of ROM
tissue (Figure 10-6). normally appears in the so-called capsular pattern
As reactivity reduces with elimination of rest pain described by Cyriax,38 as significant loss of external rota-
and pain below the elbow, and with elimination of tion and abduction, with less loss of internal rotation.
painful arc and subacromial tenderness, the patient pro-
gresses into a dynamic strengthening program that Principles of Treatment. The principles of treat-
emphasizes reestablishment of the force couple mecha- ment are similar to those of stage I with the exception
nisms at both the scapulothoracic junction and gleno- that a major goal is to restore full active and passive
humeral joint. Table 10-2 lists exercises that are ROM to prevent further impingement and tissue
normally effective at this stage. Emphasis should in- damage. Cofield and Simonet39 described how patients
clude high repetitions (3 to 5 sets of 15 repetitions for with adhesive capsulitis of the glenohumeral joint
each exercise), multiple sessions of 3 to 4 daily, working resulted in subacromial impingement. Specifically, pos-
initially in a pain-free range, and using both concentric terior capsule tightness caused the humeral head to roll
and eccentric muscle contraction. Exercises are slowly forward and superiorly into the subacromial arch and
increased to 7 to 10 different movement patterns to
isolate different muscle groups. Neer suggests that a
patient should continue this conservative approach for Table 10-2
several months before considering surgical treatment. If
the patient is an athlete, as signs and symptoms permit, SHOULDER-STRENGTHENING EXERCISES
an additional program of sport-specific exercises and
functional training should be incorporated into the Muscle Exercise
program.
Supraspinatus Prone horizontal abduction
Scaption in internal rotation
Infraspinatus Prone horizontal abduction in
external rotation
Teres minor Prone horizontal abduction in
external rotation
Subscapularis Scaption in internal rotation
Military press with dumbbell
Anterior deltoid Scaption in internal/external rotation
Posterior deltoid Prone extension
Upper trapezius Rowing (prone with dumbbell)
Shrug
Middle trapezius Prone horizontal abduction in neutral
position
Lower trapezius Prone horizontal abduction in
external rotation
Rhomboids Rowing (prone with dumbbell)
Prone horizontal abduction in neutral
Figure 10-6 Manual technique illustrating resisted position
posterior scapular depression to facilitate early recruitment of Serratus anterior Pushup with a plus
parascapular muscles.
300 SECTION III SPECIAL CONSIDERATIONS

anteroinferior acromion. Subsequent treatment should do relatively well with limited functional goals. The
be directed at restoring capsular extensibility to allow the patient progresses similarly to the previous treatment
humeral head to attain its normal center of rotation. principles. If treatment is ineffective and the patient
Several manual techniques described in Chapter 13 are continues to have pain and inability to raise the arm
effective for mobilizing the glenohumeral joint capsule. overhead, surgical options include rotator cuff debride-
The force and direction of the mobilizing force should ment and anterior acromioplasty, or a mini-open repair.
be based on the stage of reactivity and clinical mobility For those with large and massive tears, surgery is usually
testing. Treatment time in patients with a stage II patho- the most effective option followed by an extensive reha-
logic condition is longer than with stage I, and the prog- bilitation program incorporating the basic treatment
nosis and functional outcome may be more limited. principles of impingement syndrome and adherence to
soft tissue healing guidelines.
Stage III Impingement
Stage III impingement is the most difficult to treat con-
servatively and is characterized by disruption of the
rotator cuff tendons. The patient is normally older than
40 years. Clinically, muscle testing yields weakness, Table 10-3
usually for external rotation and abduction. Visual
observation indicates a “squaring” of the acromion, CLASSIFICATION OF ROTATOR CUFF TEAR BASED ON
which indicates atrophy of both the rotator cuff and DIAMETER
deltoid muscles. In significant tendon disruption, a
positive “drop-arm” or supraspinatus test will be Size Treatment Principles
present (Figure 10-7). 1 cm Conservative
1-3 cm Conservative/acromioplasty/débridement/
Principles of Treatment. Treatment principles are mini-open repair
based partly on the size and location of the tear (Table 3-5 cm Mini-open repair
10-3). Tears are classified by size, diameter, location, or 5 cm Open repair
topography.40,41 The small- and moderate-size tears can

Figure 10-7 Supraspinatus test. The arm is

abducted with internal rotation (thumb down) in plane
of the scapula. The patient is asked to resist downward
pressure on abducted arm. A test is considered positive
if patient is unable to hold the arm against resistance.
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY 301

Case Study 1: Mr. S.A. Passive range of motion (PROM): Full and pain free
Primary Impingement in all planes of motion. Accessory motion testing of the
glenohumeral joint: normal mobility and symmetrical
This case represents a typical progression for a
with the uninvolved side.
patient who has symptoms of primary impingement
Muscle Testing
syndrome. Goals and treatment are based on some of
Resisted testing: Painful and strong for resisted
the principles of treatment discussed in the previous
shoulder abduction and external rotation.
sections.
Special Tests
GENERAL DEMOGRAPHICS
Positive Neer’s impingement test.
The patient is a 22-year-old Caucasian, English-
Tenderness
speaking male who comes to the clinic with a 1-week
Palpation: Tender greater tubercle.
history of right shoulder pain. He is right-hand
Physical Therapy Clinical Impression
dominant.
Based on presenting signs and symptoms, onset,
SOCIAL HISTORY
and patient’s age, the physical therapist classified a
Mr. S.A. is single with no children. He does not
stage I primary impingement. The stage of clinical reac-
smoke and drinks approximately twice per week.
tivity was early. The patient had pain to the elbow, was
EMPLOYMENT
unable to sleep on the involved side, had a painful arc,
He is as a construction worker.
pain with manual resistance, and a positive impingement
LIVING ENVIRONMENT
sign. Resisted testing and palpation seem to indicate
Mr. S.A. lives alone in an apartment on the first floor.
primary involvement of the supraspinatus muscle
GROWTH AND DEVELOPMENT
tendon.
He is a muscular young male; no external
TREATMENT PLAN
deformities.
Initial treatment goals were to reduce and eliminate
PAST MEDICAL HISTORY (PMH)
inflammation of the supraspinatus tendon, to educate
He has no significant history of injuries to his
the patient concerning his condition and helpful and
shoulder or neck and has no medical problems aside
harmful positions of the arm, and to improve para-
from seasonal allergies.
scapular muscle control (caused by scapular winging
History of Chief Complaint
and possible weakness of the serratus anterior muscle).
Mr. S.A. enjoys lifting weights. He had an overzeal-
The patient was instructed to maintain his arm below
ous workout the previous week and attempted to
shoulder level and in front of the shoulder to prevent
perform maximum resistance during all his exercises.
impingement and stretching of the tendon. He was also
Since then, the patient has reported right-anterior and
instructed not to lift weights. He was instructed to try
lateral-shoulder pain extending to his elbow. The pain is
to maintain his arm in partial abduction and in the
described as a dull ache and sharp during shoulder ele-
scapular plane to promote perfusion to the supraspina-
vation. He has difficulty sleeping on the right shoulder
tus tendon. Early scapular exercises included manual
at night.
resistance, simple shoulder shrugs, and scapular retrac-
Prior Treatment for this Condition
tion exercises (see Figure 10-6), and were used to
His family physician prescribed Motrin and referred
promote parascapular muscle control and coordination.
him for a trial of physical therapy with a diagnosis of
Ice and pulsed ultrasound were applied along the greater
right shoulder muscle strain.
tubercle to reduce inflammation and facilitate healing.
Structural Examination
Pulse ultrasound maintained a low intensity and pro-
Visual inspection reveals no signs of swelling or
duced an acoustical streaming effect for protein synthe-
ecchymosis.
sis and cellular migration. The frequency of application
Range of Motion
was 3 MHz because of the superficial penetration that
Active range of motion (AROM): Scapulohumeral
was required for the sound waves.
elevation in the scapular plane produced a painful arc
REEXAMINATION
between 90° and 120°; bilateral scapular winging was
The patient was seen for five sessions and improved
noted.
considerably. Reevaluation indicated subjective reduc-
302 SECTION III SPECIAL CONSIDERATIONS
tion in both the intensity and area of pain, the ability
to sleep on the right shoulder at night, elimination
of painful arc, and pain with resisted abduction and
external rotation.
Treatment goals were updated to facilitate dynamic
humeral head control and muscle endurance, and to
optimize parascapular muscle control. The patient was
instructed in a program of exercises (see Table 10-2) to
be performed with 2-lb weights for 3 sets of 8 repeti-
tions. He was instructed to exercise twice daily initially
and in a pain-free range. Every two sessions, he was to
increase 1 repetition per set to 20 repetitions for 3 sets.
Ice was to be used after exercises. He was instructed
not to perform other resistance exercises until he was
completely pain free.
SUMMARY
The patient continued this program for 1 month on
a home program and was checked periodically by the
physical therapist. He did quite well, and after 1 month
returned to full activity with the warning not to overdo
his weight lifting. The approach to this case was based
partially on correct classification of the pathologic con-
dition. Often in young, active individuals, an underlying
glenohumeral joint instability is present that necessitates
a slightly different approach and is reviewed in this
chapter.
Rotator Cuff Pathology
in the Athlete
As previously noted, rotator cuff disease or impingement
that results from glenohumeral joint instability is known
generally as secondary impingement. Differentiating
primary impingement from secondary impingement is
crucial in the proper management of the two general
conditions. Secondary impingement treated as primary
impingement will fail to resolve the underlying
abnormality (instability). The following sections review
the classification of secondary impingement—which
occurs primarily in the overhead-throwing athlete—the
related clinical signs and symptoms, and approaches to
treatment.
Classification
Rotator cuff abnormality in the athlete represents a con-
tinuum of problems that may co-exist, making the
primary diagnosis difficult. General classification of
rotator cuff abnormality in athletes includes tensile over-
load, compressive impingement (Neer’s classification),
instability, and acute traumatic tears. Meister and
Andrews42 classify rotator cuff disease as: (1) primary
compressive cuff disease, (2) instability with secondary
compressive disease, (3) primary tensile overload, (4)
secondary tensile overload, and (5) macrotraumatic
failure. Primary tensile overload is the result of deceler-
ation forces in the absence of instability, while second-
ary tensile overload is precipitated by underlying
instability. Neer’s classification of compressive impinge-
ment is also observed in the athletic population and has
been described earlier in this chapter. Compressive
rotator cuff disease can occur primarily or secondarily
associated with other shoulder dysfunction. Jobe and
associates43,44 described a four-level classification of the
impingement-instability complex, which focuses on
instability as the central process. This classification
includes: (1) pure impingement without instability,
(2) impingement with instability, (3) impingement with
multidirectional instability, and (4) pure anterior insta-
bility without impingement. Finally, athletes sustain
acute traumatic tears—a topic that will be addressed in
Chapter 12.
These problems occur principally in athletes involved
in overhead sports, such as swimmers, tennis players,
baseball and softball players, and volleyball players.
Although rotator cuff dysfunction is seen most fre-
quently in overhead sport athletes, individuals may have
the same pathologic condition as a result of work-related
activity. The same deceleration forces observed serving
in tennis can be found in various work environments.
Repetitive overhead hammering or other construction
activities produce problems similar to swimming or
throwing. The underlying mechanics, which result in
overuse, must be analyzed relative to the respective signs
and symptoms.
Primary Tensile Overload
Primary tensile overload can be defined as rotator cuff
failure under tensile loads. These tensile loads are pri-
marily the result of eccentric muscle contractions and are
associated with activities such as throwing. In this case,
the rotator cuff functions to decelerate the horizontal
adduction, internal rotation, anterior translation, and
distraction forces seen during deceleration.44 During the
early cocking phase of throwing, supraspinatus elec-
tromyography (EMG) has been shown to be 40% of the
maximum manual muscle test (MMT), with increases
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY
to 45% of the MMT during late cocking.45 Peak
infraspinatus and teres minor muscle activity has
been found in the late cocking and follow-through
phases of pitching.45,46 DiGiovine and associates47 found
that supraspinatus activity peaks in the early cocking
phase at 60% of the MMT and diminishes to 49% and
51% of the MMT during the late cocking and acceler-
ation phases, respectively. Infraspinatus activity peaked
at 74% of the MMT during late cocking while teres
minor activity was found to be 71% of the MMT during
late cocking and 84% of the MMT during deceleration.
Thus, repetitive throwing will put the rotator cuff at risk
for failure. Andrews and Angelo48 describe rotator cuff
tears in throwers located from the midsupraspinatus
posterior to the midinfraspinatus, consistent with the
deceleration function of these muscles. The mechanism
of primary tensile overload is repetitive microtrauma
during decelerative functions, resulting in fatigue and
failure of the dynamic stabilizers. In addition to the
rotator cuff ’s function in deceleration and abduction, the
supraspinatus, infraspinatus, and teres minor also func-
tion to stabilize the humeral head on the glenoid. This
is the dynamic component of shoulder stability, with
static stabilization provided by the labrum and capsu-
loligamentous structures. When the rotator cuff fatigues
as a result of repetitive overload, not only is the decel-
erative function affected, but the stabilization function
is also impaired. The result may be secondary overload
on the capsulolabral structures (relative instability)
and/or secondary compressive impingement. As pain
persists, subtle changes in movement patterns can exac-
erbate the problem. Gowan and associates45 studied the
EMG patterns in amateur baseball pitchers and com-
pared the patterns with those of professional pitchers.
The professional pitchers used the shoulder muscles
more efficiently than the amateurs, who used the rotator
cuff and biceps brachii muscles during the acceleration
phase.
Evaluation of the shoulder with primary tensile
rotator cuff dysfunction reveals a stable shoulder without
true compressive impingement. Resistive testing of
the rotator cuff will be painful and may be weak with
single or multiple repetition testing. Andrews and
Giduman47,49 describe the hallmark of primary tensile
cuff disease to be a partial “undersurface” rotator cuff
tear. This type of tear is described as an “inside-outside”
tear. Frequently, no signs of compressive impingement
are found at surgery.
303
The treatment principles are embedded in the knowl-
edge of the underlying pathologic condition, the healing
process of soft tissue, and functional demands of the
shoulder. Given the premise that primary tensile over-
load is the result of excessive eccentric muscle contrac-
tions and resultant rotator cuff fatigue, the focus of
rehabilitation should address these issues. Numerous
training techniques exist that challenge the rotator cuff
eccentrically. The therapist should be familiar with these
techniques and the muscle physiology of eccentric con-
tractions. The problem can be exacerbated if eccentric
work is initiated too vigorously in the early stages.
Failure of conservative measures may result in surgery to
debride the rotator cuff tear. Subacromial decompression
is rarely necessary because associated compressive cuff
disease is uncommon.42
Secondary Tensile Overload
Secondary tensile overload, like primary tensile over-
load, is defined as rotator cuff failure under tensile loads.
In this case, excessive rotator cuff loading is caused by
underlying instability. The subscapularis, supraspinatus,
infraspinatus, and teres minor function to compress the
humeral head into the glenoid, providing dynamic sta-
bility.46,50-52 This “double function” leads to early fatigue
failure, tendinitis, and possible secondary mechanical
impingement.53
The pathomechanics of secondary tensile overload
are related to the rotator cuff ’s role in dynamic stability.
In contrast to primary tensile overload, where relative
instability may occur as a result of rotator cuff fatigue,
secondary tensile overload results from the simultaneous
demands of deceleration and stabilization. Although
both demands are present and generally tolerated in the
normal shoulder, the unstable shoulder places an addi-
tional burden on the rotator cuff. Because the static sta-
bilizers are compromised, the rotator cuff is overloaded,
resulting in dysfunction and injury.
Evaluation of the shoulder with secondary tensile
overload is similar to that of primary tensile overload,
with the addition of underlying instability. Instability
can be unidirectional or multidirectional and is
evaluated with traditional instability testing. However,
the symptoms may be those of pain rather than
instability, and careful evaluation is necessary to
delineate the underlying abnormality. Impingement
signs may be positive if secondary compressive impinge-
ment co-exists. Arthroscopic findings demonstrate
304 SECTION III SPECIAL CONSIDERATIONS
instability and an associated undersurface rotator
cuff tear.
As with primary tensile overload, the treatment prin-
ciples should address the underlying pathologic condi-
tion. In this case, emphasis on dynamic stabilization will
be the focus. Again, supraspinatus, infraspinatus, and
teres minor strengthening will be of importance because
of their role in both eccentric deceleration and stabi-
lization. Additionally, the subscapularis should be
trained because of its role in opposing superior humeral
head translation and contribution to the rotator cuff
moment.51,54 Failure of conservative treatment may
necessitate surgical intervention. Stabilization proce-
dures and debridement of a partial rotator cuff tear are
the appropriate surgical measures to address the under-
lying pathologic condition.
Instability-Impingement Complex
The scheme of instability and associated impingement
noted by Jobe and associates43,44,55 uses a four-group
classification system, with instability as the central
theme. In the young athlete, participation in overhead
sports such as throwing, swimming, tennis, and volley-
ball requires large ranges, forces, and repetitions. This
results in microtrauma to the static and dynamic struc-
tures, laxity in the anterior capsule, anterior humeral
head subluxation, and posterior capsule tightness. This
has been described as the instability-impingement
complex (IIC) and can be represented by the following
scheme45:
Instability-Subluxation-Impingement-Rotator
Cuff Tear. Individuals with pure compressive rotator
cuff impingement whose examination findings include
positive impingement signs and negative apprehension
signs constitute Group 1. Older recreational athletes are
generally found in this group, while younger athletes are
rarely in group 1. Arthroscopic examination reveals a
stable shoulder with an undersurface rotator cuff tear
and associated subacromial bursitis. The labrum and
glenohumeral ligaments will be normal. Treatment prin-
ciples are based upon clinical examination findings, and
follow the general guidelines presented in Neer’s model
of compressive cuff disease.
Group 2 consists of individuals with impingement-
associated instability with labral and/or capsular injury,
instability, and secondary impingement. Findings
include positive impingement, apprehension and reloca-
tion signs and arthroscopic findings of instability, labral
damage, and an undersurface rotator cuff tear. However,
the instability findings are often so subtle, even under
anesthesia, that the underlying abnormality may be
overlooked. As with group 1 impingement, most
individuals will respond to a conservative program that
addresses the specific mobility, strength, and endurance
deficits. Recognition of the underlying instability is the
key to successful rehabilitation. In the event of failed
conservative treatment, surgical intervention to stabilize
the shoulder and debride any rotator cuff damage pro-
vides the best results. Isolated acromioplasty can exacer-
bate underlying instability.
Those individuals classified into group 3 have hyper-
elastic soft tissue resulting in anterior or multidirectional
instability and associated impingement. Hyperelasticity
as evidenced by joint hyperextension is the distinguish-
ing characteristic between groups 2 and 3. In this case
impingement, apprehension, and relocation signs will
be positive. Arthroscopic examination reveals an unsta-
ble shoulder, an attenuated but intact labrum, and an
undersurface rotator cuff tear. Jobe and Glousman55
emphasize the difficulty in clarifying the diagnosis in
groups 2 and 3. Once the diagnosis is made and the
underlying pathologic condition is identified, appropri-
ate rehabilitation measures are generally effective in
returning the athlete to his or her sport. Group 4 con-
sists of those individuals with pure anterior instability
without associated impingement. Injury is the result of
a traumatic event, resulting in an acute partial or com-
plete dislocation. Clinical and arthroscopic examination
are consistent with an unstable shoulder, without
impingement.
Posterior Impingement
As previously described, posterior superior glenoid
impingement is an additional source of rotator cuff
abnormality, and is suggested to be the primary cause of
rotator cuff disease in athletes.30,56-58 In this case, the
rotator cuff is impinged between the greater tuberosity
and the posterior superior glenoid labrum. This often
occurs in throwers and others involved in overhead
activity. It is often associated with mild anterior insta-
bility, whereas those with significant instability do not
impinge posteriorly. Some have challenged the assump-
tion that this problem is seen primarily in athletes and
in those with mild instability, finding no statistically sig-
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY
nificant relationship between the position of contact and
mechanism of injury, range of motion, throwers versus
nonthrowers, or impingement signs.59
Patients with posterior impingement often complain
of posterior pain, which is worse when in a position of
abduction and external rotation. Anterior apprehension
testing is positive for pain, but may be negative for
instability. Relocation testing relieves the symptoms. An
arthroscopic study of patients with posterior impinge-
ment found 100% of them to have contact between the
rotator cuff and the posterosuperior glenoid rim during
apprehension testing.58 Differential diagnosis includes
posterior instability, anterior instability, and secondary
tensile overload.
Rehabilitative Issues
Overview. Jobe and Pink43 report that approxi-
mately 95% of patients with IIC will respond to con-
servative treatment. The remaining 5% will require a
surgical procedure that addresses the primary pathologic
condition. Anywhere from 2 to 3, to 6 to 12 months
of appropriate conservative rehabilitation have been
recommended before considering surgical interven-
tion, depending upon the specific impingement
problem.42,49,60,61 The rehabilitation program should be
based upon the underlying pathologic condition, the
clinical examination results, and the patient goals. The
concept that everyone with impingement should be
treated with a stretching and strengthening program
neglects the spectrum of impingement problems. Jobe
and associates44 emphasize this fact in suggesting that
stretching should be performed judiciously and only
upon demonstration of specific musculotendinous
tightness. Excessive stretching of already lax anterior
shoulder structures may exacerbate the problem.
Rehabilitative exercises have been recommended
for treating the unstable shoulder.62,63 Burkhead and
Rockwood62 treated 115 patients with 140 unstable shoul-
ders with an exercise program. Subjects had traumatic or
atraumatic recurrent anterior, posterior, or multidirec-
tional shoulder subluxation. In those individuals with
atraumatic subluxation, 83% had a good or excellent result,
compared with 15% of those with traumatic instability.
The authors emphasize the importance of continuing a
maintenance strengthening program, as several patients
had recurrent symptoms when they stopped the exercises.
Mallon and Speer63 recommend strengthening of the
rotator cuff, specifically the supraspinatus because of
305
its role in preventing inferior subluxation. Short-arc
strengthening is advocated, and stretching is generally
avoided. Kronberg and associates64 evaluated the muscle
activity and coordination in normal shoulders, and con-
cluded that muscle activity plays a significant role in sta-
bilization via coordinated activation of prime movers
and antagonists. A subsequent study analyzed shoulder
muscle activity in patients with generalized joint laxity
and shoulder instability compared with the control
groups in the previous study.65 Patient results demon-
strated increased anterior and middle deltoid activity
during flexion and abduction, and decreased subscapu-
laris activity during internal rotation as compared
with the control groups. A nonsignificant increase in
supraspinatus activity was recorded during all move-
ments except flexion, suggesting compensatory muscle
function. These findings support the role of the supra-
spinatus in stabilization, and underscore the importance
of training this muscle in rehabilitation.
Examination. The varying muscle function
throughout any upper extremity activity underscores the
importance of the evaluation process. The first and most
fundamental rehabilitation issue is clarification of the
problem through a thorough evaluation. Subjective
information should include the painful position or
motion, with estimation of the force, direction, and
magnitude of muscle activity. In addition to the primary
movers, muscles functioning as stabilizers and antago-
nists must be identified. Be aware that underlying
instability may be subtle and unrecognized by the
athlete. Moreover, instability testing may reproduce
pain, but not a feeling of apprehension. The rehabilita-
tion program will vary depending upon the absence or
presence of underlying hyperelasticity, frank instability,
and/or secondary compressive impingement. In all cases,
the primary underlying abnormality will be the focus of
rehabilitation, while simultaneously addressing second-
ary problems. This situation is clearly more difficult than
the individual who has a single problem. Many athletes
have returned to the clinic with a recurrence of impinge-
ment with a previously unrecognized underlying dys-
function. Realize that this underlying dysfunction may
not be evident in the shoulder girdle, but may be weak-
ness in another link in the kinetic chain, resulting in
excessive load on the shoulder. A lower extremity or back
injury may alter movement patterns, which are ampli-
fied at the shoulder.
306 SECTION III SPECIAL CONSIDERATIONS
Itoi and associates52 emphasize the importance of
shoulder position in kinetic and kinematic analysis, as
muscle function changes depending upon position.
Moreover, an understanding of the differences in muscle
activity between sports and among phases or positions
of the same sport is the key to designing a rehabilitation
program. Electromyographic activity has been docu-
mented in swimming, throwing, golf, and tennis, and in
painful and normal shoulders.66-72 When evaluating
electromyographic data, the type of muscle contraction
should be considered. The MMT on which EMG data
are based is generally performed isometrically, whereas
acquired EMG data may be from isometric, concentric,
or eccentric muscle contractions—depending upon the
muscle’s role at any point in time. Because of the effi-
ciency of eccentric muscle activity, the same force can be
generated with fewer motor units, resulting in a lower
percentage of MMT. Incorrect interpretation of this
data could affect rehabilitation program design. The
type of muscle contraction required at the painful posi-
tion and the number of repetitions guide rehabilitation
program design.
An important aspect of the evaluation process is the
determination of the specific return to activity goals. If
strength and endurance are the primary issues, these
should be the primary focus of rehabilitation. Dynamic
stabilization and coordination drills should be at the
program’s core in athletes with underlying instability.
Not all athletes require a plyometric program to return
to their sport, and as such, the program should differ
from one individual to the next most dramatically in the
late stages. As the rehabilitation program proceeds, the
exercise program should begin to resemble the athlete’s
sport. This includes body posture, exercise range, type
of muscle contraction, speed, load, and repetitions.
Transition to the functional progression is facilitated by
appropriate program design.
Role of the Scapula
The importance of the scapula is well documented as the
base of support for the glenohumeral joint.* The scapu-
lar stabilizing muscles place the scapula in a position for
optimal glenohumeral function and provide a stable base
for the glenohumeral primary movers. These muscles
include the rhomboid, trapezius, levator scapula, serra-
*References 27, 53, 66, 69, 73, 75.
tus anterior, and pectoralis minor. It has been suggested
that alterations in scapular positioning may contribute
to the problems seen with instability and impinge-
ment.74 As such, evaluation of scapular motion
during activity and specific muscle testing of the stabi-
lizers is an important component of the rehabilitation
program.
Several of the scapular muscles have been studied in
normal and in painful shoulders during functional activ-
ities to determine changes in firing patterns with pain.
When comparing free-style swimming EMG data
between individuals with normal and painful shoulders,
significant differences were found.69,71 The patients with
painful shoulders demonstrated the following differ-
ences when compared with normal shoulders: (1) less
anterior and middle deltoid activity at hand entry and
exit, (2) more infraspinatus activity at the end of pull-
through, (3) less subscapularis activity at midrecovery,
(4) less rhomboid and upper trapezius activity at hand
entry, and (5) more rhomboid and less serratus anterior
activity during pulling. Decreased serratus anterior
activity during the pulling phase sets the stage for
impingement symptoms because it positions the
shoulder in protraction and upward rotation to prevent
impingement. Increased rhomboid activity may partially
substitute for the serratus anterior by attempting to
create more subacromial space, while preparing the
shoulder for early hand exit. Similar findings were noted
when comparing butterfly swimmers who had pain-free
or painful shoulders.67,68 Again, the serratus anterior,
along with the teres minor, demonstrated decreased
activity, suggesting an unstable base of support and an
inability to assist with propulsion. In those with normal
shoulders, the subscapularis, serratus anterior, teres
minor, and upper trapezius maintained high levels of
activity throughout the stroke—predisposing these
muscles to fatigue. As such, training programs should
focus on increasing the endurance of these muscles.
Glousman and associates,76 in an EMG study of
pitchers with normal shoulders and those with anterior
instability, noted decreased pectoralis major, latissimus
dorsi, subscapularis, and serratus anterior muscle activ-
ity during throwing and especially during late cocking.
During this phase, the serratus anterior functions to
oppose the retractors while stabilizing and protracting
the scapula. Additionally, the serratus anterior may assist
in tipping the scapula to allow for maximal gleno-
humeral congruency during excessive external rotation.47
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY 307

Decreased serratus anterior activity in late cocking

would place additional load on the anterior static stabi-
lizers, and may contribute to anterior instability. As
such, strength and endurance of these muscles are the
keystones for shoulder rehabilitation in this population.
Moseley and colleagues27 analyzed the EMG activity
in 8 scapular muscles during 16 rehabilitation exercises.
Optimal exercises for each muscle were identified by the
criteria of greater than 50% MMT over three consecu-
tive arcs of motion. A group of four core exercises
trained each of the eight muscles at the preset criteria,
and included scaption (elevation in the scapular plane),
rowing, pushup with a plus (additional scapular protrac-
tion), and press-up. Closer evaluation of the data will
allow the therapist to make appropriate choices regard-
ing scapular strengthening activities. For example, the
criteria for the core exercise group necessitated that each
muscle be used at the predetermined minimum level.
The only qualifying exercise for the pectoralis minor was
the press-up, so it was included in the core group. The
press-up did not meet minimal criteria for any other
muscle group. Additionally, the highest EMG activity in
the middle serratus anterior was produced during flexion
and abduction, from 120° to 150°. Moreover, the stan- Figure 10-8 Scaption in internal rotation.
dard deviations of some exercises are greater than 50%
of the original value. As such, the therapist should
choose exercises judiciously based upon the examination
and activity kinetics, and should monitor the exercise
quality carefully to assure proper performance (Figures
10-8 to 10-11).

Open and Closed Chain Exercise

Closed chain exercises have been advocated for lower
extremity rehabilitation, and have recently been
suggested for the treatment of upper extremity prob-
lems.77-80 Traditional physical therapy application of the
closed kinetic chain concept assumes the distal segment
to be fixed to an object that provides considerable exter-
nal resistance, whereas in an open chain, the distal Figure 10-9 Rowing.
segment is free to move in space. The definition of “con-
siderable external resistance” could potentially be met
in a traditional open chain activity.79 Dillman and external load (MNL); (2) moveable boundary, external
associates79 suggest a new classification of this model load (MEL); and (3) fixed boundary, external load
because of inadequate standardized definitions, lack of (FEL). The MNL classification is like a traditional open
quantitative-based definitions, classification of some chain exercise, the FEL like traditional closed chain
exercises into opposing categories, and comparison of exercise, and MEL like the “gray” area. Activities repre-
exercises with different mechanics. The authors suggest sentative of the MEL classification are a resisted bench
a three-level classification of: (1) moveable boundary, no press, hack squat, or leg press. Matched MEL and FEL
308 SECTION III SPECIAL CONSIDERATIONS
Figure 10-11 Press-up.
exercises in a single subject demonstrated that exercises
with similar biomechanics result in comparable muscu-
lar activity.
Principles of closed chain exercise in the lower
extremity have been applied to the upper extremity.
Further study is necessary to determine whether this
application is appropriate. The supposition that closed
chain shoulder exercise enhances static stability during
Figure 10-10 Pushups with a plus
(additional scapular protraction).
dynamic activity via mechanoreceptor education needs
further testing.78 Specificity of exercise guidelines would
suggest little carryover from closed chain exercise to
open chain activity. The value of closed chain exercise in
the athlete participating in a closed chain sport is
evident. Closed chain exercise training in an open chain
sport may be of value for reasons yet to be clarified.
Muscular co-contraction in closed chain activity can
provide dynamic stabilization for the individual with an
unstable shoulder. Carryover of this co-contraction into
an open chain is essential for the open chain sport
athlete, and will be discussed in further detail in the next
section.
Closed chain exercise for the upper extremity
includes activities such as wall pushups, modified and
full pushups with a plus, weight shifts in weight-bearing
positions, and press-ups (Figures 10-12 to 10-14; see
also Figures 10-10 and 10-11). The progression should
be from partial weight-bearing against a wall, to increas-
ing weight-bearing on a table, to the quadrupedal posi-
tion, to the modified and full pushup positions. Exercises
may be progressed from two-arm to single-arm support,
and eventually to plyometrics. Use of gymnastic balls,
stair steppers, slide boards, treadmills, rocker boards, and
other traditional lower extremity equipment challenges
the shoulder dynamically. It is critical that the quality of
the exercise be maintained throughout. As the scapular
stabilizers fatigue, the scapulae may begin to wing,
resulting in improper motor programming and possible
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY 309

A B

Figure 10-12 A, Proper performance of wall pushup. B, Improper performance of wall pushup with excessive scapu-
lar winging. The patient should be verbally cued for proper performance.

A B

Figure 10-13 Weight-bearing reaching activities. A, Proper performance of activity with lumbar
spine neutral and proper scapular stabilization. B, Improper performance with trunk rotation and poor scapular stabiliza-
tion on the right.

A B

Figure 10-14 Modified pushup position. A, Improper performance during dynamic activity with excessive scapu-
lar winging during activity. B, Return to lower-level static activity to reinforce proper performance of exercise.
310 SECTION III SPECIAL CONSIDERATIONS

injury. The therapist and athlete alike must be aware of

and be able to recognize this situation.
The EMG activity has been well documented during
open and closed chain shoulder rehabilitation exer-
cises.81,82 Townsend and associates81 studied 9 muscles
during 17 shoulder exercises. Exercises were considered
a challenge if they produced more than 50% of the
MMT over three consecutive arcs, and four exercises
were found to load each of the nine muscles at least
once at the given criteria. These exercises included: (1)
scaption in internal rotation, (2) flexion, (3) horizontal
abduction in external rotation, and (4) press-up (Figures
10-15 and 10-16; see also Figures 10-8 and 10-11). As
with the data from Moseley and Goldie,33 closer scrutiny
can provide the therapist with a wealth of information
to guide rehabilitation. Again, the press-up was included
because of the preset criteria, while EMG activity was
noted only in the pectoralis major and latissimus dorsi.
For the therapist wanting to selectively train the rotator
cuff, other exercises tested would be more appropriate.
Although the assumption is made that the exercise
with the greatest EMG activity should be chosen to
strengthen a specific muscle, a different perspective is Figure 10-15 Shoulder flexion.
fitting. Occasionally such an activity is too strenuous for
the individual recovering from an injury or surgery. In
this case, the data from Townsend and associates81
provide the therapist with a number of different choices
that may be more appropriate. For example, if scaption

Figure 10-16 Horizontal abduc-

tion in external rotation.
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY
in internal rotation is too weak or painful, scaption in
external rotation requires less, but still a significant
amount of, supraspinatus activity.
Neuromuscular Retraining
Neuromuscular retraining has been advocated by many
in the treatment of shoulder dysfunctions, especially the
instability complex.73,83-88 Lephart and colleagues84
found decreased passive repositioning sense and thresh-
old to detection of passive motion in individuals with
anterior shoulder instability. Following reconstruction,
values for these same variables were the same as the
normal control group. The relationship between static
and dynamic structures has been explored by Cain and
associates,89 who found that contraction of the infra-
spinatus/teres minor muscles reduced strain on the
anterior-inferior glenohumeral ligament at 90° of
abduction. Guanche and associates90 noted a reflex arc
from mechanoreceptors within the glenohumeral
capsule to muscles crossing the joint. These findings
reinforce the synergistic activity of the static and
dynamic structures about the shoulder. However, Borsa
and colleagues83 suggest that damage to the mechanore-
ceptors disables the reflexive dynamic stability, increas-
ing the instability problem.
Exercises purporting to facilitate development of
proprioception should consider the multilevel aspect of
nervous system training. Reflexive patterning at the
spinal cord level occurs on a subconscious level and is
only one aspect of neuromuscular retraining. Higher
levels are involved with the planning and execution of
motor tasks. The basal ganglia are involved in the more
complex aspects of motor planning and ultimately influ-
ence the spinal motor neuron pool by forming a control
loop with motor areas of the cortex involved with the
planning and execution of voluntary motor tasks. The
cerebellum regulates some of the specific parameters of
motor control, including synergistic coordination and
background muscle tone. The question of the cognitive
role in proprioceptive training deserves attention. It has
been suggested that one purpose of a proprioceptive
rehabilitation program is to enhance cognitive appre-
ciation of the joint relative to position and motion,
and most rehabilitation programs necessitate cognitive
attention to the task.83 However, when throwing a ball,
serving a volleyball, or swimming, the athlete is unlikely
to be thinking about his or her shoulder. As such,
removal of the cognitive aspect of activity must be
311
incorporated at some time in the rehabilitation process.
Mentally attending to something besides the task at
hand will challenge the nervous system in a more real-
istic situation. Counting back by serial sevens, or engag-
ing in unrelated conversation while performing
challenging activities, will facilitate this skill. Conversion
of a conscious task to unconscious motor programming,
stored as central commands, is the goal.
Proprioceptive neuromuscular facilitation (PNF)
exercises have been advocated for the development
of kinesthetic awareness.73,78,83 Additionally, Wilk and
Arrigo73 recommend several movement awareness drills
to enhance neuromuscular control of the shoulder. These
drills are performed in the advanced phase, and place
the athlete in a position that challenges the stabilizing
mechanisms. When performing any kinesthetic or
movement awareness exercises, the therapist must
closely attend to additional information derived from
other sensory systems that may assist in proprioception.
These factors might include tactile cueing from the
supporting surface, tactile cueing from the therapist,
visual cueing, and predictability of movement pattern
and speed based upon previous experience. Additionally,
the position during exercise becomes critical when
considering the role of the cerebellum and basal ganglia
in postural set and motor programming. An activity
performed in supine position on a table does not require
the same neuromuscular coordination as when per-
formed in the standing position.
The Impulse Inertial Exercise System (IES, Newnan,
Ga.) was originally developed with neuromuscular train-
ing as the chief consideration. High-speed ballistic
activities in any number of movement patterns can be
repetitively performed on the IES. Rapid ballistic move-
ments result in different patterns of agonist muscle and
antagonist muscle contractions than do slower-speed
activities. Synchronous activation of agonists and
antagonists occurs with ballistic movements as a result
of triphasic muscle activation.91-95 The initial burst of
agonist muscle contraction initiates the activity, and this
activity ceases prior to the limb reaching its final posi-
tion. Subsequently, the antagonist fires as a braking
mechanism, and the final phase finds the agonist firing
again to “clamp” the movement toward the target.94 The
same movement pattern at a slow speed demonstrates
only agonist muscle contraction, with braking provided
by the passive viscoelastic properties of the tissue. The
timing and amplitude of antagonist activity are affected
312 SECTION III SPECIAL CONSIDERATIONS

Figure 10-17 A and B, Starting and ending positions for dynamic ballistic
horizontal abduction exercise using resistive tubing.

by the distance and speed of the movement. Small-
amplitude movements at higher speeds result in sub-
stantial overlap of burst activity in agonist and
antagonist during acceleration, while co-activation
occurred in bursts during deceleration.91 Finally, knowl-
edge of the necessity for antagonist firing affects muscle
activity. When a mechanical stop was placed in the
testing apparatus, the antagonist burst disappeared
within two to three trials, suggesting some cognitive
control over the braking mechanism. This work supports
the use of high-speed ballistic activities to train open
chain co-contraction in an unstable shoulder. Such
activities can be achieved by use of the IES or resistive
tubing (Figures 10-17 and 10-18). Any number of
movement patterns can be trained, including shoulder
rotation in abduction and PNF patterns.
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY 313

Figure 10-18 A and B, Start-

ing and ending position for dynamic
ballistic shoulder external rotation at 90°
of abduction using the Impulse Inertial
Exercise System.

Case Study 2: Ms. P.D. EMPLOYMENT AND ENVIRONMENT

Instability-Related Impingement She is a high-school student who plays volleyball
and softball.
GENERAL DEMOGRAPHICS
LIVING ENVIRONMENT
A 16-year-old Hispanic, English and Spanish speak-
She lives in a two-story house with her parents and
ing female who comes to the clinic with an 8-month
younger brother.
history of right shoulder pain. She is right-hand
PAST MEDICAL HISTORY
dominant.
She has no history of shoulder or neck problems, and
SOCIAL HISTORY
no history of medical problems.
Ms. P.D. is single with no children. She does not
smoke or drink.
314 SECTION III SPECIAL CONSIDERATIONS
History of Chief Complaint
She initially felt a sharp pain while bench pressing,
but had no pain after discontinuing the activity. Shortly
thereafter, she was moved from pitcher to center field,
requiring longer throws. She was able to manage the
remaining 2 weeks of softball. Two weeks later volley-
ball season started, and her shoulder pain increased. She
completed the volleyball season by modifying her activ-
ity level, and had minimal trouble during basketball.
However, when softball started, her symptoms increased
again. The cocking and acceleration phases of throwing
were the most painful.
Prior Treatment for this Condition
During volleyball season, the athletic trainer at her
high school placed her on a rotator cuff strengthening
program, which did not relieve her symptoms. The fol-
lowing softball season she was again placed on a rotator
cuff strengthening program of 6 weeks duration by the
athletic trainer at her high school. However, when her
symptoms failed to resolve themselves, she was referred
for formal physical therapy treatment.
STRUCTURAL EXAMINATION
Physical Therapy Examination
Visual inspection: No swelling or ecchymosis was
evident; scapular posture and muscle bulk were
symmetrical.
Range of Motion
AROM: Painful arc between 90° and 120° of eleva-
tion in the frontal plane; full range of motion.
PROM: Full and pain-free in all ranges.
Tenderness
Palpation: Tender over biceps tendon and rotator cuff
tendon.
Joint Integrity and Mobility
Accessory motion of the glenohumeral joint
increased in all directions bilaterally.
Muscle Performance
Resisted testing: 4/5 strength in resisted abduction
without pain; all other testing strong and pain free.
Special Tests
Neer’s and Hawkins impingement signs were posi-
tive; horizontal crossover testing negative; biceps tension
testing positive; apprehension and relocation testing
positive.
P.T. Clinical Impression
Given the history and physical examination of the
young athlete’s shoulder, it was determined that she had
impingement syndrome caused by underlying instabil-
ity (impingement-instability complex). This problem is
treated in a practice pattern focusing on impairments
associated with connective tissue dysfunction. The stage
of clinical reactivity was subacute. She had established
good rotator cuff strength because of her cuff-
strengthening program. However, the underlying insta-
bility had not been addressed, and was the focus of the
rehabilitation program.
TREATMENT PLAN
The initial goal was to build upon her strength base
without aggravating her secondary impingement syn-
drome. She was initiated on a high-speed, short range
of motion program with yellow resistive bands for shoul-
der external rotation and shoulder abduction, and red
bands for shoulder flexion and extension. All exercises
were performed in neutral abduction. After a warm-up,
she performed one set for 30 seconds, attempting to
perform 30 to 50 repetitions in 30 seconds. She was
instructed to add an extra set of 15 seconds or more as
tolerated during the next week.
On her return visit, she reported soreness for a day,
with no fatigue in flexion and extension exercises after
2 days. Resisted external rotation was slightly sore but
strong. Her flexion and extension exercises were pro-
gressed to 45° of abduction. One week later, she was
improving steadily. She was up to three sets for 30
seconds of all exercises. Resisted external rotation was
maintained in neutral, but progressed to red resistive
bands. Flexion, extension, and abduction were discon-
tinued, and horizontal abduction and adduction exer-
cises were initiated at 90° of abduction with green bands.
She was encouraged to try to perform up to 90 repeti-
tions in 30 seconds.
By her fourth visit, she was feeling notably better.
Internal and external rotation was initiated at 90° of
abduction, and progress was made in the resistance of
the bands. On her fifth visit, she progressed to PNF D2
flexion exercises and reproduction of the throwing
motion. She performed three sets each of more than 90
repetitions of each exercise in 30 seconds. On her sixth
and final visit, the patient was placed on a functional
progression for volleyball, and a maintenance strength
and coordination program.
SUMMARY
A 16-year-old high-school athlete was seen for a total
of six visits to treat her impingement-instability
complex. The key to successful rehabilitation was the
recognition of the underlying instability, with exercise
CHAPTER 10 IMPINGEMENT SYNDROME AND IMPINGEMENT-RELATED INSTABILITY
protocols addressing this problem. Rotator cuff
strengthening alone was ineffective in this athlete, and
the incorporation of dynamic stabilization exercises
provided the needed dynamic control of her unstable
shoulder.
Summary
Impingement syndrome of the shoulder can result in a
cascade of pathologic conditions that primarily affect
the rotator cuff and result in subacromial pain and
shoulder dysfunction. The causes of impingement pre-
sented in this chapter have multiple factors, but can be
divided into primary impingement and secondary
impingement depending on the presence of instability
and/or impingement. These categories are further sub-
divided based on the pathomechanics of injury, age of
the patient, dysfunctions, and associated abnormalities.
In the younger, athletic population the basic problem is
instability, which leads to subluxation, impingement,
and rotator cuff disease. Treatment is based on accurate
classification of the ailment and is logically focused on
the signs, symptoms, and nature of the dysfunction. For
example, treatment of impingement in younger athletes
is designed to restore shoulder stability and control, and
correcting underlying mechanical problems associated
with their sport. A systematic evaluation of the nature
and extent of the injury is imperative for the clinician to
properly classify the problem and design an effective
rehabilitation program.
ACKNOWLEDGMENTS
We are grateful to Anne Schwartz for providing the
drawings upon which we based our figures. We would
also like to thank Robert Donatelli and Jacob Irwin for
their contributions to the revision of this chapter.
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Frozen Shoulder
I n this chapter, the term frozen shoulder describes the
clinical entity in which a person has restricted
passive mobility at the glenohumeral joint, which
often results in a loss of active range of motion (ROM)
and pain. This loss of mobility can impose substantial
disability for many. The cause of frozen shoulder is
poorly understood. Much confusion exists among the
medical population concerning terminology, as the
terms adhesive capsulitis, capsulitis, and periarthritis of
the shoulder are often used synonymously. The purpose
of this chapter is to provide a historical review of liter-
ature on the painful and stiff shoulder, characterize the
clinical entity of frozen shoulder, provide a working def-
inition for frozen shoulder, and provide a description of
treatment approaches available for frozen shoulder.
Historical Review
In 1896 Duplay39 was credited with the initial descrip-
tions of the painful and restricted shoulder. He termed
the clinical entity of frozen shoulder “periarthritis scapu-
lohumerale,” theorizing the pathologic condition was in
the periarticular structures. The primary ailment was
suspected to be in the subacromial bursa. The recom-
mended treatment approach was manipulation under
anesthesia. In 1934 Codman8 coined the same disorder
as “frozen shoulder syndrome” and related the dysfunc-
tion to uncalcified tendonitis. He expressed that the
condition was “difficult to define, difficult to treat,
and difficult to explain . . . from the point of view of
pathology.”
319
11
Mollie Beyers
Peter Bonutti
Nevasier27 introduced the concept of “adhesive cap-
sulitis” in 1945, when he discovered a tight, thickened
capsule that stuck to the humerus. He described an
inflammatory reaction that led to adhesions, specifically
in the axillary fold and in the attachment of the capsule
at the anatomic neck of the humerus. Surgical explo-
ration of 10 shoulders indicated an absence of gleno-
humeral joint synovial fluid and a redundant axillary fold
of the capsule.
In 1949 Simmonds45 speculated a loss of motion at
the glenohumeral joint because of degenerative changes
and secondary inflammation of the supraspinatus
tendon. He hypothesized this was because of repetitive
wear against the acromion and coracohumeral ligament.
Many of his patients experienced functional limitation,
pain, and restriction in the shoulder for more than 5
years. Therefore he concluded it was not a self-limiting
disease process.
Quigley37 described in 1954 a “pattern of pain-free
passive motion sharply checked at about 45° of abduc-
tion and half of the normal range of motion.” He called
the entity “checkrein shoulder” to describe this condi-
tion for a subgroup of individuals with frozen shoulder,
but for whom he assigned a good prognosis. This sub-
group responded well to manipulation under anesthesia
and was described “to present with an audible and pal-
pable release” during the procedure.
In 1962 Nevasier28 described four phases of frozen
shoulder through the assistance of arthroscopic study.
These stages are defined as follows: Stage I—preadhe-
sive stage, found in patients with little to no restriction
320 SECTION III SPECIAL CONSIDERATIONS
of GH motion; Stage II—acute adhesive synovitis with
proliferative synovitis and early adhesive; Stage III—
maturation stage in which less synovitis is demonstrated
with loss of axillary fold; Stage IV—chronic stage pre-
senting with fully mature adhesions with notable restric-
tion of ROM. Nevasier discussed lack of explanation for
the disease process and suggests any condition requiring
prolonged immobilization as a causative factor.
Reeves,38 in a natural history study of frozen shoul-
der in 49 subjects conducted in 1975, reported a direct
relationship between the duration of the stiff phase and
the duration of the recovery phase. The observed popu-
lation had an onset of disease at 42 to 63 years. The
painful phase ranged from 10 to 36 weeks in length. The
stiffness phase lasted from 4 to 12 months. Recovery
of ROM ranged from 5 months to 26 months. The
reported mean duration of symptom resolution without
intervention was 30.1 months. Although Reeves38
reported no intervention when following the natural
history, the patients were instructed to use analgesics
during the painful phase, to rest and wear a sling during
the stiff phase, and “to exercise their shoulders to regain
external rotation (ER) and abduction (ABD) during the
recovery phase.” This “advice” could have altered the true
natural history.
In 1992 Itoi and Tabata,19 in a study of 91 subjects,
reported a positive correlation between abduction and
the restriction of the axillary pouch through arthro-
graphic measures.
Chi-Yin and associates7 in 1997 identified a statisti-
cally significant correlation between external rotation
ROM and increased joint capacity in a study using
arthrography following physical therapy. They identified
an increase in joint space in the acute frozen shoulder,
but not in chronic cases.
At present, “frozen shoulder” is a readily recognized
clinical grouping of signs and symptoms. Specific des-
criptions on motion, pathologic condition, treatment,
and recovery, however, are difficult to find and interpret.
Definition
Our suggested working definition for frozen shoulder is
glenohumeral joint stiffness resulting from a noncon-
tractile element unless it coexists with a noncontractile
lesion. Both active and passive motion is painful and
restricted. Passive mobility is limited in the capsular
pattern, with external rotation being most limited fol-
lowed by abduction and internal rotation. The gleno-
humeral capsular volume is less than 10 ml and plain
films are normal.
Epidemiology
The prevalence of frozen shoulder is 2% to 3% of the
U.S. population and is more common among females.21
The affliction also occurs more frequently in the non-
dominant arm. The condition is most commonly
reported between the ages of 40 and 64.22,26,38,40,51
Clinical Presentation
Frozen shoulder is a grouping of multiple symptoms.
Although not all patients follow the same course, aware-
ness of the typical clinical course of frozen shoulder may
be helpful.
Stages9
Painful or Freezing Phase. The painful or freez-
ing phase as described by Reeves39 typically lasts 10 to
36 weeks. The patient has spontaneous onset of shoul-
der pain, which is often severe and disrupts sleep. The
patient often rests the arm, noting an abatement of pain
and contributing to increased stiffness. At the end of
the painful phase, the glenohumeral capsule volume is
greatly reduced.
Stiffening or Frozen Phase. The painful phase is
often followed by a stiffening phase. This phase may last
4 to 12 months. The patient has restricted ROM in a
characteristic pattern of loss of external rotation, inter-
nal rotation, and abduction.9
Thawing Phase. The final phase is described as
thawing and is characterized by the gradual recovery of
ROM. The thawing phase will last an average of 5 to 26
months and is reportedly directly related to the length
of duration of the painful phase.9
Primary Frozen Shoulder
Primary frozen shoulder refers to the idiopathic form of
a painful, stiff shoulder. The debate continues about the
pathogenesis of idiopathic frozen shoulder. Possible
causes include immunologic, inflammatory, biochemi-
cal, and endocrine alterations.17,27,28
CHAPTER 11 FROZEN SHOULDER
Bunker and Anthony5 in 1995 reported that only 50
of 935 shoulders evaluated with restriction at the gleno-
humeral joint could be classified as primary frozen
shoulder. In these 50 cases, loss of motion occurred from
thickening and contracture of the coracohumeral liga-
ment and rotator interval, thus acting as a tight “check-
rein,” which prevented external rotation. They also
confirmed a histologic similarity between Dupuytren’s
disease and frozen shoulder.
Bunker and Esler6 in 1995 also reported an associa-
tion between hyperlipidemia, frozen shoulder, and
Dupuytren’s disease. The incidence of frozen shoulder
in the diabetic population is reported to be 10.8%.2
Janda and Hawkins20 in 1993 reported a poor outcome
in the diabetic population with frozen shoulder follow-
ing treatment with manipulation under anesthesia.
Secondary Frozen Shoulder
Secondary frozen shoulder can be indicated by a pre-
cipitating event or trauma, which can be identified to
explain the loss of motion. Examples of such events
leading to frozen shoulder include limitations following
surgery, soft tissue trauma, or fracture. The three phases
of frozen shoulder9 may not always be recognizable in
the patient having secondary frozen shoulder.
Scientific Research
As with many poorly understood medical conditions,
multiple approaches are used in the treatment of frozen
shoulder. Historically, research on treatment has in-
cluded: steroid injections, both intra-articular and extra-
capsular, with and without physical therapy; physical
therapy, including modalities, active range of motion
(AROM), stretching, exercise and mobilization, or a
combination thereof; closed manipulation, with and
without steroid injections, and with and without physi-
cal therapy; and arthroscopy and open surgical release
with physical therapy. The remainder of the chapter
focuses on reviewing the scientific literature to date
on the use/effectiveness of treatment for the frozen
shoulder.
Use of Steroid Injections With and
Without Physical Therapy
Many physicians use steroid injections in the treatment
of frozen shoulder. Most often, this treatment approach
321
is used in conjunction with physical therapy or home
exercise. Scientific research supporting and refuting this
approach will be discussed. Table 11-1 is a matrix
summary of the research.
Quigley37 conducted a prospective study on 29 sub-
jects in 1954. Subjects who were classified into the inclu-
sion for “checkrein” shoulder received manipulation,
adrenocorticotropic hormone (ACTH), and steroid
injections. The average age of the subjects was 50.5, with
a mean duration of symptoms of 5.5 months before the
intervention. Results reported were as follows: 10 sub-
jects were pain free with normal ROM; 13 subjects
reported little pain and loss of ROM or both; and 6
showed no change. Quigley concluded his definition of
checkrein shoulder would define inclusion and exclusion
criteria for those individuals who could be assigned a
good prognosis.
In 1973 and 1974 Lee and associates22,23 performed
the first study with a random clinical trial design. The
preliminary study in 1973 included four groups, with 80
subjects randomly assigned to the groups. Individuals
were included if they had periarthritis of the shoulder
and pain in the shoulder with limitation of shoulder
movement. In 1974, 45 subjects were randomly assigned
to groups. Description of treatments for each group
follows:
Group 1 active ROM and infrared heat
Group 2 intraarticular hydrocortisone acetate and
active ROM
Group 3 hydrocortisone acetate to bicipital groove
Group 4 analgesics only
Chi-square for differences showed no difference
between the groups for age, sex, or duration of symp-
toms. Physical therapy for groups 1, 2, and 3 was very
specific and included a graduated exercise program. This
included: (a) free-active exercise, 10 minutes TID (three
times a day) of the following: assisted ROM, range of
motion-gravity counterbalance, and gravity-resisted
ROM; (b) proprioceptive neuromuscular facilitation
(PNF): manual resistance and concentric contractions.
Duration of follow-up was 6 weeks. Group 4 had infe-
rior ROM results leading Lee and associates to conclude
that exercise was the beneficial component of treatment
during the 6-week time period. They also reported sig-
nificant differences in ROM, the greatest change occur-
ring in group 2. They noted the greatest improvement
in ROM during the first 3 weeks. Overall, they con-
cluded that any treatment including exercise was
322 SECTION III SPECIAL CONSIDERATIONS

Table 11-1

RESEARCH ON USE OF STEROID INJECTION AND PHYSICAL THERAPY FOR THE FROZEN SHOULDER

Use of
Author & Sample Physical
Year Size Purpose Therapy Results

Quigley TB: 1954 N = 29 To determine the effectiveness Heat, exercise 1) 10 pain free with normal ROM
of manipulation and ACTH, program 2) 13 little pain and little loss of
hydrocortisone acetate, or ROM or both
cortisone 3) 6 unimproved
Lee M, Haq N = 80 To test the value of physical Graduated 1) active ROM and infrared
AMMM, Wright therapy and local injection of active exercise 2) intraarticular hydrocortisone
V: 1973 hydrocortisone acetate in for groups acetate and active ROM
periarthritis of the shoulder 1, 2, & 3 3) hydrocortisone acetate to
bicipital groove
4) analgesic only
Improvement in ROM within
first 3 weeks; most change
occurred in intraarticular
hydrocortisone injections with
ROM exercises
No change in analgesic only group
Lee PN, Lee AM, N = 45 To test the effect of heat and Graduated ROM of other groups improved
Haq AMMM, exercise; intraarticular active exercise over analgesics only; no significant
Longton EB, hydrocortisone and exercise; for groups change between the groups
Wright V: 1974 hydrocortisone to bicipital 1, 2, & 3
groove and exercise; analgesic
control group on shoulder
movement in periarthritis of
the shoulder
Weiss JJ, Ting N = 48 To report the authors’ None 1) 16 pain free
M: 1978 experience with intraarticular 2) 11 painful
steroids and use of shoulder No increase in glenohumeral ROM
arthrography (No manipulation/ROM provided)
Binder A, Hazelman N = 40 To ascertain if a limited All performed Decreased pain in steroid group;
BL, Parr G, Roberts course of oral steroid home no difference in ROM between
S: 1986 therapy had any beneficial pendulum groups
effects and to determine the exercises
treatment favored by local
general practitioners
Dacre J, Breney N, N = 62 To determine effectiveness Physical All groups showed decrease and
Scott DL: 1989 of physical therapy, steroid therapy use ROM increased 10% to 34% at 6
injections, or both varied for head months; no differences between
for 4-6 weeks groups
CHAPTER 11 FROZEN SHOULDER 323

superior to analgesics alone and that only 3 weeks of
therapy should be prescribed with physician follow-up
to reassess the subject’s status.
In a 1978 study performed by Weiss and Ting,6 they
reported the effects of arthrographic assisted intraartic-
ular injections on glenohumeral (GH) ROM in 48 sub-
jects. These researchers reported success based on “total
shoulder movement” rather than pure GH joint motion.
The researchers did not describe the length of treatment,
the numbers of injections received, or any statistical data.
Outcomes were based on subjective reports of good, fair,
or poor relief of pain. Motion was reported as improved
or not improved, with no variance given if it was GH or
total shoulder girdle movement. Four weeks following
treatment, 16 patients reported pain-free shoulders, and
11 patients still had pain. No increase in GH motion
was noted following only an injection. These researchers
concluded that arthrographic assisted intraarticular
injections should be attempted following failure of con-
servative therapy.
Binder and associates3 in 1986 studied the effects of
oral prednisolone in treatment of frozen shoulder and
reported a statistically significant decrease in pain, but
no change in ROM when compared with noninterven-
tion groups. Both groups performed a home pendulum
exercise program.
In 1989 Dacre, Beeney, and Scott10 found no signif-
icant advantage for physical therapy and/or steroid
injection for the treatment of frozen shoulder. However,
physical therapy treatment was not consistent among the
62 subjects.
Use of Physical Therapy
The debate on the effectiveness of physical therapy in
treatment of the frozen shoulder continues. The length
of physical therapy intervention, and the stage at which
it may be appropriate, has not been justified thus far in
the research. The research that will be discussed lacks
well-controlled trials and useful outcome measurement
tools. Consistency among the studies does not exist,
making comparison difficult. Table 11-2 is a matrix
summary of the research.
Parsons, Shepard, and Fosdic34 in 1967 performed a
one-group pretest and posttest on seven subjects, report-
ing the effects of dimethyl sulfoxide (DMSO has a
vasodilation and antiinflammatory action) with ultra-
sound in frozen shoulder. The researchers concluded
that further studies needed to be performed on DMSO
as an adjunct therapy for the treatment of frozen shoul-
der. This study was terminated because of adverse effects
from the agent.

Table 11-2

RESEARCH ON USE OF PHYSICAL THERAPY FOR THE FROZEN SHOULDER

Sample Use of Physical

Author & Year Size Purpose Therapy Results

Parsons JL, Shepard N=7 Preliminary report on 5 DMSO with ultrasound 1) 4 “better”
WL, Fosdick WH: months; experimental study 2) 3 no change
1967
Hamer J, Kirk JA: N = 32 To compare the effectiveness Ice group, ultrasound No significant
1976 of ultrasound and ice on group; all performed differences
frozen shoulder active external rotation
and elevation
exercises
Rizk TE, Christopher N = 56 To describe a new method Group A: exercises B group increased
RP, Pinals RS, of therapy that has been and modalities ROM faster first
Higgins AC, Frix R: found to facilitate the Group B: pulley and 2 weeks
1983 recovery of patients with traction
adhesive capsulitis
Continued
324 SECTION III SPECIAL CONSIDERATIONS
Table 11-2
RESEARCH ON USE OF PHYSICAL THERAPY FOR THE FROZEN SHOULDER—cont’d
Sample
Author & Year Size Purpose
Bulgen DY, Binder N = 45 To study a carefully defined
AI, Hazleman BL, patient group and assess 3
Dulton J, Roberts S: treatment regimens
1984 1) Intraarticular steroids
2) Mobilization
3) Ice & PNF
4) Pendulum
Nicholson GG: 1985 N = 20 To determine the effects of
passive mobilization and
active exercises on pain and
hypomobility in patients
with painfully restricted
shoulders
Experimental group:
mobilization and active
exercises
Control: active extension only
Shaffer B, Tibone JE, N = 62 To evaluate the long-term
Kerlan RK: 1992 objective and subjective results
in a carefully selected group
of patients who had idiopathic
frozen shoulder
O’Kane JW, Jackins N = 41 To test the hypothesis that a
S, Sidles JA, Smith simple home program can
KL, Matsen FA III: improve the self-assessed
1999 shoulder function and health
status of a group of patients
with frozen shoulder
Griggs SM, Ahn A, N = 75 To evaluate the outcome of
Green A: 2000 patients with idiopathic
adhesive capsulitis who were
treated with a stretching
exercise program
Vermeulen HM, N=7 To describe the use of end
Obermann WR, range mobilization techniques
Burger BJ, Kok GJ, in the management of patients
Rozing PM, Van der with adhesive capsulitis
Ende C: 2000
Use of Physical
Therapy Results
See groups Minimal differences
between groups; injection
may benefit pain and
ROM in early stages;
biggest improvement first
4 weeks; after 6 months
decreased pain; no
significant difference in
ROM
Mobilization, passive Mean improved over 4
ROM, and weeks except internal
strengthening; home rotation with increased
exercise program gains in experimental
group
Pendulum, modalities, See text of chapter
and stretching
following manipulation
Self stretch flexion, SF 36 showed almost
abduction, external all pretreatment deficits
rotation, internal were reversed
rotation
Home exercise 1) 64 satisfactory: SF 36
program: supine cane 2) 7 not satisfied: SF 36
flexion, external 3) 5 required manipulation/
rotation, internal surgery
rotation, pendulum; 4) ROM increased
formal physical therapy 5) Pain decreased
Mobilization Reports increased ROM
and decreased pain
CHAPTER 11 FROZEN SHOULDER
In 1976 Hamer and Kirk16 performed a two-group
pretest and posttest prospective study on 32 subjects to
compare the effects of ultrasound and ice on outcome in
patients with frozen shoulder. The mean age of subjects
was 59 and the time between onset of symptoms and
discharge from physical therapy was 17.7 weeks. No
demographic differences were reported between the
groups at pretest. Both groups received active elevation
and ER exercises 2 times per day for 10 minutes until
discharge. Discharge was based on pain relief only, not
ROM gains. No significant differences were reported
between the groups. The researchers recommended
including measurements of the contralateral shoulder for
assessment of shoulder ROM gains.
Rizk and associates40 in 1983 described a new
method of therapy. Fifty subjects were assigned to
groups. Group A received conventional physical therapy,
including modalities, Codman’s exercises, wall walks,
shoulder wheel, pulley, rhythmic stabilization, and
manipulation of the GH joint. Group B used transcu-
taneous electrical nerve stimulation (TENS) + pulleys
with up to 15# 15 repetitions per exercise traction plus
intermittent 15 minutes on/5 minutes off for 2 hours.
The mean age of the subjects was 56, the duration of
symptoms ranged from 3 to 8 months before the inter-
vention. Treatment was administered for 8 weeks. The
subjects’ progress was assessed monthly for 6 months.
Both groups performed a home exercise program con-
sisting of Codman’s exercises, wall walks, and wand
ROM (five repetitions each, three times a day). Group
B progressed faster and to a greater degree than Group
A during the first 3 weeks of treatment. Both groups
demonstrated the greatest gains in the initial 3 weeks,
which was comparable to the findings of Lee and asso-
ciates.22,23 Rizk and associates concluded that the treat-
ment approach for group B was superior to conventional
physical therapy. Random assignment was not used and
no statistical analysis was reported.
Bulgen and associates4 performed random controlled
trials in 1984 comparing the following treatment groups:
intraarticular steroids, once a week for 3 weeks; mobi-
lization, three times a week for 6 weeks plus PNF three
times a week for 6 weeks; and pendulum exercises of only
2 to 3 minutes every hour. Forty-two subjects were
recruited whose mean age was 55.8, with a symptom
duration averaging 4.8 months before the intervention.
Follow-up was performed weekly for 6 weeks, then
monthly for 6 months. Statistical analysis showed no
325
differences between the groups pretreatment. Bulgen and
associates concluded that improvement in ROM was
greatest during the initial 4 weeks of treatment and that
no difference between groups was found when compar-
ing the stage at which the patient joined the study and
the severity of the subject’s outcome. A correlation was
reported between increasing age and decreasing ROM,
except for ER. Final recommendations emphasized the
need for well-designed, controlled prospective studies to
test the efficacy of commonly used interventions.
In 1985 Nicholson29 compared the effectiveness of
active exercise with joint mobilization in 20 subjects.
The mobilization group gained more internal rotation
and abduction than the exercise only group. The follow-
up measurements were taken 4 weeks after initiation of
the intervention.
Shaffer, Tibone, and Kerlan44 evaluated the long-
term subjective and objective results in 62 subjects who
had shoulder pain and restriction for at least 1 month,
AB < 100, and <50% ER. The mean age was 52, with
a mean duration of symptoms of 6 months before the
intervention. All of the subjects had previously received
supervised physical therapy or a home stretching
program. Ten received manipulation under anesthesia
and two received arthroscopic release. Conclusions from
this study are as follows:
• The average total time from onset to resolve was 12
months.
• The average time to return to nearly normal motion
(within 10° to 15°) was 6 months.
• Pain was resolved within an average of 6 months.
• Thirty-one percent of subjects had either mild
pain/stiffness of the shoulder.
• Thirty-seven percent of subjects demonstrated
restricted motion when compared with the control
group (unaffected shoulder averages).
• Seven percent interference with function was reported.
• No association was reported between functional
limitation and measurable restriction of motion.
• No association was reported between the objective
ROM and duration of symptoms with the subjective
outcome.
O’Kane and associates31 studied the effects of a home
stretching program on self-assessed function. The
researchers measured function with the Simple Shoul-
der Test and the SF 36. All deficits identified with the
SF 36 were reversed posttreatment. The duration of
follow-up was not reported.
326 SECTION III SPECIAL CONSIDERATIONS

Griggs and colleagues15 performed a prospective
study on 41 subjects using home wand active assistive
range of motion (AAROM) exercises and pendulum
exercises. The mean age of subjects was 56. The re-
searchers concluded the SF 36 was not sensitive to the
shoulder. No correlation was found between ROM gains
and improvement of function.
Vermeulen and associates47 in a case report of
four subjects observed increased ROM and decreased
pain following physical therapy intervention. Physical
therapy was provided for a maximum of 3 months.
Treatment consisted of end-ROM mobilization tech-
niques, with neither the use of modalities nor instruc-
tion in a home exercise program. All patients reported
decreased pain and increased ROM. No statistical analy-
sis was reported.
Use of Physical Therapy With Interscalene
Block or Local Anesthesia
The effectiveness of physical therapy mobilization
during interscalene brachial plexus block or local anes-
thesia has been well supported in the literature. Table
11-3 is a matrix summary of the research.
Weiser51 in 1977 reported on the treatment of frozen
shoulder with gliding mobilization while under local
anesthesia in 100 subjects. The majority of subjects were

Table 11-3

RESEARCH ON USE OF INTERSCALENE BLOCK OR LOCAL ANESTHESIA WITH PHYSICAL THERAPY TECHNIQUES

Sample Use of Physical

Author & Year Size Purpose Therapy Results

Weiser H: 1997 N = 100 To report treatment of Cane flexion, 78 no pain

frozen shoulder using abduction, internal 61 of 78 normal ROM
mobilization under rotation with 17 slight decreased ROM
local anesthesia extension/rotation
Melzer C, Wallny CJ, N = 110 To compare moderate Modalities, ROM, Physical Therapy
Hoffmann S: 1995 mobilization to mobilization, 1) Increased abduction 78%,
manipulation in stretching, isometric internal rotation 81%,
frozen shoulder strengthening adduction 54%
patients 2) Mobilization under narcosis
3) Increased abduction 66%,
internal rotation 73%,
adduction 62%
Roubal PJ, Dobritt D, N = 23 To develop and describe Supine flexion, daily Postmanipulation:
Placzek JD: 1996 an alternative method therapy, home Flexion increased 68°, abduction
that uses glide exercise program increased 77°, external rotation
manipulation under flexibility increased 49°, internal rotation
interscalene brachial increased 45°, flexion increased
plexus block 67°, abduction increased 73°,
external rotation increased 44°
Placzek JD, Roubal PJ, N = 31 To evaluate the long- Not described 1) ROM increased significantly
Freeman DC, Kulig K, term effects of 2) Pain decreased significantly
Nasser S, Pagett BT: glenohumeral joint
1998 transitional gliding,
manipulation, ROM,
pain, and function in
patients with adhesive
capsulitis
CHAPTER 11 FROZEN SHOULDER
40 to 64 years old. Forty-five subjects experienced symp-
toms less than 3 months and 55 subjects experienced
symptoms more than 4 months before the intervention.
The inclusion criteria were GH restriction only, ER less
than 55°, and flexion less than 110°. Five to 10 minutes
of grade IV mobilization was performed in all directions.
The patients performed wand exercises and were in-
structed to perform these six to eight times per day for
at least 20 minutes. Follow-up was at 2, 4, and 8 weeks.
Seventy-eight of 100 subjects were reported to have no
pain at their 2, 4, and 8-week follow-up visits. Sixty-one
of the 78 had normal ROM. Seventeen of 100 demon-
strated a slight decrease in ROM. No statistical analy-
sis was reported.
Melzer and associates25 in 1995 also studied the
effects of manipulation under general anesthesia to
“moderate mobilization.” Eighty-nine subjects, aged 34
to 78, participated. The duration of symptoms was not
reported. The average postintervention follow-up for the
two groups was 1.4 and 1.7 years, respectively. The
mobilization group showed an increase in pretreatment
to posttreatment ROM values as follows: ABD 78%,
internal rotation (IR) 81%, adduction (ADD) 54%. The
manipulation group showed an increase in pretreatment
to posttreatment ROM values as follows: ABD 66%,
IR 73%, and ADD 62%. No statistical analysis was re-
ported. The researchers concluded physical therapy
with mobilization should be used before manipulation
intervention.
Roubal and associates41 performed a similar study of
23 subjects in 1996. These researchers used an inter-
scalene brachial plexus block and a linear transi-
tional gliding manipulation. Eight subjects demon-
strated increased ROM when comparing pretest and
posttest measures of ROM. No statistical analysis was
performed.
In 1998 Placzek and associates35 performed a similar
study to Roubal and associates using linear transitional
gliding manipulation on 31 subjects. The researchers
reported a statistically significant improvement in
ROM, pain reduction, and improved functional status
at 5.3 to 14.4 weeks after the intervention. Placzek
and colleagues concluded that translational manipu-
lation was more effective than traditional angular
techniques used in manipulation. This conclusion
was drawn because of increased accessory humeral
head movement associated with translational
techniques.
327
Use of Distension Arthrography
The use of distension arthrography, with or without
the use of physical therapy, is addressed in scientific
research. This slightly invasive technique has been
attempted with local and general anesthesia. Table 11-4
is a matrix summary of scientific research.
Older and associates32 reported their experiences
using distention arthrography on six subjects.
Radiopaque contrast fluid was manually injected until
the capsule ruptured via visualization on an arthrogram.
The researchers reported full ROM at a 2.5-year follow-
up and contributed this success to their treatment. ROM
was reported as “full.” However, all patients performed
“exercises” and no attempt was made to control physical
therapy between the intervention and the follow-up.
The researchers did not perform a statistical analysis.
Arthrographic treatment progressed further when
Loyd and Loyd24 in 1983 studied the effect of local anes-
thesia, arthrographic distension, and gentle manipula-
tion in 31 subjects. The mean age of these subjects was
54, with a mean duration of 6 months for symptoms
before arthrography. Subjects were included in the study
if their capsular volume was less than 10 ml. Twenty-five
subjects reported unrestricted function, whereas nine
subjects reported continued restrictions described as
“slight weakness.” No statistical analysis was reported.
Loyd and Loyd reported the following advantages for
use of their technique: increased diagnostic accuracy,
arthrographic guided intra-articular injection, no mor-
bidity, and better pain relief than physical therapy and
analgesics only. The researchers stated that 31 of the 33
subjects reported the intervention had been beneficial
and had provided excellent relief. No reliability or valid-
ity studies were discussed in regards to the outcome
measurement tool.
Fareed and Gallivan13 in 1989 documented their
results of hydraulic distension while under local anes-
thesia and AROM. No manipulation was performed.
The mean age of the 20 subjects was 56. Subjects
included in the study demonstrated exquisite pain on
passive ER/IR/ABD and night pain. An immediate
increase in the subject’s ROM to normal function was
reported in 90% of the subjects. A 10° to 15° loss was
reported at 2 weeks, which then increased to normal
when receiving more than one intervention before the
4-week follow-up. Long-term follow up at 6 months
and 10 years showed the same results. Statistical analy-
sis was not reported.
328 SECTION III SPECIAL CONSIDERATIONS
Table 11-4
RESEARCH ON USE OF DISTENSION ARTHROGRAPHY
Sample
Author & Year Size Purpose
Older MWJ, McIntyre N=6 To report the researcher’s
JL, Lloyd GJ: 1976 experience with distension
arthrography as a treatment
of frozen shoulder
Lloyd JA, Lloyd HM: N = 31 To describe the efficacy of
1983 arthrographic diagnosis and
treatment of the frozen
shoulder
Fareed DO, Gallivan N = 20 To document the
WR: 1989 effectiveness of hydraulic
distension as a modality
of treatment for frozen
shoulder syndrome; no
manipulation
Ekelund AL, Rydell N = 22 To determine the
N: 1992 effectiveness of distension
arthrography and local
anesthesia and steroids and
manipulation
Van Royn BJ, Pavlov N = 40 To report the effectiveness
PW: 1995 of distension and
manipulation under local
anesthesia in treatment
of the frozen shoulder
Similar treatment intervention and results were
reported by Ekeland and Rydell12 in a study in 1992.
Follow-up in this study was 4 years. No attempt was
made to control activity between the intervention and
the follow-up. No statistical analysis was reported.
In a similar study in 1996, Van Royen and Pavlov46
reported similar effects with a 72% to 95% increase in
ROM with a reduction in pain. No statistical analysis
was performed.
Use of Closed-Manipulation, Arthroscopic
Release, or Open Release
Closed-manipulation, arthroscopic, or open capsular
release may be attempted upon failure of conservative
treatment. Physical therapy is prescribed most often
Use of Physical
Therapy Results
None Reported full ROM 2.5
years after intervention;
greatest change reported
with abduction
None 25 subjects reported
unrestricted function, 9
subjects reported continued
restrictions and weakness
Active external 1) 90% return of function
rotation, pendulum, and ROM after first
resistive treatment
flexion/extension/ 2) 95-100% function and
internal rotation/ ROM at 4 weeks
external rotation
Flexion/abduction All improved slightly or
External rotation/ no pain
internal rotation
none 1) ROM increased 72-95%
2) Pain absent in 15
following the intervention. Scientific research concern-
ing these more aggressive procedures is summarized
in Table 11-5, which is a matrix summary of scientific
research.
In 1988 Hill and Bogumill18 compared manipulation
under general anesthesia with the natural history of
frozen shoulder. Fifteen subjects were retrospectively
analyzed from August 1981 to November 1984. The
mean age of the subjects was 51, the mean duration of
symptoms was 5.4 months. Physical therapy interven-
tion averaged 2.2 months and the mean follow-up was
22 months after manipulation. The study included
patients who had not responded to “adequate” physical
therapy. Significant differences were found in ROM
pretreatment to posttreatment immediately following
CHAPTER 11 FROZEN SHOULDER 329

Table 11-5

RESEARCH ON CLOSED MANIPULATION AND ARTHROSCOPIC OR OPEN RELEASE IN TREATMENT OF THE FROZEN SHOULDER

Sample Use of Physical

Author & Year Size Purpose Therapy Results

Hill JJ, Bogumill H: N = 15 To report the effects Active ROM Significant difference in ROM
1988 of manipulation and pretreatment to posttreatment,
if patients of this but not posttreatment to
treatment regain full discontinue, biggest change
ROM sooner than the initially
natural recovery
Kivimaki J, Pohjolainen N = 24 To study the effects of None No enhancement with
T: 2001 manipulation with and injection
without steroid injection
Pollock RG, Duralde N = 30 To determine the Immediate ROM 1) 50% unlimited function
XA, Platow SL, effectiveness of while block active 2) 33% satisfactory function
Bigliani LU: 1994 arthroscopy and 3) 17% limited function
manipulation under
anesthesia
Segmuller HE, Taylor N = 24 To determine the In recovery 88% satisfied
DE, Hogan CS, Saies effectiveness of inferior 76% return to normal or near
AD, Hayes MG: 1995 capsular release on normal function
frozen shoulder
Ogilvie-Harris DJ, N = 40 To compare the Home exercise Manipulation group:
Bigop DJ, Fitsiabolis effectiveness of program and active 1) Pain: 8 none, 8 mild, 2
DP, Mackay M: 1995 manipulation versus assistive ROM; moderate
anterior structure physical therapy 2) ROM: abduction 11
division in frozen within first week normal, external rotation
shoulder pain, ROM, 10 normal
and function; 20 each Division group:
group, not random 1) Pain: 16 none, 4 mild
Groups: 2) ROM: abduction 17 normal,
1) manipulation with external rotation 16 normal
scope before and after
2) divided contracted
structures
Warner JJP, Allen A, N-23 To describe the results of Physical therapy 1) Flexion increase mean 49°
Marks PH, Wong P: arthroscopic release first day and 2) External rotation at 0°
1996 passive ROM; increase mean 42°
active assistive 3) External rotation at 90°
ROM; home mean increase 53°
exercise program 4) Internal rotation increase
8 spinous process levels
5) ROM increases not
significant when compared
with contralateral normal
shoulder
330 SECTION III SPECIAL CONSIDERATIONS
Table 11-5
RESEARCH ON CLOSED MANIPULATION AND ARTHROSCOPIC OR OPEN RELEASE IN TREATMENT OF THE FROZEN SHOULDER—
cont’d
Sample
Author & Year Size Purpose
Warner JJP, Allen A, N = 18 To describe the authors’
Marks PH, Wong P: experience with
1997 arthroscopic release of the
anterior shoulder capsule
in treatment of
postoperative stiffness
Watson L. Dulziel R, N = 73 To determine the
Story I: 2000 effectiveness of
arthroscopic capsulotomy
in treatment of frozen
shoulder
Gerber C, Espinosa N, N = 45 To study the outcome of
Perren TG: 2001 arthroscopic capsulotomy
for treatment of shoulder
stiffness after failure of
conservative treatment
and to determine whether
different etiologies
have a different prognosis
Omari A, Bunker TD: N = 75 To describe the
2001 effectiveness of surgical
release of frozen shoulder
in shoulders with severe
disease that fail to release
with manipulation under
anesthesia
the manipulation. No change, however, was found post-
manipulation to the time of discharge. Flexion was
found to increase significantly from pretreatment to
posttreatment, but a decrease in ROM occurred from
posttreatment to discharge. No significant differences
were found pretreatment to posttreatment with internal
or external rotation. The researchers reported that 10%
of the subjects returned to work between 2 and 6 months
following manipulation, which is of shorter duration
than the reported natural history of the condition. The
researchers did not report what “natural history” values
they used to make their comparisons.
Use of Physical
Therapy Results
Physical therapy 1) ROM mean significant
daily for ROM and increase
strengthening 2) Flexion increase 51°
3) External rotation increase
31/40°
4) Internal rotation increase 6
spinous process levels
Graduated 1) Significant decrease in pain
2) Significant increase in ROM
5.5 weeks
Passive ROM with Best results idiopathic, poorest
block 2-4 days result posttraumatic
Functional 26% increase (68%
of normal shoulder) statistically
significant
Formal physical 1) Flexion increased 97°
therapy home 2) External rotation increased 8°
exercise program 3) Internal rotation with
for ROM extension increased from
sacrum to T7
Kivimaki and Pohjolainen21 performed a random
clinical trial in 2001. Twenty-four subjects were ran-
domly exposed to manipulation under anesthesia with
or without steroid injection. No enhancement was found
with steroid injection. Twenty-two of the 23 subjects
demonstrated improved mobility. Pain was decreased in
all but three subjects. The mean follow-up period was 4
months.
Pollock and associates36 in 1994 used arthroscopy and
manipulation under anesthesia for the resistant frozen
shoulder. The mean age of the 30 subjects was 49, with
average symptom duration of 14 months before the
CHAPTER 11 FROZEN SHOULDER
intervention. The subjects received arthroscopic guided
manipulation, debridement, and decompression. The
subjects received physical therapy for ROM immedi-
ately following the procedure. The surgical procedures
were individualized for each subject. At follow-up, the
results were as follows: 50% of subjects reported unlim-
ited function (flexion [FL] 170/ER 50/IR T10), 33%
reported satisfactory function (FL 160/ER 40/IR L1,
slight pain), and 17% of subjects reported limited func-
tion (FL less than 140 degrees, moderate to severe pain).
No statistical analysis was reported.
Segmueller and associates43 studied the effect of infe-
rior capsular release without manipulation on 24 sub-
jects with frozen shoulder. The mean age of the subjects
was 50 and the mean follow-up was 13.5 months fol-
lowing intervention. Subjects were included in this study
if no progress had been reported or if ROM had been
lost during a 6-week time period of physical therapy.
Patients who had already undergone surgical procedures
on the same shoulder were excluded from the study.
Excellent results on the Constant-Murley Shoulder tests
were obtained following the procedure, with the average
score being 87%. Eighty-eight percent of the subjects
were satisfied and 76% had a return to normal or near
normal function.
Ogilvie-Harris and associates30 looked at the effec-
tiveness of manipulation versus arthroscopic anterior
structure division in frozen shoulder. Subjects were
included if they had previously received physical therapy
and cortisone injection; distension arthrography; and
continued to have difficulty for more than 1 year fol-
lowing intervention. Forty subjects, divided into two
equivalent groups, were studied. One group received
manipulation with arthroscopy before and after the pro-
cedure, while the other group underwent arthroscopic
release of contracted anterior structures. All subjects
performed hourly AAROM physical therapy and con-
ducted 6 weeks of outpatient physical therapy. No dif-
ferences were reported between the groups for ROM.
Significant differences were reported for improved func-
tion in the division group. Follow-up was reported in a
range of 2 to 5 years. The researchers theorized that a
significant difference in ROM between the groups
would be found using a larger sample size, thus increas-
ing the impact of the study.
In 1996 Warner and colleagues48 described similar
increases in ROM in 23 subjects. The mean age of the
subjects was 48 and the mean duration of symptoms was
331
48 months. Subjects included in the study had failed
conservative treatment and closed manipulation. Fol-
lowing arthroscopic release of chronic refractory frozen
shoulder, increases were reported in both function and
ROM. In a similar study in 1997, Warner and associ-
ates49 reported similar results using arthroscopic release
in secondary frozen shoulder following rotator cuff tear
repair.
Watson and associates50 performed arthroscopic cap-
sulotomy on 73 subjects with a mean age of 52. The
average duration of symptoms was 19.7 months before
the intervention. Physical therapy intervention consisted
of pendulum exercises, stretching, and AROM on days
one through four. Modalities and massage were initiated
on day 10. Mobilization and isometrics were initiated at
2 weeks, and isotonic strengthening was initiated at 4
weeks. Follow-up was reported on average 8.9 weeks fol-
lowing the intervention. Increased ROM and decreased
pain were reported at 5.5 weeks. No statistical analysis
was reported.
Gerber and colleagues14 compared arthroscopic out-
comes for the following: idiopathic, postsurgical, and
posttraumatic frozen shoulder groups. The mean age of
the 45 subjects was 50.8. The average follow-up
occurred 26 months after the intervention. The
researchers concluded that those with an idiopathic
frozen shoulder responded the best to arthroscopic treat-
ment of frozen shoulder, with a 26% increase in func-
tion. The posttraumatic group demonstrated the worst
outcome.
Omari and Bunker33 reported improvements in pain
and ROM following open release in patients who failed
to release under closed manipulation. Seventy-five sub-
jects, mean age 52.6 years, were followed for an average
of 19.52 months. These subjects demonstrated a mean
increase in flexion of 97°, external rotation of 8°, and
internal rotation by 10 spinous process levels. Formal
physical therapy was prescribed, but was not controlled.
A significant increase in function was also reported. No
statistical analysis was provided.
Through this review of scientific research, it appears
that in the very early stages of frozen shoulder, physical
therapy—consisting of AROM exercises and end-ROM
linear translation/mobilization techniques, especially
under local or interscalene brachial plexus block—is
beneficial.* Traction using TENS was noted in one case
*References 15, 25, 29, 34, 41, 47, 51.
332 SECTION III SPECIAL CONSIDERATIONS
report, with improvements in ROM and pain.40 Weiss
and Ting52 conducted arthrographic assisted intraartic-
ular injections and reported no benefit on ROM.
However, use of intraarticular steroid injections in the
first 3 weeks of therapy may be beneficial for pain
control.18,22,23,29,40 Following failure of conservative treat-
ment, distension arthrography—especially with gentle
manipulation/mobilization and AROM exercises—led
to successful increases in ROM.2,13,24,32 Other measures
may be needed for pain control.32
Closed manipulation of the GH joint has been
studied extensively. Much controversy exists over the
possible maladies associated with this intervention, such
as fracture and nerve injury.* Two studies evaluated the
effects of steroid injection during manipulation and the
usefulness of oral steroids. No enhancement of ROM
was reported with either treatment.37,49 Surgical treat-
ment, both arthroscopic and open capsular release,†
offered favorable results. However, the sample sizes were
small. Researchers who are prosurgical release‡ argue
against closed manipulation because of inconsistent
results and unpredictable release of capsular structures.
Arthroscopic and open controlled release is becoming
favored by many surgeons to prevent the morbidities
reported with closed manipulation.
The lack of a working definition of frozen shoulder
has led to inconsistencies among inclusion and exclusion
criteria used in scientific research. Most studies reviewed
reported no or minimal statistical analysis making com-
parison difficult and the credibility of results question-
able. The sample size in most studies was small,
decreasing power. All studies reviewed were missing
discussion about sources of secondary variance. The
outcome measurement tools that were used were not
consistent among the studies. Furthermore, the outcome
measures used had no reliability or validity studies to
support their use. Carefully controlled clinical trials need
to be performed to further evaluate treatment efficacy of
the frozen shoulder.
Treatment Objectives
The studies demonstrate that various forms of treatment
are effective in increasing ROM and reducing pain in
*References 14, 24, 30, 33, 43, 48-50
†
References 14, 30, 33, 36, 43, 48-50.
‡
References 12, 14, 30, 33, 36, 43, 48-50.
patients with frozen shoulder. Physical therapy should
play a major role in the initial treatment of frozen shoul-
der. After careful assessment and objective evaluation to
confirm the diagnosis of frozen shoulder, the current
stage of the condition, and identification of any causal
factors, physical therapists should be prepared to design
an individual treatment program based on their assess-
ment. The physician, in conjunction with the physical
therapist, should direct each case if physical therapy is
to be used alone or with other medical or surgical treat-
ment.
The treatment objective during the painful phases are
pain control and reduction of inflammation. A com-
bination of medical pharmaceutical management and
exercise with modalities may help accomplish them. The
physical therapist should encourage the patient to use
his or her arm as aggressively as the condition allows. A
home exercise program should be recommended that
promotes ROM in the pain-free range, especially in
internal and external rotation. Promotion of elevation
with compensatory scapular motion can increase
impingement and inflammation, often causing a loss of
glenohumeral mobility. The patient should be educated
on glenohumeral elevation within a range to prevent
impingement and compensatory motion. The physical
therapist may provide gentle mobilization to promote
accessory joint motion.
Heat application may be used to promote soft tissue
pliability and pain reduction. Other investigators rec-
ommend heating the joint capsule before stretching,
with the belief that increased circulation acts as an anal-
gesic.9 Cryotherapy may also be used before stretching
to provide an analgesic effect or following stretching to
prevent increased inflammation. This may be especially
beneficial in the painful phase of frozen shoulder.
During the stiff/frozen and thawing phases, treat-
ment objectives should focus on pain reduction and
regaining ROM within a pain-free range. Exercise pre-
scription should include active-assistive, active, and iso-
metric activities. The physical therapist should provide
mobilization to attempt to restore joint mobility. End-
range linear translation/gliding techniques have been
supported in research for treatment efficacy over tradi-
tional manipulative techniques.35,41,47,51 Target-specific
mobilization should be performed with prepositioning
of the GH joint to address specific structures such as
the posterior-inferior capsule or the coracohumeral
ligament. The patient’s capsular restrictions must be
CHAPTER 11 FROZEN SHOULDER
carefully assessed to determine the most effective
techniques.
When designing any treatment program, the physi-
cal therapist should consider patient alignment and
movement impairments so that optimal biomechanics
can be achieved around the joint. Sahrmann42 has cate-
gorized key tests and signs that may assist the physical
therapist in evaluation and treatment of frozen
shoulder.
Movement impairments, which are especially helpful
to identify to optimize the proper biomechanics of the
shoulder, are as follows:
1. Loss of both passive and active ROM in all
directions, most commonly in the capsular pattern
2. Pain increases toward the limitations of motion
3. Excessive humeral superior glide during shoulder
abduction and flexion
4. Decreased glenohumeral crease just distal to the
acromion with the arm overhead
5. Compensatory movement—excessive scapular
motion
6. Impairments of muscle recruitment—dominance of
the deltoid over the rotator cuff; dominance of the
upper trapezius over the lower trapezius
7. Impairments in muscle strength—weakened rotator
cuff
Other Treatment
The patient is often required to perform a home stretch-
ing program to increase glenohumeral joint motion.
STRESS RELAXATION (SR)
-CONSTANT DISPLACEMENT- VARIABLE FORCE
Force
Displacement
Time
Figure 11-1 Loading conditions.
333
Joint Active Systems ( JAS), Effingham, Indiana pro-
vides an orthosis that is patient applied and directed,1
for contracture stretching of the shoulder. This is used
as an adjunct to traditional physical therapy. This system
of stretching is based on the principles of stress-
relaxation (Figure 11-1) and static progressive stretch-
ing (Figure 11-2). The system provides an external
rotation stretch, from a range of neutral to 90° of abduc-
tion in the scapular plane. Impingement often associated
with stretching into elevation can be avoided with use
of this orthosis. The treatment protocol is 30 minutes
one time a day the first week, two times daily the second
week, and never more than three times a day following
the third week. Donatelli and associates,11 following a
pretreatment, posttreatment study of 30 subjects,
reported an increase of 1.5° of elevation for every degree
gained into external rotation. Both groups received
physical therapy, while group I performed a home exer-
cise program in three planes of motion, and group II
used the JAS shoulder orthosis twice a day for 30
minutes. Group II demonstrated twice the gain of ROM
in external rotation and elevation compared with group
I. The researchers also reported greater patient com-
pliance, attributing this to shorter wearing times. The
researchers concluded that the JAS shoulder orthosis is
a useful adjunct at home for treatment of frozen shoul-
der (Figure 11-3).
STATIC PROGRESSIVE STRETCH (SPS)
-INCREMENTAL AND PROGRESSIVE APPLICATION OF SR
Hold
Stretch
Hold
Stretch
Stretch
Hold
Stretch
Time
Figure 11-2 Static progressive stretch. Incremental
and progressive application of stress relaxation (SR).
334 SECTION III SPECIAL CONSIDERATIONS
Figure 11-3 A and B, Joint active systems ( JAS) shoulder arthrosis as a useful adjunct for treatment of frozen
shoulder.
Conclusion
This chapter has described the distinct clinical entity of
frozen shoulder and the confusion that exists about this
condition. Clearly, in the clinical setting, the condition
of frozen shoulder can be painful and debilitating to
many patients. By understanding a typical presentation
of primary frozen shoulder, and the literature support-
ing various treatment approaches, one can apply this
knowledge to make treatment decisions based on evi-
dence. The evidence at present supports varied treat-
ment approaches, which are largely dependent on the
stage of presentation for treatment and the failure of
previous treatments. More clinical trials, with a clarified
working definition for inclusion and exclusion criteria,
will assist in promoting evidence-based practice and
treatment of frozen shoulder.
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18. Hill JJ, Bogumill H: Manipulation in the treatment of frozen
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19. Itoi E, Tabata S: ROM and arthrography in the frozen
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20. Janda DH, Hawkins R: Shoulder manipulation in patients
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22. Lee M, Haq AMMM, Wright V: Periarthritis of the shoul-
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44. Shaffer B, Tibone JE, Kerlan RK: Frozen shoulder: a
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47. Vermeulen HM, Obermann WR, Burger BJ, et al: End
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51. Weiser H: Painful primary frozen shoulder, mobilization
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Etiology and Evaluation
of Rotator Cuff
Pathologic Conditions
and Rehabilitation
T he integral functions of the rotator cuff muscu-
lature, combined with the large multiplanar
movement patterns inherent in both activities
of daily living and sport activity in the glenohumeral
joint, make the rotator cuff vulnerable to injury—
commonly requiring treatment in both orthopedic and
sports physical therapy. The rotator cuff musculature
functions to stabilize the glenohumeral joint in four
primary ways: (1) by its passive bulk, (2) by developing
muscle tension, which compresses the joint surfaces
together, (3) by moving the humerus with respect to the
glenoid and thus tightening the static stabilizers (capsu-
lar-ligamentous restraints), and (4) by limiting the arc
of motion of the glenohumeral joint by muscle tension.1
As one of the primary dynamic stabilizing structures of
the glenohumeral joint, high-intensity concentric and
eccentric rotator cuff muscular activity has been reported
during simple elevation in the scapular plane,2 and
during the tennis serve3-5 and throwing motion.6,7 To
better understand the rehabilitation process required to
restore normal shoulder joint arthrokinematics and
pain-free glenohumeral joint function, the etiology and
classification must first be developed for rotator cuff
injury.
337
12
Todd S. Ellenbecker
Etiology and Classification of
Rotator Cuff Injury
The etiology of the again—take out “the” rotator cuff
pathologic conditions can be described along a contin-
uum, ranging at one end from overuse microtraumatic
tendonosis to macrotraumatic full-thickness rotator cuff
tears (Box 12-1). A second continuum of rotator cuff
etiology consists of glenohumeral joint instability and
primary impingement or compressive disease.8 The clin-
ical challenge of treating the patient with a rotator cuff
injury begins with a specific evaluation and clear under-
standing of the underlying stability and integrity of not
only the components of the glenohumeral joint, but also
the entire upper extremity kinetic chain.
There are several ways of classifying rotator cuff
injury. One classification method is based upon the sus-
pected or proposed pathophysiology.9 For the purpose
of this chapter, four classifications of rotator cuff
pathologic conditions will be discussed: primary com-
pressive disease, secondary compressive disease, tensile
disease/injury, and macrotraumatic failure. Additionally,
this discussion will involve the relatively new concept of
undersurface or posterior impingement.
338 SECTION III SPECIAL CONSIDERATIONS
Box 12-1
Etiologic Factors Associated With Rotator Cuff
Pathologic Conditions
Microtrauma
Tendonosis
Instability
Macrotrauma
Rotator cuff tear
Compressive disease
Primary Compressive Disease
Primary compressive disease or impingement is a direct
result of compression of the rotator cuff tendons
between the humeral head and the overlying anterior
third of the acromion, coracoacromial ligament, cora-
coid, or acromioclavicular joint.10,11 The physiologic
space between the inferior acromion and superior
surface of the rotator cuff tendons is termed the sub-
acromial space. It has been measured using anteropos-
terior radiographs and found to be 7 to 13 mm in size
in patients with shoulder pain12 and 6 to 14 mm in
normal shoulders.13
Biomechanical analysis of the shoulder has produced
theoretical estimates of the compressive forces against
the acromion with elevation of the shoulder.14-16 Poppen
and Walker14 calculated this force at 0.42 times body
weight, with Lucas15 estimating this force at 10.2 times
the weight of the arm. Peak forces against the acromion
were measured between 85° and 136° of elevation,16 a
position inherent in sport-specific movement patterns7,17
and commonly incurred in ergonomic and daily activi-
ties. The position of the shoulder in forward flexion,
horizontal adduction, and internal rotation during the
acceleration and follow-through phases of the throwing
motion are likely to produce subacromial impingement
caused by abrasion of the supraspinatus, infraspinatus,
or biceps tendon.7 These data provide scientific ration-
ale for the concept of impingement or compressive
disease as a cause of rotator cuff injury.
Neer10,11 has outlined three stages of primary
impingement as it relates to rotator cuff injury. Stage I,
edema and hemorrhage, results from the mechanical
irritation of the tendon because of an impingement that
occurs with overhead activity. This is characteristically
observed in younger patients who are more athletic and
is described as a reversible condition with conservative
physical therapy. The primary symptoms and physical
signs of this stage of impingement or compressive
disease are similar to the other two stages and consist of
a positive impingement sign, painful arc of movement,
and varying degrees of muscular weakness.11
The second stage of compressive disease outlined by
Neer is termed fibrosis and tendonitis. This occurs from
repeated episodes of mechanical inflammation, and can
include thickening or fibrosis of the subacromial bursae.
The typical age range for this stage of injury is 25 to 40
years. Neer’s stage III impingement lesion is termed
bone spurs and tendon rupture and is the result of
continued mechanical compression of the rotator cuff
tendons. Full-thickness tears of the rotator cuff, partial-
thickness tears of the rotator cuff, biceps tendon lesions,
and bony alteration of the acromion and acromioclavic-
ular joint may be associated with this stage.10,11 In
addition to bony alterations, which are acquired with
repetitive stress to the shoulder, the native shape of the
acromion is relevant.
The specific shape of the overlying acromion process,
termed acromial architecture, has been studied in relation
to full-thickness tears of the rotator cuff.18,19 Bigliani and
associates18 described three types of acromions: type I
(flat), type II (curved), and type III (hooked). A type III
or hooked acromion was found in 70% of cadaveric
shoulders with a full-thickness rotator cuff tear, whereas
type I acromions were only associated with 3% of cada-
veric shoulders.18 In a series of 200 clinically examined
patients, 80% with an abnormal arthrogram had a type
III acromion.19
Surgical treatment for primary compressive disease
generally consists of decompression of 8 mm of the ante-
rior acromion, with preservation of the insertion of the
deltoid, and beveling of approximately 2 cm posteriorly
to provide additional space for the inflamed tendons.9
Open repairs of associated full-thickness tears of the
rotator cuff are routinely performed along with the
decompression acromioplasty to address the offending
overlying acromion and repair the full-thickness defect
in the rotator cuff. The method of open repair has spe-
cific ramifications on the postoperative rehabilitation.
Specifically, the type of open surgical approach can
either detach the deltoid origin from the lateral aspect
of the clavicle and acromion, which can be referred to
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION
as the “traditional anterior approach,” or the deltoid can
be split vertically along the direction of its fibers, which
is commonly referred to as the “deltoid splitting” or
“mini-open” approach. The preservation of the deltoid
origin used during the “deltoid splitting” approach is
of benefit as rehabilitation can commence sooner with
active assistive and active range of motion as compared
with the traditional deltoid detachment approach. The
traditional approach often necessitates 6 to 8 weeks
without active or resistive exercise to protect not only
the healing rotator cuff, but also the healing deltoid
origin, which is reattached following rotator cuff repair.
Knowledge of the specific surgical technique used on a
patient referred to physical therapy following an open
rotator cuff repair of a full-thickness rotator cuff tear is
imperative for optimal progression in postoperative
rehabilitation.
Secondary Compressive Disease
Impingement or compressive symptoms may be second-
ary to underlying instability of the glenohumeral joint.8,9
Attenuation of the static stabilizers of the glenohumeral
joint, such as the capsular ligaments and labrum from
the excessive demands incurred in throwing or overhead
activities, can lead to anterior instability of the gleno-
humeral joint. Because of the increased humeral head
translation, the biceps tendon and rotator cuff can
become impinged secondarily to the ensuing instabil-
ity.8,9 A progressive loss of glenohumeral joint stability
is created when the dynamic stabilizing functions of the
rotator cuff are diminished from fatigue and tendon
injury.9 The effects of secondary impingement can lead
to rotator cuff tears as the instability and impingement
continue.8,9
Tensile Overload
Another etiologic factor in rotator cuff injury is repeti-
tive intrinsic tension overload. The heavy, repetitive
eccentric forces incurred by the posterior rotator
cuff musculature during the deceleration and follow-
through phases of overhead sport activities can lead to
overload failure of the tendon.9,20 The pathologic
changes referred to as “angiofibroblastic hyperplasia” by
Nirschl20 occur in the early stages of tendon injury and
can progress to rotator cuff tears from the continued
tensile overload.9
Recent research by Kraushaar and Nirschl21 in a his-
tologic study of the extensor carpi radialis brevis, the
339
primary tendon involved in lateral humeral epicondyli-
tis, has identified specific characteristics inherent in an
injured tendon. Based on their histopathologic study,
they recommend the term tendonosis be used rather
than tendonitis to more accurately describe tendon
injury. Histopathologic study of tendons taken from
areas of chronic overuse in the human body do not
show large numbers of macrophages, lymphocytes,
or neutrophils. “Rather, tendonosis appears to be a
degenerative process, which is characterized by the
presence of dense populations of fibroblasts, vascular
hyperplasia, and disorganized collagen.”21 Kraushaar
and Nirshl point out that it is unknown why
tendonosis is painful, given the absence of acute inflam-
matory cells, nor is it known why the collagen fails to
mature.
In the biomechanical study of highly skilled
pitchers,7 the tensile stresses incurred by the rotator cuff
during the arm deceleration phase of the throwing
motion—to resist joint distraction, horizontal adduc-
tion, and internal rotation—are reported to be as high
as 1090 N. The presence of either acquired or congeni-
tal capsular laxity and labral insufficiency can greatly
increase the tensile stresses to the rotator cuff muscle
tendon units.8,9
Macrotraumatic Tendon Failure
Unlike the previously mentioned rotator cuff classifica-
tions, cases involving macrotraumatic tendon failure
usually entail a previous or single traumatic event in the
clinical history.9 Forces encountered during the trau-
matic event are greater than the normal tendon can tol-
erate. Full-thickness tears of the rotator cuff, with bony
avulsions of the greater tuberosity, can occur from single
traumatic episodes. According to Cofield,22 injuries to
normal tendons do not occur easily because 30% or more
of the tendon must be damaged to produce a substan-
tial reduction in strength. Although a single traumatic
event, which resulted in tendon failure, is often reported
by the patient in the subjective exam, repeated micro-
traumatic insults and degeneration over time may have
created a substantially weakened tendon. The tendon
ultimately failed under the heavy load described by the
patient. Full-thickness rotator cuff tears require surgical
treatment and aggressive rehabilitation to achieve a
positive functional outcome.9,11 Further specifics of
rotator cuff surgical treatment are discussed later in this
chapter.
340 SECTION III SPECIAL CONSIDERATIONS
Posterior or “Undersurface” Impingement
One additional cause for the undersurface tear of the
rotator cuff in the young athletic shoulder is termed pos-
terior, inside, or undersurface impingement.23,24 This
phenomenon was originally observed by Walch during
shoulder arthroscopy with the shoulder placed in the
90/90 position. Placement of the shoulder in a position
of 90° of abduction and 90° of external rotation causes
the supraspinatus and infraspinatus tendons to rotate
posteriorly. This more posterior orientation of the
tendons aligns them such that the undersurfaces of the
tendons rub on the posterior-superior glenoid lip and
become pinched or compressed between the humeral
head and the posterior-superior glenoid rim (Figure 12-
1).23 Individuals having posterior shoulder pain brought
on by positioning of the arm in 90° of abduction and 90°
or more of external rotation, typically from overhead
positions in sport or industrial situations, may be
considered as potential candidates for undersurface
impingement.
The presence of anterior translation of the humeral
head with maximal external rotation and 90° of abduc-
tion, which has been confirmed arthroscopically during
the subluxation relocation test, can produce mechanical
Figure 12-1 Schematic representation of posterior-
superior glenoid impingement between the posterior edge of
the glenoid and the deep surface of the supraspinatus and
infraspinatus tendons. (From Loehr JF, Helmig P, Sojbjerg JO, et al:
Shoulder instability caused by rotator cuff lesions: an in vitro study, Clin
Orthop 303:84, 1994.)
rubbing and fraying on the undersurface of the rotator
cuff tendons. Additional harm can be caused by the
posterior deltoid if the rotator cuff is not functioning
properly. The posterior deltoid’s angle of pull pushes
the humeral head against the glenoid, accentuating the
skeletal, tendinous, and labral lesions.23 Walch and asso-
ciates24 arthroscopically evaluated 17 throwing athletes
with shoulder pain during throwing and found under-
surface impingement that resulted in 8 partial-thickness
rotator cuff tears and 12 lesions in the posterior-
superior labrum. Impingement of the undersurface of
the rotator cuff on the posterior-superior glenoid labrum
may be a cause of painful structural disease in the over-
head athlete.
Additional research confirming the concept of poste-
rior or undersurface impingement in the overhead
athlete has been published.25,26 Halbrecht and associ-
ates25 have confirmed, via magnetic resonance imaging
(MRI) performed in the position of 90° of abduction
and 90° of external rotation, contact of the undersurface
of the supraspinatus tendon against the posterior-
superior glenoid in baseball pitchers with the arm placed
in 90° of external rotation and 90° of abduction. Ten col-
legiate baseball pitchers were examined and in all 10
pitchers, physical contact was encountered in this posi-
tion. Paley and associates26 also published a series on
arthroscopic evaluation of the dominant shoulder of 41
professional throwing athletes. With the arthroscope
inserted in the glenohumeral joint, they found that 41
of 41 dominant shoulders evaluated had posterior un-
dersurface impingement between the rotator cuff and
posterior-superior glenoid. In these professional throw-
ing athletes, 93% had undersurface fraying of the rotator
cuff tendons and 88% showed fraying of the posterior-
superior glenoid.
Additional Etiologic
Factors in Rotator Cuff
Pathologic Conditions
In addition to the etiologic factors already mentioned for
rotator cuff pathologic conditions, other factors inher-
ent in the rotator cuff have relevance with respect to
injury. The vascularity of the rotator cuff, specifically the
supraspinatus, has been extensively studied beginning in
1934 by Codman.27 In his classic monograph on rup-
tures of the supraspinatus tendon, Codman described
a critical zone of hypovascularity located 0.5 inch
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION
proximal to the insertion on the greater tuberosity.27
This region appeared anemic with the appearance of an
infarction. The biceps long head tendon was found to
have a similar region of hypovascularity in its deep
surface 2 cm from its insertion.28 Rathburn and
MacNab29 reported the effects of position on the
microvascularity of the rotator cuff. With the gleno-
humeral joint in a position of adduction, a constant area
of hypovascularity was found near the insertion of the
supraspinatus tendon. This consistent pattern was not
observed with the arm in a position of abduction. These
authors termed this the “wringing out phenomenon” and
also noticed a similar response in the long head tendon
of the biceps. This positional relationship has clinical
ramifications for both exercise positioning and immobi-
lization. Brooks and colleagues30 found no significant
difference between the tendinous insertions of the
supraspinatus and infraspinatus tendons, with both
being hypovascular with quantitative histologic analysis.
Contradictory research published by Swiontowski
and associates31 does not support this region of hypo-
vascularity or critical zone. Blood flow was greatest in
the critical zone in living patients with rotator cuff ten-
donitis from subacromial impingement measured with
Doppler flowmetry.
Anatomic Description of
Rotator Cuff Tears
There are several primary types of rotator cuff tears
commonly described in literature. Full-thickness tears in
the rotator cuff consist of tears that comprise the entire
thickness (from top to bottom) of the rotator cuff
tendon or tendons. Full-thickness tears are often initi-
ated in the critical zone of the supraspinatus tendon and
can extend to include the infraspinatus, teres minor, and
subscapularis tendons.32 Often associated with a tear in
the subscapularis tendon is subluxation of the biceps
long head tendon from the intertubercular groove, or
either partial or complete tears of the biceps tendon.
Histologically, full-thickness rotator cuff tears show a
variety of findings ranging from almost entirely acellu-
lar and avascular margins to neovascularization with
cellular infiltrate.32
The effects of a full-thickness rotator cuff tear on
glenohumeral joint stability were studied by Loehr and
associates.33 Changes in stability of the glenohumeral
joint were assessed with selective division of the
341
supraspinatus and/or infraspinatus tendons. Their find-
ings indicated that a one-tendon lesion of either the
supraspinatus or infraspinatus did not influence the
movement patterns of the glenohumeral joint, whereas
a two-tendon lesion induced notable changes compati-
ble with instability of the glenohumeral joint.33 There-
fore patients with full-thickness rotator cuff tears may
have additional stress and dependence placed on the
dynamic stabilizing function of the remaining rotator
cuff tendons because of increased humeral head transla-
tion and the ensuing instability.
Additional research on full-thickness rotator cuff
tears has had notable clinical ramifications. Miller and
Savoie34 examined 100 consecutive patients with full-
thickness tears of the rotator cuff to determine the inci-
dence of associated intraarticular injuries. Seventy-four
of 100 patients had one or more coexisting intraarticu-
lar abnormalities, with anterior labral tears occurring in
62 and biceps tendon tears in 16. The results of this
study clearly indicate the importance of a thorough clin-
ical examination of the patient with a rotator cuff injury.
A second type of rotator cuff tear is an incomplete or
partial-thickness tear. Partial-thickness tears can occur
on the superior surface (bursal side) or undersurface
(articular side) of the rotator cuff. Although both bursal
and articular side tears are partial-thickness tears of the
rotator cuff, notable differences in causes are proposed
for each.9
Neer10,11 and Fukoda and associates35 have both
emphasized that superior surface (bursal side) tears in
the rotator cuff are the result of subacromial impinge-
ment. In the classification scheme listed earlier in this
chapter, tears on the superior or bursal side of the rotator
cuff are generally associated with both primary and sec-
ondary compressive disease and macrotraumatic tendon
failure. The progression of the mechanical irritation
on the superior surface can produce a partial-thickness
tear, which can ultimately progress to a full-thickness
tear.9-11
Partial-thickness tears on the undersurface or articu-
lar side of the rotator cuff are generally associated with
tensile loads and glenohumeral joint instability.9,36 Tears
on the undersurface of the rotator cuff are commonly
found in overhead-throwing athletes, where anterior
instability, capsular and labral insufficiency, and dynamic
muscular imbalances are often reported. To further
understand the differing causes of rotator cuff tears,
Nakajima and colleagues36 performed a histologic and
342 SECTION III SPECIAL CONSIDERATIONS
biomechanical study of the rotator cuff tendons. Bio-
mechanically, their results showed greater deformation
and tensile strength of the bursal side of the supraspina-
tus tendon. The bursal side of the supraspinatus tendon
was composed of a group of longitudinal tendon
bundles, which could disperse a tensile load and gener-
ate greater resistance to elongation than the articular or
undersurface of the tendon. These authors found the
articular surface to be composed of a tendon, ligament,
and joint capsule complex that elongated poorly and tore
more easily.36 The results of this study further reinforce
the proposed cause of the tensile stresses producing
undersurface rotator cuff tears.
One final type or classification of rotator cuff tear is
the intratendinous or interstitial rotator cuff tear. This
tear develops between the bursal and articular side layers
of the degenerated tendon.37 Shear within the tendon
appears to be responsible in the pathogenesis of this
rotator cuff tear.
Rotator cuff injury has several underlying etiologic
factors, as evidenced by the classification schemes and
scientific research in literature. Although it is imperative
to understand the common causes and classifications of
rotator cuff injury and types of rotator cuff tears, it is of
paramount importance that a structured, scientifically
based evaluation procedure is used not only to diagnose
rotator cuff injury, but also to ultimately identify the cause.
Clinical Evaluation of the
Shoulder for Rotator
Cuff Injury
It is beyond the scope of this chapter to completely cover
a comprehensive evaluation of the shoulder. This is pro-
vided in Chapter 4. A brief discussion is warranted,
however, on the specific aspects of the evaluation
process, which are of critical importance in identifica-
tion and delineation of rotator cuff injury. The multiple
causes and specific types of rotator cuff ailments are
reflected in the types of clinical tests routinely employed.
During the subjective examination, specific question-
ing—particularly for the overhead athlete—can greatly
assist in understanding the probable cause and type of
rotator cuff injury. Merely establishing the patient has
pain with overhead throwing or during the tennis serve
does not provide the optimal level of information as
would more specific questioning aimed at identifying
the stage or phase of the overhead activity. Specific
muscular activity patterns and joint kinetics inherent in
each stage of these sports activities can assist in the iden-
tification of compressive disease or tensile-type injuries.
The presence of instability, however subtle, during the
cocking phase of overhead activities can produce
impingement or compressive symptoms.9,23,24 A feeling
of instability or loss of control, however, during the
follow-through phase and during the predominantly
eccentric loading can indicate a tensile rotator cuff
injury.9 Additional questions regarding a change in sport
equipment, ergonomic environment, and training
history provide information that is imperative in under-
standing the stresses leading to injury.
Scapular Examination
Objective examination of the patient with rotator cuff
injury must include postural testing and observation.38
Tests are indicated to diagnose scapular posterior dis-
placement in multiple positions (waist level and 90° of
flexion or greater) with an axial load via the arms.
Testing for scapular dyskinesia can be performed using
the Kibler scapular slide test in both neutral and 90° ele-
vated positions.39 A tape measure is used to measure the
distance from a thoracic spinous process to the inferior
angle of the scapula. A difference of more than 1 to
1.5 cm is considered abnormal, and may indicate scapu-
lar muscular weakness and poor overall stabilization of
the scapulothoracic joint.39
Greater understanding of the importance the scapu-
lothoracic joint plays in rotator cuff injury has led to the
development of a more advanced and detailed clas-
sification system of scapular dysfunction. Kibler and
associates39 have outlined three primary scapular dys-
functions. This classification system proposed by Kibler
can assist the clinician in evaluating the patient with
more subtle forms of scapular malady. Zeier41 described
the massive disassociation of the scapula from the tho-
racic wall that occurs with injury to the long thoracic
nerve. This massive disassociation of the scapula from
the thoracic wall has been termed scapular winging.41
However, few patients with a rotator cuff condition clin-
ically display true scapular winging.
To address and better define the types of scapular
pathologic conditions seen clinically in patients with
rotator cuff injury, Kibler has developed a classification
system for subtle scapular dysfunction. This classifica-
tion system consists of three primary scapular conditions
and is named for the portion of the scapula that is most
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION 343

pronounced or most prominently visible when viewed superior scapular dysfunction as described by Kibler
during the clinical examination. The scapular examina- involves early and excessive superior scapular elevation
tion valuation recommended by Kibler includes visual during arm elevation (Figure 12-4). This typically results
inspection of the patient from a posterior view in resting from rotator cuff weakness and force couple im-
stance; again in the hands on hips position (hands placed balances.39
upon the hips such that the thumbs are pointing back- Kibler tested his scapular classification system using
ward on the iliac crests); and during active movement videotaped evaluations of 26 individuals with and
bilaterally in the sagittal, scapular, and frontal planes.40 without scapular dysfunction.40 Four evaluators, each
These scapular dysfunctions are termed inferior angle, blinded to the other evaluators’ findings, observed indi-
medial border, and superior.40 viduals and categorized them as having one of the three
In the inferior angle scapular dysfunction, the Kibler scapular dysfunctions or normal scapulohumeral
patient’s inferior border of the scapula is very prominent function. Intertester reliability measured using a kappa
(Figure 12-2). This results from an anterior tipping of
the scapula in the sagittal plane. It is most commonly
seen in patients with rotator cuff impingement as the
anterior tipping of the scapula causes the acromion to
be positioned in a more offending position relative to an
elevating humerus.40 The medial border dysfunction
results in the patient’s entire medial border being poste-
riorly displaced from the thoracic wall (Figure 12-3).
This occurs from internal rotation of the scapula in the
transverse plane, and is most often witnessed in patients
with glenohumeral joint instability. The internal rotation
of the scapula results in an altered position of the
glenoid—commonly referred to as “antetilting,” which
allows for an opening up of the anterior half of the
glenohumeral articulation.39 The antetilting of the
scapula has been shown by Saha42 to be a component of
the subluxation/dislocation complex in patients with
microtrauma-induced glenohumeral instability. Finally, Figure 12-3 Medial border scapular dysfunction.

Figure 12-2 Inferior angle scapular dysfunction. Figure 12-4 Superior scapular dysfunction.
344 SECTION III SPECIAL CONSIDERATIONS
coefficient was slightly lower (kappa = 0.4) than
intrarater reliability (kappa = 0.5). Kibler’s results
support the use of this classification system to catego-
rize subtle scapular dysfunction via careful observation
of the patient in static stance positions and during active
goal-directed movement patterns.
Glenohumeral Joint Range of
Motion Measurement
A detailed, isolated assessment of glenohumeral joint
range of motion is a key ingredient to a thorough
evaluation. Selective loss of internal rotation range of
motion on the dominant extremity was consistently
reported in elite tennis players43,44 and professional base-
ball pitchers. (Ellenbecker TS: unpublished data, 1991).
A goniometric method using an anterior containment
force by the examiner (Figure 12-5) to minimize the
scapulothoracic contribution and or substitution is rec-
ommended by Ellenbecker. The loss of internal rotation
range of motion is notable for two reasons. The rela-
tionship between internal rotation range of motion loss
(tightness in the posterior capsule of the shoulder) and
increased anterior humeral head translation has been
scientifically identified. The increase in anterior humeral
shear reported by Harryman and colleagues45 was man-
ifested by a horizontal adduction cross-body maneuver
similar to that incurred during the follow-through of
the throwing motion or tennis serve. Tightness of the
posterior capsule has also been linked to increased
superior migration of the humeral head during shoulder
elevation.46
Figure 12-5 Goniometric measurement of internal
rotation range of motion.
Recent research by Koffler and associates47 studied
the effects of posterior capsular tightness in a functional
position of 90° of abduction and 90° or more of exter-
nal rotation in cadaveric specimens. They found that
humeral head kinematics were changed or altered with
imbrication of either the inferior aspect of the posterior
capsule or imbrication of the entire posterior capsule. In
the presence of posterior capsular tightness, the humeral
head will shift in an anterior-superior direction as com-
pared with a normal shoulder with normal capsular rela-
tionships. With more extensive amounts of posterior
capsular tightness the humeral head was found to shift
posterosuperiorly.
Anterior translation of the humeral head and supe-
rior migration are two key factors indicated in rotator
cuff injury.8,9 Loss of internal rotation range of motion
has also been consistently identified in a population of
patients with glenohumeral joint impingement.48
Careful assessment of glenohumeral joint range of
motion is an important part of the clinical evaluation.
Measurement of active and passive internal and external
rotation at 90° of abduction—along with scapular plane
elevation, forward flexion, and abduction—is performed
during the examination of the patient with rotator
cuff injury. Documentation of combined functional
movement patterns (Apley’s scratch test),49 such
as internal rotation with extension, and abduction
and external rotation, is important. But specific, isolated
testing of glenohumeral joint motion is necessary
to identify important glenohumeral joint motion
restrictions.43
Recent research performed on elite junior tennis
players and professional baseball pitchers using a new
concept called the total rotation range of motion concept
has clinical ramifications for clinicians treating overhead
athletes with glenohumeral joint injury.50 Ellenbecker
and associates50 measured internal rotation, external
rotation, and total rotation range of motion with 90° of
glenohumeral joint abduction in 163 asymptomatic
overhead athletes (117 elite junior tennis players, 46 pro-
fessional baseball pitchers). The total rotation range of
motion is obtained simply by summing the internal and
external rotation measures together. Results indicated
significantly greater dominant-arm external rotation
range of motion (103° dominant arm vs. 94° nondomi-
nant arm) and significantly less internal rotation range
of motion (42° dominant arm vs. 54° nondominant arm)
in the professional baseball pitchers. However, despite
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION 345

these significant differences in internal and external for the infraspinatus and teres minor muscles is done
rotation, the total rotation range of motion was not sig- with resisting external rotation in both the neutral
nificantly different between extremities (145° vs. 146°).50 adducted and 90° abducted position.51 Resisted internal
In the elite junior tennis players, significantly less rotation in the neutral adducted position is generally
internal rotation range of motion was found on the recommended for the subscapularis.51 Care must be
dominant arm (45° vs. 56°), as well as significantly less taken when interpreting normal grade static manual
total rotation range of motion on the dominant arm muscle tests of the internal and external rotators.52
(149° vs. 158°).50 Normal grade 5/5 muscular strength has shown large
This total rotation range of motion has specific clin- variability when compared with isokinetic testing in
ical ramifications for treating athletes from this popula- patients with rotator cuff injury and in normal control
tion. If during the initial examination of a high-level groups.52 Regardless of this reported variability, the con-
baseball pitcher, the clinician finds a range of motion sistent application of manual muscle testing is highly
pattern of 120° of external rotation and only 30° of inter- recommended for the rotator cuff, deltoid, scapular sta-
nal rotation, some uncertainty may exist as to whether bilizers, and distal upper extremity muscle groups. For
that represents a range of motion deficit in internal rota- the patient with subtle symptoms and apparently normal
tion that requires rehabilitative intervention via stretch- muscular strength, more specific, dynamic, isokinetic
ing and specific mobilization. However, if measurement testing is indicated to better diagnose muscular weak-
of that patient’s nondominant extremity rotation reveals ness or unilateral strength imbalances.53 It is beyond the
90° of external rotation and 60° of internal rotation, the scope of this chapter to fully outline the specific isoki-
current recommendation based on the total rotation netic testing principles and interpretation of isokinetic
range of motion concept would be to avoid extensive tests for evaluation and rehabilitation of the patient
mobilization and passive stretching of the dominant with rotator cuff dysfunction. The reader is referred to
extremity since the total rotation range of motion in
both extremities is 150° (120° ER + 30° IR = 150° dom-
inant arm/90° ER and 60° IR = 150° total rotation non-
dominant arm). In elite-level tennis players, the total
active rotation range of motion can be expected to be up
to 10° less on the dominant arm.50
This total rotation range of motion concept can be
used as illustrated to guide the clinician during rehabil-
itation, specifically in the area of application of stretch-
ing and mobilization. This allows the clinician to best
determine which glenohumeral joint requires additional
mobility and which extremity should not have additional
mobility because of the obvious harm induced by
increases in capsular mobility and increases in humeral
head translation during aggressive upper extremity
exertion.

Muscular Strength Testing

Determination of isolated and gross muscular strength
during the examination of the patient with rotator cuff
injury not only has a major impact on the determination
of the underlying cause, but assists in the formulation
of a specific, objectively based rehabilitation program.
Isolated testing in the “empty can” position for the
supraspinatus is performed in the scapular plane, 30°
anterior to the coronal plane (Figure 12-6).42,51 Testing Figure 12-6 Supraspinatus MMT position.
346 SECTION III SPECIAL CONSIDERATIONS
reference 54 for a detailed isokinetic review for shoulder
rehabilitation.
Special Tests
The classic tests for evaluation of a patient with rotator
cuff injury are the impingement tests. The impingement
test reported by Neer10,11 places the shoulder in full
forward flexion with overpressure. This places the
supraspinatus under the coracoacromial arch and can
compress the tendon and reproduce the patient’s symp-
toms. A second impingement test, reported by Hawkins
and Kennedy,55 involves 90° of forward flexion with full
internal rotation. This test passes the rotator cuff under
the coracoacromial arch, with pain and a facial grimace
being indicative of an abnormality. A final impingement
test is the crossed-arm adduction test, which involves
horizontally adducting the humerus starting in 90° of
elevation. These impingement tests primarily indicate
the presence of rotator cuff injury from compression or
impingement.10,55
Tests to determine the integrity of the static stabiliz-
ers of the glenohumeral joint are a vital part of the com-
prehensive evaluation.8,9 Rotator cuff injury caused by
instability of the glenohumeral joint is a common occur-
rence in younger individuals and in overhead athletes.8,9
Clinical tests for instability must be routinely per-
formed on the patient with rotator cuff injury to deter-
mine the underlying mobility status and/or degree of
instability in the glenohumeral joint. Clinical tests for
instability of the glenohumeral joint include the appre-
hension and multidirectional instability (MDI) sulcus
signs, and the fulcrum, load and shift, and subluxation
relocation tests. (Further description of these clinical
tests can be found in Chapter 4.) The subluxation relo-
cation test popularized and originally described by
Jobe8,23 is performed with the patient supine, with 90°
of glenohumeral joint abduction and 90° of external
rotation. The examiner pushes the humeral head
forward, using one hand on the posterior aspect of the
patient’s shoulder. This places tension on the anterior
capsule and can produce a subtle anterior subluxation of
the humeral head, often reproducing the patient’s shoul-
der pain.8 The relocation portion of the test consists of
a posteriorly directed force produced by the examiner,
by placing the heel of the hand over the humeral head
anteriorly. This posterior force centralizes the humeral
head in the glenoid fossa. A positive subluxation/
relocation sign consists of provocation of the patient’s
symptoms—with the anterior translation in the position
of 90° of abduction and external rotation—with cessa-
tion of the symptoms with the relocation (posterior cen-
tralization force). Modification of the relocation test has
been recommended by Hamner and associates,56 who
recommend using the position of 90° of abduction and
full end range external rotation rather than only 90° of
external rotation as Jobe originally described to further
provoke the rotator cuff. Additionally, testing is per-
formed with subluxation and relocation forces not only
in 90° of abduction, but also at 110° and 120° of abduc-
tion. Arthroscopic confirmation of contact between the
undersurface of the rotator cuff and the posterior-
superior glenoid was confirmed using the modified sub-
luxation relocation test in overhead athletes with
shoulder dysfunction.56 This test is the primary one used
to diagnose individuals with posterior or undersurface
impingement of the rotator cuff.
Capsular mobility testing—with the patient supine at
30°, 60°, and 90° of abduction—is also performed with
both anterior and posterior stresses imparted. The ante-
rior stress applied at 30°, 60°, and 90° of abduction tests
the integrity of the superior, middle, and inferior gleno-
humeral ligaments, respectively.57 The degree of transla-
tion of the humeral head relative to the glenoid, and the
end feel, are bilaterally compared and recorded.9,58
Ellenbecker and colleagues57 tested the intrarater and
interrater reliability of the anterior humeral head trans-
lation test at 90° of abduction. Significantly greater
intrarater and interrater reliability was achieved when
examiners simply graded the movement of the humeral
head relative to whether the head traversed the glenoid
rim. Estimating end feel and further delineation of
humeral head translation grades complicated and jeop-
ardized both intrarater and interrater reliability.
Research recommendations call for the primary delin-
eation during humeral head translation tests to be
whether the humeral head stayed within the glenoid
when stress was applied (Grade I), or if the head tra-
versed up and over the glenoid rim with spontaneous
reduction upon removal of anterior load or stress (Grade
II). Capsular mobility testing with the shoulder in 90°
of abduction is particularly important because of the
important hammocklike stabilizing function of the infe-
rior glenohumeral ligament complex. The anterior band
of the inferior glenohumeral ligament provides critical
reinforcement against anterior translation of the
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION
humeral head (subluxation) with the arm in a position
of 90° of abduction and 90° of external rotation.57
An additional test to determine the degree of ante-
rior capsular laxity is the Lachman test of the shoulder.9
With the patient supine and the shoulder abducted
90°—with 45° of external rotation—an anterior force is
applied to the humeral head to assess anterior transla-
tion of the glenohumeral joint and to note the end point
of the anterior capsule.9
The consistent use of these instability tests will
provide the clinician with greater insight into the rela-
tionship, if any, between the patient’s rotator cuff injury
and glenohumeral joint instability. The identification
of either anterior or multidirectional glenohumeral
joint laxity should lead to a treatment plan addressing
the instability.9 The special tests listed above are by no
means comprehensive. Many other areas of emphasis are
of paramount importance, such as tests to determine the
integrity of the biceps and glenoid labrum. Interpreta-
tion of the results of a comprehensive evaluation will
allow the clinician to develop an objectively based reha-
bilitation program for rotator cuff injury.
Biomechanical Concepts for
Rehabilitation of Rotator
Cuff Injury
Several biomechanical concepts have notable applica-
tions in the formulation and application of rehabilitative
exercise for the patient with rotator cuff injury. One
important concept is the force couple. A force couple
consists of a pair of forces acting on an object, which
tends to produce rotation, even though the forces may act
in opposite directions.60 An example of a force couple in
the shoulder is the deltoid rotator cuff force couple out-
lined by Inman and colleagues.61 The force vector of the
deltoid is superior, if contracting unopposed, which
would create superior migration of the humeral head.62
The supraspinatus muscle has a compressive function
while contracting, creating an approximation of the
humerus into the glenoid (Figure 12-7). The infraspina-
tus, teres minor, and subscapularis produce a caudal force
that resists the superior migration of the humeral head.
One factor of key importance when clinically interpret-
ing the force couple concept is the muscle’s force poten-
tial in relation to its physiologic cross-sectional area.60
Research shows the subscapularis to have the greatest
force potential, followed closely by the infraspinatus teres
347
Figure 12-7 Deltoid rotator cuff force couple.
minor group.60 The smallest physiologic cross-sectional
area is exhibited by the supraspinatus. These small
rotator cuff cross-sectional areas pale in comparison to
the larger force-generating capacities of the deltoid
muscle. The presence of a force couple imbalance is often
identified on initial evaluation of the patient with rotator
cuff injury.38,48 Weakness of the rotator cuff, coupled with
hypertrophy or training enhancement of the deltoid
through uneducated exercise prescription by the patient
using traditional “large shoulder muscle group domi-
nant” resistive training exercises, further perpetuates this
force couple imbalance.
Further application of this deltoid rotator cuff force
couple was presented in research comparing normal
subjects with patients with primary glenohumeral
joint impingement.48 Electromyogram (EMG) analysis
showed a substantial reduction in infraspinatus and sub-
scapularis EMG activity during the critical first stage of
elevation of the shoulder in the scapular plane between
30° and 60°. Further decreases in infraspinatus EMG
activity were noted between 60° and 90° of elevation in
the impingement group. The study by Reddy and asso-
ciates63 showed decreases in the inferior force vector pro-
vided by the rotator cuff in patients with subacromial
impingement.
The coordinated interplay between the rotator cuff
and deltoid musculature is further demonstrated in
EMG analysis by Kronberg and colleagues.2 This study
illustrates that all of the rotator cuff muscles are
348 SECTION III SPECIAL CONSIDERATIONS
involved, to some extent, with basic shoulder move-
ments. They act to assist movement and counterbalance
the micromotions of the humeral head to keep it stable
within the glenoid.
Additional force couples described in literature8,60 are
the serratus anterior trapezius and internal/external
rotator couples. The serratus anterior trapezius force
couple is also important in rotator cuff injury because it
produces upward rotation of the scapula,8 moving the
overlying acromion superiorly out of the path of the ele-
vating proximal humerus. The internal/external rotator
force couple is another commonly imbalanced pair in
the overhead athlete because of selective development
of internal rotation strength, which overpowers the
controlling and decelerating influence of the external
rotators.60,64,65
Cain and associates66 and Blaiser1 demonstrated
further evidence of the rotator cuff ’s vital function in
glenohumeral joint arthrokinematics in cadaveric
studies. These studies have shown the rotator cuff ’s
ability to reduce the strain on the anterior capsule (infe-
rior glenohumeral ligament) with the shoulder in 90° of
abduction and external rotation. This important stabi-
lizing function of resisting anterior translation demon-
strates the rotator cuff ’s critical contribution to joint
stability. Additional biomechanical research by Clark
and colleagues67 identifies the intimate, adherent associ-
ation of the rotator cuff to the capsuloligamentous struc-
tures. It also identifies the ability of rotator cuff muscular
contraction to create tension and affect the orientation
of the capsuloligamentous complex. Muscular force
vectors have been studied with the shoulder in the
functional position of 90° of abduction and external
rotation.68 In this abducted position, the subscapularis
functions as a flexor and internal rotator, the supraspina-
tus as an extensor, and the infraspinatus as an adductor.
This study demonstrates the importance of working the
dynamic stabilizers of the shoulder in both neutral and
functional positions to most closely simulate the actual
muscular length, tension, and contraction specificity
incurred in activities of daily living (ADL) and overhead
sport movement patterns.
Rehabilitation of Rotator
Cuff Injury
Both nonoperative and postoperative rehabilitation of
the rotator cuff involve the following principles.
Reduction of Overload and
Total Arm Rehabilitation
The initial goal of any treatment program includes the
reduction of pain and inflammation by protection of
the extremity from stress, but not complete function.20
Application of modalities, or modification or complete
cessation, is often required in sport and ergonomic
movement patterns. Care should be taken to identify the
presence of any compensatory actions in the upper
extremity kinetic chain, such as excessive scapular move-
ment and/or elbow kinematics.69 Early use is indicated
for the distal strengthening of the elbow, forearm, and
wrist, particularly in postoperative cases in which the
degree and length of immobilization are greater. Mobi-
lization of the scapulothoracic joint and submaximal
strengthening of the scapular stabilizers are indicated,
taking great care not to impart inappropriate stresses or
loads onto the injured tissues. One early technique that
I use throughout rehabilitation phases is pictured in
Figure 12-8. It involves a side-lying position and spe-
cific hand placements to resist scapular protraction and
retraction without stress applied via the glenohumeral
joint. This technique, performed with manual resistance
and a pillow to place both a barrier between the patient
and therapist and to place the glenohumeral joint in
slight abduction and forward flexion during scapular
motion, is performed using a relatively low initial resist-
ance level. It emphasizes increased repetitions to build
local muscular endurance of the serratus anterior during
protraction, particularly the lower trapezius and rhom-
boids during retraction.
Restoration of Normal Joint
Arthrokinematics
Thorough evaluation to determine the degree of hyper-
mobility or hypomobility of the glenohumeral joint,
coupled with isolated joint range of motion measure-
ments, predicates the progression of and inclusion of
stretching and joint mobilization in treatment. The pres-
ence of increased anterior capsular laxity and underlying
instability of the glenohumeral joint, a finding consis-
tently found in overhead athletes, contraindicates the
application of joint accessory mobilization and stretch-
ing techniques that attenuate the anterior capsule. Pos-
terior capsular mobilization and stretching techniques
are often indicated and applied to improve internal rota-
tion range of motion. The consequences of posterior cap-
sular tightness have been outlined earlier in the chapter.
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION
A B
Figure 12-8 Side-lying manual scapular protraction (A) and retraction (B) resistance exercise to
promote scapular stabilization.
In postoperative rehabilitation of rotator cuff repairs,
the use of joint mobilization techniques is recommended
to both retard and address the effects of immobilization.
In addition to the posterior capsular mobilization
described, specific emphasis on the caudal glide in
varying positions of abduction is applied assertively to
stress the inferior capsule and prevent both adhesions
and functional elevation range of motion loss.38
Promotion of Muscular Strength Balance
and Local Muscular Endurance
The addition of resistive exercise is begun as inflamma-
tion and pain levels allow. Early submaximal resistance
exercise in the rotator cuff and scapular muscles is
initiated in the form of multiple-angle isometrics,
progressing rapidly to submaximal isotonic exercises
because of their inherent dynamic characteristics.53 The
presence or lack of pain over the joint or affected
tendon(s) determines the speed of progression and
intensity of exercise. Resistive exercises are used that
emphasize concentric and eccentric muscular contribu-
tions from the key dynamic stabilizers of the shoulder.
Movement patterns are applied that require high acti-
vation levels from the rotator cuff based on EMG con-
firmation via biomechanical study.70-72 The proper use of
these patterns using a low-resistance (never greater than
5 lb and typically initiated with either no weight or as
little as 1 lb), high-repetition format is recommended to
enhance local muscular endurance74 of the rotator cuff
musculature. The movement patterns pictured in Figure
12-5 have been biomechanically studied and produce
high levels of rotator cuff activation. These positions
neither place the shoulder in a potential position of
349
impingement, nor do they place excessive stress to the
often attenuated anterior capsuloligamentous complex.
The movement patterns recommended for strengthen-
ing the rotator cuff do not place the shoulder in eleva-
tion beyond 90° or posterior to the coronal plane.
Recent research has confirmed the use of the rotator
cuff exercise patterns outlined in Figure 12-9. Moncrief
and associates73 studied the effects of a 5 times per week
training program performing the exercises for 2 sets of
15 repetitions for 1 month in healthy, uninjured subjects.
Subjects were pretested and posttested on an isokinetic
dynamometer to objectively quantify internal and exter-
nal rotation strength. Results of the 1-month rotator
cuff training program showed 8% to 10% gains in iso-
kinetically measured internal and external rotation
strength in the training arms and no significant
improvement in strength in the control group arms. This
fine study shows the effectiveness of using a low-
resistance, high-repetition format with specific exercises
that create high levels of activation in the rotator cuff
muscles.
Similar positional limitations are applied in this stage
of rehabilitation for strengthening the scapular stabiliz-
ers. Patterns resisting scapular protraction and retrac-
tion, elevation, and depression produce considerable
muscular activity in the serratus anterior, trapezius, and
rhomboids.75 Use of closed-chain exercise, which
approximates the glenohumeral joint and produces co-
contraction of the proximal stabilizing musculature of
the scapulothoracic joint, is also recommended for both
nonpostoperative and postoperative rehabilitation of the
rotator cuff. Progression to advanced-level plyometric
exercises is also indicated for the upper extremity.
350 SECTION III SPECIAL CONSIDERATIONS
Figure 12-9 Rotator cuff exercises predicated on
electromyographic research.
Common applications are medicine balls and therapeu-
tic Swiss balls in exercise patterns that use the stretch-
shortening cycle of the scapulothoracic musculature,
such as chest passes, and various throw and catch
maneuvers that alter the position of the glenohumeral
joint.76
Resistive exercises, with emphasis on the biceps
muscle, are recommended in rotator cuff rehabilitation
because of the glenohumeral joint stabilizing and
humeral head depression actions.77-79 Strengthening of
the biceps in neutral and 90° of shoulder flexion is rec-
ommended, with concentric and eccentric contractions
implemented.
The use of isokinetic exercise is warranted in later
stages of both nonpostoperative and postoperative reha-
bilitation. As patients tolerate medium-resistance elastic
tubing exercises, and can perform isolated rotator cuff
exercises with a 2- to 3-lb weight, they are considered
for this progression. The Davies modified base position
is initially used for all patients for internal and external
rotation.38,53,54 Submaximal intensities at speeds ranging
from 210° to 300°/sec are used in active athletic patients
with a more intermediate contractile velocity range of
120° to 210°/sec for less active and general orthopedic
patients. Specific emphasis is placed on the external
rotators because of their important role in functional
activities3,5,7 and in the maintenance of dynamic gleno-
humeral joint stability.1,67
Progression from the modified position in patients
who will return to aggressive overhead activity is
observed, using tissue tolerance as the guide. Isokinetic
internal and external rotation in the scapular plane, with
80° to 90° of abduction using fast contractile velocities,
has been used successfully as an end-stage rotator cuff
exercise to prepare the rotator cuff musculature for the
demands of overhead activity (Figure 12-10).
Interpretation of isokinetic test data typically focuses
on bilateral comparisons and unilateral strength
ratios.53,54 Unilaterally dominant upper extremity ath-
letes often demonstrate 15% to 30% greater internal
rotation strength on the dominant arm, with bilaterally
symmetric external rotation strength.38,53,54,64,65
Although bilateral comparison does provide important
baseline comparison for the individual, the unilateral
strength ratio may be of even greater importance.38,53,54
The unilateral external/internal rotation ratio in healthy
shoulders has been reported at 66% throughout the
velocity spectrum.53,54 A goal in rehabilitation of patients
with rotator cuff injury is to bias this ratio to range
between 66% and 75%. This has been referred to as a
posterior dominant shoulder and ensures that the
strength of the external rotators is present to stabilize
the humeral head in the glenoid and provide sta-
bility.54 Patients with rotator cuff impingement and
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION 351

A B

Figure 12-10 A and B, Isokinetic internal/external rotation with 90° of abduction in the scapular plane.

glenohumeral joint instability have significant alter-
ations of this normal 66% ratio.48 The unilateral strength
ratio is also altered (<66%) in the dominant arm in over-
head throwing and racquet sport athletes because of
the selective internal rotation strength develop-
ment.38,53,54,64,65 Isokinetic exercise and isolated joint
testing are objectively quantifiable methods to address
the force couple imbalances often inherent in the shoul-
der with rotator cuff injury.
Specific Factors Influencing
the Rehabilitation of Rotator
Cuff Tears
Surgical Approach
As mentioned earlier in this chapter, the type of surgi-
cal approach used during open repairs of rotator cuff
tears has a considerable influence on several aspects of
the rehabilitative process. Two surgical approaches com-
monly seen in rehabilitation will be discussed briefly.
The “traditional anterior approach” consists of an
anterolateral incision beginning just below the middle
one third of the clavicle. It crosses the coracoid tip and
continues distally in an oblique lateral fashion to the
anterior aspect of the humerus.80 Almost all anterior sur-
gical procedures can be accomplished using this surgical
exposure, including open rotator cuff tears. In most
cases, use of this anterior surgical exposure of the shoul-
der necessitates detachment of the deltoid origin from
the anterior aspect of the acromion.81 This is particularly
common if an open subacromial decompression is per-
formed. The subacromial decompression is used to
remove a portion of the overlying offending structure,
and provide both protection for the rotator cuff and
prevention of further disease progression following its
repair.81
Another commonly used surgical exposure for rotator
cuff repair is the lateral “deltoid splitting” approach. This
352 SECTION III SPECIAL CONSIDERATIONS
surgical approach begins with a transverse incision
through the skin, 4 to 6 cm in length, beginning at the
anterolateral corner of the acromion and continuing
posteriorly to the posterolateral corner.82 A straight lon-
gitudinal incision, based off the lateral aspect of the
acromion and along the line of the deltoid fibers, is also
frequently used. Regardless of the orientation of the skin
incision, the deltoid is then split in line with its fibers
near the anterolateral corner of the acromion. The
deltoid’s origin is protected and not detached. The
deltoid is not split farther distally than 5 cm to avoid
damage to the axillary nerve.82
The type of surgical approach used in an open rotator
cuff repair dictates the progression of both range of
motion and resistance exercise following surgery. With
the anterior deltopectoral approach (where the deltoid
can be detached from its origin), restrictions regarding
the application of active or resistive exercise are normally
given to allow the deltoid’s origin to heal and become
viable before applying the larger stresses of active or
resistive movements. Active-assistive movement follow-
ing surgery with the mini-arthrotomy or “mini-open”
technique, using the lateral deltoid splitting approach,
can normally commence on the first postoperative day.82
Preservation of the deltoid’s origin allows more aggres-
sive range of motion and earlier application of strength-
ening exercises during the rehabilitation process. My
protocol for rehabilitation following open rotator cuff
repair with a deltoid splitting surgical approach is given
in Case Study 2 later in this chapter.
Progression of both range of motion and resistive
exercise is much faster following arthroscopic rotator
cuff debridement (Case Study 1). Active, active-
assistive, and passive range of motion all commence on
the first postoperative day following arthroscopy unless
associated surgical procedures were performed such as
anterior plication, repair of a Bankart or SLAP (supe-
rior labrum anterior posterior) lesion with suture tacks,
laser capsulorrhaphy, or extensive subacromial decom-
pression. Submaximal intensity resistive exercise is also
initiated rapidly, following debridement of partial
rotator cuff tears. Because arthroscopic approaches to
the shoulder do not disturb the deltoid origin or the
trapezo-deltoid fascia, resistive exercise using a low-
resistance, high-repetition format is recommended early
to retard atrophy and begin to normalize muscular
strength imbalances.82
Length of Immobilization
The degree and length of immobilization of the shoul-
der following rotator cuff repair can greatly affect early
rehabilitation emphasis. Traditional immobilization in a
sling, or sling and swathe, for up to 6 weeks following
open rotator cuff repairs results in a capsular pattern of
range of motion limitation that necessitates extensive
joint mobilization and passive stretching. Extensive lim-
itation in active and passive elevation, and external rota-
tion of the shoulder, is commonly present following this
degree and length of immobilization. Patients seen fol-
lowing arthroscopic debridement of partial rotator cuff
tears often receive no immobilization other than a sling
for 1 to 2 postoperative days. They often require
minimal accessory mobilization to restore normal joint
arthrokinematics. The common finding of associated
instability and capsular laxity in the overhead athlete
with partial undersurface rotator cuff tears, coupled with
minimal immobilization time following arthroscopic
debridement, often deemphasizes the importance of
accessory joint mobilization, especially of the anterior
capsule. As stated earlier, the loss of internal rotation
range of motion does indicate the application of poste-
rior capsular mobilization and passive stretching tech-
niques in this population.45,46
Surgical Procedure
Debate exists in literature regarding the surgical man-
agement of rotator cuff tears. Open repair of the torn
rotator cuff tendon versus arthroscopic debridement and
subacromial decompression are two frequently discussed
options.83-85 Rockwood and Burkhead83 observed 93
patients who underwent open debridement and sub-
acromial decompression for irreparable rotator cuff tears.
Minimal deterioration in function and no degenerative
changes were reported with an 8-year average follow-up
evaluation. Burkhart85 studied 25 patients who under-
went arthroscopic debridement and subacromial decom-
pression of massive rotator cuff tears with an average
30-month follow-up. Eighty-eight percent of the
patients in this series were found to have good or excel-
lent results, with no deterioration over time. Finally,
Montgomery and associates84 compared the results of
open surgical repair with arthroscopic debridement in 87
consecutive patients with full-thickness rotator cuff
tears. A 2- to 5-year follow-up indicated that the open
surgical repair group had superior results as compared
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION
with the arthroscopic group. The literature contains an
extensive array of research demonstrating the efficacy of
various surgical procedures for rotator cuff injury, which
is far beyond the scope of discussion of this chapter. One
consistent finding is the important role of physical
therapy in both the conservative treatment86,87 and post-
operative management of rotator cuff disease.
Factors Influencing the
Results of Nonoperative
Rehabilitation of Rotator
Cuff Tears
Several factors are consistently reported in literature as
having a notable relationship to the outcome of nonop-
erative treatment of rotator cuff disease. Clinical find-
ings and prognostic factors associated with unfavorable
clinical outcomes in a sample of 136 patients with
impingement syndrome and rotator cuff disease were:
(1) a rotator cuff tear greater in size than 1 cm,2 (2) a
history of pretreatment symptoms greater than 1 year,
and (3) significant functional impairment at initial eval-
uation.87 Itoi and Tabata86 reported on the clinical
outcome of conservative treatment of 124 shoulders
with a full-thickness rotator cuff tear with a follow-up
of 3 years. The primary factors relating to an unsatis-
factory result were identified in their sample as limited
abduction range of motion and significant abduction
muscular weakness on initial evaluation of the patient.
Factors not associated with clinical outcome included
patient age, gender, occupation, associated instability,
dominance, and chronicity of onset.
Summary
Rehabilitation of rotator cuff pathologic conditions
necessitates an extensive, objectively based evaluation
and thorough understanding of the complex biome-
chanical principles and etiologic factors associated with
rotator cuff injury. A rehabilitation program aimed at
restoring normal joint arthrokinematics and normal
muscular strength, endurance, and balance is supported
by the scientific principles currently present in literature.
Isolated treatment and evaluative focus on the rotator
cuff and glenohumeral joint must be combined with a
more global upper extremity kinetic chain approach to
comprehensively address rotator cuff injury.
353
Case Study 1
Rehabilitation Following
Arthroscopic Rotator Cuff
Debridement of an Undersurface
Tear of the Supraspinatus
SUBJECTIVE INFORMATION
The patient is a 27-year-old professional baseball
pitcher who started having left anterior shoulder pain in
early April following a normal, uneventful spring train-
ing. Although the patient denies any particular incident
of injury, he reported initially decreased recovery fol-
lowing pitching and pain in the anterior aspect of his
shoulder during the acceleration phase and continued
pain during follow-through of his pitching motion. In
addition to localized anterior left shoulder pain, the
patient complained of weakness, loss of velocity in his
throwing, and eventually an inability to tolerate repeated
repetitions of overhead activity. His pertinent history
includes previous bouts of what he calls impingement
dating back to his high school and collegiate baseball
years. He denies any dislocations of his left shoulder.
After 2 months of nonoperative treatment, including
nonsteroidal antiinflammatory medication and physical
therapy for rotator cuff and general upper extremity
strengthening, he was scheduled for further diagnostic
testing.
Diagnostic testing revealed an undersurface (articu-
lar side) tear in the supraspinatus tendon. He underwent
an arthroscopic procedure to debride the margins of the
partial-thickness tear. He is referred to physical therapy
1 day following arthroscopic surgery.
INITIAL FINDINGS
Examination of the patient postoperatively shows no
obvious atrophy with the exception of a hollowing in the
infraspinous fossa on the left. Passive motion on the
second day following surgery is 120° in forward flexion,
100° of abduction, 75° of external rotation, and 20° of
internal rotation. Good distal strength is present along
with confirmation of intact neurologic status. Passive
accessory mobility of the patient’s left shoulder indicates
a 2+ anterior translation at 60° and 90° of abduction, as
compared with a 1+ on the right uninjured shoulder.
Posterior and caudal mobility are equal bilaterally. Addi-
tional special tests, such as labral and impingement, are
deferred because of the patient’s early postoperative
nature.
354 SECTION III SPECIAL CONSIDERATIONS
TREATMENT
Week 1
Modalities are applied (electric stimulation and ice)
to decrease pain and swelling, with a primary goal ini-
tially of restoring normal joint motion. Passive, active
assistive, and active range of motion (ROM) are used as
tolerated to terminal ranges. Accessory mobilization is
applied in the posterior and caudal directions to facili-
tate the return of flexion, abduction, and internal rota-
tion ROM. Anterior glides are not indicated because of
the hypermobility assessed on initial evaluation. Appli-
cation of isometric and manually resisted rotator cuff
strengthening is initiated along with scapular stabiliza-
tion techniques (rhythmic stabilization, manual protrac-
tion/retraction). At the end of the first postoperative
week, the patient has 175° of forward flexion and abduc-
tion, 90° of external rotation, and 35° of internal rota-
tion measured with 90° of abduction.
Weeks 2 to 4
Continued use of ROM techniques is indicated at
terminal ranges of motion, with posterior glides and
emphasis on stretching of the posterior musculature to
increase internal rotation. Progression of the patient’s
rotator cuff strengthening program includes concentric
and eccentric isotonic exercise using the patterns with
high levels of scientifically documented rotator cuff acti-
vation. Initially, a 1-lb weight is tolerated with progres-
sion to 3 lb by the third week after surgery. Advancement
of the patient’s scapular strengthening program includes
the use of closed-chain Swiss ball exercise, seated rows,
shrugs, and serratus anterior dominant activities, includ-
ing a protraction punch movement pattern with tubing
and manual resistance. Distal strengthening is of key
importance, and biceps/triceps and forearm/wrist iso-
tonics are performed both in the clinic and in the home
program. Continued progress of this patient is noted
with average range of motion (AROM) of the left
shoulder at 175° of forward flexion and abduction, 95°
of external rotation, and 40° of internal rotation.
Weeks 4 to 8
Addition of isokinetic exercise in the modified base
position is warranted with this patient. Tolerance of a
minimum of 3-lb isolated rotator cuff exercises, normal
results from impingement tests, and functional ROM
make him a candidate for isokinetic exercise between 4
and 6 weeks postoperatively. A submaximal introduction
to the isokinetic form of resistance is recommended,
with an isokinetic test to document internal and exter-
nal rotation strength applied during this time frame.
Results of the patient’s initial isokinetic test show 10%
to 15% greater internal rotation strength when com-
pared with the uninjured extremity and 5% to 10%
weaker external strength at 5 weeks postoperatively.
External/internal rotation ratios range between 45% and
50%, revealing a relative weakness or imbalance of exter-
nal rotation strength on the dominant extremity. A ply-
ometric program, with medicine balls to simulate
functional muscular contractions and facilitate scapu-
lothoracic strength, is initiated during this stage.
Weeks 8 to 12
Continued mobilization and passive range of motion
(PROM) are performed to normalize glenohumeral
joint motion, with continued emphasis on the posterior
capsule and posterior musculature. Isotonic rotator cuff
exercise is progressed to not more than 5 lbs, and
advancement of the scapular programs in isotonic,
closed-chain, and plyometric venues continues. Isoki-
netic testing at 8 to 9 weeks postoperatively shows 25%
greater internal rotation strength and equal external
rotation strength measured in the modified position. At
this time the patient progresses to an interval-throwing
program carried out at the clinic on alternate days begin-
ning with tossing at a 30-foot distance and progressing
during the next 3 to 4 weeks to 60-, 90-, and 120-foot
distances. Once the patient tolerates 120 feet with as
many as 75 to 100 repetitions, he is progressed to throw-
ing off the mound at 50% intensities. The isokinetic
strengthening progresses to a more functional 90°
abducted position in the scapular plane. The continua-
tion of a total arm strength program is followed both in
the clinic and at home.
Case Study 2
Open Rotator Cuff Repair
(Deltoid Splitting Approach)
SUBJECTIVE HISTORY
The patient is a 51-year-old male competitive tennis
player with a 1-year history of shoulder tendonitis/
impingement symptoms reported as intermittent based
CHAPTER 12 ETIOLOGY AND EVALUATION OF ROTATOR CUFF PATHOLOGIC CONDITIONS AND REHABILITATION 355

on his level of activity. One month ago the patient was active-assistive ROM. The use of overhead pulleys
hitting a serve early in a match with minimal warm-up and the upper body ergometer are added within the
and felt a deep, sharp pain in the anterolateral aspect of listed ROM restrictions. Submaximal multiple-angle
his shoulder as his arm was accelerating forward just isometrics are performed for shoulder internal rota-
before hitting the ball. He was unable to continue tion/external rotation (IR/ER) as is manual resistance
playing and was unable to abduct or flex his arm more exercise for the biceps and triceps, scapular protrac-
than 90°. Continuous pain was reported, even with rest tors/retractors and elevators, and distal forearm and
and sleep, and he was examined by an orthopedic wrist musculature.
surgeon 2 days later. An MRI was scheduled, which PHASE II: TOTAL ARM STRENGTH
showed a full-thickness tear of the supraspinatus
tendon. He subsequently underwent an open surgical Weeks 6 to 12
repair using a deltoid-splitting approach and was
The patient’s ROM is advanced from active-assistive
referred for rehabilitation 2 days following surgery.
to active, and terminal ranges of flexion, abduction, and
INITIAL FINDINGS
internal and external rotation are included. Current
The patient appears with his right arm immobilized
ROM of the patient is 120° of flexion, 105° of abduc-
in a sling. Initial treatment called for PROM for the
tion, 60° of external rotation, and 60° of internal rota-
initial 2 weeks within the limitations of 100° of flexion
tion. Continued mobilization of the glenohumeral joint
and abduction, 30° to 40° external rotation. The patient
is combined with end-range passive stretching tech-
has no distal radiation of symptoms and full light touch
niques to restore normal joint arthrokinematics. Initia-
sensation and strong distal grip. The initial examination
tion of resistive exercise in the form of isotonic internal
consists primarily of a neurologic screening and PROM
and external rotation, prone extension, horizontal
measurement. The patient’s contralateral extremity
abduction, and eventually scaption is performed with no
has a 1° load and shift, and anterior translation. The
resistance. The resistance level progresses as tolerated.
patient expressly denies any instability in either shoul-
Advancement of the scapular strengthening program to
der before this injury. Instability or impingement tests
include plyometrics, with a Swiss ball and eventually a
are not performed on the postoperative shoulder at this
medicine ball, is included during this time frame. Con-
time.
centric and eccentric muscular work are performed using
INITIAL PHASE
surgical tubing and controlled execution of the resistive
Weeks 1 to 6 exercise patterns with isotonic resistance. At 10 days
postoperatively, this patient has 155° of forward flexion,
Modalities consisting of electric stimulation and ice
145° of abduction, and 85° of external rotation with 90°
are applied as needed to control pain and increase local
of abduction. Sixty degrees of internal rotation is present
blood flow. Passive range of motion is performed using
with 90° of abduction. Tolerance is demonstrated using
the above guidelines as maximum ranges. Evaluation of
3-lb isolated rotator cuff exercises (mentioned earlier).
the patient’s accessory movement shows a decreased
The patient progresses to isokinetic internal and exter-
caudal glide and posterior glide relative to the con-
nal rotation in the modified base position for a trial of
tralateral extremity. Accessory mobilizations are applied
submaximal isokinetic exercise. Continued home exer-
using the caudal and posterior directions along with
cise for the rotator cuff using tubing, and tubing and a
passive stretching. Scapulothoracic joint mobilization
counterbalanced weight for a forearm and wrist
also is used. Passive stretching of the elbow, particularly
program, is employed to begin to prepare the distal
into extension because of the continued use of a sling
upper extremity for the return to tennis play in the later
for immobilization, is indicated as is the use of grip putty
stages of rehabilitation.
to prevent disuse atrophy of the forearm and wrist
RETURN TO ACTIVITY PHASE
musculature during the immobilization period. The
patient’s initial ROM at 1 week after open rotator cuff Weeks 12 to 16
repair is 90° of flexion and abduction, 50° of internal
rotation, and 30° of external rotation. During the third Continued accessory mobilization to achieve full
postoperative week, PROM exercise progresses to range of elevation is applied to this patient as is passive
356 SECTION III SPECIAL CONSIDERATIONS
stretching in physiologic ROM patterns. An isokinetic
test is performed in the modified base position, indicat-
ing equal internal rotation strength bilaterally, with a
35% external rotation deficit identified. The patient’s
ER/IR ratio is 54%, well below the desired 66% balance.
Range of motion for this patient has continued to
improve to 175° of flexion and 160° of abduction, 95°
of external rotation, and 60° of internal rotation.
Advancement of the patient’s strengthening program
includes the 90° abducted position for both isokinetic
IR/ER and surgical tubing strengthening. Plyometric
exercise with medicine balls intensifies, as does the entire
scapular program, including the use of closed chain
push-ups and step-ups with emphasis on protraction
for serratus strengthening. The patient continues with
rehabilitative exercise and close adherence to a home
program to reinforce the concepts of total arm strength
in preparation for the interval return to playing tennis.
Achievement of greater external rotation muscular
strength and endurance is recommended before this
patient begins the interval tennis program. The guided
return to tennis will include ground stroke activity ini-
tially, with progression to volleys and serving based on
tolerance to the forehand and backhand ground strokes.
Typically the interval program following an open repair
of a full-thickness rotator cuff tear takes up to 6 to 8
weeks before protected match play can resume. Empha-
sis is on continued use of the rotator cuff and scapular-
strength maintenance program following discharge of
the patient from formal physical therapy.
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34. Miller C, Savoie FH: Glenohumeral abnormalities associated
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38. Ellenbecker TS: Rehabilitation of shoulder and elbow injuries
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55. Hawkins RJ, Kennedy JC: Impingement syndrome in ath-
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56. Hamner DL, Pink MM, Jobe FW: A modification of the
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57. Obrien SJ, Neves MC, Arnoczky SJ, et al: The anatomy and
histology of the inferior glenohumeral ligament complex of
the shoulder, Am J Sports Med 18:449, 1990.
58. Altchek DW, Skyhar MJ, Warren RF: Shoulder arthroscopy
for shoulder instability. In instructional course lectures. The
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59. Ellenbecker TS, Bailie DS, Mattalino AJ, et al: Intrarater and
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der Elbow Surg 11:470-475, 2002.
60. Dillman CJ: Biomechanics of the rotator cuff, Sports Med
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61. Inman VT, Saunders JB, de CM Abbot LC: Observations on
the function of the shoulder joint, J Bone Joint Surg 26A:1,
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62. Weiner DS, MacNab I: Superior migration of the humeral
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64. Ellenbecker TS: Shoulder internal and external rotation
strength and range of motion of highly skilled junior tennis
players, Isokinet Exercise Sci 2:1, 1992.
65. Ellenbecker TS, Mattalino AJ: Concentric isokinetic shoul-
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glenohumeral joint: a dynamic model, Am J Sports Med
15:144, 1987.
67. Clarke J, Sidles JA, Matsen FA: The relationship of the gleno-
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68. Bassett RW, Browne AO, Morrey BF, et al: Glenohumeral
muscle force and moment mechanics in a position of shoul-
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outcome in the treatment of rotator cuff disease, Clin Orthop
308:90, 1994.

Visceral Referred Pain
to the Shoulder
A n important component of the initial ortho-
pedic evaluation is the differentiation of the
causes of your patient’s pain complaints as
musculoskeletal in origin versus a visceral pathologic
condition or disease. Screening for visceral disease is
important for several reasons including: (1) many dis-
eases mimic orthopedic pain and symptoms, and a sub-
sequent delay in diagnosis and treatment may lead to
severe morbidity or death; (2) there is a notable increase
in the number of people over age 60 seeking orthopedic
medical care, and this patient population is at the great-
est risk for visceral disease; (3) 35 states currently have
direct access with 48 states allowing physical therapists
to perform an initial evaluation without a referral from
a physician;1 (4) our profession is committed to entry-
level doctor of physical therapy degree programs and
complete autonomous practice by the year 2020;1 (5) an
aggressive managed care environment in some states
encourages primary care physicians to limit the number
of referrals to specialists, as well as limiting the referrals
for diagnostic testing; and finally (6) comorbid medical
problems are important to identify so that the clinician
can take note of these potential additional strains on
the shoulder and be able to modify the rehabilitation
plan accordingly to ensure a safe and successful treat-
ment session. The physical therapist in an outpatient
orthopedic setting is evaluating and treating patients
who may have greater morbidity and may be more
acutely ill than the patients who were referred for phys-
ical therapy 15 to 20 years ago. Boissonnault and Koop-
meiners2 found in their study that approximately 50% of
359
13
John C. Gray
all the patients referred for outpatient orthopedic phys-
ical therapy have at least one of the following
diagnoses: high blood pressure, depression, asthma,
chemical dependency, anemia, thyroid problems,
cancer, diabetes, rheumatoid arthritis, kidney problems,
hepatitis, or heart attack.
Pain may be defined as an unpleasant sensory and
emotional experience associated with actual or potential
tissue damage.3 True visceral pain can be experienced
within the involved viscus.4,5 It is often described as
deep, dull, achy, colicky, and poorly localized.4-6 Visceral
injury or disease can elicit a strong autonomic reflex phe-
nomenon, including sudomotor changes (increased
sweating), vasomotor responses (blood vessel), changes
in arterial pressure and heart rate, and an intense psychic
or emotional reaction.3,5,7 Viscera are innervated by noci-
ceptors (Plate 13-1).4,8 These free nerve endings are
found in the loose connective tissue walls of the viscus,
including the epithelial and serous linings, and the walls
of the local blood vessels in the viscus.4 After activation
of these nociceptors by sufficient chemical or mechani-
cal stimulation, neural information is transmitted along
small unmyelinated type C nerve fibers within sympa-
thetic and parasympathetic nerves.4,8-10 This information
is subsequently relayed to the mixed spinal nerve, dorsal
root, and into the dorsal horn of the spinal cord (see
Plate 13-1). Second-order neurons in the dorsal
horn project into the anterolateral system.8 Within
the anterolateral system, nociceptive impulses ascend
through the spinothalamic, spinoreticular, and spino-
mesencephalic tracts.8 The targets in the brain for these
360 SECTION III SPECIAL CONSIDERATIONS
tracts are the thalamus, reticular formation, and mid-
brain, respectively.8
Chemical stimulation of nociceptors may result from
a buildup of metabolic end products, such as bradykinins
or proteolytic enzymes, secondary to ischemia of the
viscus.4 Prolonged spasm or distention of the smooth
muscle wall of viscera can cause ischemia secondary
to a collapse of the microvascular network within the
viscus.4 Chemicals, such as acidic gastric fluid, can leak
through a gastric or duodenal ulcer into the peritoneal
cavity—resulting in local abdominal pain.4,11 Mechani-
cal stimulation of visceral nociceptors can occur second-
ary to torsion and traction of the mesentery, distention
of a hollow viscus, or impaction.3-7 Distention may result
from a local obstruction, such as a kidney stone, or from
local edema caused by infection or inflammation.4
Spasm of visceral smooth muscle may also be a sufficient
mechanical stimulus to activate the nociceptors of the
involved viscus.4,6,11
Visceral pain is not uncommon in patients suffering
from neoplastic disease. Pain complaints from cancer
patients have several origins. Somatic pain occurs as a
result of activation of nociceptors in cutaneous and deep
tissues (tumor metastasis to bone for example) and is
usually constant and localized.3 Visceral pain results
from stretching and distending, or from the production
of an inflammatory response and the release of algesic
chemicals in the vicinity of nociceptors.3-5 This inflam-
mation can provoke a central sensitization phenomenon
(see Chapter 5) that results in a lowering of the thresh-
old of activation of neurons in the dorsal horn, which
can subsequently produce referred hyperalgesia (exag-
gerated response to a painful stimulus).12 Metastatic
tumor infiltration of bone, and gastrointestinal and
genitourinary tumors that invade abdominal and pelvic
viscera, are very common causes of pain in cancer
patients.3 Deafferentation pain results from injury to the
peripheral and/or central nervous system as a result of
tumor compression or infiltration of peripheral nerves or
the spinal cord. It also results from injury to peripheral
nerves as a result of surgery, chemotherapy, or radiation
therapy for cancer.3 Examples are metastatic or
radiation-induced brachial or lumbosacral plexopathies,
epidural spinal cord and/or cauda equina compression,
and postherpetic neuralgia.3
The observation has been made that visceral disease
produces not only orthopedic-like pain, but true ortho-
pedic dysfunction.13,14 For example, pain referred to the
T4 spinal segment from cardiac tissue (angina) may
cause reflex muscle guarding of the tonic muscles sur-
rounding T4, and therefore interfere with its normal
mobility. This may then produce movement around a
nonphysiologic axis at that segment, which will predis-
pose it to injury. Even in the absence of an acute injury,
the hypomobility at T4, induced from the muscle guard-
ing, can inhibit full flexion and abduction at the
shoulder. Subsequently, this could initiate a cascade of
events leading to shoulder impingement and rotator
cuff tendinopathy (see Figure 5-3, B). This patient, for
example, with signs and symptoms consistent with
supraspinatus tendinosis, may experience a prolonged
rehabilitation effort if his T4 dysfunction and his cardiac
symptoms are not addressed.
Two important aspects of the orthopedic evaluation,
which will help detect visceral pathology or disease,
are a careful history and palpation. Below is a list
of questions that should be a part of your standard
interview.
1. Describe the first and last time you experienced
these same complaints.
2. Are your symptoms the result of a trauma, or are
they of a gradual or insidious onset?
3. Was it a macrotrauma (motor vehicle accident,
fall, sports injury) or repeated microtrauma
(overuse injury, cumulative trauma disorder)?
4. What was the mechanism of injury?
5. Do you have any other complaints of pain
throughout the rest of your body: head, neck,
temporomandibular joint (TMJ), chest, back,
abdomen, arms, or legs?
6. Do you have any other symptoms throughout the
rest of your body: headaches, tinnitus, vision
changes, nausea, vomiting, dizziness, shortness of
breath, weakness, fatigue, fever, bowel or bladder
changes, numbness, tingling, pins or needles?
7. Is your pain worse at night or while sleeping?
8. Are there positions or activities that change your
pain, either aggravating or relieving your
symptoms?
9. Does eating or digesting a meal affect your pain?
10. Does bowel or bladder activity affect your pain?
11. Does coughing, laughing, or deep breathing affect
your pain?
12. Does your shoulder pain get worse with exertional
activities (climbing stairs, for example) that do not
directly involve your shoulder?
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
The following are some warning signs, gathered
during the history and interview, that may indicate a
possible visceral pathologic condition or disease.4,15
1. Pain is constant.
2. The onset of pain is not related to trauma or
chronic overuse.
3. Pain is described as throbbing, pulsating, deep
aching, knifelike, or colicky.
4. There is no relief of pain or symptoms with rest.
5. Constitutional symptoms are present: fever, night
sweats, nausea, vomiting, pale skin, dizziness,
fatigue, or unexplained weight loss.
6. Pain is worse at night and during sleep.
7. Pain does not change with changes in body
position or activity.
8. Pain changes in relation to organ function (eating;
bowel or bladder activity; coughing or deep
breathing).
9. Indigestion, diarrhea, constipation, or rectal
bleeding is present.
10. Shoulder pain increases with exertion that does
not stress the shoulder (walking or climbing stairs,
for example).
A self-administered patient questionnaire (Figure
13-1) is useful as a quick screen for a possible visceral
pathologic condition or disease. For example, if a patient
has a few checks under the “yes” column for pulmonary,
then refer to the section below titled “lung.” This will
allow you to analyze the patient’s signs and symptoms
to see if they correlate with a possible medical disorder
in the lung. The idea is not to diagnose visceral disease,
which should be left to the physician, but to assess
whether the patient’s symptoms are orthopedic in origin
or to acknowledge comorbid disease.
The second important aspect of the evaluation is
palpation. Palpation should include the lymph nodes
(for infection or neoplasm)—which are normally 1 to
2 cm—in the cervical (medial border of sternocleido-
mastoid (SCM), anterior to upper trapezius muscle),
supraclavicular, axillary, and femoral triangle regions.4,16
Abnormal findings are swollen, tender, or immovable
lymph nodes.16 Palpate the abdomen for muscle rigidity
and significant local tenderness (possible visceral
disease), or a large pulsatile mass (indicative of an aortic
aneurysm).4,16,17 Palpation in the right upper abdominal
quadrant will uncover abnormalities in the liver, gall-
bladder, and portions of the small and large intestines
(Plate 13-2). Palpation of the left upper abdominal
361
quadrant will show abnormalities in the stomach, spleen,
tail of the pancreas, and portions of the small and large
intestines (see Plate 13-2).17 The kidneys lie deep pos-
teriorly in the left and right upper abdominal quadrants.
The appendix and large intestine are found in the right
lower quadrant, while other portions of the large intes-
tine may be found in the left lower quadrant.17 A tender
mass in the femoral triangle or groin area may indicate
a hernia.17 When evaluating abdominal tenderness, it is
important to differentiate the source as originating from
the superficial myofascial wall or from the deep viscera.
If palpable tenderness is elicited at rest and again with
the abdominal wall contracted, then the symptoms are
probably originating from the myofascial abdominal
wall.17 If, however, the palpable tenderness disappears
in the above situation, then you should suspect deep
visceral pathology.17 Again the objective is not to
diagnose medical disease, but to know when to refer
your patient for medical follow-up. Even though
your patient’s shoulder pain may not be visceral in
origin, you may be the first to discover a comorbid
medical problem.
The ability to palpate and interpret peripheral pulses
is another important diagnostic tool for the physical
therapist. Palpating the arterial pulses can help to iden-
tify cardiovascular and peripheral vascular disease. The
arterial pulses may be palpated in the upper extremity
(axillary artery in the axilla, brachial artery in the cubital
fossa, ulnar and radial arteries at the wrist) and lower
extremity (femoral artery at the femoral triangle,
popliteal artery at the popliteal fossa, posterior tibialis
artery posterior to the medial malleolus, and dorsal pedis
artery at the base of the first and second metatarsal
bones).4,16,18,19 When palpating a pulse, the therapist
needs to compare the amplitude and force of pulsations
in one artery with those in the corresponding vessel on
the opposite side.18 Palpation of the artery should be
performed with a light pressure and a sensitive touch. If
the pressure is firm, then there is a risk of not being able
to perceive a weak pulse or misinterpreting your own
pulse as that of your patient’s.18 Pulsations may be
recorded as normal (4), slightly (3), moderately (2), or
markedly reduced (1), or absent (0).18
Be alert and aware of your elderly patients who have
osteoarthritis, degenerative joint disease, degenerative
disk disease, or spondylosis. Many asymptomatic elderly
persons have abnormal radiographs for these diseases. It
is the elderly in our society that are at a greater risk for
362 SECTION III SPECIAL CONSIDERATIONS

Figure 13-1 A and B, A self-administered patient questionnaire. Continued

CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER 363

Figure 13-1, cont’d.

364 SECTION III SPECIAL CONSIDERATIONS
visceral abnormalities and disease. In addition, previ-
ously healed orthopedic injuries may become sympto-
matic simply because of facilitation from a segmentally
related visceral organ in a diseased state.20,21
Theories on Visceral
Referred Pain
1. Referred pain is pain experienced in tissues that are
not the site of tissue damage and whose afferent or
efferent neurons are not physically involved in any
way.22
2. Pain happens within the central nervous system,
not in the damaged tissue itself. Pain does not
really happen in your hands, feet, or head. It
happens in the images of your hands, feet, or
head.22
3. Referred pain from deep somatic structures is often
indistinguishable from visceral referred pain.23
4. Visceral pain fibers constitute less than 10% of the
total afferent input to the lower thoracic segments
of the spinal cord and are activated rarely.8 In this
way, a visceral stimulus may be mistaken for the
more familiar somatic pain.8
5. Visceral referred pain may be caused by
misinterpretation by the sensory cortex.24 Over the
years, specific cortical cells are repeatedly stimulated
by nociceptive activity from a specific area of the
skin. When nociceptors of a viscus are eventually
stimulated chemically or mechanically, these same
sensory cortex cells may become stimulated with
the cortex interpreting the origin of this sensory
input based on past experience. The pain therefore
is perceived to arise from the area of skin that has
repeatedly stimulated these cortical cells in the past.
The referred pain may lie within the dermatome of
those spinal segments that receive sensory
information from the viscera.24
6. Sensory fibers dichotomize as they “leave” the
spinal cord, one branch passing to a viscus as the
other branch travels to a site of reference in muscle
or skin (Figure 13-2).25,26
Figure 13-2 Schematic drawing
of a single afferent nerve fiber receiving
input from both skin and viscera.
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
7. Visceral nociceptor activity converges with input
from somatic nociceptors into common pools of
spinothalamic tract cells in the dorsal horn of the
spinal cord. Visceral pain is then referred to remote
cutaneous sites because the brain “misinterprets” the
input as coming from a peripheral cutaneous
source, which frequently bombards the central
nervous system with sensory stimuli (Figure 13-
3).3,5-8,17,23,27-29
Viscera Capable of Referring
Pain to the Shoulder
Diaphragm
Although the diaphragm is a musculotendinous struc-
ture and not a viscus, it is interesting in terms of the dis-
tance it refers its pain to the shoulder. Also, many viscera
(lung, esophagus, stomach, liver, and pancreas) can refer
pain to the shoulder through contact with the
Figure 13-3 Schematic drawing
of a visceral afferent nerve and a somatic
afferent nerve converging onto the same
spinothalamic tract cell in the dorsal horn
of the spinal cord.
365
diaphragm (Plate 13-3 and Figure 13-4; see also Plate
13-2).4 The central portion of the diaphragm, which
is segmentally innervated by cervical nerves C3 to C5
via the phrenic nerve, can refer pain to the shoulder
(see Plate 13-3).4,25,29-36 The peripheral portion of the
diaphragm is innervated by the lower six or seven inter-
costal nerves.37 In the rat, cervical (C3, C4) dorsal root
ganglion cells were seen that had collateral nerve fibers,
which emanated from both the diaphragm and the skin
of the shoulder (see Figure 13-2).25
Symptoms. Pain in the shoulder is most often felt
at the top or posterior portions of the shoulder; that is,
at the superior angle of the scapula, in the suprascapu-
lar region, or along the upper trapezius muscle.30,31 The
upper arm and anterior portions of the shoulder are not
common areas of referred pain for the diaphragm. Nor-
mally there are no complaints of pain in the region of
the diaphragm, unless the patient suffered trauma or a
musculoskeletal strain to the surrounding tissues.
366 SECTION III SPECIAL CONSIDERATIONS
Signs. There is usually a history of direct or indi-
rect, severe twisting motions—for example, trauma to
the rib cage and diaphragm. Shoulder pain is reproduced
or exacerbated by deep breathing, coughing, or sneez-
ing.32,35,36 There may be local tenderness or shoulder
pain during palpation of the diaphragm. Full active and
passive shoulder elevation in standing may cause pain
because this motion changes the shape of the rib cage
and subsequently puts tension on the diaphragm.32
Repeating these motions seated, with the thoracic spine
flexed to minimize stress to the diaphragm, should now
be pain free.
Pneumoperitoneum
Pneumoperitoneum, or air in the peritoneal cavity, can
refer pain to the shoulder caused by pressure on the
central portion of the diaphragm (see Plate 13-3 and
Figure 13-4).30-32,38-43 Air may become trapped within
the peritoneal cavity in a number of different ways. Per-
foration of an abdominal viscus can release air into the
peritoneum.30,40,44 Examples of this are a peptic ulcer,
acute pancreatitis, perforated appendix, and a splenic
Figure 13-4 Schematic drawing
of an afferent nerve from the diaphragm
converging onto the same spinothalamic
tract cell as is a somatic afferent nerve
from the skin of the shoulder.
infarct or rupture.32,40,44 Abdominal or vaginal surgeries
that allow free air to enter and become trapped within
the peritoneal cavity, or surgeries that necessitate insuf-
flation of the peritoneum, are another source of referred
pain to the shoulder.45 Although a rare occurrence,
certain activities for females during pregnancy, within
6 weeks postpartum, or following abdominal or vaginal
surgery can lead to a pneumoperitoneum. These include
menstruation, effervescent vaginal douching, vigorous
sexual intercourse, orogenital insufflation, and knee to
chest stretching exercises.38,39,41,42 The last three acti-
vities, although rare, can be fatal because of an air
embolism.38,39,41-43 To create a pneumoperitoneum under
these circumstances, air must first enter the vagina
before it passes through a patent os cervix to enter the
body cavity of the cervix and subsequently travel through
the uterine tube before escaping into the peritoneal
cavity (Figure 13-5).
Symptoms. The patient may complain of acute or
spasmodic shoulder and/or abdominal pain, especially in
the case of a perforated abdominal viscus. In the case of
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
Figure 13-5 Schematic drawing
of the pathway that air must travel to create
a pneumoperitoneum.
a splenic infarct or rupture, the pain will be in the left
shoulder.44 There will be a variety of symptoms depend-
ing on which viscus have been perforated.
Pain in the shoulder is most often felt at the top or
posterior portions of the shoulder; that is, at the supe-
rior angle of the scapula, in the suprascapular region, or
along the upper trapezius muscle.30,31 The upper arm and
anterior portions of the shoulder are not common areas
of referred pain for the diaphragm. Normally there are
no complaints of pain in the region of the diaphragm,
unless the patient suffered trauma or a musculoskeletal
strain to the surrounding tissues.
Signs. There will be a history of acute visceral
pain (before perforation), recent abdominal or vaginal
surgery, current pregnancy, or a recent parturition.
Shoulder pain may be reproduced or exacerbated by
deep breathing, coughing, or sneezing.32,35,36 There
should be no local tenderness or shoulder pain during
palpation of the diaphragm. Full active and passive
shoulder elevation in standing may cause pain because
this motion changes the shape of the rib cage and sub-
sequently puts tension on the diaphragm.32 Repeating
these motions seated, with the thoracic spine flexed
to minimize stress to the diaphragm, should now be
pain free. In the case of a perforated viscus, pain and/or
367
rigidity will be noted with abdominal palpation.
An upright plain anterior-posterior radiograph will
demonstrate free intraperitoneal air under one or
both hemidiaphragms.38
Lung
The lung, which is innervated by thoracic nerves T5 to
T6, is capable of referring pain from two distinct dis-
eases to the shoulder.* The first is pulmonary infarction,
which is often secondary to a pulmonary embolism. The
second is a Pancoast’s tumor.32,49
Pulmonary Infarction. The most common cause
of pulmonary embolism is a deep venous thrombosis
(DVT) originating in the proximal deep venous system
of the lower legs.49 Risk factors for DVT include blood
stasis caused by bed rest, endothelial (blood vessel)
injury from surgery or trauma, and a state of hyperco-
agulation.49 Other risk factors include congestive heart
failure, trauma, surgery (especially of the hip, knee, and
prostate), more than 50 years of age, infection, diabetes,
obesity, pregnancy, and oral contraceptive use.49 Pain is
normally referred to the shoulder because of contact
*References 4, 30, 32, 33, 36, 46-59.
368 SECTION III SPECIAL CONSIDERATIONS
with the central portion of the diaphragm (see Plate 13-
3 and Figure 13-4).30-32
Symptoms. In cases where the inferior lobe of the
lung is involved and in contact with the diaphragm, the
referred pain is most often felt at the top or posterior
portions of the shoulder; that is, at the superior angle of
the scapula, in the suprascapular region, or along the
upper trapezius muscle.30,31 The upper arm and anterior
portions of the shoulder are not common areas of
referred pain for the diaphragm. The region surround-
ing the diaphragm may be free of pain. In cases where
the diaphragm is not involved, pain may be referred to
the scapula and/or interscapular region. Patients will
usually report the relief of pain when lying on the
involved shoulder. Symptoms related directly to the pul-
monary embolism may include swollen and painful legs
with walking, acute dyspnea or tachypnea, chest pain,
tachycardia, low-grade fever, rales, diffuse wheezing,
decreased breath sounds, persistent cough, restlessness,
and acute anxiety.49-51
Signs. A history of recent surgery is most common.
Full active and passive shoulder elevation in standing
may cause pain because this motion changes the shape
of the rib cage and subsequently puts tension on the
diaphragm.32 Shoulder pain may be reproduced or exac-
erbated in cases with diaphragmatic irritation by deep
breathing, coughing, or sneezing.32,35 There is often no
local tenderness or shoulder pain during palpation of
the diaphragm. Chest radiographs, arterial blood gas
studies, pulmonary angiography, and ventilation-
perfusion (V/Q ) scintigraphy are diagnostic tools avail-
able for the physician.52 Plain radiographs can miss the
pulmonary infarct if it is in the inferior lobe of the lung
and hidden by the dome of the diaphragm.32 This is a
potentially fatal condition, which necessitates rapid
referral for emergency medical attention.
Pancoast’s Tumor. Pancoast’s tumor occurs in the
apical portion of the lung (Plate 13-4).* Lung cancer is
the most common fatal cancer in both men and
women.53 It commonly refers pain to the supraclavicu-
lar fossa, usually on the right side.32 Pain from Pancoast’s
tumor may be referred to the shoulder because of the
involvement of the upper ribs.54 Shoulder and arm pain
may also occur secondary to contact between the can-
cerous lobes of the lung with the eighth cervical (C8)
*References 30, 32, 36, 46, 48, 49, 53, 54.
and first thoracic (T1) nerves. This results in shoulder
and upper extremity symptoms similar to a myocardial
infarction, brachial plexus lesion, thoracic outlet syn-
drome, ulnar neuropathy, and C8 or T1 nerve root
injury.* The chest wall and subpleural lymphatics are
often invaded by the tumor.54 Other structures that may
be involved include the subclavian artery and vein, inter-
nal jugular vein, phrenic nerve, vagus nerve, common
carotid artery, recurrent laryngeal nerve, sympathetic
chain, and stellate ganglion.46,48,54 Cancer can metasta-
size to the lungs from carcinomas in the kidney, breast,
pancreas, colon, or uterus.49
The lung itself is a common source of metastatic
cancer to the bone, liver, adrenal glands, and brain.49,53
Symptoms associated with cancer of the spine include a
deep, dull ache that may be unrelieved by rest.53 Pain
often precedes a pathologic fracture.53 If a fracture is
present, then the pain may be sharp, localized, and asso-
ciated with swelling.53 Pain is often reproduced with
mechanical stress, thereby simulating a pure muscu-
loskeletal dysfunction. Neurologic signs and symptoms
will be present in some patients caused by compression
of the spinal cord, C8, or T1 nerves. Percussion of a
spinous process, with a reflex hammer, will exacerbate
pain from the involved vertebrae.53 A tuning fork may
also be used to elicit symptoms from the involved
vertebrae.
Symptoms. Shoulder pain is the symptom present in
more than 90% of patients with Pancoast’s tumor.46,49
Arm pain is also common, often involving the medial
aspect of the forearm and hand, including the fourth and
fifth digits.46,48,54 Paresthesia may be felt in the arm and
hand because of compression of the subclavian artery
and vein or the lower portions of the brachial plexus.54
Patients will often report relief of pain when lying on
the involved shoulder. Associated symptoms include
Horner’s syndrome (contraction of the pupil, partial
ptosis of the eyelid, loss of sweating over the affected
side of the face, and recession of the eyeball back into
the orbit; see Plate 13-4), supraclavicular fullness,
atrophy of the intrinsic muscles of the hand, and dis-
coloration or edema of the arm.32,46,48,49,54 Also, some
patients will complain of a sore throat, fever, hoarseness,
bloody sputum, unexplained weight loss, chronic cough,
dyspnea, and/or wheezing.36,48-50
*References 36, 46, 48, 49, 53, 54.
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
Signs. In cases of advanced disease, the clinical
examination may show positive results for special tests
and signs related to a brachial plexus lesion, thoracic
outlet syndrome, ulnar neuropathy, or C8 and T1 nerve
root injury. Smoking is a risk factor.36,49 Peak incidence
occurs in smokers around 60 years of age.36 The patient
should be referred for a chest radiograph (see Plate 13-
4). However, a bone lesion of the spine may be detected
before lung lesion on plain radiograph as lung cancer
metastasizes to the bone early.49,53
Esophagus
The esophagus, which is segmentally innervated by
thoracic nerves T4 to T6, is able to refer pain to the
shoulder through contact with the central portion of the
diaphragm (see Figure 13-4).4,17,55 Esophageal pain is
transmitted via afferents in the splanchnic and thoracic
sympathetic nerves.8 The primary afferent fibers, both
A-delta and C fiber neurons, pass through the paraver-
tebral sympathetic chain and the rami communicans to
join the spinal nerve and enter the dorsal root ganglia
before entering the dorsal horn of the spinal cord (see
Plate 13-1).8 Referred pain is thought to occur through
convergence of visceral (cardiac and esophageal) and
somatic afferents onto the same dorsal horn neurons (see
Figure 13-3).8,56
Symptoms. In cases where the diseased esophagus
is in contact with the diaphragm, the referred pain is
most often felt at the top or posterior portions of the
shoulder; that is, at the superior angle of the scapula, in
the suprascapular region, or along the upper trapezius
muscle.30,31 The upper arm and anterior portions of the
shoulder are not common areas of referred pain for the
diaphragm. The region surrounding the diaphragm may
be free of pain. In cases where the diaphragm is not
involved, pain may be referred to the scapula and/or
interscapular region. Patients often report that the pain
in the shoulder is exacerbated during or following
meals.4 They may also complain of substernal chest,
neck, or back pain.50 Other symptoms include difficulty
swallowing, weight loss, and (in the late stages) drool-
ing.50 Symptoms associated with esophageal cancer are
bloody cough, hoarseness, sore throat, nausea, vomiting,
fever, hiccups, and bad breath.50 Symptoms associated
with reflux esophagitis are regurgitation, frequent vom-
iting, and a dry nocturnal cough.50 The patient will com-
plain of heartburn—which is aggravated by strenuous
369
exercise, or by bending over or lying down—and is
relieved by sitting up or taking antacids.50
Signs. Physician-ordered tests include a positive
result from 24-hour intraesophageal pH and pressure
recordings, acid perfusion, edrophonium stimulation,
balloon distention, and ergonovine stimulation.4,57,58
There may be no local tenderness or shoulder pain
during palpation of the diaphragm. Full active and
passive shoulder elevation in standing may cause pain
because this motion changes the shape of the rib cage
and subsequently puts tension on the diaphragm.32
Shoulder pain, in cases with diaphragmatic irritation,
may be reproduced or exacerbated by deep breathing,
coughing, or sneezing.32,35,36
Heart
The heart, which is innervated by thoracic nerves T1 to
T5, is capable of referring pain to the shoulder (see Plate
13-3).4,30-33,55,59 Cardiac afferent fibers have shown evi-
dence of convergence with esophageal afferents and
somatic afferents in the upper thoracic spinal cord.23 In
fact, esophageal chest pain is known to mimic angina
pectoris.57 In addition, convergence has been demon-
strated between cardiac afferents, abdominal visceral
afferents (gallbladder, for example), and somatic affer-
ents in the lower thoracic spinal cord.23,56 Convergence
has also been noted with proximal somatic afferents
(shoulder), phrenic (diaphragm), and cardiopulmonary
spinal afferents onto the cervical spinothalamic tract
neurons (Figure 13-6).29 This explains how diaphrag-
matic disease and cardiac disease are both able to refer
pain to the shoulder and to other cervical-related
dermatomes.
Symptoms. The patient may complain of pain in
the left shoulder that is often associated with reports of
numbness and tingling in the left hand.19,31,50,60 Pain may
also be felt in the chest, neck, arm (usually the left, and
a C8 and T1 distribution), jaw, posterior thorax, or epi-
gastrium.19,36,50,60 The patient may describe tightness,
pressure sensations, throbbing, cramping, or aching in
the above areas.19,36 Other symptoms include exertion
and nocturnal dyspnea, ankle edema, palpitations, easy
fatigability, syncope, weakness, anxiety, profuse sweat-
ing, nausea, vomiting, tachycardia, or bradycardia.19,36,50
Signs. A history of shoulder or chest pain (angina)
on effort or exercise, such as a brisk walk, not associated
370 SECTION III SPECIAL CONSIDERATIONS
with movements of the shoulder.19 Symptoms are
relieved with rest.19 There may be a resting pulse greater
than 100 or less than 50 beats per minute.36 Blood pres-
sure consistently higher than 160/90 is a positive sign.36
Nitroglycerin will provide immediate relief of symp-
toms. Refer for electrocardiogram (EKG), blood test
(increased creatine phosphokinase (CPK) levels), tread-
mill with echocardiogram, and/or angiography. Heart
disease is most common in men over 40 and is associ-
ated with smoking, obesity, high blood pressure, dia-
betes, and physical inactivity.36,60 Timely recognition of
a cardiac problem cannot be overstated. Coronary artery
disease may show up as angina, myocardial infarction,
heart failure, or sudden death.36
Pericarditis
The heart, which is innervated by thoracic nerves T1 to
T5, is capable of referring pain to the shoulder in cases
of pericarditis (see Plate 13-3).4,36,60 Pericarditis is an
inflammation of the sac surrounding the heart.36,60
Figure 13-6 Schematic drawing of a
somatic afferent nerve (shoulder), a phrenic nerve
(diaphragm), and a cardiopulmonary afferent nerve
all converging onto the same spinothalamic tract
neuron.
Symptoms. There is usually a sharp burning pain
in the chest or left shoulder.36,50,60 Pain may be evoked
by deep breathing, coughing, or lying flat, and relieved
by sitting up and leaning forward.19,36,50,60 Other symp-
toms include fever, tachycardia, and dyspnea.50 Symp-
toms of chronic pericarditis include pitting edema of the
arms and legs, serous fluid in the peritoneal cavity,
enlarged liver, distended veins in the neck, and a
decrease in muscle mass.50
Signs. There will often be a pericardial friction rub
(the sound of two dry surfaces rubbing against each
other), which has different characteristics than a heart
murmur, noted during auscultation of the thorax.19,50
Patients with chronic pericarditis will demonstrate
pulsus paradoxus, which is an exaggerated decline in
blood pressure during inspiration.50 There are a variety
of causes including viral and bacterial infection, trauma,
cancer, collagen vascular disease, uremia, post–cardiac
surgery, myocardial infarction, radiation therapy, and
aortic dissection.19,36,60
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
Bacterial Endocarditis
Bacterial endocarditis is another source of pain in the
region of the shoulder.60-62 It is an inflammation of the
cardiac endothelium overlying a heart valve that is
caused by a bacterial infection.19,60 If left undiagnosed
and untreated, bacterial endocarditis can be fatal.61,62
Pain is most common in the glenohumeral, sternoclav-
icular, or acromioclavicular joints, and symptoms are
usually confined to one joint.60-62 Symptoms are not
caused by referred pain, therefore the patient will have
a positive musculoskeletal examination of the involved
joint. Articular involvement is thought to be secondary
to deposition of large particulate masses (emboli) that
contain immune complexes.60-62
Symptoms. Pain is often localized to one of the
three true joints of the shoulder. Low back pain, which
may mimic a herniated disk and sacroiliac joint pain, is
often reported.60 In approximately 25% of patients, mus-
culoskeletal complaints are the first symptoms of this
disease.60-62 There may be an abrupt onset of intermit-
tent shaking chills with fever.50,60 The patient may also
complain of dyspnea and chest pain with cold and
painful extremities.60 Other symptoms include pale skin,
weakness, fatigue, night sweats, tachycardia, and weight
loss.19,50,60
Signs. The patient’s history will often indicate no
trauma or previous occurrence of these symptoms. Pal-
pation of the involved joint will reveal warmth, redness,
and tenderness.60-62 An acute synovitis in a single joint,
especially the metacarpophalangeal, sternoclavicular,
or acromioclavicular joints, which are not commonly
involved in other diseases, should raise suspicions of
bacterial endocarditis.61,62 There will be a heart murmur,
positive results from a blood test for anemia, elevated
erythrocyte sedimentation rate (ESR), decrease in serum
albumin levels, increase in serum globulin concentration,
and microhematuria (blood in the urine).61,62 There is
relief of symptoms with antibiotics. Fever will be present
at some time during the illness.60-62 Associated signs are
dyspnea, peripheral edema, fingernail clubbing, enlarged
spleen, anorexia, Roth’s spots (small white spots in the
retina, usually surrounded by areas of hemorrhage),
petechiae (small purplish hemorrhagic spots on the
skin), and Janeway lesions (small red-blue macular
lesions) on the palm of the hands or the soles of the
feet.50 Diagnosis may be difficult in elderly patients,
371
who have a higher frequency of nonpathologic heart
murmurs and are less likely to have a fever develop in
response to infection.60-62 A plain radiograph may show
destructive changes within the joint (glenohumeral,
acromioclavicular, or sternoclavicular) indicative of an
infection.61,62 Risk groups for this illness include patients
with abnormal cardiac valves, congenital heart disease,
or degenerative heart disease (calcific aortic stenosis);
parenteral drug abusers; and those with a history of bac-
teremia.60-62 Treatment is with antibiotics.60-62
Vascular
Aneurysm. An aneurysm within a subclavian
vessel, or an aortic orifice of a subclavian vessel, can
result in pain at the shoulder.30-32,50,55 This is a poten-
tially dangerous arterial condition.36 An aneurysm is an
abnormal widening of the arterial wall caused by the
destruction of the elastic fibers of the middle layer of
that wall or by a tear in the inner lining of the arterial
wall that allows blood to flow directly into the wall and
subsequently widen it.36 Aortic aneurysms can enlarge
and compress pain-sensitive structures in the upper
mediastinum, leading to shoulder pain.30 They generally
occur in the elderly and slowly enlarge over a period of
many years.36 Rapid morbidity or mortality are expected
if an aneurysm ruptures.36
Symptoms. Pain in the shoulder may include throb-
bing and cramping. The patient may also report pares-
thesia, neck pain, and/or chest pain.50 Other symptoms
include night sweats, pallor, nausea, weight loss,
Raynaud’s phenomenon, diplopia, dizziness, and
syncope.50 Symptoms may be aggravated by an increase
in activity level (climbing stairs, fast walk, or upper
extremity repetitive motions), and relieved by rest.32
Signs. There will be a prolonged capillary refill time
for the fingers, systemic hypotension, and a weak or
absent distal pulse (radial and ulnar arteries at the
wrist).50 Bilateral dilation of the pupils will occur late.50
A plain radiograph of the chest may or may not allow
visualization of the aneurysm.
Arterial Occlusion. Arterial occlusion—usually
caused by atherosclerosis or compression of an artery,
such as the subclavian artery in thoracic outlet syn-
drome—can show up as a deep constant pain in the
shoulder or lead to ischemic pain with exercise.30,63
Symptoms. Patients will complain of pain in the
region of the shoulder, which may mimic a nerve
372 SECTION III SPECIAL CONSIDERATIONS

root compression.64 Other symptoms include pares-
thesia, coldness, weakness, and fatigue in the involved
extremity.50,64
Signs. Systolic blood pressure will be higher while
diastolic blood pressure remains unchanged in the
involved extremity.50 There will be a weak or absent
distal pulse (radial and ulnar arteries at the wrist).50,64
The extremity will be cool, cyanotic, and demonstrate a
prolonged capillary refill time.50 Tachycardia and angina
pectoris may also be present.50 Contrast angiography will
demonstrate arterial occlusion, which is best seen with
the extremity elevated.64 In the case of thoracic outlet
syndrome, results from one of the following tests will be
abnormal: Adson’s, costoclavicular, hyperabduction,
pectoralis minor stress test, or the 3-minute flap-arm
test.63-65
Thrombophlebitis. Thrombophlebitis of the
axillary and subclavian veins can also cause shoulder
pain (Figure 13-7).30,55,66-69 Thrombophlebitis is an
inflammation of a vein in the presence of a blood clot.
This is a serious situation, because emboli may break free
and travel to the lung, a potentially fatal condition. The
risk of pulmonary embolization for persons with a sub-
clavian thrombosis is approximately 12%.66 Deep vein
thrombosis of the upper extremity is often caused by
venous trauma from repetitive motions of the shoulder,
referred to as effort thrombosis, in persons with an
abnormal thoracic outlet.66-68 The most common site of
compression is between the clavicle, the costocoracoid
ligament, and the first rib.67,68 Repeated compression of
the vein can lead to injury and inflammation, which will
then put the vein at risk for the formation of a throm-
bus.67,68 Other causes of venous thrombosis include the
presence of indwelling venous catheters (central lines
or pacemaker leads), local compression, radiation, or
hypercoagulability.66-68
Symptoms. The patient will usually complain of a
dull pain in the shoulder and down the arm, which may
include paresthesia. Fever and chills may be present.50

Figure 13-7 Thrombosis of the subclavian vein at the level of the tho-
racic outlet. (From Rohrer MJ: Vascular problems. In Pappas AM, editor: Upper extremity
injuries in the athlete, New York, 1995, Churchill Livingstone.)
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
The patient may complain of cold and swollen fingers.67
Patients with effort thrombosis complain of the sudden
onset of swelling and cyanosis involving the entire arm.66
These patients will often report a history of upper
extremity exertion such as weightlifting or prolonged
repetitive motions.66-68 Symptoms of shortness of breath,
pleuritic chest pain, hemoptysis (expectoration of
blood), or a new nonproductive cough are suggestive of
a pulmonary embolus.66
Signs. Edema, coldness, and cyanosis may be noted
in the fingers, hand, or upper arm.50,66-69 Distention of
the superficial veins is usually seen in the hand, upper
arm, shoulder, or anterior chest wall.66-69 Effort throm-
bosis is usually seen in young, healthy individuals with
an athletic physique.66,67 It is also seen frequently in
hikers who carry backpacks.66 Exertion of the involved
extremity will lead to a notable exacerbation of the pain
and swelling.66 There may be a loss of range of motion
(ROM) at the shoulder. Conservative treatment usually
consists of heat, elevation, and anticoagulation medica-
tion. The heat is used to dilate the veins so that the fluid
may get by the thrombus. Physician-ordered tests
include duplex ultrasound scanning and venography.67
Thoracic outlet tests and arteriograms will show no
abnormalities.
Additional diagnostic tests, which may be indicated
for a variety of vascular disorders, include Allen’s test of
the radial and ulnar arteries at the wrist, Doppler ultra-
sonic flow detector, systolic blood pressure, pulse volume
recording, angiography, and auscultation of the major
arteries.18,65
Liver
The liver, which is segmentally innervated by thoracic
nerves T7 to T9, is able to refer pain to the right shoul-
der through its contact with the central portion of the
diaphragm (see Plates 13-2 and 13-3; see Figure 13-
4).4,17,32,55,70 Cancer of the liver is more common in men
and women over the age of 50.4 The liver is one of the
most common sites of metastasis from primary cancers
elsewhere in the body (colorectal, stomach, pancreas,
esophagus, lung, and breast cancers).70 Hepatitis, or
inflammation of the liver, can range from the subclini-
cal to the rapidly progressive and fatal stage.17,70
Symptoms. The referred pain is most often felt
at the top or posterior portions of the right shoulder;
that is, at the superior angle of the scapula, in the
373
suprascapular region, or along the upper trapezius
muscle.30,31 The upper arm and anterior portions of the
shoulder are not common areas of referred pain for the
diaphragm. The region surrounding the diaphragm may
be free of pain. Right shoulder pain may be acute or
spasmodic in nature.4 The patient may also complain of
headache, myalgia, and arthralgia.17 Other symptoms
include indigestion, nausea, vomiting, unexplained
weight loss, and fatigue.4,17,50,70 Pain from cancer of the
liver may also be described as deep, gnawing, and poorly
localized to the upper abdomen or back.4
Signs. Full active and passive shoulder elevation in
standing may cause pain because this motion changes
the shape of the rib cage and subsequently puts tension
on the diaphragm.32 Shoulder pain may be reproduced
or exacerbated—in cases with diaphragmatic irrita-
tion—by deep breathing, coughing, or sneezing.32,36
There is often no local tenderness or shoulder pain
during palpation of the diaphragm. However, there may
be a mass in the upper right abdominal quadrant (liver),
an enlarged liver, and/or the liver may be tender to pal-
pation.4,17,50,70 Associated signs are jaundice, pale skin,
purpura (red and purple hemorrhage into the skin),
ecchymosis, spider angiomas (hemorrhagic pattern in
the skin), palmar erythema, anorexia, and the accumu-
lation of serous fluid in the peritoneal cavity.17,50,70 Refer
the patient for a plain radiograph, diagnostic ultrasound,
computed tomography (CT) scan, or magnetic reso-
nance imaging (MRI) of the abdomen.70
Pancreas
The pancreas, which is segmentally innervated by
thoracic nerves T6 to T10, can refer pain to the left
shoulder through contact with the central portion of the
diaphragm (see Plates 13-2 and 13-3, and Figure 13-
4).4,17,30,55 Pancreatitis, or inflammation of the pancreas,
may be caused by heavy alcohol use, gallstones, viral
infection, or blunt trauma.17,44 Acute pancreatitis can be
fatal.44
Symptoms. Shoulder pain is usually referred to the
left scapula, supraspinous area, mid epigastrium, and/or
back.17,44 Patients with a pancreatic abscess, cancer, or
pancreatitis may complain of fever, weight loss, jaundice,
tachycardia, nausea, and/or vomiting.44,50 Patients with
a pancreatic abscess may also report an abrupt rise in
temperature, diarrhea, and hypotension.50 Patients with
374 SECTION III SPECIAL CONSIDERATIONS
pancreatic cancer may also complain of fatigue, weak-
ness, and gastrointestinal bleeding.50 A patient with pan-
creatitis will often bend forward or bring the knees to
the chest to relieve the pain.44,50 These patients will
report an exacerbation of pain with walking or lying
supine.44 In addition, these latter patients will complain
of a waxing and waning pain in the epigastric and left
upper quadrant of the abdomen.17 Pain will be exacer-
bated by eating, alcohol intake, or vomiting.17
Signs. Pancreatic cancer has been linked to dia-
betes, alcohol use, a history of pancreatitis, and a high-
fat diet.44 Full active and passive shoulder elevation in
standing may cause pain because this motion changes
the shape of the rib cage and subsequently puts tension
on the diaphragm.32 Shoulder pain may be reproduced
or exacerbated—in cases with diaphragmatic irrita-
tion—by deep breathing, coughing, or sneezing.32,36
There is often no local tenderness or shoulder pain
during palpation of the diaphragm. However, there may
be an abdominal mass, enlarged liver or spleen, or ten-
derness in the epigastric area.4,17,50 Cancer of the pan-
creas is more common in men and women older than 50
years of age.4 Diagnostic ultrasound, CT scan, or MRI
may be necessary for an accurate diagnosis.
Gallbladder
The gallbladder, which is innervated by thoracic nerves
T7 to T9, is capable of referring pain to the right shoul-
der (see Plate 13-2 and Figures 13-2 and 13-3).* Affer-
ent fibers (T6 to T11) from the gallbladder pass into
hepatic and celiac plexuses and then enter the major
splanchnic nerves, through which they pass to the sym-
pathetic chain into the spinal cord.27 Common diseases
of the gallbladder include cholecystitis (inflammation)
and cholelithiasis (stones).4 Risk factors for the latter
include age (increases with age), sex (more common in
women), pregnancy, oral contraceptive use, obesity, dia-
betes, a high-cholesterol diet, and liver disease.70
Symptoms. Cramping pain or a deep, gnawing,
poorly localized pain in the back of the right shoulder
may be the first symptoms of gallbladder involve-
ment.4,17,50,70 Pain is usually referred to the right
scapula.4,17,70 Other symptoms include chronic epigastric
or right upper abdominal pain after meals, nausea,
*References 4, 17, 30-32, 50, 55, 70.
vomiting, and fever.17,50,70 Patients suffering with
cholelithiasis, the passage of a stone through the bile or
cystic duct, will complain of sudden and severe paroxys-
mal pain in addition to chills and restlessness.50
Signs. Gallbladder cancer is more common in men
and women over the age of 50. More specifically, it is
most common in obese women over 40 years of age.4,17
Gallbladder cancer is characterized by weight loss,
anorexia, and/or jaundice.50,70 Patients with cholecystitis
will have a fever, jaundice, tenderness over the gall-
bladder, and abdominal rigidity.50,70 Cholelithiasis will
produce a low-grade fever in the patient.17,50 Fatty or
greasy foods will exacerbate the symptoms of gallblad-
der disease.4,70 There will be tenderness, and occasion-
ally a palpable mass, in the right upper abdominal
quadrant.17 The patient should be referred for a plain
radiograph, diagnostic ultrasound, and/or CT scan.70
Kidney
Though rare, the kidney, which is innervated by thoracic
nerves T10 to L1, may refer pain to the shoulder region
(see Plate 13-2 and Figures 13-2 and 13-3).4,32,71 There
are several pathologic conditions to consider with
respect to the kidney, including cancer, perinephric
abscess, and other disease processes such as kidney
stones. Associated disorders are pyelonephritis, nephri-
tis, nephropathy, nephrotic syndrome, renal artery
occlusion, renal failure, renal infarction, and renal
tuberculosis.50
Symptoms. Some of the following complaints may
be noted: acute or spasmodic ipsilateral shoulder, lower
abdominal, groin, low back, or flank pain; weakness,
fatigue, or generalized myalgia; unexplained weight loss;
nausea, vomiting, or chills; or painful, frequent, and
urgent urination with or without hematuria.4,50,71,72
Signs. Tenderness will be noted at the costoverte-
bral angle and, in the case of inflammation, there will be
a fever.50,71 Musculoskeletal pain is rarely the primary
complaint. Cancer of the kidney is most common
between the ages of 55 and 60.53 It can metastasize to
the lung, brain, or liver.53 Metastasis to bone occurs late
in the disease process.53
In patients with a perinephric abscess, there is no ten-
derness over the renal areas of the back, and only mild
distention is noted during abdominal palpation.72 The
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
ESR (erythrocyte sedimentation rate), white cell count,
and fever will all be elevated.72 A plain anteroposterior
KUB (view of the kidney, ureters, and bladder) radio-
graph will demonstrate the following: (1) difficulty iden-
tifying the psoas stripe, (2) absence of the renal outline,
and (3) curvature of the spine towards the side of the
disease.72 Your patient should be referred for an intra-
venous pyelogram and/or CT scan. Kidney stones may
produce a severe cramping pain.4 Chronic kidney disease
may be associated with poor calcium deposits in bone,
which will lead to a weak bone structure.4 For all of the
diseases of the kidney that have been discussed, patients
may benefit by referrals for diagnostic ultrasound, CT
scan, or MRI.
Stomach
The stomach, which is segmentally innervated by tho-
racic nerves T6 to T10, can refer pain to the shoul-
der through contact with the central portion of the
diaphragm (see Plates 13-2 and 13-3, and Figure 13-
4).4,30 Risk factors for an ulcer or gastritis include heavy
alcohol use, smoking, and the use of nonsteroidal anti-
inflammatory drugs (NSAIDs).17,44
Symptoms. Pain is most often felt in the right
shoulder at the superior angle of the scapula, in the
suprascapular region, and in the upper trapezius
muscle.30,31,44 The patient may also complain of epigas-
tric or right upper abdominal quadrant pain.17,44 Patients
with cancer, an ulcer, or gastritis may complain of weight
loss, night pain, or chronic dyspepsia (painful digestion),
a sense of fullness after eating, heartburn, nausea,
vomiting, and a loss of appetite.17,44,50 Patients with
stomach cancer may complain of a deep, gnawing, and
poorly localized pain in the upper abdomen or back.4
Persons with an ulcer may also complain of gastroin-
testinal bleeding and epigastric pain 1 to 2 hours after a
meal, which may occur with vomiting, fullness, or
abdominal distention.44,50 Patients with gastritis may
also report belching, fever, malaise, anorexia, or bloody
vomit.50
Signs. Full active and passive right shoulder eleva-
tion in standing may cause pain because this motion
changes the shape of the rib cage and subsequently puts
tension on the diaphragm.32 Right shoulder pain may be
reproduced or exacerbated by deep breathing, coughing,
or sneezing.32,36 Cancer of the stomach is more common
375
in men and women over 50 years of age.4 There may be
an abdominal mass or tenderness noted with palpa-
tion.4,50 Abdominal CT scan or MRI may be necessary
for an accurate diagnosis.
Colon and Large Intestine
The colon and large intestine, which is innervated by
thoracic and lumbar nerves T11 to L1, are capable of
referring pain to the right shoulder—although this is a
rare event (see Plates 13-1 and 13-2, and Figures 13-2
and 13-3).4,73 The gastrointestinal tract (GI) has dual
innervation (see Plate 13-1). There are afferent fibers
that join sympathetic nerves and afferent fibers that join
parasympathetic nerves.74 Pain from the GI track is pre-
dominantly mediated by afferent activity in sympathetic
nerves, such as the splanchnic and hypogastric nerves.74
These afferent nerve fibers have their cell bodies in tho-
racolumbar spinal ganglia and their central projections
enter the spinal cord at levels between T2 and L3.74 Dis-
orders relevant to this region include ulcerative colitis,
irritable bowel syndrome, spastic colon, obstructive
bowel disease, diverticulitis, and cancer. Colon cancer
is the most frequently diagnosed cancer in the United
States.17 Cancer in this region is most common in men
and women over the age of 50.4,53 Metastasis to the
spine, liver, and lung is common.17,53 Smoking, alcohol,
NSAIDs, and caffeine may increase the risk of disease.4
NSAIDs may also mask the symptoms.4 Other risk
factors include a prior history of inflammatory bowel
disease, prior cancer of another organ, and benign polyps
of the colon.17
Symptoms. Pain is referred to the right shoulder
from the hepatic flexure of the colon (see Plate 13-2).73
A cramping pain is often described in the lower mid-
abdominal region.17,44,50 There may also be a fluctuation
of pain with eating habits, painful bowel movements,
diarrhea, indigestion, nausea, vomiting, change in bowel
habits, bloody stools, jaundice, and weight loss.4,50 Irri-
table bowel syndrome is the most common gastroin-
testinal disorder in Western society.44 Symptoms are
aggravated or precipitated by emotional stress, fatigue,
or alcohol, or by eating a large meal with fruit, roughage,
or a high fat content.44 In addition to the above symp-
toms, there may be constipation, foul breath, and flatu-
lence.44 The predominant symptoms with ulcerative
colitis are rectal bleeding and diarrhea.44 With obstruc-
tive bowel disease, the patient will complain of consti-
376 SECTION III SPECIAL CONSIDERATIONS
pation, rapid heart rate, and short episodes of intense
cramping pain.50 Diverticulitis, an inflammation in the
wall of the colon, will produce constant left lower
abdominal pain with radiation commonly to the low
back, pelvis, or left leg.17 In cases of cancer, there may
be a change in the frequency of bowel movement, a sense
of incomplete evacuation, bloody stools, unexplained
weight loss, weakness, fatigue, exertional dyspnea, and
vertigo.17,50,53
Signs. Patients may exhibit signs of abdominal dis-
tention, abdominal tenderness, rectal bleeding, anorexia,
and abnormal bowel sounds.50 Diagnosis is confirmed by
a positive result from a colonoscopy.
Case Studies
The case studies in this chapter have been modified
slightly for instructional purposes and to fit the format
of the Guide to Physical Therapist Practice.
Case Study 1
DEMOGRAPHICS
Robbie is a 24-year-old, right-handed, white male
college graduate whose primary language is English. He
came to physical therapy Feb. 13, 1999, without a physi-
cian’s diagnosis or referral, and complaining of periodic
left shoulder pain. He denied previous treatment of any
kind for his current complaints.
SOCIAL HISTORY
He shares an apartment with two of his friends.
Robbie denies any cultural or religious beliefs that he
thinks may affect his care with us. He has been unem-
ployed for 3 months.
LIVING ENVIRONMENT
Robbie lives in a three-bedroom apartment on the
second floor. He denies the existence of any major obsta-
cles in and around his apartment. He ascends and
descends one flight of stairs every day. He does not use
assistive devices of any kind for his activities of daily
living (ADL).
GENERAL HEALTH STATUS
He states that he is in excellent health and has had
no major life changes in the past year. The medical
screening questionnaire that he completed did not
produce any notable “red flags” to indicate visceral
involvement (Figure 13-8).
SOCIAL/HEALTH HABITS
Robbie reports that he eats a healthy diet that
excludes red meat. He takes a multivitamin and protein
shake daily and denies any substantial intake of caffeine
or tobacco. He drinks a few beers on the weekends. He
states that he is a competitive racquetball and volleyball
player. He also surfs and lifts weights occasionally.
FAMILY HISTORY
Both his parents and grandparents are still alive. Both
his father and his grandfather each have suffered heart
attacks. His grandmother had a cerebrovascular accident
(CVA). He notes that his mother and grandmother both
suffer from rheumatoid arthritis.
MEDICAL/SURGICAL HISTORY
1998—Muscle injury to the left side of his rib cage
after a weekend volleyball tournament
1997—Muscle injury to the left side of his rib cage
after a weekend volleyball tournament
1994—Low back muscle injury from racquetball
He denies a history of surgery. The only illness or
other complaints he has had in the past year are related
to the flu, which he had 6 to 9 months ago.
CURRENT CONDITION(S)/CHIEF COMPLAINT(S)
Robbie comes to physical therapy complaining of
periodic, severe (2/10—7/10), localized left shoulder
pain at the acromioclavicular joint (Figure 13-9). He
reported a constant low-intensity ache (2/10), which
never went away regardless of what he did. He was able,
however, to produce a sudden and sharp pain with
certain movements. The movements that consistently
reproduced his pain were full flexion or full abduction
of his shoulder overhead. He also reported sharp pain
with powerful or forceful movements, such as hitting a
racquetball hard or spiking a volleyball. He was able to
sleep on his left side without much difficulty. He denied
neck pain, headaches, dizziness/vertigo, vision changes,
tinnitus, nausea, upper extremity symptoms (radiating
pain, weakness, or paresthesia), night pain, and short-
ness of breath (SOB). He reported there was no change
in his shoulder pain related to eating, bowel or bladder
activity, or during exertional activities (light jog) that
did not directly involve his shoulder. He also denied
having constitutional symptoms (fever, night sweats,
nausea/vomiting, dizziness, fatigue, or unexplained
weight loss). He stated that the sharp pain was not con-
stant and that he could get immediate relief if he rested
his shoulder. He admitted there was shoulder pain if he
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER 377

Figure 13-8 Patient questionnaire for Case Study 1.

378 SECTION III SPECIAL CONSIDERATIONS
Figure 13-9 Pain diagram from a 24-year-old, right-
handed male experiencing left shoulder pain.
laughed out loud or took a deep breath. He was not sure
if coughing was a problem. He denies a history of a
motor vehicle accident (MVA), fractures, or falls. His
pain started 6 days ago. He denied any incidents of
specific trauma. Nine days ago he participated in a
2-day walleyball (volleyball on a racquetball court) tour-
nament; and 6 days ago, he was involved in two com-
petitive racquetball league matches.
FUNCTIONAL STATUS/ACTIVITY LEVEL
Before the onset of his shoulder pain, Robbie was a
competitive racquetball and volleyball player who played
either sport three to four times a week. He also surfed
and lifted weights occasionally. Robbie scored 92 out of
a possible maximum score of 100 on the Sharp Func-
tional Activity Survey (Sharp FAS) for the Neck &
Shoulder region (Sharp HealthCare, San Diego, 1998).
He reported no difficulties performing all of his ADL.
He did state, however, that he had severe difficulty
playing volleyball and racquetball at a competitive level
because of the periodic sharp pains in his left shoulder.
MEDICATIONS
Robbie denied taking any medications, prescription
or nonprescription, of any kind.
OTHER CLINICAL TESTS
There were no clinical tests of any kind performed
on our patient in the past year. He has never had any
imaging studies performed on his shoulder or neck.
Robbie did have x-rays taken of his low back in 1994,
which he reported were read as normal.
CARDIOVASCULAR/PULMONARY SYSTEM
Although it is well known that the heart and lungs
can refer pain to the left shoulder, there was no indica-
tion that our patient’s symptoms might be cardiopul-
monary in origin. Robbie was a very fit and very young
(24-year-old) man with no risk factors, and no specific
symptoms of heart or lung disease. His medical screen-
ing questionnaire did not raise any “red flags” for the
pulmonary and cardiovascular sections (see Figure 13-
8). Subsequently, a physical examination was deferred on
his cardiopulmonary system.
INTEGUMENTARY SYSTEM
Robbie’s skin appeared healthy, with a good continu-
ity of color and no significant changes in temperature.
There was no joint effusion, soft tissue edema, or scars
noted.
COMMUNICATION, AFFECT, COGNITION, LEARNING STYLE
There were no known learning barriers identified for
our patient. Robbie reported that he learned best when
given a demonstration of the procedure or exercise. He
did not show any deficits with regard to his cognition,
orientation, or ability to effectively communicate.
MUSCULOSKELETAL SYSTEM
Posture
In standing, he had good posture with only a slight
forward head and a slight increase in his lumbar
lordosis.
Range of Motion
Cervical spine ROM:
Active and passive ROM were within normal limits
(WNL) and pain free.
Shoulder ROM:
Left shoulder active and passive ROM were WNL.
Pain was reproduced at the end ROM in active flexion
or abduction, with our patient standing. Passive range of
motion (PROM), tested in the sitting position, was pain
free.
Scapula and elbow ROM:
Active and passive ROM were WNL and pain free.
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER 379

Thoracic spine ROM: Cervical Spine (Negative Tests)

Active and passive thoracic ROM were minimally Compression testing of the cervical spine in flexion,
limited in flexion and extension. Sharp left shoulder neutral, and extension (see Figure 5-13)
pain, however, was noted with movement into the end Cervical quadrant test in flexion and extension (see
range of active or passive flexion or extension. Figure 5-17)
Rib ROM: Valsalva
Active deep inhalation reproduced the patient’s left Shoulder (Positive Tests)
shoulder pain. Passive lower rib cage compression was None
normal. Shoulder (Negative Tests)
Lumbar active range of motion (AROM): Distraction/compression of the glenohumeral (GH)
There was a moderate restriction in the upper joint
lumbar region with active flexion and a mild sharp angu- Hawkins impingement sign
lation into extension at approximately the L4-5 Load and shift test (anterior and posterior instability)
segment. Distraction/compression of the acromioclavicular (AC)
Muscle Performance joint
There was no reproduction of symptoms during resist- O’Brien test (SLAP)
ed testing in each of the shortened, mid, and lengthened Crank test (labrum)
ranges for muscles of the cervical and thoracic spine, Empty can (supraspinatus tendon)
shoulder, or rib cage. Specific myotome testing was Speed’s (biceps tendon)
deferred to save time and because there were no neuro- Thoracic Spine (Positive Tests—Shoulder Pain)
logic complaints. Thoracic quadrant tests in flexion to the left and
Sensory Integrity extension (right > left)
This part of the examination was deferred to save Thoracic Spine (Negative Tests)
time. Our patient denied having any neurologic Segmental joint mobility and provocation testing
symptoms. (prone posterior to anterior glides) (see Figure
Reflex Integrity 5-21)
This part of the examination was deferred to save T1 nerve root tension test (see Figure 5-22)
time. Our patient denied having any neurologic Ribs (Positive Test—Shoulder Pain)
symptoms. Coughing and deep inhalation
Pain Ribs (Negative Tests)
There was no tenderness or reproduction of symp- Lateral compression of mid and lower ribs (supine)
toms with palpation of musculoskeletal structures Mobility and provocation testing of first rib (see
throughout the cervical and thoracic spine, chest, shoul- Figure 5-24)
der, and upper ribs. Palpation of the lymph nodes in the Cervical rotation lateral flexion “CRLF” test (see
cervical, supraclavicular, and axillary regions was normal. Figure 5-26)
Palpation of the abdomen indicated local pain and ten- Mobility and provocation testing of ribs R2-5
derness along the left anterolateral border of the anteriorly (see Figure 5-25)
diaphragm and costal margin, just under the rib cage. JOINT INTEGRITY AND MOBILITY
Palpation of this peripheral portion of the diaphragm Cervical spine: Deferred to save time because patient
did not reproduce the patient’s shoulder pain. The had full cervical AROM without pain. (Will examine
central portion of the diaphragm was out of reach for during a future appointment as needed.)
palpation. Palpation of Robbie’s upper extremity pulses Shoulder
was deferred because he reported no symptoms during Glenohumeral: Normal (grade 3) in all directions, no
his history or on his medical screening questionnaire complaints of pain.
suggestive of cardiovascular disease. Sternoclavicular: Normal (grade 3) in all directions,
Special tests: no complaints of pain.
Cervical Spine (Positive Tests) Acromioclavicular: Normal (grade 3) in all directions,
None no complaints of pain.
380 SECTION III SPECIAL CONSIDERATIONS
Scapulothoracic: Normal (grade 3) in all directions,
no complaints of pain.
Thoracic spine: Slight hypomobility (grade 2) in mid
and lower thoracic spine in extension, with muscle
guarding and no pain.
Ribs: Slight hypomobility (grade 2) of R7-10 on the
left, with muscle guarding and no pain.
NEUROMUSCULAR SYSTEM
Robbie had no gross gait, locomotion, or balance
disorders.
IMAGING STUDIES: RADIOGRAPHS
Lumbar (1994): The films and the radiologist’s report
were not available.
DIAGNOSIS
Musculoskeletal Pattern D: Impaired joint mobility,
motor function, muscle performance, and ROM associ-
ated with connective tissue dysfunction.
This is a 24-year-old, right-handed male with signs
and symptoms consistent with an extrinsic source of
shoulder pain. Shoulder AROM at the end of range for
flexion or abduction, which deforms the rib cage and can
put stress on the diaphragm, was the only test of the
shoulder that gave rise to pain. All other tests of the
shoulder—palpation, PROM, resisted testing, special
tests, and specific mobility tests—were negative. This
extrinsic source appeared to be from an irritation of his
central left hemidiaphragm, with subsequent referred
pain to the left shoulder. Although end ROM of the
thoracic spine, thoracic quadrant tests, coughing, and
deep inhalation produced shoulder pain, motions that
also deform the rib cage and produce stress on the
diaphragm, there were no collaborative findings of tho-
racic or rib injury from resisted testing, palpation, special
tests, or specific mobility testing of the thoracic spine
and ribs.
There is a high suspicion, in cases involving the
diaphragm, of visceral disease or tumor-induced inflam-
mation of the diaphragm. Even though there were no
signs, symptoms, patient history, or family history to
suggest that there might be a medical disease involving
the diaphragm, it has to be part of the differential
diagnosis.
PAIN: The primary pain generator for this patient
appears to be his left hemidiaphragm.
STRAIN: The strains that may be exacerbating the
pain and dysfunction are mild hypomobilities in the
thoracic spine and ribs with possible lumbar
instability. The latter will be more fully assessed at
his next appointment.
BRAIN: The patient has experienced his current pain
episode for only 1 week. He is in the early stage of
healing and has not demonstrated any signs of fear,
anger, or frustration. There is no indication of a
primary central sensitization disorder or adverse
forebrain activity at this time.
PROGNOSIS
Robbie has a very good prognosis for returning to
competitive volleyball and racquetball.
PLAN OF CARE
Anticipated goals:
1. Robbie’s goal: “Get back to a competitive level of
volleyball and racquetball.”
2. Patient will be independent with his home exercise
program.
3. Thoracic spine and rib mobility will return to WNL.
4. His Sharp FAS score will be ≥95 with minimal
pain (3/10) and no analgesics or NSAIDs.
5. Patient will return to competitive volleyball and
racquetball with minimal discomfort (3/10).
INTERVENTIONS
Robbie received a comprehensive treatment program
incorporating the W.O.M.E.N. (wisdom, optimism,
manual therapy, exercise, and nutrition) plan of care
concept that was outlined in Chapter 5. He was expected
to achieve at least a 50% reduction in pain after 7 to
10 days. If not, the clinician was prepared to refer
the patient to an internal medicine specialist for
further medical evaluation. Fortunately, our patient
was 90% improved with respect to his symptoms after
1 week. He was able to play racquetball at a competitive
level after 2 weeks with only minimal discomfort.
At a 1-year follow-up with our patient, he reported that
his left shoulder pain had not returned and he had
reported no illnesses or adverse symptoms over the
past year. Although it is hard to verify for sure the source
of our patient’s pain, the only structure that seemed a
likely candidate was his diaphragm. Instances of
diaphragmatic inflammation from physical strain, not
surgical, visceral, or tumor related, are rare. Therefore it
is strongly suggested that with a similar patient presen-
tation, serious consideration should be given to a differ-
ential diagnosis of visceral disease or musculoskeletal
tumor.
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
Case Study 2
DEMOGRAPHICS
Annem is a 66-year-old, right-handed Hispanic
female college professor whose primary language is
Spanish—although she is fluent in English. She was
referred to us May 31, 1994, from her primary care
physician with a diagnosis of “frozen shoulder.” She
denied previous treatment of any kind for her current
complaints.
SOCIAL HISTORY
Annem lives at home with her husband of 34 years.
She denies any cultural or religious beliefs that she
thinks may affect her care with us. She is employed as a
professor of biology at a local university. Her job requires
her to reach overhead and perform repetitive motions
with her arm elevated, including writing on the chalk-
board, lifting and carrying less than 10 lb, prolonged
sitting, and prolonged standing. She has not missed any
time from work because of her current complaints.
LIVING ENVIRONMENT
Annem lives in a two-story house in which she
ascends and descends one flight of stairs every day. She
denies the existence of any major obstacles in and
around her house. She does not use assistive devices of
any kind for her ADL.
GENERAL HEALTH STATUS
Annem rates her general health as fair. In the past
year, both her sister and her father died of cancer. The
medical screening questionnaire that Annem filled out
on her first visit indicated a family history of cancer
(Figure 13-10). Her grandmother died from throat
cancer, her father died from prostate cancer, and her
sister died from pancreatic cancer. Questioning her on
her smoking habits uncovered that she is a 50-pack-year
smoker (1 pack per day ¥50 years of smoking). The mis-
cellaneous questions of the medical screening question-
naire documented a significant number of items that
may not be related to somatic injury and dysfunction,
including unexplained weight change, history of cancer,
extensive family history of cancer, insidious onset of
pain, constant pain, and pain that is worse at night—
therefore raising a red flag. In addition, half of the ques-
tions under the pulmonary section of the questionnaire
were answered yes—again raising a red flag. The car-
diovascular section was only of mild concern since the
items checked were not strong indicators of cardiovas-
381
cular disease. At this point, we should have concerns
about our patient’s pulmonary system and how this
might relate to her family’s history of cancer and her
history as a heavy smoker. If her symptoms correlate
with a known visceral disease, and we are unable to
provoke her symptoms and come up with a meaningful
musculoskeletal explanation, then we will have to refer
our patient for further medical evaluation.
SOCIAL/HEALTH HABITS
Annem reports that she has smoked approximately
one pack of cigarettes a day for the past 50 years (50-
pack-year smoker). She takes a multivitamin pill daily,
drinks one to two cups of coffee a day, and has two to
three glasses of wine each week. She is not a vegetarian
and eats at least two meals a day, usually skipping break-
fast. Her normal physical activity level involves walking
5 days a week for approximately 40 minutes. She does
not participate in sports or any other forms of physical
exercise.
FAMILY HISTORY
She reports that three members of her family have
died from various forms of cancer and congestive heart
failure has been diagnosed in one other. Her parents are
both deceased.
MEDICAL/SURGICAL HISTORY
1994—Surgery to right TMJ 2 months ago for a
malignant melanoma
1992—Osteoporosis was diagnosed
1991—Fell on right shoulder, no fracture; symptoms
resolved in 4 months
1975—Lumbar disk surgery
In the past year, she has had episodes of chest pain,
cough, SOB, pain at night, loss of appetite, weight loss,
and nausea.
CURRENT CONDITION(S)/CHIEF COMPLAINT(S)
Annem came to physical therapy May 31, 1994, with
a diagnosis of “frozen shoulder.” Her main complaint
was constant severe (7/10-9/10) right shoulder pain that
radiated down her arm and along the ulnar border of her
forearm and hand, and included the third through fifth
digits (Figure 13-11). Approximately 6 weeks before her
evaluation she reported an episode in which her whole
right arm felt numb. This symptom did not return. She
did report, however, a periodic mild tingling sensation
along the ulnar border of her right hand. Upon further
discussion, she admitted that she forgot to tell her
physician about the tingling. She denied neck pain,
382 SECTION III SPECIAL CONSIDERATIONS

Figure 13-10 Patient questionnaire for Case Study 2.

CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
Figure 13-11 Pain diagram from a 66-year-old,
right-handed woman with a diagnosis of “frozen shoulder.”
headaches, chest pain, dizziness/vertigo, vision changes,
tinnitus, nausea, and upper extremity weakness. She
reported there was no change in her shoulder pain
related to eating, bowel or bladder activity, or during
exertional activities (light jog) that did not directly
involve her shoulder. Laughing, coughing, or taking a
deep breath did not seem to alter her constant severe
pain. She also denied having constitutional symptoms
(fever, night sweats, nausea/vomiting, dizziness, or
fatigue). She denied a history of neck pain, fracture, or
MVA. Other than what she had stated above, Annem
denied any other complaints or symptoms throughout
the rest of her body. She stated that her shoulder pain
started gradually, with no trauma or overuse noted,
sometime in January 1994. Her pain is evoked by reach-
ing into the back seat of her car from the driver’s seat.
She gets relief when she lies down on her right side.
FUNCTIONAL STATUS/ACTIVITY LEVEL
Her normal physical activity level involves walking 5
days a week on her lunch hour for approximately 40
383
minutes. She does not participate in sports or any other
forms of physical exercise. She reports moderate diffi-
culties with her job, looking up or reaching overhead,
dressing, and her domestic duties around the house.
MEDICATIONS
Prescription: Fosamex (osteoporosis)
Nonprescription: Advil and Tylenol daily for the past
6 months.
OTHER CLINICAL TESTS
1992—She underwent a CT bone density scan of the
spine: T-score of -2.7 (osteoporosis)
1991—Cervical spine and right shoulder plain
radiographs showed a “normal cervical spine” and a
“normal right shoulder” according to the radiologist.
CARDIOVASCULAR/PULMONARY SYSTEM
Heart rate (resting): 75 beats per minute
Respiratory rate (resting): 16 breaths per minute
(shallow)
Blood pressure: 130/80
Edema: None
INTEGUMENTARY SYSTEM
Annem’s skin appeared healthy with a good continu-
ity of color and no significant changes in temperature.
There was very mild swelling and a surgical scar around
her right TMJ, and mild swelling was also noted in the
right supraclavicular fossa. A well-healed, thin white
scar was noted in her lower lumbar spine.
COMMUNICATION, AFFECT, COGNITION, LEARNING STYLE
There were no known learning barriers identified for
our patient. She stated that she learned best when given
a diagram and a demonstration. Annem did not display
any deficits with regard to her cognition, orientation, or
ability to effectively communicate.
MUSCULOSKELETAL SYSTEM
Posture
In standing, she had a forward head, rounded and
protracted shoulders, and a moderately increased tho-
racic kyphosis. Her iliac crest was high on the right, with
right genu recurvatum, collapsed arches bilaterally, and
bilateral hallux valgus (R > L).
Range of Motion
Cervical spine ROM:
Active and passive extension or right rotation repro-
duced her shoulder pain. Both motions were limited by
pain.
Shoulder ROM:
Active and passive ROM were equally limited.
Abduction and ER were moderately limited with
384 SECTION III SPECIAL CONSIDERATIONS
minimal limitations in IR and flexion. Minimal shoul-
der pain, but no arm pain, was reproduced at the end
ROM in all directions.
Scapula and elbow ROM:
Active and passive ROM were WNL and pain free.
Thoracic spine ROM:
Active and passive thoracic ROM were severely
limited in extension and moderately limited in side
bending and rotation. There was no reproduction of our
patient’s primary complaint.
Rib ROM:
Active deep inhalation was limited and accompanied
by a cough and a dull ache in her shoulder. Gentle
(because of Annem’s age and diagnosis of osteoporosis),
passive mid and lower rib cage compression was normal.
Lumbar AROM:
There were moderate restrictions in all directions,
without complaints of pain.
Muscle Performance
Shoulder and arm pain were reproduced with re-
sisted testing of the cervical spine when the neck was
held in extension (shortened position for the neck exten-
sors and lengthened position for the neck flexors) or
right side bending (shortened position for the scalenus
and upper trapezius on the right and lengthened posi-
tion for the scalenus and upper trapezius on the left).
There was no reproduction of symptoms for all the car-
dinal directions tested in each of the shortened, mid, and
lengthened ranges for muscles of the thoracic spine
and shoulder. Manual muscle testing—isometric (5/5 =
WNL)—of the upper extremities was as follows: right
triceps (4/5), wrist flexion and extension (4/5), and the
intrinsics of the hand were 3/5.
Sensory Integrity
Her sensation to light touch and pinprick was
decreased in the right C8 and T1 dermatomes.
Reflex Integrity
Her deep tendon reflexes (DTR) were 2+ and equal
at the biceps, brachioradialis, and triceps tendons. The
right abductor digiti minimi tendon reflex was 1+. The
scapulohumeral reflex (SHR) and Hoffman’s sign
showed normal results. Both of these tests are used to
help rule out cervical myeloradiculopathy.
Pain
Palpation: Swelling and tenderness were noted in the
right supraclavicular fossa and right TMJ. There was no
edema or skin discoloration noted in the extremities.
Palpation of the lymph nodes (SCM, supraclavicular,
and axillary), arterial pulses (brachial and radial), and
abdomen was normal.
Special Tests
Cervical Spine (Positive Tests—Reproduction
of Symptoms)
Cervical quadrant test in extension to the right or
flexion to the left (see Figure 5-17)
Compression testing of the cervical spine was positive
only in extension (see Figure 5-13)
Upper limb neurodynamic testing (ULNT) brachial
plexus/median nerve and ulnar nerve bias
techniques
Cervical Spine (Negative Tests)
Cervical quadrant test in flexion to the right or
extension to the left
ULNT radial nerve bias technique
Thoracic outlet syndrome (TOS)
Valsalva
Shoulder (Positive Tests—Reproduction
of Symptoms)
Hawkins impingement sign
Shoulder (Negative Tests)
Distraction/compression of the GH joint
Load and shift test (anterior and posterior instability)
Distraction/compression of the AC joint
O’Brien test (SLAP)
Crank test (labrum)
Empty can (supraspinatus tendon)
Speed’s (biceps tendon)
Thoracic Spine (Positive Tests—Reproduction
of Symptoms)
T1 nerve root tension test (see Figure 5-22)
Thoracic Spine (Negative Tests)
Segmental joint mobility and provocation testing
(prone P/A glides) (see Figure 5-21)
Thoracic quadrant tests
Ribs (Positive Test)
Mobility and provocation testing of the right first rib:
local pain and muscle guarding (see Figure 5-24)
Cervical rotation lateral flexion “CRLF” test: limited
mobility on the right (see Figure 5-26)
Ribs (Negative Tests)
Mobility and provocation testing of ribs R2-5
anteriorly (Figure 5-25)
Lateral compression of mid and lower ribs (supine)
Coughing and deep inhalation
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
Joint Integrity and Mobility
Cervical spine: There was a loss of segmental mobil-
ity in all directions throughout the mid and lower cer-
vical spine. Severe limitations (grade 1) were evident,
with pain and muscle guarding from C6 to T1 in exten-
sion, right side bending, and right rotation. There was a
positive disk shear test at C5-6 (see Figure 5-14)
Shoulder:
Glenohumeral: Normal (grade 3) in all directions
except distraction (grade 2)—muscle guarding and pain.
Sternoclavicular: Normal (grade 3) in all directions,
no complaints of pain.
Acromioclavicular: Normal (grade 3) in all directions
without primary complaint of pain.
Scapulothoracic: Normal (grade 3) in all directions
without primary complaint of pain.
Thoracic spine: Severe hypomobility (grade 1) at all
levels in extension; upper segments associated with local
pain and muscle guarding.
Ribs: Slight hypomobility (grade 2) of R1 on the
right, with pain.
Neuromuscular System
Annem had no gross gait, locomotion, or balance
disorders.
Imaging Studies
Cervical (1991): A review of Annem’s cervical spine
x-rays revealed the following: mild degenerative disk
disease (DDD) at C5-6 and degenerative joint disease
(DJD) at C5-6 and C6-7.
Shoulder, right (1991): A review of her shoulder x-
rays revealed the following: WNL with a Type II
acromion.
DIAGNOSIS
Musculoskeletal Pattern F: Impaired joint mobility,
motor function, muscle performance, ROM, and reflex
integrity associated with spinal disorders and/or Neuro-
muscular Pattern F: Impaired peripheral nerve integrity
and muscle performance associated with peripheral
nerve injury. Also, Musculoskeletal Pattern A: Primary
prevention/risk reduction for skeletal demineralization
and Musculoskeletal Pattern B: Impaired posture.
PAIN: The primary pain generator for this patient
appeared to be her right C8 and/or T1 nerve root(s)
or nerve(s).
STRAIN: The strains that may be exacerbating the
pain and dysfunction are heavy smoking,
osteoporosis, posture, hypomobility—in the cervical
385
and thoracic spine, and ribs—and signs of possible
pulmonary disease or dysfunction.
BRAIN: The patient has experienced her symptoms
only for a few weeks and she has no overt signs of
anger, frustration, hopelessness, depression, or
denial. There is no indication of a primary central
sensitization disorder or adverse forebrain activity at
this time.
Suspicions were raised with respect to the insidious
onset of symptoms, age of the patient, constant pain,
night pain, family history of cancer, patient history of
cancer, pulmonary symptoms, and a 50-pack-year
smoking history.
PROGNOSIS
Prognosis is uncertain and dependent on the presence
or absence of visceral disease.
PLAN OF CARE
Anticipated Goals:
1. Annem’s goal: “Get rid of the pain!”
2. Minimal restrictions, less than a 15° loss, with
active and passive shoulder abduction and ER.
3. Improve active and passive thoracic extension so
that the restrictions are no longer severe.
4. Minimal difficulty (3/10) with her job and ADL.
5. Independent with a comprehensive home exercise
program (HEP).
Interventions
Annem’s primary physician was contacted and made
aware of our concerns regarding her pulmonary status.
She received 5 treatments (W.O.M.E.N.) in physical
therapy while waiting for her follow-up visit with her
physician. Minimal progress was made during this initial
course of physical therapy. Following a chest radiograph
and further medical examination, a Pancoast tumor was
diagnosed in her right lung. After radiation treatment
and surgery to remove the cancerous tumor from her
lung, Annem reported a moderate decrease in her com-
plaints of neck and right upper extremity symptoms. Of
note is that our patient did not have Horner’s syndrome.
Case Study 3
DEMOGRAPHICS
Bula is a 48-year-old, obese, left-handed, Caucasian
male architect whose primary language is English. He
was referred to physical therapy Dec. 11, 1994, by his
386 SECTION III SPECIAL CONSIDERATIONS
primary care physician with a diagnosis of “shoulder
pain—bursitis.” He received approximately six treat-
ments from a chiropractor without relief. The treatments
consisted of massage and ultrasound to his shoulder fol-
lowed by a chiropractic adjustment to his cervical spine
at each visit.
SOCIAL HISTORY
Bula is recently divorced and has 50% custody of his
two children, whom he sees mainly on weekends. He
denies any cultural or religious beliefs that he thinks may
affect his care with us. He is employed as an architect,
a job that requires him to sit for a prolonged time. He
occasionally has periods of driving and prolonged stand-
ing at construction sites. He lifts and carries up to 20 lb,
but rarely has to reach over his head and normally does
not perform repetitive motions. He does, however, spend
hours at a time on his computer. He has not missed any
time from work because of his current complaints.
LIVING ENVIRONMENT
He lives in a two-bedroom condominium on the
fourth floor and has the choice of stairs or an elevator
when he comes and goes. He denies the existence of any
major obstacles in and around his house. He does not
use any assistive devices for his ADL.
GENERAL HEALTH STATUS
Bula rates his general health as good. In the past year,
he went through a painful and costly divorce, a beloved
family pet died, and he moved into a condominium in
a different part of town. The medical screening ques-
tionnaire, which Bula filled out on his first visit, was
notable in the pulmonary and cardiovascular sections
(Figure 13-12). At the time of his evaluation, he was a
33-pack-year smoker, had a history of heart problems
(palpitations and tachycardia), and both his father and
grandfather died prematurely of heart attacks. If his
symptoms correlate with a known visceral disease and
we are unable to provoke his symptoms and come up
with a meaningful musculoskeletal explanation, then we
will refer our patient for further medical evaluation.
SOCIAL/HEALTH HABITS
Bula reports that he has smoked an average of one
pack of cigarettes a day since he was 15 years old (33-
pack-year smoker). He drinks one to two cups of coffee
in the morning, and has a couple of beers or other type
of alcohol usually just once during the week. He is not
a vegetarian, does not skip any meals, does not take any
vitamins or supplements, and usually eats at a fast food
restaurant several times a week. Bula does not partici-
pate in regular physical activity or sports other than
playing “catch” with his sons on the weekends.
FAMILY HISTORY
His mother is still alive and in reasonably good
health. His grandmother died from a pulmonary
embolus, at the 65 years of age, following hip surgery.
Both his father (56 years old) and grandfather (46 years
old) died prematurely of heart attacks. Diabetes and
rheumatoid arthritis appear to “run” in his family.
MEDICAL/SURGICAL HISTORY
1993—Arthroscopic surgery to the right knee: lateral
meniscectomy, still stiff and painful per patient
1993—Fell and sprained left shoulder; resolved in 3
months
1992—High cholesterol (345 mg/dl) was diagnosed
1988—Noninsulin-dependent diabetes mellitus (Type
II DM) was diagnosed
1985—Lumbar disk surgery
In the past year, he has reported fatigue, SOB, sweat-
ing with pain, difficulty sleeping, chest pain, and dizzi-
ness without vertigo or blackouts.
CURRENT CONDITION(S)/CHIEF COMPLAINT(S)
Bula is a 48-year-old, obese, left-handed male who
came to physical therapy Dec. 11, 1994, with a diagno-
sis of “shoulder pain-bursitis” and complaining of peri-
odic moderate (0–6/10) pain in his left shoulder (Figure
13-13). He stated that the pain was not constant and
did not radiate down his arm. He did admit that his left
hand “tingled” every once in a while. He denied neck
pain, headaches, nausea, tinnitus, dizziness/vertigo,
vision changes, upper extremity numbness, and upper
extremity weakness. He also denied chest pain, but
admitted to muscle soreness in his chest after playing
“catch” with his sons. He denied a change in symptoms
after eating a greasy meal, bowel movement, coughing,
laughing, or with a deep inhalation. He also reported
that there was no change in his shoulder pain related to
eating or bowel and bladder activity. He noted that exer-
tional activity—climbing four flights of stairs to his con-
dominium—gave him SOB, fatigue, and an ache in his
left shoulder. He denied having the following constitu-
tional symptoms: fever, night sweats, nausea/vomiting,
dizziness, or unexplained weight loss. Other than what
was reported above, he denied any other complaints or
symptoms throughout the rest of his body. Bula reported
that his symptoms started 2 days after an afternoon of
throwing and catching a football with his sons approx-
imately 2 months ago. He reports that his shoulder pain
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER 387

Figure 13-12 Patient questionnaire for Case Study 3.

388 SECTION III SPECIAL CONSIDERATIONS
Figure 13-13 Pain diagram from a 48-year-old, left-
handed man with a diagnosis of “shoulder pain—bursitis.”
is made worse by activities such as waxing his car or car-
rying groceries. He states his symptoms change with his
activity level, but not with changes in his posture. He
notes that with repeated overhead use he has shoulder
pain and fatigue, which is quickly resolved if he stops
that particular activity.
FUNCTIONAL STATUS/ACTIVITY LEVEL
Bula does not participate in regular physical activity
or sports other than playing “catch” with his sons on the
weekends. He used to use the four flights of stairs up to
his condominium as a source of exercise; however, he
had to give that up a couple of months ago because of
SOB and significant fatigue. Bula reports that he can
throw 8 or 10 good passes with the football without
pain. Then his shoulder rapidly fatigues and begins to
ache. He states that he can lift 10 lb or more over his
head without difficulty, but has problems with repeated
overhead activities such as painting his garage or
washing and drying his camper. He has difficulty carry-
ing groceries if his car is parked too far away from the
grocery store and he has noted fatigue and shoulder pain
if he vacuums more than one room of his condominium.
He reports no difficulties with sleeping, looking up or
reaching overhead, driving, dressing, personal care, or
work.
MEDICATIONS
Prescription: Lipitor (high cholesterol), insulin (Type
II DM)
Nonprescription: Tylenol (acetaminophen)
OTHER CLINICAL TESTS
Per his last physician visit 2 weeks ago, Bula’s blood
sugar level was WNL. His cholesterol level was high,
but much improved at 250 mg/dl. No imaging studies
have been performed on Bula’s cervical or thoracic spine
or shoulder. In 1985 he had a plain radiograph of his
lumbar spine followed by a MRI (films and radiologist’s
report were not available). In 1993 he also had a plain
radiograph and MRI of his right knee (films and radi-
ologist’s report were not available).
CARDIOVASCULAR/PULMONARY SYSTEM
Heart rate (resting): 80 beats per minute
Respiratory rate (resting): 18 breaths per minute
Blood pressure: 135/88
Edema: None
INTEGUMENTARY SYSTEM
Bula’s skin appeared healthy, with a good continuity
of color and no significant changes in temperature.
White, well-healed scars were noted around the right
knee and the lower lumbar spine. No swelling was noted.
COMMUNICATION, AFFECT, COGNITION, LEARNING STYLE
There were no known learning barriers identified for
our patient. He stated that he could remember things
best if they are clearly explained to him with a good
rationale and if he is allowed to take notes. Bula did not
reveal any deficits with regard to his cognition, orienta-
tion, or ability to effectively communicate.
MUSCULOSKELETAL SYSTEM
Posture
In standing, he had a slight forward head, flat tho-
racic and lumbar spine, a protruding belly (obese), slight
genu valgum bilaterally, and bilateral pes planus.
Range of Motion
Cervical spine ROM:
Active and passive ROM were WNL and pain free.
Shoulder ROM:
Active and passive ROM were WNL and pain free.
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER 389

Scapula and elbow ROM: Shoulder (Positive Tests)

Active and passive ROM were WNL and pain free. None
Thoracic spine ROM: Shoulder (Negative Tests)
Active and passive ROM were pain free. Mild to Distraction/compression of the GH joint
moderate limitations were noted in flexion. Hawkins impingement sign
Rib ROM: Load and shift test (anterior and posterior
Active and passive ROM were WNL and pain free. instability)
Lumbar AROM: Distraction/compression of the AC joint
Active ROM was painful and limited in extension O’Brien test (SLAP)
and left side bending. Pain was localized to the lower Crank test (labrum)
lumbar spine. Empty can (supraspinatus tendon)
Muscle Performance Speed’s (biceps tendon)
There was no reproduction of symptoms for all of the Thoracic Spine (Positive Tests)
cardinal directions tested in each of the shortened, mid, None
and lengthened ranges for muscles of the cervical and Thoracic Spine (Negative Tests)
thoracic spine and left shoulder. Manual muscle Segmental joint mobility and provocation testing
testing—isometric (5/5 = WNL)—of the upper extrem- (prone P/A glides) (see Figure 5-21)
ities was WNL (5/5). T1 nerve root tension test (see Figure 5-22)
Sensory Integrity Thoracic quadrant tests
Upper extremity light touch and pinprick sensation Ribs (Positive Test)
was WNL. None
Reflex Integrity Ribs (Negative Tests)
Upper extremity deep tendon reflexes were equal and Mobility and provocation testing of ribs R2-5
brisk (2+). The SHR and Hoffman’s sign were normal. anteriorly (see Figure 5-25)
Pain Mobility and provocation testing of right first rib (see
Palpation Figure 5-24)
There was no reproduction of symptoms with palpa- Cervical rotation lateral flexion “CRLF” test (see
tion of musculoskeletal structures throughout the cervi- Figure 5-26)
cal and thoracic spine, chest, shoulder, and upper ribs. Lateral compression of mid and lower ribs (supine)
There was no edema or skin discoloration noted in the Coughing and deep inhalation
extremities. Palpation of the lymph nodes (SCM, su- Joint Integrity and Mobility
praclavicular, and axillary), arterial pulses (brachial and Cervical spine: Deferred (full gross active and passive
radial), and the abdomen was normal. ROM without pain; will examine segmental mobility at
Special Tests future appointment as needed).
Cervical Spine (Positive Tests–Reproduction Shoulder:
of Symptoms) Glenohumeral: Normal (grade 3) in all directions, no
TOS: Roo’s 3-minute flap arm test reproduced left complaints of pain.
shoulder pain Sternoclavicular: Normal (grade 3) in all directions,
Cervical Spine (Negative Tests) no complaints of pain.
Compression testing of the cervical spine in flexion, Acromioclavicular: Normal (grade 3) in all directions,
neutral, and extension (see Figure 5-13) no complaints of pain.
TOS: Adson’s, costoclavicular, and the pectoralis Scapulothoracic: Normal (grade 3) in all directions,
minor stress test no complaints of pain.
Cervical quadrant test in flexion and extension (see Thoracic spine: Deferred to save time, will examine
Figure 5-17) at future appointment as needed.
ULNT ¥ 3 Ribs: Normal (grade 3) for first ribs bilaterally, no
Valsalva complaints of pain.
390 SECTION III SPECIAL CONSIDERATIONS
Neuromuscular System
Bula had no gross gait, locomotion, or balance
disorders.
Imaging Studies
No imaging studies were taken of our patient’s cer-
vical or thoracic spine or shoulder.
DIAGNOSIS
Bula’s symptoms did not appear to be musculoskele-
tal in origin. The patient’s symptoms were not repro-
duced during a thorough musculoskeletal examination.
A return to the interview process revealed that the
patient periodically felt a tightness or pressure on his
chest at the same time he felt the shoulder pain. Both
symptoms rapidly went away when he sat down and
relaxed. Of concern was the number of yes answers on
his medical screening questionnaire under the sections
for pulmonary and cardiovascular disease. He also had
risk factors related to cardiovascular disease, such as his
age (48), sex (male), diet (fast food), smoker (33-pack-
year), high cholesterol, diabetes, and family history
(father and grandfather died from myocardial infarc-
tion). In addition, he noted that exertional activities gave
him SOB, fatigue, and a shoulder ache. Finally, he
had reported cardiovascular type symptoms in the past
year: SOB, fatigue, sweating with pain, chest pain, and
dizziness.
PAIN: The primary pain generator in this case appears
to be non-musculoskeletal in origin.
STRAIN: The strains that may be exacerbating Bula’s
pain and dysfunction are restricted mobility in the
thoracic spine, smoker, obesity, lack of regular exer-
cise, and signs of possible cardiopulmonary disease.
BRAIN: Because his symptoms are not chronic, a
primary central sensitization disorder was not
suspected initially. However, since a majority of his
musculoskeletal examination was negative, the
possibility of a central sensitization disorder will
need to be re-examined if there is no visceral disease
or medical condition to explain his symptoms. Bula
did not exhibit any overt signs of fear, anger, or
frustration. He has, however, had several recent and
significant life-changing events (divorced, moved to
a new residence, pet died). To facilitate the
rehabilitation process, Bula may benefit from
counseling.
PROGNOSIS
Prognosis is uncertain and dependent on the presence
of visceral disease.
PLAN OF CARE
Intervention
The patient was referred back to his primary care
physician for follow-up to rule out cardiopulmonary
disease. Subsequently, myocardial ischemia, with associ-
ated angina pectoralis, was diagnosed. His shoulder
symptoms disappeared immediately with the use of
nitroglycerin.
Case Study 4
DEMOGRAPHICS
Vinaka is a 64-year-old, right-handed Fijian female
interpreter who speaks fluent English, French, and
several Fijian dialects. She was referred Sept. 16, 1993,
for a consultation and second opinion on her right
shoulder pain by a physical therapist at another facility.
She denied previous treatment of any kind for her
current complaints.
SOCIAL HISTORY
She is married with five adult children and six grand-
children. Vinaka states that she comes from a very
modest culture with strict religious beliefs. If she were
to receive ongoing care, then she would feel more com-
fortable with a female therapist. Because of the nature
of her job as an interpreter, she spends approximately 6
months in Fiji, 3 months in Europe, and 3 months in
the United States each year.
LIVING ENVIRONMENT
In Fiji she lives in a modest, one-story, two-bedroom
house. In Europe she lives in a one-bedroom apartment
on the second floor, and in the United States she divides
her time between a two-bedroom condominium on the
first floor and a one-bedroom apartment on the third
floor. She denies the existence of any major obstacles in
and around any of her living quarters, except for the
stairs leading up to her apartments. She does not use any
assistive devices for her ADL.
GENERAL HEALTH STATUS
Vinaka states that she is in very good health for her
age. In the past year, she learned that cancer was diag-
nosed in her sister. She has had no other major life
changes and she states that she enjoys the amount of
traveling her job requires. The medical screening ques-
tionnaire, which Vinaka filled out on her first visit, was
notable for the general and cardiovascular sections
(Figure 13-14). Specifically, the patient questionnaire
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER 391

Figure 13-14 Patient questionnaire for Case Study 4.

392 SECTION III SPECIAL CONSIDERATIONS

revealed recent surgery, fever, SOB, and a prosthetic dizziness/vertigo, vision changes, tinnitus, nausea, radi-
cardiac valve. Upon further questioning, our patient ating arm pain, upper extremity paresthesia, and upper
admitted to an episode of chest pain 2 weeks ago, but extremity weakness. She denied a history of right shoul-
she related this to muscle soreness from washing her der pain, neck pain, falls, fractures, or MVA. She
windows. If her symptoms correlate with cardiac disease, reported there was no change in her shoulder pain
and we are unable to provoke her symptoms and come related to eating, bowel or bladder activity, coughing,
up with a meaningful musculoskeletal explanation, then laughing, deep inspiration, or during exertional activities
we will have to refer her for further medical evaluation. (long walks for example) that did not directly involve her
SOCIAL/HEALTH HABITS shoulder. She also denied having the following consti-
Vinaka reports that she has never used tobacco prod- tutional symptoms: night sweats, nausea/vomiting,
ucts. She drinks a cup of decaffeinated coffee in the dizziness, fatigue, or unexplained weight loss. Other
morning and has approximately three sodas with caf- than what she reported above, she denied any other
feine throughout the day. She does not drink alcohol. complaints or symptoms throughout the rest of her
She takes a multivitamin supplement, extra calcium, fish body. She reported the sudden onset, without trauma, of
oil tablets, and glucosamine sulfate. She is not a vege- right shoulder and upper trapezius pain approximately 1
tarian, but she avoids red meat in favor of chicken or month before her initial evaluation (Figure 13-15).
seafood, and has a limited intake of dairy products. FUNCTIONAL STATUS/ACTIVITY LEVEL
Vinaka does not participate in any sports or regular Vinaka does not normally participate in any sports or
forms of physical activity other than her daily walks regular forms of physical activity other than her daily
between 1 and 2 miles. walks between 1 and 2 miles. She works full time as an
FAMILY HISTORY
Vinaka’s grandfather died, at the age 65, of a myocar-
dial infarction and her grandmother died, at the age
of 77, following her second cerebrovascular accident
(CVA) in 2 years. Her mother died of breast cancer at
the age of 69; her father died of a massive myocardial
infarction at age 73; non-Hodgkin’s lymphoma was
diagnosed in her 62-year-old sister; and her brother, 66
years old, received coronary artery bypass surgery—
involving 4 arteries—10 years ago.
MEDICAL/SURGICAL HISTORY
1993—Surgery (August) root canal
1993—Surgery (March) implant of prosthetic heart
valve
1986—High blood pressure/hypertension (HTN) was
diagnosed
1986—High cholesterol (300 mg/dl) was diagnosed
1975—Hysterectomy
In the past year, she has reported fatigue, SOB,
swelling in the extremities, heart palpitations, difficulty
sleeping, nausea, and dizziness without vertigo or
blackouts.
CURRENT CONDITION(S)/CHIEF COMPLAINT(S)
Vinaka, a 64-year-old, right-handed woman, came to
physical therapy Sept. 16, 1993, with a complaint of
constant severe (7/10—10/10) right shoulder pain. She
reported that she had had a low-grade fever for the past Figure 13-15 Pain diagram from a 64-year-old,
2 weeks. She denied neck pain, headaches, chest pain, right-handed woman with a diagnosis of “right shoulder pain.”
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
interpreter, which involves a lot of traveling (planes,
trains, and automobiles), prolonged standing, and a
moderate degree of sitting. Her job does not require her
to stress her shoulders or upper extremities to any sig-
nificant degree. However, she is required to carry a brief-
case and a suitcase when traveling, which does put stress
on her shoulder. She cannot sleep on her right side
and has moderate difficulties with all ADL (reaching
overhead, driving, dressing, personal care, lifting/carry-
ing, and domestic duties) because of pain in her right
shoulder.
MEDICATIONS
Prescription: Lotensin (HTN), ibuprofen (NSAID),
Lescol (high cholesterol)
Nonprescription: Tylenol (acetaminophen)
OTHER CLINICAL TESTS
At her last visit to her primary care physician 2
months ago, her blood pressure was 125/85 and her total
cholesterol was 245 mg/dl. Vinaka has had no imaging
studies, other than those at the dentist’s office, in the
past 10 years.
CARDIOVASCULAR/PULMONARY SYSTEM
Heart rate (resting): 75 beats per minute
Respiratory rate (resting): 15 breaths per minute
Blood pressure: 130/90
Edema: Mild bilateral ankle edema.
INTEGUMENTARY SYSTEM
Vinaka’s skin appeared generally healthy. The area
surrounding her right sternoclavicular joint was slightly
swollen, warm, red, and tender. A well-healed surgical
scar was noted across her sternum. Mild bilateral ankle
edema was noted.
COMMUNICATION, AFFECT, COGNITION, LEARNING STYLE
There were no known learning barriers identified for
our patient. She stated that she could remember things
best if they were written down clearly and, in the case
of home exercises, if she was also given a chance to
perform them under supervision for the first time.
Vinaka did not reveal any deficits with regard to her cog-
nition, orientation, or ability to effectively communicate.
MUSCULOSKELETAL SYSTEM
Posture
In standing, she had a slight forward head; slight sco-
liosis (concave right through the mid thoracic spine); an
elevated and slightly winging left scapula, left iliac crest
high, left posterior superior iliac spine (PSIS) high, left
gluteal high, left popliteal fossa high, and pronated left
foot with moderate hallux valgus.
393
Range of Motion
Cervical spine ROM:
Active and passive ROM was limited slightly in
flexion and left side bending with complaints of a
“stretching ache” in the region of the right upper trapez-
ius only during left side bending. The patient was able
to perform pain free cervical left side bending, through
a full ROM, with the right scapula passively elevated
and the upper trapezius placed on slack.
Shoulder ROM:
Active and passive flexion, extension, abduction, hor-
izontal adduction, and horizontal abduction reproduced
pain. AROM in these directions was minimally limited;
PROM was WNL.
Scapula ROM:
Active and passive elevation, depression, protraction,
and retraction also reproduced our patient’s complaints
of pain. AROM was limited, mild, in all directions.
PROM was WNL.
Elbow ROM:
Active and passive ROM were WNL and pain free.
Thoracic spine ROM:
Active and passive ROM were pain free. In general,
there were moderate limitations noted in left sidebend-
ing, right rotation, and extension.
Rib ROM:
Active and passive ROM were WNL and pain free
for general inhalation/exhalation and passive compres-
sion. First rib mobility on the right was slightly hypo-
mobile, grade 2, but pain free.
Lumbar AROM:
Active ROM was pain free, but limited in all
directions.
Muscle Performance
There was no reproduction of symptoms for all the
cardinal directions tested in each of the shortened, mid,
and lengthened ranges for muscles of the cervical and
thoracic spine and right shoulder. Since our patient
reported no history of upper extremity symptoms sug-
gestive of neurogenic injury or irritation, specific manual
muscle testing was deferred on the myotomes of the
upper extremity.
Sensory Integrity
Tests were deferred because no neurogenic symptoms
were reported and to save time.
Reflex Integrity
Tests were deferred because no neurogenic symptoms
were reported and to save time.
394 SECTION III SPECIAL CONSIDERATIONS
Pain
Palpation: The right sternoclavicular joint was
slightly swollen, warm, red, and exquisitely tender. A
palpable band of tender tissue was noted in the right
upper trapezius muscle. Palpation of the lymph nodes
(SCM, supraclavicular, and axillary), arterial pulses
(brachial and radial), and abdomen was normal. There
were no petechiae or Janeway lesions on her skin. Ankle
edema was noted bilaterally.
Special Tests
Cervical Spine (Positive Tests—Reproduction
of Symptoms)
Cervical quadrant test in flexion left: “stretch” pain in
the right upper trapezius (see Figure 5-17)
Cervical quadrant test in extension left: pain in right
sternoclavicular joint (see Figure 5-17)
Cervical Spine (Negative Tests)
Compression testing of the cervical spine in flexion,
neutral, and extension (see Figure 5-13)
Cervical quadrant test in flexion right and extension
right (see Figure 5-17)
Valsalva
Shoulder (Positive Tests—Pain at SC Joint)
Hawkins impingement sign
AC joint compression (horizontal adduction of
humerus)
Shoulder (Negative Tests)
Distraction/compression of the GH joint
Load and shift test (anterior and posterior instability)
O’Brien test (SLAP)
Crank test (labrum)
Empty can (supraspinatus tendon)
Speed’s (biceps tendon)
Thoracic Spine (Positive Tests)
None
Thoracic Spine (Negative Tests)
Segmental joint mobility and provocation testing
(prone P/A glides) (see Figure 5-21)
Thoracic quadrant tests
Ribs (Positive Test)
Mobility and provocation testing of right first rib:
hypomobile with local tenderness (see Figure
5-24)
Cervical rotation lateral flexion “CRLF” test:
hypomobile on the right (see Figure 5-26).
Ribs (Negative Tests)
Mobility and provocation testing of ribs R2-5
anteriorly (see Figure 5-25)
Lateral compression of mid and lower ribs (supine)
Coughing and deep inhalation
Joint Integrity and Mobility
Cervical spine: Hypomobile, severe (grade 1), at C6
in extension, left side bending, and left rotation; without
pain. Hypermobile, mild (grade 4), at C5 in extension
and left rotation; without pain. The disk shear test was
positive at C5 (see Figure 5-14).
Shoulder:
Glenohumeral: Normal (grade 3) in all directions,
without pain
Sternoclavicular: Hypomobile, mild (grade 2) in all
directions, with pain
Acromioclavicular: Normal (grade 3) in all directions,
without pain
Scapulothoracic: Normal (grade 3) in all directions,
without pain
Thoracic spine: Hypomobile, mild (grade 2), from T1
to T4 for left side bending and right rotation, without
pain; hypomobile, severe (grade 1), from T1 to T7 in
extension, without pain
Ribs: Hypomobile, mild (grade 2) for right first rib,
without complaints of shoulder pain
Neuromuscular System
Vinaka had no gross gait, locomotion, or balance
disorders.
Imaging Studies
No imaging studies were taken of our patient’s cer-
vical or thoracic spine or shoulder.
DIAGNOSIS
Musculoskeletal Pattern E: Impaired joint mobility,
motor function, muscle performance, and ROM associ-
ated with localized inflammation.
Our patient’s signs and symptoms were consistent
with an irritable, and probably inflamed, right sterno-
clavicular joint. She demonstrated classic signs of
inflammation: pain, tenderness, swelling, warmth, and
redness. Because of the multiple yes answers under the
cardiovascular section of her medical screening ques-
tionnaire—and her history of prosthetic valve surgery,
recent surgery, recent illness, SOB, fever, chest pain, and
the sudden onset of pain without trauma—the plan was
to refer her back to her primary care physician to rule
out cardiac symptoms and disease. If nothing else, this
was thought to be a musculoskeletal problem with
comorbid cardiac disease.
PAIN: The primary pain generator for this patient
appeared to be her right sternoclavicular joint.
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
STRAIN: The strains that may be exacerbating her
pain and dysfunction at the sternoclavicular joint are
possible heart disease, posture, segmental instability
of the cervical spine, and hypomobilities in the first
rib and thoracic spine.
BRAIN: The patient has experienced her symptoms
only for a few weeks and she has no overt signs of
anger, frustration, hopelessness, depression, or
denial. There is no indication of a primary central
sensitization disorder or adverse forebrain activity at
this time.
PROGNOSIS
Prognosis is uncertain and dependent on the
presence of visceral disease and whether the visceral
disease is comorbid or the primary generator of her
symptoms.
PLAN OF CARE
Anticipated goals:
1. Vinaka’s goal: “Learn an exercise program I can do
on my own.”
2. Cervical AROM will return to WNL.
3. Minimal restrictions for thoracic spine motion.
4. Minimal difficulty (3/10) with ADL.
5. Independent with a comprehensive HEP.
INTERVENTION
Since Vinaka was referred to us for a consultation and
second opinion, treatment was not initiated. She was
referred back to her primary care physician with con-
cerns regarding her cardiac status. A report was sent to
her primary physical therapist with a recommendation
to hold physical therapy until after Vinaka sees her
physician. After a referral to a rheumatologist and then
a cardiac specialist, bacterial endocarditis was eventually
diagnosed. After a week on antibiotics, her right shoul-
der pain was minimal (3/10) and she was scheduled to
begin physical therapy elsewhere in approximately 1
week.
Case Study 5
DEMOGRAPHICS
Sheila is a 51-year-old, right-handed, obese, African
American female patent attorney whose primary lan-
guage is English. She was referred for physical therapy
by her primary care physician May 21, 2000, with a
395
diagnosis of “right shoulder strain.” She denied previous
treatment of any kind for her current complaints.
SOCIAL HISTORY
Sheila is single, never married, and lives with her
partner. She denies any cultural or religious beliefs that
she thinks may affect her care with us. She works as a
patent attorney, which involves prolonged sitting and
long periods on her computer. There is minimal physi-
cal stress, however, in terms of lifting, carrying, and over-
head activities.
LIVING ENVIRONMENT
She lives in a two-story, three-bedroom house. She
denies the existence of any major obstacles in and
around her house. She denies the use of assistive devices
during her ADL.
GENERAL HEALTH STATUS
Sheila reports that she is in “pretty fair” health. She
states she started her own law firm 6 months ago and
has only recently been able to keep her workweek under
60 hours. The medical screening questionnaire, which
Sheila filled out on her first visit, was notable for the
general and gastrointestinal sections (Figure 13-16).
Further questioning revealed that she had a low-grade
fever for the 3 weeks before her evaluation in physical
therapy. In addition, she also admitted to having occa-
sional upper abdominal and right shoulder blade pain
after meals.
SOCIAL/HEALTH HABITS
Sheila reports that she stopped smoking 10 years ago.
Before then she had smoked a half to a full pack of cig-
arettes a day for approximately 26 years. She drinks two
to three cups of coffee and two to three cans of soda with
caffeine a day. She drinks a beer or glass of wine three
to four nights a week. She takes a multivitamin and extra
calcium. She is not a vegetarian, eats red meat several
times a week, dairy products daily, and shellfish occa-
sionally. Lately, she has been avoiding greasy or fried
foods. Her only form of exercise—she does not partici-
pate in athletic activities or sports—is walking on a
treadmill for 20 minutes three times a week.
FAMILY HISTORY
Her father died at the age of 71 from progressive
heart failure. Her mother is still alive, but diabetes,
lupus, and rheumatoid arthritis have been diagnosed.
Her sister, who is 54 years old, has fibromyalgia.
MEDICAL/SURGICAL HISTORY
1999—Arthroscopic decompression of right shoulder
(August)
396 SECTION III SPECIAL CONSIDERATIONS
Figure 13-16 Patient questionnaire for Case Study 5, modified to show notable portions of both pages.
1998—Hepatitis was diagnosed
1995—MVA with diagnosis of cervical sprain/strain,
whiplash; resolved
1988—Diagnosis of noninsulin-dependent diabetes
mellitus (type II DM)
In the past year, Sheila has complained of joint pain,
difficulty sleeping, nausea, indigestion, diarrhea, unex-
plained weight change, headaches, and fever.
CURRENT CONDITION(S)/CHIEF COMPLAINT(S)
Sheila, a 51-year-old, right-handed, obese woman
came to our office on May 21, 2000, with a diagnosis of
“right shoulder strain.” She complained of a periodic
severe (0—8/10), deep, and generalized ache across the
back of her right shoulder (Figure 13-17). She reported
that her right shoulder pain was worse at night. After
asking her directly, she did admit that there seemed to
be an exacerbation of her right shoulder pain an hour or
so after lunch. Sheila reported that she often had lunch
with clients at a local restaurant. Her lunchtime meals
varied between hamburger with fries, fried chicken and
mashed potatoes, to the occasional soup and salad. She
denied neck pain, headaches, temporomandibular
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
Figure 13-17 Pain diagram from a 51-year-old,
right-handed woman with a diagnosis of “right shoulder
strain.”
dysfunction (TMD), chest pain, dizziness/vertigo, vision
changes, tinnitus, radiating right arm pain, paresthesia
in the right upper extremity, and right upper extremity
weakness. She reported no change in her right shoulder
pain related to bowel and bladder activity, or during pro-
longed walks or climbing stairs. She admitted to having
the following constitutional symptoms: fever, unex-
plained weight change, night pain, indigestion, diarrhea,
and nausea. She denied night sweats, vomiting, dizzi-
ness, and fatigue. Sheila reported the sudden onset of a
severe ache in her right shoulder after a day of house-
cleaning 2 weeks ago. She also admitted to a long history
(5 years) of headaches, neck pain, and left shoulder pain
with tingling in her left hand. The symptoms in her neck
and left shoulder did not change after cleaning her
house, and they remained mild in intensity. The pain in
her left shoulder was not the same as the pain in the
right. The left shoulder pain was sharp, shooting, and
397
localized. She did admit that there was an occasional
ache in her right shoulder blade during the past 2
months before she came to physical therapy. She denied
a history of falls or fractures. Other than what she
reported above, she denied any other complaints or
symptoms throughout the rest of her body.
FUNCTIONAL STATUS/ACTIVITY LEVEL
Sheila’s only form of exercise—she does not partici-
pate in athletic activities or sports—is walking on a
treadmill for 20 minutes three times a week. She scored
58* out of a possible maximum score of 100 on the
Sharp FAS for the Neck & Shoulder region (© Sharp
HealthCare 1998). Since she has been taking medica-
tions specifically for her neck and shoulder pain,
her Sharp FAS score has an asterisk next to it. The aster-
isk symbolizes that her FAS score, because of the
medication she is taking, overstates her true functional
abilities; that is, her functional abilities would be
much less without the use of the medications. She
reports severe difficulty looking up or reaching overhead;
moderate difficulty with sleeping, driving, dressing,
personal care, lifting/carrying, and domestic duties; and
minimal difficulty with leisure activities and work.
She is working full time and has not had to miss
any time from work because of her neck and shoulder
complaints.
MEDICATIONS
Prescription: Celebrex (NSAID), Vicodin (anal-
gesic), Soma (sleep) and Elavil (antidepressant)
Nonprescription: Maalox prn
OTHER CLINICAL TESTS
She has regular tests for blood sugar levels. Her most
recent test was 3 weeks ago and was reported as WNL.
A mammogram last year was reported as normal per our
patient. A plain radiograph of the cervical spine 4 years
ago indicated “mild to moderate spondylosis throughout
the cervical spine” per the radiologist. A plain radio-
graph of the right shoulder last week was reported as
“normal right shoulder” per the radiologist.
CARDIOVASCULAR/PULMONARY SYSTEM
Although it is well known that the heart and lungs
can refer pain to the left shoulder, and cause indigestion
and nausea, the right shoulder is an extremely rare region
of the body for referred cardiac pain and symptoms.
There was no clear indication that our patient’s symp-
toms might be cardiopulmonary in origin. Her medical
screening questionnaire did not raise any “red flags” in
the pulmonary or cardiovascular sections (see Figure 13-
398 SECTION III SPECIAL CONSIDERATIONS
16). Subsequently, a specific physical examination was
deferred on her cardiopulmonary system.
INTEGUMENTARY SYSTEM
Sheila’s skin appeared healthy, with a good continu-
ity of color and no significant changes in temperature.
There was no swelling present. White, well-healed sur-
gical scars were noted around her right shoulder.
COMMUNICATION, AFFECT, COGNITION, LEARNING STYLE
There were no known learning barriers identified for
our patient. She stated that she could remember things
best if they were explained clearly and she was given a
good rationale to back up the advice or instruction.
Sheila did not reveal any deficits with regard to her cog-
nition, orientation, or ability to effectively communicate.
MUSCULOSKELETAL SYSTEM
Posture
In standing, she had a slight forward head, exagger-
ated lumbar lordosis, and bilateral pes planus.
Range of Motion
Cervical spine ROM:
Active and passive cervical extension, left side bend-
ing, or left rotation reproduced neck and left shoulder
pain. There was no reproduction of right shoulder pain.
Shoulder ROM (right):
Active and passive ROM of the right shoulder did
not reproduce pain, although mild restrictions were
noted with flexion, abduction, and external rotation.
Scapula and elbow ROM (right):
Active and passive ROM were WNL and pain free.
Thoracic spine ROM:
Active and passive ROM were pain free. Moderate
limitations were noted in upper thoracic left side
bending and extension.
Rib ROM:
Active and passive ROM were WNL and pain free
for general inhalation/exhalation and passive compres-
sion. First rib mobility on the left was slightly hypomo-
bile (grade 2).
Lumbar AROM:
Active ROM was pain free, with a moderate limita-
tion in flexion and extension, and a mild limitation in
all other directions.
Muscle Performance
There was no reproduction of right shoulder pain for
all the cardinal directions tested in each of the short-
ened, mid, and lengthened ranges for muscles of the cer-
vical and thoracic spine, and right shoulder. Left cervical
and shoulder symptoms were reproduced with resisted
testing when the cervical spine was extended, side bent
left, or rotated left. Specific manual muscle testing—iso-
metric (5/5 = WNL)—of the upper extremities was
WNL (5/5).
Sensory Integrity
Increased sensitivity to light touch and pinprick was
noted in the left C6 dermatome.
Reflex Integrity
Hyperreflexia (3+) was noted for the left brachiora-
dialis DTR. The biceps brachialis, triceps, and abductor
digiti minimi were equal (2+) bilaterally. The SHR result
was negative. Hoffman’s sign showed a positive result on
the left.
Pain
Palpation: Mild tenderness, without reproduction of
significant shoulder pain, was noted in the left upper
trapezius, left middle trapezius, left rhomboids, and
right infraspinatus muscle belly. Palpation of the lymph
nodes (SCM, supraclavicular, and axillary) was normal.
Palpation of the abdomen indicated rigidity and exqui-
site tenderness in the right upper abdominal quadrant.
There was no joint effusion or soft tissue edema noted.
Palpation of her upper extremity pulses was deferred
since her symptoms and medical screening questionnaire
did not indicate the possibility of cardiovascular disease.
Special Tests
Cervical Spine (Positive Tests*)
Cervical quadrant test in extension left: left cervical
and left shoulder pain with “tingling” in the left
hand (see Figure 5-17)
Compression testing of cervical spine in extension
only: left cervical and left shoulder pain only (see
Figure 5-13)
Cervical quadrant test in flexion right: left cervical and
left shoulder pain only
Valsalva: left shoulder pain
Cervical Spine (Negative Tests)
None
Shoulder Right (Positive Tests)
None
Shoulder Right (Negative Tests)
Distraction/compression of the GH joint
Hawkins impingement sign
Load and shift test (anterior and posterior instability)
Distraction/compression of the AC joint
*None of the cervical provocational tests reproduced right shoul-
der pain.
CHAPTER 13 VISCERAL REFERRED PAIN TO THE SHOULDER
O’Brien test (SLAP)
Crank test (labrum)
Empty can (supraspinatus tendon)
Speed’s (biceps tendon)
Thoracic Spine (Positive Tests)
None
Thoracic Spine (Negative Tests)
Segmental joint mobility and provocation testing
(prone P/A glides) (see Figure 5-21)
Thoracic quadrant tests
Ribs (Positive Test*)
Mobility and provocation testing: left first rib tender
and hypomobile (see Figure 5-24)
Cervical rotation lateral flexion “CRLF” test:
hypomobile on the left (see Figure 5-26)
Coughing: left cervical and left shoulder pain
Ribs (Negative Tests)
Mobility and provocation testing of ribs R2-5
anteriorly (see Figure 5-25)
Lateral compression of mid and lower ribs (supine)
Deep inhalation
Joint Integrity and Mobility
Cervical spine: Tests deferred to save time. Previous
portions of the evaluation have not implicated the cer-
vical spine as a source of the right shoulder pain. In addi-
tion, there is a strong suspicion of gastrointestinal
disease.
Shoulder (right):
Glenohumeral: Hypomobile, mild (grade 2) in all
directions, with muscle guarding; no pain.
Sternoclavicular: Hypomobile, mild (grade 2) in dis-
traction and inferior glide; no pain.
Acromioclavicular: Normal (grade 3) in all directions;
no pain.
Scapulothoracic: Normal (grade 3) in all directions;
no pain.
Thoracic spine: Tests deferred to save time; same
rationale as noted for the cervical spine.
Ribs: Hypomobile, mild (grade 2) for left first rib;
with muscle guarding.
Neuromuscular System
Sheila had no gross gait, locomotion, or balance
disorders.
*None of the rib provocational tests reproduced right shoulder
pain.
399
Imaging Studies
Cervical (1996): A review of the films revealed the
following: mild DDD at C3-4 and C4-5, moderate at
the C5-6 and C6-7 levels with mild posterior vertebral
osteophytes. Facet DJD at same levels and degrees noted
above. Moderate foraminal stenosis at left C5-6, mild at
left C4-5. Loss of the normal cervical spine lordosis.
Incidental note of an incomplete ponticulus ponticus on
the posterior arch of the atlas.
Shoulder, right (2000): A review of the films revealed
the following: normal shoulder with a Type I acromion.
DIAGNOSIS
Sheila’s right shoulder symptoms did not appear to be
musculoskeletal in origin. Although mild chronic joint
dysfunction was noted in the right shoulder girdle, our
patient’s signs and symptoms were inconsistent with an
active orthopedic injury of the right shoulder. The cervi-
cal and thoracic spine and ribs did not appear to be a
source of her right shoulder symptoms. Of concern was
the patient’s history of diabetes, hepatitis, fever, shoulder
pain associated with greasy meals (lunch), and the exqui-
site tenderness in the right upper abdominal quadrant.
The left shoulder and hand symptoms were thought to
be secondary to a mild and chronic left cervical radicu-
lopathy. (Musculoskeletal Pattern F: Impaired joint
mobility, motor function, muscle performance, ROM,
and reflex integrity associated with spinal disorders.)
PAIN: The primary pain generator in this case appears
to be non-musculoskeletal in origin.
STRAIN: The strains that may be exacerbating
Sheila’s pain and dysfunction are her chronic neck
and left upper extremity symptoms, restricted
mobility in the thoracic spine, diet (excessive
caffeine, red meat, shellfish, and dairy) and signs of
possible GI disease.
BRAIN: Because she has had chronic neck and left
upper extremity symptoms and the physical examina-
tion of her right shoulder was mostly negative, Sheila
is likely to have a component of central sensitization
aggravating her symptoms—especially if her right
shoulder symptoms cannot be attributed to a visceral
disease or medical condition. Although she did not
exhibit any overt signs of fear, anger, or frustration, it
should be noted that Sheila is under a lot of stress at
work and is working long hours.
PROGNOSIS
Prognosis is uncertain and dependent on the presence
of visceral disease and whether the visceral disease
400 SECTION III SPECIAL CONSIDERATIONS
is comorbid or the primary generator of her
symptoms.
PLAN OF CARE
Intervention
Sheila was referred back to her primary care physi-
cian to rule out any gastrointestinal problems. Chole-
cystitis secondary to gallstones was diagnosed in the
patient. Her gastrointestinal symptoms and right shoul-
der pain were reduced approximately 50% on a con-
trolled diet. The right shoulder blade pain did not
disappear, however, until after she had a cholecystec-
tomy. She continued to report chronic neck and left
upper extremity symptoms, but was never referred back
for physical therapy to address these symptoms.
Summary
The best way to determine if your patient’s symptoms
may be caused by visceral disease is to first eliminate all
possible musculoskeletal tissue as a source of their symp-
toms. This requires skill, confidence, and experience in
performing a thorough and comprehensive orthopedic
evaluation. If you cannot reproduce your patient’s symp-
toms or have difficulty identifying a tissue in lesion, or
if your patient does not respond to treatment, then
ruling out a visceral pathologic condition becomes
imperative. A patient who is referred to physical therapy
with an orthopedic diagnosis, but who demonstrates
signs and symptoms of visceral disease, can be saved
from severe morbidity—and sometimes death—by an
early referral to the appropriate level of medical care.
Of course, it should also be mentioned that many of
our patients have known comorbid visceral disease; i.e.,
both orthopedic and visceral problems. In this case, a
positive musculoskeletal examination did not eliminate
the possibility of an unrelated viscus injury or disease.
Comorbid visceral disease is important to identify since
this will most likely put a strain on the orthopedic
injury/dysfunction and should therefore necessitate a
change in your normal plan of care and prognosis
accordingly.
ACKNOWLEDGMENTS
I wish to thank Ola Grimsby, AnneMarie Kaiser, and
Jim Rivard for their contributions and support.
REFERENCES
1. Massey BF Jr: 2002 APTA presidential address: what’s all the
fuss about direct access? Phys Ther 82:1120, 2002.
2. Boissonnault WG, Koopmeiners MB: Medical history
profile: orthopaedic physical therapy outpatients, J Orthop
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3. Payne R: Cancer pain: anatomy, physiology, and pharmacol-
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4. Boissonnault WG, Bass C: Pathological origins of trunk and
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5. Procacci P, Maresca M: Clinical aspects of visceral pain, Funct
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6. Cervero F: Mechanisms of acute visceral pain, Br Med Bull
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8. Lynn R: Mechanisms of esophageal pain, Am J Med 92:11S,
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9. Cousins M: Introduction to acute and chronic pain: implica-
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12. Galea MP: Neuroanatomy of the nociceptive system.
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13. Lewit K: The contribution of clinical observation to neurobi-
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14. Patterson M: A model mechanism for spinal segmental facil-
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15. Goodman CC, Snyder TEK: Introduction to differential
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ical therapy, ed 2, Philadelphia, 1995, WB Saunders.
16. Boissonnault WG, Janos SC: Screening for medical disease:
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sonnault WG, editor: Examination in physical therapy practice:
screening for medical disease, ed 2, New York, 1995, Churchill
Livingstone.
17. Koopmeiners MB: Screening for gastrointestinal system
disease. In Boissonnault WG, editor: Examination in physical
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18. Abramson DI, Miller DS: Clinical and laboratory tests of
arterial circulation. In Vascular problems in musculoskeletal dis-
orders of the limbs, New York, 1981, Springer-Verlag.
19. Michel TH, Downing J: Screening for cardiovascular system
disease. In Boissonnault WG, editor: Examination in physical
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therapy practice: screening for medical disease, ed 2, New York,
1995, Churchill Livingstone.
20. Natkin E, Harrington G, Mandel M: Anginal pain referred
to the teeth: report of a case, Oral Surg 40:678, 1975.
21. Henry J, Montuschi E: Cardiac pain referred to site of previ-
ously experienced somatic pain, Br Med J 9:1605, 1978.
22. Grieve G: Clinical features. In Common vertebral joint prob-
lems, New York, 1981, Churchill Livingstone.
23. Lewis T, Kellgren J: Observations relating to referred pain,
visceromotor reflexes and other associated phenomena, Clin
Sci 4:47, 1939.
24. Cyriax J: Referred pain. In Textbook of orthopaedic medicine.
Diagnosis of soft tissue lesions, ed 8, London, 1982,
Bailliere Tindall.
25. Laurberg S, Sorensen K: Cervical dorsal root ganglion cells
with collaterals to both shoulder skin and the diaphragm: a
fluorescent double labeling study in the rat—a model for
referred pain? Brain Res 331:160, 1985.
26. Bahr R, Blumberg H, Janig W: Do dichotomizing afferent
fibers exist which supply visceral organs as well as somatic
structures? A contribution to the problem of referred pain,
Neurosci Lett 24:25, 1981.
27. Doran F: The sites to which pain is referred from the common
bile duct in man and its implication for the theory of referred
pain, Br J Surg 54:599, 1967.
28. Hobbs S, Chandler M, Bolser D, et al: Segmental organiza-
tion of visceral and somatic input onto C3-T6 spinothalamic
tract cells of the monkey, J Neurophysiol 68:1575, 1992.
29. Bolser D, Hobbs S, Chandler M, et al: Convergence of
phrenic and cardiopulmonary spinal afferent information on
cervical and thoracic spinothalamic tract neurons in the
monkey: implications for referred pain from the diaphragm
and the heart, J Neurophysiol 65:1042, 1991.
30. Campbell S: Referred shoulder pain: an elusive diagnosis,
Postgrad Med 73:193, 1983.
31. Calliet R: Visceral referred pain, In: Shoulder pain, ed 3,
Philadelphia, 1981, FA Davis.
32. Leland J: Visceral aspects of shoulder pain, Bull Hosp Jt Dis
14:71, 1953.
33. Capps J: An experimental and clinical study of pain in the pleura,
pericardium, and peritoneum, New York, 1932, Macmillan.
34. Bateman J: Applied physiology of the shoulder and neck. In:
The shoulder and neck, Philadelphia, 1978, WB Saunders.
35. Walsh RM, Sadowski GE: Systemic disease mimicking mus-
culoskeletal dysfunction: a case report involving referred
shoulder pain, J Orthop Sports Phys Ther 31(12):696, 2001.
36. Boissonnault W, Bass C: Pathological origins of trunk and
neck pain: disorders of the cardiovascular and pulmonary
system, J Orthop Sports Phys Ther 12:208, 1990.
37. Williams PL, Warwick R, Dyson M, et al, editors: Myol-
ogy. In: Gray’s anatomy, ed 37, New York, 1989, Churchill
Livingstone.
38. Angel J, Sims C, O’Brien W, et al: Postcoital pneumoperi-
toneum, Obstet Gynecol 71:1039, 1988.
39. Christiansen W, Danzl D, McGee H: Pneumoperitoneum
following vaginal insufflation and coitus, Ann Emerg Med
9:480, 1980.
401
40. Rucker C, Miller R, Nov H: Pneumoperitoneum secondary
to perforated appendicitis: a report of two cases and a review
of the literature, Am J Surg 33:188, 1967.
41. Lozman H, Newman A: Spontaneous pneumoperitoneum
occurring during postpartum exercises in the knee chest posi-
tion, Am J Obstet Gynecol 72:903, 1956.
42. Aronson M, Nelson P: Fatal air embolism in pregnancy
resulting from an unusual sex act, Obstet Gynecol 30:127, 1967.
43. Quigley J, Gaspar I: Fatal air embolism on the eighth day of
puerperium, Am J Obstet Gynecol 32:1054, 1936.
44. Goodman CC, Snyder TEK: Overview of gastrointestinal
signs and symptoms. In: Differential diagnosis in physical
therapy, ed 2, Philadelphia, 1995, WB Saunders.
45. Sarli L, Costi R, Sansebastiano G, et al: Prospective ran-
domized trial of low-pressure pneumoperitoneum for reduc-
tion of shoulder-tip pain following laparoscopy Br J Surg
(England), 87(9):1161-1165, 2000.
46. Vargo M, Flood K: Pancoast’s tumor presenting as cervical
radiculopathy, Arch Phys Med Rehabil 71:606, 1990.
47. Welch WC, Erhard R, Clyde B, et al: Systemic malignancy
presenting as neck and shoulder pain, Arch Phys Med Rehabil
75:918, 1994.
48. Kovach SG, Huslig EL: Shoulder pain and Pancoast’s tumor:
a diagnostic dilemma, J Manipulative Physiol Ther 7:25,
1984.
49. Goodman CC, Snyder TEK: Overview of pulmonary signs
and symptoms. In: Differential diagnosis in physical therapy, ed
2, Philadelphia, 1995, WB Saunders.
50. Loeb S: Professional guide to signs and symptoms, Springhouse,
Pennsylvania, 1993, Springhouse Corp.
51. Arnall D, Ryan M: Screening for pulmonary system disease.
In Boissonnault WG, editor: Examination in physical therapy
practice: screening for medical disease, ed 2, New York, 1995,
Churchill Livingstone.
52. Niethammer JG, Hubner KF, Buonocore E: Pulmonary
embolism: how V/Q scanning helps in diagnosis, Postgrad
Med 87:263, 1990.
53. Boissonnault W, Bass C: Pathological origins of trunk and
neck pain: diseases of the musculoskeletal system, J Orthop
Sports Phys Ther 12:216, 1990.
54. Netter FH: Diseases and pathology. In: The Ciba collection of
medical illustrations: respiratory system, ed 2, West Caldwell,
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55. Coventry MB: Problem of painful shoulder, JAMA 151:177,
1953.
56. Ammons W: Cardiopulmonary sympathetic afferent input to
lower thoracic spinal neurons, Brain Res 529:149, 1990.
57. Nevens F, Janssens J, Piessens J, et al: Prospective study on
prevalence of esophageal chest pain in patients referred on an
elective basis to a cardiac unit for suspected myocardial
ischemia, Dig Dis Sci 36:229, 1991.
58. Lagerqvist B, Sylven C, Beermann B: Intracoronary adeno-
sine causes angina pectoris like pain: an inquiry into the
nature of visceral pain, Cardiovasc Res 24:609, 1990.
59. Askey JM: The syndrome of painful disability of the shoul-
der and hand complicating coronary occlusion, Am Heart J
22:1, 1941.
402 SECTION III SPECIAL CONSIDERATIONS
60. Goodman CC, Snyder TEK: Overview of cardiovascular
signs and symptoms. In: Differential diagnosis in physical
therapy, ed 2, Philadelphia, 1995, WB Saunders.
61. Churchill M, Geraci J, Hunder G: Musculoskeletal manifes-
tations of bacterial endocarditis, Ann Intern Med 87:754,
1977.
62. Hunder G: When musculoskeletal symptoms point to endo-
carditis, J Musculoskel Med 9:33, 1992.
63. Abramson DI, Miller DS: Clinical entities with both
vascular and orthopedic components. In: Vascular problems
in musculoskeletal disorders of the limbs, New York, 1981,
Springer-Verlag.
64. Wilgis EFS: Compression syndromes of the shoulder girdle
and arm. In: Vascular injuries and diseases of the upper limb,
Boston, 1983, Little, Brown.
65. Wilgis EFS: Diagnosis. In: Vascular injuries and diseases of the
upper limb, Boston, 1983, Little, Brown.
66. Rohrer MJ: Vascular problems. In Pappas AM, editor: Upper
extremity injuries in the athlete, New York, 1995, Churchill
Livingstone.
67. Abramson DI, Miller DS: Vascular complications of muscu-
loskeletal disorders produced by trauma. In: Vascular problems
in musculoskeletal disorders of the limbs, New York, 1981,
Springer-Verlag.
68. O’Leary MR, Smith MS, Druy EM: Diagnostic and thera-
peutic approach to axillary-subclavian vein thrombosis, Ann
Emerg Med 16:889, 1987.
69. Jiha JG, Laurito CE, Rosenquist RW: Subclavian vein com-
pression and thrombosis presenting as upper extremity pain,
Anesth Analg 85:225, 1997.
70. Goodman CC, Snyder TEK: Overview of hepatic and biliary
signs and symptoms. In: Differential diagnosis in physical
therapy, ed 2, Philadelphia, 1995, WB Saunders.
71. Goodman CC, Snyder TEK: Overview of renal and urologic
signs and symptoms. In: Differential diagnosis in physical
therapy, ed 2, Philadelphia, 1995, WB Saunders.
72. Davidson R, Lewis E, Daehler D, et al: Perinephrenic abscess
and chronic low back pain, J Fam Pract 15:1059, 1982.
73. Swarbrick E, Hegarty J, Bat L, et al: Site of pain from the
irritable bowel, Lancet 1980:443, 1980.
74. Cervero F: Neurophysiology of gastrointestinal pain, Baillieres
Clin Gastroenterol 2:183, 1988.

Manual Therapy
Techniques
T he primary goals of the clinician are to opti-
mize function, decrease pain, restore proper
mechanics, facilitate healing, and assist regen-
eration of tissue. Manual therapy has been demonstrated
clinically to be an important part of rehabilitation and
assessment of restricted joint movement. Clinical appli-
cation of manual techniques is based on an understand-
ing of joint mechanics, tissue histology, and muscle
function. Notable advancement has been made in
describing the benefits of passive movement by such
researchers as Akeson, Woo, Mathews, Amiel, and
Peacock.1-3 With this knowledge in hand the clinician
can apply manual therapy techniques during critical
stages of wound healing to influence the extensibility
of scar tissue, reduce the development of restrictive
adhesions, and provide foundations of neuromuscular
mechanisms to restore homeostasis.1 Through an
understanding of the effects of immobilization and soft
tissue healing constraints we can establish criteria for
phases of manual therapy techniques.
This chapter focuses on manual therapy for the
shoulder complex from a basic science and problem-
solving approach. Manual therapy is discussed in rela-
tion to soft tissue and joint mobilization and muscle
reeducation. A variety of manual therapy techniques will
be described. Management of the shoulder patient is
discussed from a perspective of protective versus non-
protective injuries. Evidence-based practice is presented
for the use of manual therapy for the shoulder.
Normal joint function includes a dynamic combina-
tion of arthrokinematics (intimate mechanics of joint
surfaces), osteokinematics (the movement of bones),
405
14
Timothy J. McMahon
Robert A. Donatelli
muscle function, fascial extensibility, and neurobio-
mechanics (see Chapter 6). Dysfunction and pain of the
shoulder can result from altered function of any or all
of these systems. A detailed sequential evaluation
that hypothesizes particular impairments dictates which
particular manual therapy strategy is appropriate.
Please refer to Chapter 4 for shoulder evaluation
procedures. Clearing the cervical and thoracic spine
and brachial plexus is reviewed in Chapters 5 and 8.
Manual techniques discussed will focus on the shoulder
complex.
Definitions
Several terms must be defined when discussing manual
therapy. Articulation, oscillation, distractions, manipula-
tion, and mobilization all describe a specialized type of
passive movement.
Manual therapy is defined by the Guide to Physical
Therapy Practice as “skilled hand movements intended to
improve tissue extensibility; increase range of motion;
induce relaxation; mobilize or manipulate soft tissue and
joints; modulate pain; and reduce soft tissue swelling,
inflammation, or restriction.4”
Articulatory techniques are derived from the osteo-
pathic literature. They are defined as passive movement
applied in a smooth rhythmic fashion to stretch con-
tracted muscles, ligaments, and capsules gradually.5 They
include gentle techniques designed to stretch the joint
in each of the planes of movement inherent to the
joint.5 The force used during articular techniques is
usually a prolonged stretch into the restriction or tissue
limitation.
406 SECTION IV TREATMENT APPROACHES
Oscillatory techniques are best defined by Maitland—
who describes oscillations as passive movements to the
joint, which can be a small or large amplitude and applied
anywhere in a range of movement, and which can be per-
formed while the joint surfaces are held distracted or
compressed.6 There are four grades of oscillations. Grade
1 is a small-amplitude movement performed at the
beginning of a range. Grade 2 is a large-amplitude move-
ment performed within the range, but not reaching the
limit of the range. Grade 3 is a large-amplitude move-
ment up to the limit of a range. Grade 4 is a small-ampli-
tude movement performed at the limit of a range.6
Grades 1 and 2 are used primarily for neurophysiologic
effects and do not engage detectable resistance. Grades 3
and 4 are designed to initiate mechanical changes in the
tissue and do engage tissue resistance.
Distraction is defined as “separation of surfaces of a
joint by extension without injury or dislocation of the
parts.7” Distraction techniques are designed to separate
the joint surface attempting to stress the capsule.
Manipulation is defined by Dorland’s Illustrated
Medical Dictionary as “skillful or dextrous treatment by
the hand. In physical therapy, the forceful passive move-
ment of a joint beyond its active limit of motion.8”
Maitland describes two manipulative procedures.
Manipulation is a sudden movement or thrust, of small
amplitude, performed at a speed that renders the patient
powerless to prevent it.6 Manipulation under anesthesia
is a medical procedure used to restore normal joint
movement by breaking adhesions.
Mobilization is defined as “the making of a fixed or
ankylosed part movable, or restoration of motion to a
joint.7” To the clinician, mobilization is passive move-
ment that is designed to improve soft tissue and joint
mobility. It can include oscillations, articulations, dis-
tractions, and thrust techniques.
Mobilization, in this chapter, is defined as a special-
ized passive movement, attempting to restore the
arthrokinematics and osteokinematics of joint move-
ment. Mobilization includes articulations, oscillations,
distractions, and thrust techniques. The techniques are
built on active and passive joint mechanics and are
directed at the periarticular structures that have become
restricted secondary to trauma and immobilization.
These same techniques can be effective tools in assess-
ment of specific joint impairments.
Soft tissue mobilization (STM) for purposes of this
chapter will be as defined by Johnson: “STM is the
treatment of soft tissue with consideration of layers and
depth by initially evaluating and treating superficially
proceeding to bony prominence, muscle, tendon, and
ligament.9”
Evidence-Based Practice
Several studies to date have investigated the efficacy of
manual therapy interventions for shoulder dysfunction.
Some studies have focused on physiologic parameters in
response to particular mobilization techniques10-12 while
others focus on randomized controlled studies13-17 com-
paring physical therapy to other traditional treatment
approaches.
The highest level of evidence to support use of an
intervention is through controlled randomized studies.
Systematic reviews of randomized clinical trials before
1996 showed studies had too small sample sizes and
poor study design to make any conclusions about the
effectiveness of physical therapy for patients with shoul-
der soft tissue disorders.13
Some studies have compared the effectiveness of
alternative methods of treatment with physical therapy
for treatment of painful stiff shoulders. A randomized
study by Van der Windt and associates investigated cor-
ticosteroid injections versus physiotherapy for treatment
of painful stiff shoulders.15 Primary outcome measures
were the patient’s main complaint and the pain and
shoulder disability questionnaire. Early results indicated
significant improvement in all outcomes for the corti-
costeroids group over the physical therapy group. The
difference, however, between the groups at weeks 26 and
52 was small. In a follow-up of 76% of the participants
in the original study, investigators found as many as half
of the patients experienced recurrent complaints across
groups.14 The study concluded that in the long term
there were no significant differences between treatment
groups.
More recent randomized clinical trials demonstrate
the effectiveness of manual therapy for shoulder disor-
ders. A randomized clinical study by Bang and Deyle
compared the effectiveness of supervised exercise for
shoulder impingement syndrome with and without
manual therapy intervention.16 The subjects in the
manual therapy group received joint and soft tissue
mobilization to the involved shoulder complex and the
involved upper quarter based on a clarifying examina-
tion. The study used pain (visual analog scale for func-
tion and brake tests), isometric strength tests, and the
CHAPTER 14 MANUAL THERAPY TECHNIQUES
functional assessment questionnaire to determine the
effectiveness of interventions. Participants were assessed
after 2 months of treatment. Results of the study
demonstrated a decrease in pain and an increase in func-
tion for both groups, but there was significantly more
improvement in the manual therapy intervention
group.16 Strength was also significantly improved in the
manual therapy group, but not in the supervised
strengthening group.
In a similar study, investigators compared the effect
of comprehensive treatment (hot packs, active range of
motion (AROM), physiologic stretching, muscle
strengthening, soft tissue mobilization, and patient edu-
cation) with and without joint mobilization in patients
with primary impingement syndrome.17 The results of
the study indicated improved 24-hour pain measure and
an improved subacromial compression test, but there
were no significant differences in range of motion and
function.
Several investigations have looked at specific effects
of joint mobilization on range of motion (ROM) meas-
ures and periarticular structures. A recent study using
cadavers demonstrated that end range mobilization
techniques were more effective in improving gleno-
humeral abduction ROM than those techniques per-
formed at the middle of the range.10 Vermeulen and
associates demonstrated in a multisubject case report
that the end range mobilization techniques in patients
with adhesive capsulitis resulted in increases in the
passive range of motion (PROM) and AROM, and in
the arthrographic assessment of joint capacity.12 These
changes were still present during a follow-up 9 months
later.
Further randomized controlled studies comparing
treatment methods for different shoulder impairment
classifications are needed to guide clinical decision
making, improve outcomes, and reduce use of inefficient
costly treatment.
Effects of Passive Movement
on Scar Tissue: Indications
and Contraindications
for Mobilization
Research indicates mobilization is most effective in
reversing the changes that occur in connective tissue fol-
lowing immobilization.1 Mobilization must be carefully
analyzed after trauma and/or surgery. When is it safe to
407
apply stress to scar tissue? How much stress should be
applied to the scar to promote remodeling? In what
direction should stress be applied? These important
questions must be answered before we can determine the
indications for mobilization of scar tissue. Indications
for mobilization will be discussed in regard to protective
and nonprotective categories of shoulder injuries. A case
study format will be used for each category to illustrate
changes in treatment and discuss the rationale of each
phase.
Case Study 1
PROTECTIVE INJURY
The Guide to Physical Therapist Practice describes
the preferred practice patterns for protective shoulder
injuries under Practice Pattern 4I—Impaired Joint
Mobility, Motor Function, Muscle Performance, and
Range of Motion Associated with Bony or Soft Tissue
Surgery.4 Protective injuries are from surgery and/or
trauma, with substantial soft tissue (muscle, ligament,
tendon, capsule) damage or repair. Examples of protec-
tive injuries include anterior capsular shift, Bankart
repair, rotator cuff repair, and shoulder dislocation.
Rehabilitation for patients with protective injuries is
divided into six phases: maximum protection, protected
mobilization, moderate protection, late moderate pro-
tection, minimum protection, and return to function.
This case study illustrates the concepts of phased reha-
bilitation in a patient with a protective shoulder injury.
EXAMINATION
History
A 16-year-old female basketball player was referred
for postoperative rehabilitation of a right anterior
capsulolabral reconstruction. The procedure performed
was a mini-open procedure, which includes a rotator
cuff interval reduction and anterior capsular shift
with labral cartilage repair. Before surgery, the patient
had recurrent anterior dislocations for the past 3 years.
Functional limitations included weakness and instabil-
ity, especially with basketball activities, and difficulty
sleeping on the affected side. Additional past medical
history includes previous arthroscopic surgery to
repair torn cartilage to the same shoulder 2 years
ago with little change in symptoms. The patient had
stiffness, weakness, and some mild pain 2 weeks after
the operation.
408 SECTION IV TREATMENT APPROACHES

SYSTEMS REVIEW EVALUATION

Integumentary System Adolescent female athlete has a protective shoulder
Decreased fascial mobility of suture and along fascia of injury and reconstructive capsular surgery. Patient is
inferior clavicle currently in the protective mobilization phase. Patient
Hypermobility of wrist, knee, elbow bilaterally, and appears to have anterior pectoral tightness and middle
left shoulder joints trapezius stretch weakness. The patient has inherent lig-
Musculoskeletal System ament laxity throughout other joints.
Palpable tenderness and trigger points on Phase 1: Maximum Protection Phase
subscapularis, serratus anterior, levator scapulae,
pectoralis minor, and lower portions of longus colli 1 to 10 Days Postwound
muscles
Intervention
Scapular gliding along pectoralis major and minor
tightness, and excessive mobility of the scapula in an Patient was immobilized in a sling postoperatively for
anterior direction the first 5 to 7 days. AAROM and PROM were in the
TEST AND MEASURES following protected ranges: Up to 90° of flexion, 45° of
Posture internal rotation, 90° of abduction, and neutral external
Slightly elevated and protracted rotation to be started 1 to 2 weeks postoperatively. Ice
Right scapula right upper extremity (RUE) held in and rest with arm was advised for pain reduction.
slight internal rotation
ROM Rationale
See Table 14-1 for ROM measurements. Immobilization during the first 3 to 5 days is critical
to allow the inflammatory and proliferation stages to
proceed. The inflammatory stage begins 1 hour post-
Table 14-1 wound and continues for 72 hours, during which vasodi-
latation, edema, and phagocytosis of debris in and
PROTECTIVE INJURY CASE STUDY 1: SUMMARIZATION OF around the wound are occurring.18 The matrix and cel-
RANGE OF MOTION MEASUREMENTS lular proliferative stage begins 24 hours postwound and
is characterized by endothelial capillary buds, with
Weeks Postoperatively fibroblasts synthesizing the extracellular matrix.18,19
The scar is still quite cellular with the presence
2 4 6 8 16
of macrophages, mast cells, and fibroblasts. Little to no
PROM (degrees) motion should occur during the first 3 to 5 days to
Flexion 80 130 140 165 176 protect the newly forming network of capillaries.2
Abduction 58 90 102 160 170 Excessive motion too early can result in a prolonged
External rotation, -5 14 25 45 64 inflammatory stage and excessive scarring. Heat should
neutral position also be avoided secondary to vascular stress on capillary
External rotation, 45° -10 18 30 53 75 budding. Ice can be used to control swelling and pain.
abd. position Gentle stress to the tissue is initiated by the seventh
External rotation, 90° NT NT 38 56 80 to tenth day postwound. The fibroblastic stage of healing
abd. position has already begun with presence of fibroblasts in the
Internal rotation, 45° 43 63 63 65 70 wound.18,19 Gentle early motion, such as with grades 1
abd. position
and 2 joint mobilization and PROM in protected posi-
Extension NT NT 60 69 78
tions, helps to facilitate alignment of newly formed col-
AROM (degrees) lagen fibers, aid muscle relaxation, and prevent adhesion
Flexion NT NT 125 160 170 formation. In protected injuries with surgical involve-
Scaption NT NT 130 165 175 ment, it is helpful to have an operative report to inform
the therapist of the specific tissues involved in the pro-
NT, Not tested. cedure. For this case study, the anterior capsule, a small
CHAPTER 14 MANUAL THERAPY TECHNIQUES
portion of the subscapularis, and the labrum were
primarily involved.
Phase 2: Protected Mobilization
10 Days to 3 Weeks
Intervention
Continued grades 1 and 2 joint mobilization are pro-
gressing toward grades 3 and 4 by 3 weeks. Scapular
gliding passive and active assistive. Strain counterstrain
an indirect positional release technique20 to spinal and
rib dysfunctions. PROM and AAROM in protected
positions described in the previous phase.
(See Table 14-1 for current ROM measures.)
Rationale
The goal of this phase is to promote a functional scar
and attempt to decrease other compensatory or con-
tributing dysfunctions. Early mobilization is critical in
affecting scar tissue length, glide, and tensile strength.
As the inflammatory phase ends, the fibroplasia stage of
healing has already begun. The production of scar tissue
begins on the fourth day of wound healing and increases
rapidly during the first 3 weeks.2,21 Peacock has substan-
tiated this peak production of scar tissue by the increased
quantities of hydroxyproline.2 Hydroxyproline is a
byproduct of collagen synthesis.2,22 Collagen production
begins and continues to increase for up to 6 weeks.2,18,19
The newly synthesized collagen fibrils are weak
against tensile force. Intramolecular and intermolecular
cross-linking of collagen develops,6 and is designed to
resist tensile forces.2,22 The first peak in tensile strength
occurs around the 21st day postwound.2
Gentle mobilization techniques can be effective
during early fibroplasia because of the immaturity of the
collagen tissue. Arem and Madden demonstrated that
after 14 weeks of scar maturation, elongation of scar was
no longer possible.23 In contrast, the 3-week-old scar
was substantially lengthened when subject to the same
tension.23 Peacock hypothesizes that the mechanism by
which the length of the scar is increased becomes criti-
cal for the restoration of the gliding mechanism.2
Stretching, or an increase in length of the scar, is a result
of straightening or reorientation of the collagen fibers,
without a change in their dimensions.2 For this to occur,
the collagen fibers must glide on each other. The gliding
mechanism is hampered in unstressed scar tissue by the
development of abnormally placed cross-links and a
409
random orientation of the newly synthesized collagen
fibrils.21 Early gentle passive motion starting around the
10th day and progressing to the 21st day facilitates the
development of tissue tensile strength by helping align
newly synthesized collagen. Additionally, improved ten-
sile strength allows for early AROM in the next phase.
Phase 3: Moderate Protection Phase
3 to 6 Weeks
Reexamination
Continued muscle guarding of subscapularis. Serra-
tus anterior, first rib, longus colli, and scalenes with little
to no tenderness. Subjective reports of decreasing sore-
ness and pain of glenohumeral joint at rest. Sutures have
been removed and superficial closure complete. Patient
continues with anterior chest muscle tightness and
decreased scapular excursion. See Table 14-2 for PROM
measures.
Intervention
PROM stretching and physiologic oscillations to 30°
of external rotation in neutral and 45° abducted posi-
tions, joint mobilization glenohumeral joint with grades
3 and 4 in a posteroanterior (PA) direction, and gentle
posterior capsule stretching. STM to superficial scar
(suture), inferior clavicle, fascial restrictions between
pectoralis major and minor and between rib cage and
pectoralis minor. Muscle reeducation initiated with
proprioceptive neuromuscular facilitation (PNF) and
scapular techniques with active, eccentric, and concentric
patterns (primarily posterior elevation and depression).
Gentle AAROM and AROM initiated, but continuing
to avoid combination of external rotation and abduction.
At 5 weeks, isometrics are initiated in the plane of the
scapula (30° to 45° anterior to frontal plane) for internal
and external rotation, extension, and abduction.
Rationale
The moderate protection phase allows for more
AAROM progressing toward AROM by the fourth
week. Collagen production continues to be high until
the sixth week.2,18,19 The goal of rehabilitation at this
stage is to further facilitate extensibility of newly syn-
thesized collagen, realign randomly oriented collagen,
and enhance fiber glide between collagen fibers. Tensile
strength has reached its first peak, allowing gentle
AROM as early as 3 weeks2 in protected positions
410 SECTION IV TREATMENT APPROACHES

Table 14-2

SUMMARIZATION OF PHASES OF REHABILITATION FOR PROTECTIVE SHOULDER INJURIES

Late
Maximum Protected Moderate Moderate Minimum Return to
Phases Protection Mobilization Protection Protection Protection Function

Time 1-10 days 10 days to 3 3-6 weeks 6-12 weeks 12-16 weeks +16 weeks
weeks
Stage of Inflammatory, Early Fibroplasia, Maturation Maturation Maturation
healing proliferative fibroplasia maturation
early fibroplasia
Goals Protect newly Facilitate Enhance Stress scar; Same as Return to
formed scar functional tensile restore force previous phase; function
scar, aligning strength of couples; progressively
new collagen scar proximal, increase
fibers; clear distal strength
spinal and rib rotator cuff,
dysfunction parascapular
muscles
Manual 7-10 days Joint mobs As previous, Scapular PNF UE As needed for
therapy postwound, grades 1 and 2 STM to release tech.; patterns with any deficits
techniques grades 1 and 2 progress to 3, suture, PNF UE significant
joint mobs 4; STM scapular patterns; resistance;
surrounding release tech.; low-load low-load
tissue; PNF PNF scapular prolonged prolonged
scapular patterns stretch stretch if
patterns; needed
protected
PROM
Other Position Home Codman Isokinetics in Same as Progressive
therapeutic education; program of exercises, protected previous, return to sport
interventions antiinflamma- PROM in T-bar, Swiss ROM submax; increasing drills, light
tory modalities; protected ball, foam active effort and recreational
ice ranges roller; scapular ROM; activities
AAROM stabilization plyoball
and AROM exercises; throwing
exercises PREs

STM, Soft tissue mobilization; PNF, proprioceptive neuromuscular facilitation; PROM, passive range of motion; UE, upper extremity;
AROM, active range of motion.

(rotation before elevation especially in contractile com-
ponent injuries). STM to sutures and surrounding
fascial planes facilitates suture scar extensibility and
proper muscle function, and decreases pain.
An additional goal of rehabilitation for this phase is
to prevent muscle atrophy, inhibition, and the effects of
immobilization. PNF scapular patterns with a progres-
sion towards resisted patterns during this phase foster
activation and restoration of scapular muscle activity,
providing dynamic proximal stability. Progressive iso-
metric exercises in protected positions can be used
around 5 weeks by the patient at home or work to stim-
ulate inhibited muscle and provide dynamic tension to
healing soft tissue.
CHAPTER 14 MANUAL THERAPY TECHNIQUES
Phase 4: Late Moderate Protection
6 to 12 Weeks
Reexamination
Decreased tenderness and improved fascial glide of
suture scar and surrounding superficial fascia. Scapular
mobility is within normal limits (see Table 14-1 for
ROM measures).
Intervention
Six to 8 weeks PROM stretching with emphasis on
external ROM in the plane of the scapula and 45°
abducted position. Continuing PNF scapular patterns
working on any areas of weakness. AROM PNF pat-
terns for upper extremity initiated with some resistance
in weak aspects of the pattern. Active scapular stabiliza-
tion and movement patterns incorporating closed
kinetic chain exercises.
At 8 to 12 weeks, AROM exercises begun in unre-
stricted ROM (no loading of joint in external and
abduction). Progressive resistive exercises (PREs) in
protected ROM with emphasis on rotator cuff strength-
ening progressing to overhead exercises. Submaximal
isokinetic internal/external rotation in the plane of the
scapula (limited external rotation to 45°).
Rationale
At 6 weeks, collagen production tapers off. The mat-
uration or remodeling phase of healing begins around
3 weeks and continues for up to 12 to 18 months.18
Maximizing scar extensibility is essential because by
14 weeks scar deformability may be greatly decreased.22
Strengthening is emphasized more during this phase.
Some strengthening has already begun using PNF
scapular patterning to reestablish balance of function of
the parascapular muscles in the previous phase. During
the first 2 to 3 weeks of this phase, active and reactive
scapular stabilization activities are initiated. These exer-
cises help to restore force couples around the scapula and
usually involve some co-contraction or synergy patterns
of the rotator cuff. During the last 3 to 4 weeks of this
phase, emphasis shifts toward strengthening the rotator
cuff throughout the full range of movement. Through
the progressions described, proximal stability and force
couples are established before distal force couples. Low-
level weights or theraband resistance for this case study
for internal and external rotation effect healing
411
subscapularis tendon and enhance dynamic gleno-
humeral joint stability.
Phase 5: Minimal Protection
12 to 16 Weeks
Reevaluation
Patient demonstrating some elevation of scapula with
late elevation phase. Excessive scapular elevation in-
creased with resistance. Activities of daily living (ADL)
within normal limits. No pain with most activities and
exercises. (See Table 14-1 for ROM measurements.)
Intervention
Continued progression of weights and repetitions of
previous phase of exercises. Chest pass throwing against
plyotrampoline with 2.5-lb ball. STM performed to
apparent remaining fascial restrictions along the inferior
clavicle followed by manual and PRE strengthening
of lower trapezius and serratus anterior. PNF resistive
patterns performed close to end range abduction and
external rotation.
Rationale
Multiple repetitions in unrestricted ROM continue
to provide stress to the maturing scar. Manual tech-
niques during this phase are used to further fine-tune
function and clear any remaining restrictions. Neuro-
muscular control at end range abduction and external
rotation is essential to help protect capsular reconstruc-
tion and return to sport.
Phase 6: Return to Function
More Than 16 Weeks
Reevaluation: Tests and Measures
Isokinetic testing shows external/internal rotators
ratio at 81% and 20% stronger than uninvolved side.
Intervention
Patient began progressive basketball shooting and
drill activities at 18 weeks. Patient was instructed not to
begin team play until 22 weeks postoperatively. Patient
was discharged at 18 weeks with an extensive program
of rotator cuff strengthening and scapular stabilization
exercises.
Rationale
The return to function phase begins usually around
16 weeks if elements of movement are free of abnormal
412 SECTION IV TREATMENT APPROACHES
patterns and pain. This phase happens sooner based on
patient response, specific trauma, and the required level
of function. Exercises are more functionally based and
maximal efforts are used. Isokinetic testing of rotator
cuff muscles informs the therapist of any deficits, in par-
ticular internal to external ratios that may indicate an
increased hazard for return to function. Currently reim-
bursement issues and managed care policies may not
allow physical therapists to observe a patient completely
through all phases of rehabilitation. Proper education of
progressive activities and appropriate time frames for
return to full function need to be outlined for patients
with limited follow-up.
In summary, protected shoulder injuries can be safely
progressed through a phased program of rehabilitation
based on stages of soft tissue healing. Table 14-2 sum-
marizes the various stages. Manual therapy techniques
used at specific stages of healing can enhance the
strength and extensibility of scar tissue, reestablish force
couples, and restore functional movement patterns.
Case Study 2
NONPROTECTIVE INJURY
The Guide to Physical Therapist Practice describes the
preferred practice patterns for nonprotective shoulder
injuries under Preferred Practice Patterns 4 B, C, D, E,
and G.4 Nonprotective shoulder injuries are primarily
shoulder dysfunctions that have no significant soft tissue
healing constraints. Examples of nonprotective injuries
include postacromioplasty, prolonged immobilization,
adhesive capsulitis, and impingement syndromes. These
patients frequently had pain, stiffness, and limited func-
tion. This case study will illustrate the concepts of reha-
bilitation for a patient with a nonprotective injury.
EXAMINATION
History
A 46-year-old female homemaker has left shoulder
pain and stiffness. Patient was referred 5 days after
arthroscopic surgery and closed manipulation. Patient
began having pain and stiffness several months before,
possibly caused by overworking in her yard. Left shoul-
der became increasingly stiff and painful the 5 to 6
weeks before surgery. The diagnosis given was adhesive
capsulitis. Past medical history: “stiff neck” 2 to 3 years
ago. Subjective functional complaints: patient is unable
to reach overhead, fasten bra. Moderate difficulty with
dressing and placing hand behind back, and washing
opposite axilla.
SYSTEMS REVIEW
Musculoskeletal System
Tenderness and muscle spasm: Posterior cervical spine
C1-2, anterior cervical spine along longus colli
muscles at C5-6 L; posterior aspects of ribs 2-4 L,
L subscapularis, supraspinatus, infraspinatus, teres
minor, and levator scapulae
All other systems unremarkable
TEST AND MEASURES
Posture
L scapula protracted, downwardly rotated, and with
winging
Slight forward head position with increased tone of
sternocleidomastoid muscle bilaterally
ROM
See Table 14-3 for initial shoulder ROM
measurements.
Upper quarter screening: Extension and side bending
L of cervical spine were limited by 50% and painful
actively and passively with over pressure.
Special Tests
Capsular testing revealed restricted motion in all
directions.
EVALUATION
Patient has a nonprotective shoulder injury. Adhesive
capsulitis with strong muscle guarding and possible
adaptive shortening of subscapularis. Currently, unable
to fully assess capsular restrictions secondary to muscle
guarding of rotator cuff and subscapularis muscles.
INITIAL PHASE
Intervention
Indirect techniques, such as strain and counterstrain,
used on cervical, rib, and shoulder musculature. PROM
stretching to tolerance in external and internal rotation,
flexion and abduction with scapula stabilized. Joint
mobilizations of grades 1 and 2 to glenohumeral joint.
Patient instructed in positioning comfort for L shoulder
and cervical spine.
Rationale
The initial phase of rehabilitation for nonprotected
injuries primarily focuses on antiinflammatory modali-
ties, grades 1 and 2 joint mobilization, and education.
Patients often will perform habitual patterns of move-
ment, maintaining current state of dysfunction. Correc-
tion, modification, or cessation of predisposing activities
is essential. Goals of rehabilitation during this phase are
CHAPTER 14 MANUAL THERAPY TECHNIQUES 413

Table 14-3

NONPROTECTIVE INJURY CASE STUDY 2: SUMMARIZATION OF RANGE OF MOTION MEASUREMENTS

Time Initial 2 Weeks 4 Weeks 6 Weeks 10 Weeks

PROM (DEGREES)
Flexion 102 112 140 150 174
Abduction 70 80 120 150 170
External rotation, neutral position -20 5 30 36 62
External rotation, 45° abd. position 10 20 45 56 70
External rotation, 90° abd. position NT NT 40 46 75
Internal rotation, 45° abd. position 52 54 52 53 71
Hyperextension 48 50 53 53 71

AROM (DEGREES)
Scaption 70 90 112 132 155

NT, Not tested.

to reduce inflammation and pain, restore proximal sta-

bility to the spine, scapular muscle activity, and avoid
painful positions. Clearing spinal and rib dysfunctions
that contribute to or are source problems for shoulder
signs and symptoms is essential during this phase for an
optimal functional outcome.
INTERMEDIATE PHASE
Reevaluation
By the third treatment, the patient reports decreased
soreness of the L shoulder at rest. Still experiencing pain
with reaching and overhead activities. Decreased pain
and stiffness of cervical spine, but ROM still restricted.
Continued abnormal position of L scapula. (See Table
14-3 for ROM measurements.)
Intervention Figure 14-1 Proprioceptive neuromuscular facilita-
Continued PROM stretching, joint mobilization as tion.
previous. Patient started on low-load prolonged stretch
with heat in the plane of the scapula using theraband
and a 1-lb weight initially for 10 minutes progressing to with emphasis on posterior depression, as illustrated in
20 minutes during a series of four to five treatment ses- Figure 14-1.
sions. High-speed (200°/s) isokinetics were initiated for Rationale
internal and external rotation in the plane of the scapula The intermediate phase of rehabilitation begins when
in the available ROM. Scapular release techniques used patient reactivity allows for more aggressive progression
to mobilize fascial restrictions within subscapularis, ser- of techniques. Goals of this phase are to maximize
ratus anterior, and levator scapulae. Joint mobilization ROM of all components of shoulder movement and
and myofascial release techniques used to address facet normalize force couples of scapula and glenohumeral
joint irritation C5-6 and suboccipitally. PNF scapular joint. Emphasis is placed on restoring rotation at the
patterns progressing from passive to resistive movements glenohumeral joint and then on elevation.
414 SECTION IV TREATMENT APPROACHES
Traditional manual therapy techniques used to treat
limited shoulder ROM have followed the arthrokine-
matic movements of joint surfaces occurring at the
glenohumeral. Kaltenborn determined the appropriate
method of applying a gliding mobilization technique by
the convex concave rule.24 For example, sliding of the
convex humeral head on a concave glenoid surface
occurs in the opposite direction of the humerus. There-
fore during elevation of the shoulder, the humeral head
is sliding inferiorly as the bone moves superiorly.
However, data are now available that challenge the
concave-convex rule of arthrokinematic motion.
Poppen and Walker25 report a movement of the
humeral head in a superior and inferior direction during
elevation of the shoulder. Howell and colleagues demon-
strated translatory motion of the head of the humerus
to be opposite of that predicted by the concave-convex
rule. Only patients with instability had demonstrated
translation in the direction predicted by the concave-
convex rule.26 Soft tissue tension of the capsular and
ligament components rather than joint surface geome-
try may be a greater determinant of the arthrokinematics
of the glenohumeral joint.
The type and frequency of force used to mobilize
depend on the implicated tissue. In this case study, the
implicated tissue of restriction is the anterior and infe-
rior capsule, glenohumeral ligaments, and subscapularis.
The authors advocate the use of low-load prolonged
stretch in addition to oscillation techniques for more
substantial soft tissue restrictions. Connective tissue
structures such as ligaments, tendons, and capsules
respond to mechanical stress in a time-dependent or
viscoelastic manner.27-30 Viscoelasticity is a mechanical
property of materials that describes the tendency of a
substance to deform at a constant rate. The rate of defor-
mation is not dependent on speed of the external force
applied. If the amount of deformation does not exceed
the elastic range, the structure can return to the original
resting length after the load is removed. If loading is
continued into the plastic range, passing the yield point,
failure of the tissue will occur. Failure is thought to be a
function of breaking intermolecular cross-links rather
than rupture of the collagen tissue.31
If a permanent increase in ROM is a goal of treat-
ment, then manual therapy should be aimed at produc-
ing plastic deformation. Taylor and associates32 showed
that there is an increased risk of tissue trauma and injury
with rapid stretch rates. Rapidly applied forces may
cause material to react in a stiff, brittle fashion, causing
tissue tearing. Gradually applied loads could result in
tissue responding in a more yielding manner with plastic
deformation. If the tissue is held under a constant
external load and at a constant length, force relaxation
occurs.33
In addition to increasing extensibility of gleno-
humeral capsular and ligamentous structures, muscle
extensibility must also be addressed. Clinically the
authors have found the subscapularis to be commonly
restricted in shoulder dysfunction. The subscapularis is
the most stabilizing factor during external rotation of
the glenohumeral joint in 0° of abduction.25 Addition-
ally, most patients tend to guard or immobilize a painful
shoulder by adducting and internally rotating the gleno-
humeral joint, thus shortening the subscapularis.
In prolonged immobilization and dysfunction, such
as adhesive capsulitis, the subscapularis may acclimate to
a shortened position. Muscles respond to immobiliza-
tion by degeneration of myofilaments, a change in
sarcomere alignment and configuration, a decrease in
mitochondria, and a decreased ability to generate
tension.35 Muscles acclimate to immobilization in a
shortened position by losing sarcomeres. Tabary and
associates found that muscles immobilized in a short-
ened position for 4 weeks had a 40% decrease in total
sarcomeres and displayed an increased resistance to
passive movement.36 Muscles immobilized in a length-
ened position had 20% more sarcomeres and demon-
strated no change in resistance to passive motion.
Functionally, limited subscapularis extensibility may
affect functional elevation. Otis and associates37 have
reported the importance of restoring rotation to the
glenohumeral joint to facilitate elevation. It was demon-
strated that the contribution of the infraspinatus
moment arm to abduction is enhanced with internal
rotation while that of the subscapularis is enhanced with
external rotation.37 Low-load prolonged stretch and
rotational exercises in the plane of the scapula in our case
study are an attempt to reverse the effects of immobil-
ity, increasing the extensibility and strength of the sub-
scapularis. Restrictions of the subscapularis tend to also
affect parascapular muscles secondary to the altered
scapulohumeral rhythm.
Scapular release techniques and STM (described
later in this chapter and in Chapter 16) can be used to
release fascial restrictions that have developed as a result
of abnormal movement patterns. In this particular case
CHAPTER 14 MANUAL THERAPY TECHNIQUES 415

the patient had excessive protraction and downward
rotation of the scapula with myofascial trigger points in
the levator scapulae, serratus anterior, and pectoralis
minor. Warwick and Williams38 report a possible fusion
of the serratus anterior and levator by their fascial con-
nection. Excessive tone of pectoralis minor effectively
depresses the scapula and restricts the scapular rotation
necessary for proper elevation. Furthermore, the serra-
tus anterior and levator scapulae work as a force couple
to rotate the scapula. Increasing the extensibility of the
fascia of these three muscles would allow proper func-
tioning of parascapular force couples during elevation.
RETURN TO FUNCTION PHASE
Reevaluation
All ADLs without pain and patient has started
working in the yard without limitations. Patient without
cervical pain, but ROM cervical spine three-quarters
normal side bending right and left. (See Table 14-3 for
10-week ROM measurements.)
Intervention
Patient instructed in exercise progressions for next 2
months, with emphasis on rotator cuff and parascapular
muscle exercises. Patient allowed to progress back to
swimming and gardening activities to tolerance.
Rationale
Once ROM and strength are optimized, a home
program is finalized to further facilitate physiologic
changes—such as increased sarcomeres and remodeling
of periarticular tissue. In the competitive and industrial
athlete, form, technique, and training error correction
are essential to prevent recurrence of dysfunction.
In summary, rehabilitation of nonprotective injuries
depends on the implicated tissue or systems in dysfunc-
tion or restriction. Table 14-4 summarizes the phases

Table 14-4

SUMMARY OF PHASED REHABILITATION FOR NONPROTECTIVE SHOULDER INJURIES

Phases Initial Intermediate Return To Function

Signs and symptoms Pain at rest; difficulty
(reactivity) sleeping; pain before
resistance
Goals Decrease pain
Manual therapy techniques Grades 1 and 2 joint mobs
Other therapeutic Antiinflammatory
interventions modalities; positioning and
activity education
No pain at rest; pain with ROM maximized;
resistance; moderate functional movement pain
reactivity; limited rot and free; muscle imbalances
elevation; weakness of resolving
rotator cuff and/or
parascapular muscles
Restore rotation ROM and Return to function
strength of parascapular
muscles and rotator cuff
Grades 3 and 4 joint mobs; Fine-tuning of functional
STM; scapular release patterns with PNF
techniques; PNF scapular
and UE patterns; low-load
prolonged stretch
Heat with stretch; isokinetic Home program, correct
and isotonics working technique and training
rotation before elevation in errors
POS; isometrics; AAROM
with T bars, Swiss balls,
foam rollers; glenohumeral
joint and scapular taping
techniques

ROM, Range of motion; STM, soft tissue mobilization; PNF, proprioceptive neuromuscular facilitation; UE, upper extremity.
416 SECTION IV TREATMENT APPROACHES
of rehabilitation. Glenohumeral joint arthrokinematics
may be strongly influenced by periarticular tissue exten-
sibility and muscle function rather than pure joint geom-
etry. Manual techniques must comply with the type of
tissue or system response desired. Continual reassess-
ment of subjective, functional, and objective measures
assists the therapist in evaluating treatment effectiveness.
Role of Mobilization
The primary role of joint mobilization is to restore joint
mobility and facilitate proper biomechanics of involved
structures. Joint mobilization has two proposed ratio-
nales—neurophysiologic and biomechanical.
The neurophysiologic effect is based on the stimula-
tion of peripheral mechanoreceptors and the inhibition
of nociceptors (pain fibers). Nociceptors are unmyeli-
nated nerve fibers, which have a higher threshold of
stimulation than mechanoreceptors.39,40 There is evi-
dence that stimulation of peripheral mechanoreceptors
blocks the transmission of pain to the central nervous
system (CNS).39 Wyke postulates that this phenomenon
is because of a direct release of inhibitory transmitters
within the basal spinal nucleus, inhibiting the onward
flow of incoming nociceptive afferent activity. Joint
mobilization is one method of enhancing the frequency
of discharge from the mechanoreceptors, thereby dimin-
ishing the intensity of many types of pain.
The biomechanical effect of joint mobilization is
focused on the direct tension of periarticular tissue to
prevent complications resulting from immobilization
and trauma. The lack of stress to connective tissue results
in changes in normal joint mobility. A recent study using
cadavers demonstrated that end range mobilization
techniques were more effective in improving gleno-
humeral abduction ROM than those performed at the
middle of the range of abduction.10 Vermeulen and col-
leagues demonstrated in a multisubject case report that
the end range mobilization techniques in patients with
adhesive capsulitis resulted in increases in PROM and
AROM, and in arthrographic assessment of joint capac-
ity.12 The changes were still visible in a follow-up 9
months later.
The periarticular tissue and muscles surrounding the
joint demonstrate significant changes after periods of
immobilization. Akeson and associates have substanti-
ated a decrease in water and glycosaminoglycans (GAG,
the fibrous tissue lubricant), an increase in fatty fibrous
infiltrates (which may form adhesions as they mature
into scar), an increase in abnormally placed collagen
cross-links (which may contribute to the inhibition of
collagen fiber gliding), and the loss of fiber orientation
within ligaments (which significantly reduces their
strength).1,3 Passive movement or stress to the tissue can
help to prevent these changes by maintaining tissue
homeostasis.2 The exact mechanisms of prevention are
uncertain.
Contraindications
We can understand contraindications to joint mobiliza-
tion by becoming aware of the common abuses of passive
movement. The abuses of passive movement can be
broken down into two categories: creating an excessive
trauma to the tissue and causing undesirable or abnor-
mal mobility.1 Improper techniques, such as extreme
force, poor direction of stress, and excessive velocity, may
result in serious secondary injury. In addition, mobiliza-
tion to joints that are moving normally or that are hyper-
mobile can create or increase joint instability.
Ultimately, selection of a specific technique will
determine contraindications. For example, the very
gentle grade 1 oscillations, as described by Maitland,
rarely have contraindications. These techniques are
mainly used to block pain. They are of small amplitude
and controlled velocity. In contrast, manipulative
techniques have many contraindications. Haldeman
describes the following conditions as major contraindi-
cations to thrust techniques: arthritides, dislocation,
hypermobility, trauma of recent occurrence, bone weak-
ness and destructive disease, circulatory disturbances,
neurologic dysfunction, and infectious disease.41
Principles of Joint Mobilization Techniques
The mobilization techniques are designed to restore
intimate joint mechanics. Several general principles
should be remembered during application of the
techniques.
Hand Position. The mobilization hand should be
placed as close as possible to the joint surface, and the
forces applied should be directed at the periarticular
tissue. The stabilization hand counteracts the movement
of the mobilizing hand by applying an equal but oppo-
site force, or by supporting or preventing movement at
surrounding joints. Excessive tension in the therapist’s
CHAPTER 14 MANUAL THERAPY TECHNIQUES
hands during joint mobilization can result in the patient
guarding against the mobilization.
Direction of Movement. The direction of move-
ment of mobilization should take into account the
mechanics of the joint mobilized, the arthrokinematic
and osteokinematic impairments of the dysfunction, and
the current reactivity of the involved tissue.
The direction of forces to the joint is also determined
based on the desired response. Neuromuscular relaxation
and pain modulation effects will be appreciated if the
direction of force is opposite the pain. Biomechanical
effects will be appreciated if forces are directed towards
resistance, but to patient tolerance. The resistance
represents the direction of capsular or joint limitation.
Movement into the restriction is an attempt to make
mechanical changes within the capsule and the sur-
rounding tissue. The mechanical changes may include
breaking up of adhesions, realignment of collagen, or
increasing fiber glide. Certain movements stress specific
parts of the capsule. For example, arthrogram studies
demonstrated that external rotation of the glenohumeral
joint stresses the anterior recess of the capsule.42
Body Mechanics. Proper body mechanics are
essential in application of mobilization techniques. The
therapist is able to impart desired direction and force of
movement if working from a position of stability. The
therapist should stand close to the area being mobilized
and use weight shifting through legs and trunk to assist
movement in the vector of mobilization. The therapist’s
A B
Figure 14-2 A, Low-load prolonged stretch (LLPS) with a Theraband. B, LLPS external rotation with weight.
417
hands and arms should be positioned to act as fulcrums
and levers to fine-tune mobilization.
Duration and Amplitude. Several animal model
studies have been performed using different loads and
loading time to determine the most effective technique
for obtaining permanent elongation of collagenous
tissue. The studies used rat tendons under varied loads
to demonstrate the elongation of tissue. A high-load,
short-duration treatment (105 g to 165 g for 5 minutes)
was compared with a low-load, long-duration treatment
(5 g for 15 minutes).43,44 The results indicated that a low-
load, long-duration stretch was more effective in obtain-
ing a permanent elongation of the tissue. In humans,
Bonutti and associates45 determined that the optimal
method to obtain plastic deformation and reestablish
ROM is static progressive stretch (SPS). One to two 30-
minute sessions per day of SPS for 1 to 3 months pro-
duced an overall average increase in motion of elbow
contractures of 69%, with excellent compliance by the
patients. As previously noted, the authors advocate the
use of low-load prolonged stretch with heat to facilitate
plastic deformation of shoulder capsular restrictions.
Figures 14-2, A, B, and 14-3 depict a method of low-
load prolonged stretch for external rotation and internal
rotation, respectively. The patient needs to be in a sub-
acute stage of reactivity and the stretch is to patient tol-
erance. Heat used in conjunction with the stretch has
been found to be more effective than stretch alone.46,47
The patient’s shoulder is placed in the plane of the
scapula with a wedge or stack of towels. The stretch is
418 SECTION IV TREATMENT APPROACHES

Figure 14-3 Low-load prolonged stretch internal Figure 14-4 Inferior glide of the humerus.
rotation.

performed by using Theraband resistance to assist with

positioning, and/or the use of a hand weight and gravity
to stretch periarticular structures. Duration of stretch
can be gradually progressed from 10 to 30 minutes.
Little research has been performed on joint mobi-
lization to determine the optimum duration of oscilla-
tion. Often the duration is determined by the change
desired by the therapist. For example, glenohumeral
joint mobilization of grades 1 or 2 performed to facili-
tate neuromuscular relaxation could be performed until
muscle guarding was reduced and ROM increased.

Glenohumeral Joint Figure 14-5 Longitudinal distraction—inferior glide

Techniques of the humerus.

Figure 14-4: Inferior Glide of the Humerus
Patient Position. Supine, with the involved
extremity close to the edge of the table. A strap may be
used to stabilize the scapula. The extremity is abducted
to the desired range.
Therapist Position. Facing the lateral aspect of the
upper arm. Cephalad hand web space is placed on supe-
rior glenohumeral inferior to acromion. Assisting hand
supports the weight of the arm by holding the distal
upper arm superior to epicondyles and bracing patient’s
arm against therapist. Assisting hand/arm can also
impart distractive force and change amount of rotation.
The mobilizing hand glides the head of the humerus
inferiorly, attempting to stress the axillary pouch or infe-
rior portion of the glenohumeral capsule.
Figure 14-5: Longitudinal Distraction—
Inferior Glide of the Humerus
Patient Position. Supine, with the involved
extremity as close as possible to the edge of the table.
Therapist Position. Facing the joint, with inner
hand up into the axilla pressing against scapuloglenoid.
The outer mobilizing hand grips the epicondyles of the
humerus and imparts a distractive force stressing the
CHAPTER 14 MANUAL THERAPY TECHNIQUES 419

Figure 14-6 Postcapsule stretch.

inferior capsule. To increase the efficiency of the pull,

the therapist can weight shift and rotate the body
slightly away from the patient. A prolonged stretch is
often effective with this technique.

Figure 14-6: Posterior Glide of the Humerus

Patient Position. Supine, with arm slightly
abducted and flexed into plane of the scapula and resting
on the therapist’s thigh.
Therapist Position. Sitting on treatment table at
45° turn from sagittal plane. Mobilizing hand is placed
on anterior humeral head, with a wedge or rolled towel
under lateral scapula. Assisting hand supports distal
extremity to facilitate relaxation. The mobilization is
directed posteriorly along the plane of the glenoid. This
technique is useful for reactive shoulders with posterior
capsule tightness.
Figure 14-7: Posterior Glide of the Humerus
Patient Position. Supine with involved shoulder
flexed 90° and horizontally adducted to first tissue
resistance.
Therapist Position. Opposite side of patient’s
shoulder. Mobilizing hand is same as involved shoulder.
Therapist cups patient’s elbow in mobilizing hand and
assists mobilization with therapist’s sternum. Assisting
hand stabilizes the scapula under patient. Mobilization
movement is along 35° of glenoid tilt. The level of
Figure 14-7 Posterior glide of the humerus.
flexion can be changed to work the most restricted part
of the capsule. This technique is useful with subacute
and chronic posterior capsule tightness.
Figure 14-8: Posterior Glide of the Humeral
Head in Side Lying
Patient Position. Patient is positioned in side lying
with the involved shoulder facing upward.
Therapist Position. Facing the patient, the thera-
pist’s cephalad hand contacts the proximal humerus and
the caudal hand holds the involved extremity by the
elbow. The mobilization is a force couple motion with
the proximal hand providing the primary mobilizing
force in an anterior to posterior direction while the
caudal hand provides a slight circumduction motion
usually opposite that of the proximal hand.
420 SECTION IV TREATMENT APPROACHES
Figure 14-9: Lateral Distraction of the
Humerus
Patient Position. Supine, close to edge of table,
with the involved extremity flexed at the elbow and
glenohumeral joint.The extremity rests on the therapist’s
shoulder. A strap and the table stabilize the scapula.
Therapist Position. Facing laterally, both hands
grasp the humerus as close as possible to the joint. The
therapist should assess which vector of movement is
most restricted by starting laterally with mobilization
Figure 14-8 Posterior glide of the humeral head in
side lying.
Figure 14-10 Anterior glide of the head of the humerus.
and proceeding caudally. To improve delivery of oscilla-
tion or stretch, the therapist should align his or her trunk
along vector of mobilization.
Figure 14-10: Anterior Glide of the Head of
the Humerus
Patient Position. Prone, with the involved extrem-
ity as close as possible to the edge of the table. The head
of the humerus must be off the table. A wedge or towel
roll is placed just medial to joint line under the coracoid
process. The extremity is abducted and flexed into the
plane of the scapula.
Therapist Position. Distal to the abducted shoul-
der facing cephalad. The outer hand applies slight
Figure 14-9 Lateral distraction of the humerus.
CHAPTER 14 MANUAL THERAPY TECHNIQUES
distractive force while the inner mobilizing hand glides
the head of the humerus anteriorly, stressing the ante-
rior capsule. The tendon of the subscapularis is also
stressed with this technique. The mobilization can be
fine-tuned by changing the angle of the anterior force
to the most restricted area.
Figure 14-11: Anterior-Posterior Glide of the
Head of the Humerus
Patient Position. Prone, with the involved extrem-
ity over the edge of the table abducted to the desired
range. A strap may be used to stabilize the scapula.
Therapist Position. Facing laterally in a sitting
position, with the forearm of the involved extremity held
Figure 14-11 Anterior-
posterior glide of the head of the
humerus.
Figure 14-12 Anterior-posterior
glide of the head of the humerus.
421
between the therapist’s knees. Both hands grasp the
head of the humerus and apply anteroposterior move-
ment oscillating the head of the humerus. Grades 1 and
2 are mainly used with this technique to stimulate
mechanoreceptor activity.
Figure 14-12: Anterior-Posterior Glide of the
Head of the Humerus
Patient Position. Supine, with the involved
extremity supported by the table. A towel roll, pillow, or
wedge is placed under the elbow to hold the arm in the
plane of the scapula.
Therapist Position. Facing laterally in a sitting
position. The fingertips hold the head of the humerus
422 SECTION IV TREATMENT APPROACHES

Figure 14-13 External rotation of

the humerus.

while a gentle up-and-down movement is applied. This

technique is used with grades 1 and 2 oscillations.

Figure 14-13: External Rotation of

the Humerus
Patient Position. Supine, with the involved
extremity supported by the table. The arm is held in the
plane of the scapula.

Therapist Position. Facing laterally with caudal

mobilizing hand grasping the distal humerus, the heel
of the cephalad mobilizing hand over the lateral aspect
of the head of the humerus. Force is applied through
both hands. The caudal hand rotates the humerus exter- Figure 14-14 External rotation, abduction, inferior
nally and provides long-axis distraction while the cepha- glide of the humerus.
lad hand pushes the head of the humerus in a posterior
direction.

Figure 14-14: External Rotation/Abduction/
Inferior Glide of the Humerus
Patient Position. Supine, with the involved
extremity supported by the table. The arm is abducted
in the plane of the scapula.
Therapist Position. Facing laterally with the
caudal hand holding the distal humerus and the heel of
the cephalad hand over the head of the humerus. The
caudal hand abducts the arm and externally rotates the
humerus while maintaining the POS. The cephalad
hand simultaneously pushes the head of the humerus
into external rotation and slight inferior glide. The force
can be oscillated, thrusted, or a prolonged stretch.
Sternoclavicular and
Acromioclavicular Techniques
Figure 14-15: Superior Glide of the
Sternoclavicular Joint
Patient Position. Supine, with the involved
extremity close to the edge of the table.
CHAPTER 14 MANUAL THERAPY TECHNIQUES 423

Figure 14-15 Superior glide of

the sternoclavicular joint.

Figure 14-16 Inferior-pos-

terior glide of the sternoclavicular
joint.

Therapist Position. Facing cranially. The volar
surface left thumb pad is placed over the inferior surface
of the most medial aspect of the clavicle. The right
thumb reinforces the dorsal aspect of the left thumb.
Both thumbs mobilize the clavicle superiorly. Graded
oscillations are most successful with this technique.
Figure 14-16: Inferior-Posterior Glide of the
Sternoclavicular Joint
Patient Position. Supine, with the patient’s head
supported on a pillow. The patient’s cervical spine side
bent toward and rotated away from involved side 20°
to 30°.
424 SECTION IV TREATMENT APPROACHES
Therapist Position. At the head of the patient,
using thumb pad or pisiform contact on the most medial
portion of the clavicle. Mobilization is performed in an
inferior/posterior/lateral direction parallel to the joint
line. Elevating the involved shoulder to a position of
restriction and then performing mobilization the sterno-
clavicular joint may assist the rotational component of
clavicle motion joint.
Figure 14-17: Anterior Glide of the
Acromioclavicular Joint
Patient Position. Supine, at a diagonal to allow the
involved acromioclavicular joint to be over the edge of
the table.
Therapist Position. Mobilizing force is performed
with both thumbs (dorsal surfaces together). The ther-
apist places the distal tips of the thumbs posteriorly to
the most lateral edge of the clavicle. Both thumbs push
the clavicle anteriorly. Graded oscillations are mainly
used with this technique.
Figure 14-18: Gapping of the
Acromioclavicular Joint
Patient Position. Sitting close to the edge of the
table.
Therapist Position. Facing laterally with the heel
of the left hand over the spine of the scapula and the
Figure 14-17 Anterior glide of the acromioclavicu-
lar joint.
thenar eminence to the right hand over the distal clav-
icle. The force is applied simultaneously. Both hands
push the bones in opposite directions, obtaining a
general stretch to the capsular structures of the acromio-
clavicular joint. Oscillations or a prolonged stretch are
used with this technique.
Soft Tissue Mobilization and
Scapulothoracic Release
Techniques
Soft tissue mobilization for purposes of this chapter will
be as defined by Johnson: “STM is the treatment of soft
tissue with consideration of layers and depth by initially
evaluating and treating superficially, proceeding to bony
prominence, muscle, tendon, ligament, etc.”9 The goals
of STM in the patient are similar to those of joint
mobilization: development of functional scar tissue,
elongation of collagen tissue, increase in GAGs, and
facilitation of lymphatic drainage.48
In overuse syndromes, trauma, postsurgical condi-
tions, and abnormal movement patterns of the shoulder,
areas of tenderness and restricted extensibility of con-
nective tissue may develop. Adhesions within the fascia
may reduce the muscle’s ability to broaden during con-
traction and lengthen during passive elongation.48
Abnormal compensations may occur, possibly leading to
breakdown of compensating tissue.
Within the shoulder complex several areas are impor-
tant to evaluate for fascial restrictions. Scapulothoracic
Figure 14-18 Gapping of the acromioclavicular
joint.
CHAPTER 14 MANUAL THERAPY TECHNIQUES 425

releasing techniques will also be described because of the stabilizes the lateral border of the scapula. Both move-
musculotendinous and fascial characteristics of this ments occur simultaneously in a slight arcing fashion.
articulation. The following is a description by muscle(s)
or space between structures to evaluate and mobilize.
Box 14-1 defines the types of techniques referred to in Figure 14-21: Side Lying Subscapularis,
the figure legends. Teres Major Stretch
Patient Position. Side lying facing the therapist
Figure 14-19: Subscapularis
with hips flexed to about 45° to stabilize the patient.
Patient Position. Supine, with the shoulder
abducted to tolerance. Therapist Position. Facing the patient, the thera-
pist’s caudal hand and upper extremity (UE) skin lock
Therapist Position. Facing axilla with mobilizing
fingers on muscle belly of subscapularis. Parallel mobi-
lization or perpendicular strumming or direct oscillation
may be used. Assistive techniques are sustaining pres-
sure while elevating and adducting the shoulder as
shown in Figure 14-19, B.

Figure 14-20: Subscapularis Arc Stretch

A
Patient Position. Supine.
Therapist Position. Cephalad hand simultane-
ously elevates, externally rotates, and distracts the
involved shoulder, while the caudal hand (thenar side)

BOX 14-1

Treatment Hand Techniques

Sustained pressure: Pressure applied directly to

restricted tissue at the desired depth and direction
of maximal restriction
Direct oscillations: Repeated oscillations on and off a
restriction with uptake of slack as restriction
resolves B
Perpendicular mobilization: Direct oscillations and/or
sustained pressure techniques performed
perpendicular to muscle fiber or soft tissue play
Parallel mobilization: Pressure applied longitudinally
to restrictions along the edge of the muscle belly
or along bony contours
Perpendicular (transverse) strumming: Repeated
rhythmical deformations of a muscle belly to
improve muscle play and reduce tone

Modified from Johnson GS: Soft tissue mobilization. In Donatelli

R, Wooden MJ, editors: Orthopaedic physical therapy, New York, Figure 14-19 A, Subscapularis. B, Subscapularis arc
1994, Churchill Livingstone. stretch.
426 SECTION IV TREATMENT APPROACHES

on the inferior border of the scapula. The cephalad hand

and UE wrap around the patient’s humerus and the
therapist’s elbow and proximal arm control the amount
of external rotation. The forces from the therapist UEs
are in opposite directions or one hand can stabilize and
one can be the primary mobilizer. This technique can
also be used with contract-relax stretching to increase
contractile component extensibility.

Figure 14-22: Pectoralis Minor

Patient Position. Supine or side lying, with arm
slightly abducted and flexed.

Therapist Position. Mobilizing fingers glide along

in a superficial vector along ribs 3 to 5 lateral to medial
underneath pectoralis major. Often pectoralis minor is
bound down and tender in shoulder dysfunction. STM
techniques used: direct oscillation, sustained pressure,
perpendicular and parallel deformations. Assistive tech-
niques are inhalation and contract-relax with shoulder
protraction.

Figure 14-23: Serratus Anterior—Upper

Portion
Patient Position. Side lying, with involved side up.

Figure 14-20 Subscapularis arc stretch. Therapist Position. Standing posterior to patient’s
shoulder. Caudal hand elevates the scapula in a cepha-
lad and anterior direction off the rib cage. The therapist
can use the fingers of the top hand to roll over and
palpate the superior fibers of the serratus anterior that
attach to the first and second ribs, and the fascial
attachments between levator scapularis and serratus
anterior.38 STM techniques: sustained pressure, direct
oscillation. Assistive techniques: resistive PNF diagonal
contract-relax, deep breath.

Figure 14-24: Serratus Anterior—Lower

Portion
Patient Position. Side lying.
Therapist Position. Place mobilizing fingers along
an interspace of ribs 2 to 8 on interdigitations of serra-
tus anterior. STM techniques used: parallel techniques
Figure 14-21 Sidelying subscapularis, teres major along rib contours medial to lateral or lateral to medial.
stretch.
Assistive techniques: deep breath, contract-relax with
scapular depression, rotation of the thoracic spine to the
CHAPTER 14 MANUAL THERAPY TECHNIQUES 427

Figure 14-22 Pectoralis minor.

Figure 14-23 Serratus anterior—upper portion.

same side. Restrictions may be evident with previous
history of rib fracture or abdominal surgery.
Figure 14-25: Inferior Clavicle
Patient Position. Supine with involved extremity
supported by a pillow.
Therapist Position. Same side as involved shoul-
der. Palpating medial to lateral or vice versa along infe-
rior clavicle, look for fascial restrictions and tenderness
especially at the costoclavicular ligament, the subclavius
muscle, and the conoid and trapezoid ligaments. This
region is important to evaluate and treat in shoulder
428 SECTION IV TREATMENT APPROACHES

Figure 14-24 Serratus anterior—lower portion.

Figure 14-25 Inferior clavicle.

CHAPTER 14 MANUAL THERAPY TECHNIQUES 429

A B

Figure 14-26 A and B, Scapular distraction.

patients who have protracted and externally rotated

scapulae with adaptive shortening of anterior chest
musculature.

Figure 14-26: Scapular Distraction

Patient Position. Side lying close to the edge of
the table, with the involved extremity accessible to the
therapist. A pillow may be placed against the patient’s
chest to provide anterior support.

Therapist Position. In Figure 14-26, A, the book-

binder illustrates the tilting aspect of the scapula before
attempting to lift the scapula off the thoracic wall.
Figure 14-26, B shows the tilting of the scapula. Facing
the patient with the caudal hand underneath the infe-
rior angle of the scapula and the cephalad hand grasp-
ing the vertebral border of the scapula. The therapist’s
anterior sternum is the third contact point assisting the
scapular tilt. Both hands tilt the scapula away from the
thoracic wall along with the distraction of the scapula
by the therapist leaning backward.
Figure 14-27: Scapular Distraction,
Posterior Approach
Patient Position. Side lying as previous, but closer
to the posterior edge of the table.
Therapist Position. Posterior to the patient with
the therapist’s hips in perpendicular orientation to the
patient’s trunk. Therapist’s adjacent leg on the treatment
Figure 14-27 Scapular distraction, posterior
approach.
table with knee bent and placed along midthoracic
spine. Outer mobilizing hand grasps the vertebral border
of the scapula. Inner hand supports the anterior gleno-
humeral joint. Once hand placement is achieved, the
therapist leans back, distracting the scapula away from
the thoracic wall. Sustained stretch most effective with
this technique.
Figure 14-28: Scapular External Rotation
Patient Position. Side lying, with the involved
extremity accessible to the therapist.
430 SECTION IV TREATMENT APPROACHES

Figure 14-28 Scapular external rotation.

Figure 14-29 Scapular external rotation with soft tissue stretch.

Therapist Position. Facing the patient with the
caudal hand under the extremity through the axillary
area. The cephalad hand grasps the superior aspect of
the scapula while the caudal hand grasps the inferior
angle. The force is applied simultaneously, producing an
external rotation of the scapula. Figure 14-29 demon-
strates external rotation of the scapula with soft tissue
technique using the therapist’s elbow to mobilize upper
trapezius and levator scapulae. Assistive techniques
include patient actively rotating cervical spine toward
and away from involved side, and spray and stretch to
upper trapezius trigger points.
CHAPTER 14 MANUAL THERAPY TECHNIQUES
Figure 14-30
Figure 14-30: Scapular Distraction, Prone
Patient Position. Prone, with the involved extrem-
ity supported by the table.
Therapist Position. Facing cephalad, outer hand
under the head of the humerus and the adjacent mobi-
lizing hand web space under the inferior angle of the
scapula. The forces are applied simultaneously. The outer
hand lifts the glenohumeral joint while the adjacent
hand lifts the inferior angle of the scapula.
Summary
Rehabilitation of shoulder injuries using manual tech-
niques is based on an understanding of stages of soft
tissue healing; normal and abnormal arthrokinematics
and osteokinematics of the shoulder complex; effects of
biomechanical stress on various tissue; and muscle func-
tion. The application of manual techniques for the
shoulder is dependent on a thorough sequential exami-
nation and continuous reevaluation. Indications and
contraindications for mobilization are based on an
understanding of the histology of immobilized and trau-
matized tissue. Clinical management of shoulder
injuries has been discussed from a perspective of pro-
tective versus nonprotective injuries, and phased pro-
grams of rehabilitation have been presented. Recent
431
Scapular distraction, prone.
clinical research is beginning to demonstrate the posi-
tive effects of manual therapy in patients with shoulder
dysfunction, but further studies must be advanced, and
traditional concepts and techniques should comply with
current and future discoveries.
ACKNOWLEDGMENTS
We would like to thank Aimee Reiss, MPT, and David
Ciganek, ATC, for their assistance with the manual
technique pictures.
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Muscle Length Testing and
Electromyographic Data
for Manual Strength
Testing and Exercises
for the Shoulder
T he shoulder girdle is composed of complex con-
nections relying not only on static stability from
ligamentous structures, but also on the dynamic
stability provided by a highly organized series of muscle
actions. Normal shoulder function depends on coordi-
nated muscular action in the presence of a normal joint.
The examination of the patient with a shoulder
problem typically involves some component of manual
muscle testing and muscle length assessment. The
intervention plan may incorporate a strengthening
component and other measures such as stretching,
neuromuscular-control exercises, or the use of physical
agents. The primary focus of this chapter will be to
present an overview of shoulder muscle length assess-
ment, manual muscle testing, and strengthening exer-
cises that may be used for rehabilitation of the shoulder.
Muscle Length
Because of their ability to change length, skeletal
muscles can create movement. Each skeletal muscle has
an ideal resting length, which correlates with its ability
435
15
Richard A. Ekstrom
Roy W. Osborn
to generate force during contraction.1 The optimal
muscle length of the agonist and antagonist permits a
full range of joint motion to occur. Several factors can
create a change in this ideal length and result in
decreased muscle excursion. Trauma to the muscle or to
the connective tissue can lead to extensive formation of
scar tissue or myositis ossificans. Changes in the length
of a bone because of trauma, injury to a motor nerve,
operative procedures, and prolonged immobilization can
lead to muscle length changes. In addition, it has been
shown that muscle length can change as a result of pos-
tural habits, including prolonged positioning of a muscle
in either a shortened or a lengthened position.2-4
Stretching exercises can also lead to muscle lengthening
over a certain period by the addition of sarcomeres.4,5
Muscle shortening or a lengthening can affect the func-
tion of either the agonist or the antagonist, or both, and
consequently the movement or stabilization available at
the joint(s) that these muscles act upon. Therefore as cli-
nicians attempting to develop appropriate intervention
programs for patients with shoulder problems, recogni-
tion of muscle length imbalances may be important.
436 SECTION IV TREATMENT APPROACHES
The scapular-resting position has received atten-
tion.3,4,6-8 The scapular-resting position in 19- to 21-
year-old females without a history of shoulder pathology
was recently studied by Sobush and associates.9 They
found that the medial scapular border is on the average
8.8 cm (31/2 inches) from the spine and essentially paral-
lel to the spinous processes. Kendall and colleagues6 indi-
cate the distance between the scapulae should be 3 to 4
inches, whereas Sahrmann4 suggests the distance from
the spinous processes to the scapula should be 3 inches.
Assessment of the scapular-resting position and
movement patterns requires close scrutiny of the
axioscapular, axiohumeral, and scapulohumeral muscu-
lature because of their direct and indirect influence on
the scapular position. The axioscapular muscles are the
trapezius, levator scapulae, rhomboid major and minor,
pectoralis minor, and serratus anterior muscles that can
have a direct effect on the scapular position on the tho-
racic wall. The axiohumeral muscles are the pectoralis
major and latissimus dorsi muscles and they have an
indirect influence on scapular position and a direct effect
on humeral position within the glenohumeral joint.
Structural conditions such as scoliosis and kyphosis
must also be accounted for because of their effect on the
scapular position on the chest wall.
Length Assessment of
Individual Muscles
Axioscapular Muscles
The axioscapular muscles have their origin on the axial
skeleton (skull, vertebrae, pelvis, sternum, and ribs) with
their insertion on the scapula. These muscles are respon-
sible for positioning and stabilizing the scapula to permit
upper limb movements such as reaching, grasping, and
lifting. Sahrmann4 believes that most patients with
shoulder pain develop their condition as a result of move-
ment impairments of the scapula, which disrupts the
relationship between the humeral head and the glenoid
fossa. Changing postures of the scapula may cause
lengthening and shortening of axioscapular muscles. The
assessment of postural changes of the scapula and the
implications of muscle shortening and lengthening are
described by Sahrmann. In addition, there is also a review
of the function of the axioscapular muscles.
Trapezius. Concentric contraction of the upper
trapezius muscle with the spine fixed creates elevation of
the scapula through its attachment to the clavicle. If the
scapula is fixed or the ipsilateral upper extremity load is
heavy, the trapezius muscle can create ipsilateral rotation
of the cervical vertebrae through its attachment to the
ligamentum nuchae. The middle fibers of the trapezius
muscle adduct the scapula with concentric contraction
or assist the rhomboid muscles with control of scapular
abduction when contracting eccentrically. The lower
fibers of the trapezius muscle depress the scapula with
concentric contraction. When combined with concentric
contraction of the upper trapezius and serratus anterior
muscles, a force couple is produced, causing scapular
upward rotation.10
If an individual performs repetitive, unilateral carry-
ing of heavy loads or other habitual activities with the
upper trapezius muscle in a lengthened position, the
muscle can stretch, causing scapular downward rotation
at rest.4 The patient’s appearance is that of a long,
sloping shoulder (Figure 15-1). This position of down-
ward rotation of the scapula may contribute to shoulder
dysfunction in part because of a change in the length-
tension curve for the trapezius and serratus anterior
muscles, and may change the resting position of the
glenohumeral joint. Because of the downward rotation
position of the scapula, the scapula must upwardly rotate
an increased amount to achieve shoulder elevation.
Levator Scapulae. Concentric contraction of the
levator scapulae muscle with the spine fixed will cause
elevation, adduction, and downward rotation of the
scapula.4 According to Sahrmann,4 this muscle is a syn-
ergist with the upper trapezius for scapular elevation and
adduction, but an antagonist for scapular rotation.
Shortness of this muscle may elevate the medial portion
of the scapula, but not the acromial end, producing
downward rotation of the scapula. Differentiating
between shortness of the levator scapulae and rhomboid
muscles (scapula adducted and downwardly rotated)
versus upper trapezius muscle lengthening (scapula
abducted and downwardly rotated) is extremely impor-
tant in designing a corrective therapeutic intervention
program.4
Rhomboid Major and Minor. The rhomboid
muscles work with the trapezius muscle during concen-
tric contraction to retract the scapula, and with the
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA
Figure 15-1 Subject in relaxed stance demonstrating
an abducted scapula with a lengthened upper trapezius muscle.
levator scapulae and pectoralis minor muscles to create
downward scapular rotation. Shortening or tightness of
the rhomboid muscles could position the scapula closer
to the spinous processes (Figure 15-2) and may result in
downward rotation of the scapula. Figure 15-3 demon-
strates restricted scapular upward rotation in this
individual as a result of rhomboid muscle shortness.
Normally, the inferior angle of the scapula should reach
the mid-axillary line during full shoulder flexion.4
Serratus Anterior. Concentric contraction of the
serratus anterior muscle causes scapular abduction/pro-
traction and upward rotation of the scapula. When the
scapula is habitually abducted, this muscle may undergo
shortening together with the pectoralis minor muscle
(see Figure 15-1). Conversely, when the rhomboid and
levator scapulae muscles are short, the serratus anterior
437
Figure 15-2 Subject in relaxed stance demonstrating
an adducted scapular position.
muscle is placed in an elongated position together with
the pectoralis minor muscle. If elongated, a change in
the length-tension curve may result in weakness of this
muscle because it contracts during scapular upward rota-
tion during shoulder elevation.
Pectoralis Minor. The pectoralis minor muscle
can assist the serratus anterior muscle in protracting the
scapula during a concentric contraction. In addition, it
creates scapular downward rotation when concentric
contraction is combined with the levator scapulae and
rhomboid muscles.11 Tightness of this muscle can create
a forward “tipping” of the scapula, which may be noted
as a prominence of the inferior angle of the scapula
(Figure 15-4). Shortening of the pectoralis minor
muscle may be combined with shortening of the serra-
tus anterior muscle. Shortening of the pectoralis minor
438 SECTION IV TREATMENT APPROACHES

muscle may impede the upward rotation of the scapula

during elevation of the arm and may limit shoulder-
flexion range of motion. When the patient with a short
pectoralis minor is positioned supine, it is apparent that
the acromion process is elevated off the table to a greater
degree than normal (Figure 15-5). The lateral border of
the spine of the scapula should be no more than 1 inch
off the table.4 Pressure over the anterior shoulder in the
area of the coracoid process will stretch this muscle
(Figure 15-6). The patient with tightness in this muscle
should describe a “pull” in the anterior chest in line with
the muscle fibers when stretched.

Axiohumeral Muscles
The axiohumeral muscles originate on the axial skeleton
with their insertion on the humerus. They have a direct
effect on the glenohumeral joint and an indirect effect
on the scapular position because of their proximal
attachments on the humerus.

Pectoralis Major. This muscle is a powerful medial

rotator and adductor of the arm. Shortness of this
muscle will restrict glenohumeral abduction and exter-
nal rotation, and will place the scapula in an abducted
position. In addition, shortness of this muscle will limit
the extent of shoulder horizontal abduction. To assess
the length of the sternocostal head of this muscle, the
Figure 15-3 Subject with restricted upward rotation
of the scapula.

Figure 15-4 Subject in relaxed

stance demonstrating prominence of the
inferior angle of the scapula because of a
shortening of the pectoralis minor muscle.
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 439

Figure 15-5 Supine resting position that demonstrates shortening of the

pectoralis minor muscle. The right shoulder is elevated off the table.

Figure 15-6 Testing the flexibility of the pectoralis minor muscle.

subject should be lying supine with the arm at maximum
elevation and in lateral rotation, with the hand supinated
(Figure 15-7).4 In this position, the subject’s posterior
arm should be able to make contact with the table
surface. The subject in Figure 15-7 demonstrates short-
ness of the sternocostal fibers of the pectoralis major
muscle because the upper arm is unable to make contact
with the table. This tightness is commonly found in sub-
jects who demonstrate an abducted (protracted) scapula
and a medially rotated humerus (Figure 15-8).
Latissimus Dorsi. This muscle is capable of per-
forming adduction, medial rotation, and extension of the
humerus. To assess the length of this muscle, the subject
440 SECTION IV TREATMENT APPROACHES

Figure 15-7 Assessment of pec-

toralis major (sternocostal portion) muscle
length.

is positioned supine with the hips and knees flexed to

flatten the lumbar spine. The subject then raises the arm
into shoulder flexion, maintaining lateral rotation of the
humerus while the therapist observes restricted-passive
elevation and possible compensatory movement in the
lower spine4 (Figure 15-9). In a subject with shortening
of the latissimus dorsi muscle, shoulder flexion will be
limited and the lumbar spine may elevate off the table
as the latissimus dorsi muscle becomes taut. This muscle
is capable of indirectly influencing the scapular position
because of its attachment to the humerus.

Scapulohumeral Muscles
The scapulohumeral muscles have their origin on the
scapula and insertion on the humerus. They consist of
the supraspinatus, infraspinatus, teres minor, teres major,
and subscapularis muscles. The supraspinatus, infra-
spinatus, teres minor, and subscapularis comprise the
rotator cuff muscles of the shoulder. The rotator cuff
muscles provide the “fine tuning” or “steering” of the
humeral head in the glenoid fossa because the upper
limb is positioned to perform various tasks.

Subscapularis. When contracting concentrically,

the subscapularis muscle is a medial rotator of the
humerus. This muscle also functions as a humeral head
Figure 15-8 Subject in a relaxed stance demonstrating depressor with the other rotator cuff muscles during
an abducted scapula with shoulder medial rotation on the right. overhead activities. To assess the length of the
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 441

Figure 15-9 Assessment of latissimus dorsi muscle length.

Figure 15-10 Assessment of subscapularis muscle length.

subscapularis muscle, the subject is positioned supine
with the elbow held against the trunk while the humerus
is rotated into lateral rotation (Figure 15-10). Perform-
ing this motion bilaterally permits the examiner to
quickly compare the two extremities.
Infraspinatus and Teres Minor. Concentric con-
traction of the infraspinatus and teres minor muscles
produces lateral rotation of the humerus. Co-contrac-
tion of the external rotators and subscapularis muscle
results in humeral head depression during overhead
activities. Shortness of the infraspinatus and teres minor
muscles results in a decrease in medial rotation of the
humerus. Muscle length assessment for these muscles
can be performed with a single motion. The subject is
positioned supine with the humerus abducted 90° and
442 SECTION IV TREATMENT APPROACHES
Figure 15-11 Assessment of infraspinatus and teres minor muscle length.
the elbow positioned at 90° of flexion (Figure 15-11).
The examiner stabilizes the scapula by pushing posteri-
orly on the head of the humerus with one hand while
the other hand rotates the arm into medial rotation.
When the examiner feels the scapula elevate off the table
or feels tissue tension increase during medial rotation,
the end has been reached on the available glenohumeral
joint range of motion. Figure 15-11 shows a subject with
shortness of the infraspinatus and teres minor muscles
using this method. Normal medial rotation is about 70°
when the arm is abducted to 90°.4
Teres Major. Concentric contraction of the teres
major produces medial rotation, adduction, or extension
of the shoulder. To assess the length of the teres major
muscle, the subject is positioned supine so the table can
assist with stabilization of the scapula. The subject per-
forms shoulder flexion, as is also performed with the
latissimus dorsi muscle length test (see Figure 15-9).
The examiner observes the amount of shoulder flexion
achieved and the position of the inferior angle of the
scapula. If the inferior angle of the scapula protrudes
more than 1/2 inch beyond the lateral wall of the trunk
(excessive scapular abduction), a short teres major
muscle is suspected.4 To verify, the examiner has the
subject bring his or her arm down toward the side of
the body and repeat the shoulder flexion motion while
the examiner stabilizes the inferior angle of the scapula
at the lateral chest wall to prevent excessive scapular
abduction. If the subject has less shoulder flexion com-
pared with the previous attempt, the teres major muscle
is further implicated. To further confirm the decreased
length of the teres major muscle, the examiner instructs
the subject to medially rotate the shoulder and maintain
the position of shoulder flexion with the scapula stable.
If the subject is able to gain additional shoulder flexion,
the teres major is short.4 In addition, tightness of the
subscapular will prevent disassociation of the humerus
from the scapula during the final 40° of elevation. The
lack of disassociation of the humerus from the scapula
will cause abduction of the scapula or protrusion of the
inferior angle beyond the lateral wall of the trunk (see
Chapter 2).
General Comments
During the observation component of the examination
for a patient with a shoulder problem, it is helpful to
determine the degree of shoulder-medial or -lateral
rotation in an upright, relaxed, and standing position. To
assess the direction of shoulder rotation, the therapist
stands behind the subject and observes the position of
the olecranon process of the elbow.4 In a subject with
scapular abduction (protraction) coupled with medial
rotation of the shoulder, the elbow will appear more
lateral in position as shown in Figure 15-8. The
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA
therapist should then correct the scapular position and
reassess the position of the olecranon process.4
Although the aforementioned techniques are valu-
able for identifying muscles having a change in length,
the clinician should be aware that joint capsular tissue
can also be shortened concurrently with muscles. The
clinician is advised to assess capsular mobility to ensure
optimal intervention planning that addresses both
muscle and capsular length changes.
Manual Muscle Testing
Manual muscle testing is an integral part of the physi-
cal examination of the shoulder and provides informa-
tion that is useful in the management of shoulder
ailments. Several textbooks have been published on
manual muscle testing techniques.6,12-15 To become pro-
ficient at manual muscle testing, a clinician must prac-
tice and must be meticulous with patient positioning
and stabilization.
Manual muscle testing positions have been generally
based on anatomic knowledge of muscle origins and
insertions, and expected muscle action. Electromyo-
graphic (EMG) analysis can help verify whether a
muscle is contracting maximally during a muscle test. It
has been used in studies to quantify the muscle activity
during manual muscle testing and exercises.16-23 Ideally,
a muscle test would create maximum EMG activity
in the muscle being tested with minimal activity in the
synergistic muscles. However, rarely can one particular
muscle be completely isolated from other muscle activ-
ity. When available, we will report on the published
EMG data pertinent to manual muscle testing.
It has been demonstrated that the intratester and
intertester reliability of manual muscle testing is high for
identifying a grade of strength when rated on a numer-
ical scale.24-26 However, manual muscle testing remains
problematic because there can be a wide range of muscle
strength within muscle grades.27,28 Many times consid-
erable weakness must be present before it can be
detected. In large muscle groups, patients with up to a
50% loss of absolute force when compared with the
normal extremity, as measured by dynamometry, are
often rated as normal using manual muscle testing.27,29,30
Agre and Rodriquez31 found that muscles producing
forces as low as 8% compared with the opposite normal
limb were graded as good (4/5) during a manual
muscle test. Others have found that dynamometer
443
measurements detect increases in strength over time,
with no change in manual muscle test scores.32,33
Because manual muscle testing will not provide precise
objective measurements of strength deficits, we recom-
mend the use of a hand-held dynamometer during
manual muscle testing of the shoulder.
Dynamometry data can provide objective measure-
ments of strength (force) in comparing extremities or as
a measure of progress in strengthening during rehabili-
tation. Most studies have found high levels of intratester
reliability in hand-held dynamometry testing.33-37 An
examiner inexperienced with hand-held dynamometer
use may want to perform muscle testing with and
without the dynamometer. When the dynamometer is
interposed between the examiner and the subject, it may
reduce the sensitivity of the examiner.
Another consideration is that the isometric hold
during manual muscle testing should be held for at least
4 seconds to allow for maximum-tension development.38
A longer hold may reveal weakness not detectable with
a 1- to 2-second hold.
It may be important to test a muscle in both a short-
ened and a lengthened position because the length of
the muscle at the time of the examination can affect the
force produced by the muscle. A muscle held in a chron-
ically lengthened position as the result of postural habits
or other reasons may test weak in a shortened position,
but may be strong in a more lengthened position.4 This
is due to a change in the normal length-tension curve.
Other muscles may be weak at any point in the range of
motion because of disuse atrophy. Whether the muscle
is tested in a shortened or lengthened position, the
clinician is provided with valuable information when
developing a corrective-strengthening program.
Strength Testing of
Specific Muscles
Supraspinatus
Jobe and Moyne39 recommended that the supraspinatus
muscle should be tested with the shoulder medially
rotated and abducted to 90° in the plane of the scapula
(“empty can” or Jobe position). Worrell and associates40
compared the Jobe position with the position recom-
mended by Blackburn and colleagues.41 The Blackburn
test is performed with the subject prone, and the
444 SECTION IV TREATMENT APPROACHES

shoulder abducted 100° and laterally rotated with the is often due to pain production that inhibits muscle
thumb up. They found that significantly more EMG contraction.
activity was produced when the supraspinatus muscle
was tested in the Blackburn position. In a similar study, Infraspinatus and Teres Minor
Malanga and associates23 did not find a significant dif-
Electromyographic studies have demonstrated there is
ference in EMG activity in the supraspinatus muscle
no significant difference in the muscle activity of the
when comparing the two positions.
infraspinatus when shoulder lateral rotation is per-
Later, Kelly and colleagues16 performed an EMG
formed during exercises or muscle tests at 0°, 45°, or 90°
study comparing muscle tests with the shoulder at a 90°
of shoulder abduction.16,20,22 It has been found that
abduction in the plane of the scapula and in various
the infraspinatus muscle activity is best isolated from the
degrees of rotation. They did not find a significant dif-
supraspinatus and posterior deltoid muscles with the
ference in the EMG activity in the supraspinatus
shoulder in 0° of abduction and medially rotated about
muscle. However, they recommended that the test with
45° (Figure 15-13).16 We recommend testing the lateral
lateral rotation (thumb up or “full can” position) be used
rotator muscles in this position and at the end range of
because this is a position in which less subacromial
shoulder lateral rotation with 90° of abduction (Figure
impingement, and therefore less pain, would be expected
15-14). In the second position, the glenohumeral joint
(Figure 15-12). Itoi and associates42 verified there is less
is less stable and requires more activity from posterior
pain produced in the “full can” position compared with
deltoid and other rotator cuff muscles.16
the “empty can” position when testing supraspinatus
tendon tears in patients. Therefore we recommend test-
ing the supraspinatus muscle in the “full can” position Subscapularis
(see Figure 15-12). Greis and associates18 and Kelly and colleagues16 found
One must be aware that one may not be able to deter- that the EMG activity of the subscapularis muscle is
mine specific supraspinatus muscle weakness because maximal and best isolated from the other shoulder inter-
the deltoid muscle is always active with the supraspina- nal rotators with the Gerber lift-off test (Figure 15-
tus muscle. Weakness detected with this muscle test 15).43 This muscle test is performed with the maximal

Figure 15-12 Manual muscle testing of the supraspinatus muscle in the

“full can” position.
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 445

Figure 15-13 Manual muscle testing of the infraspinatus and teres minor
muscles.

Figure 15-14 Manual muscle testing for the infraspinatus and teres minor
muscles with the arm abducted.

internal shoulder rotation, with the hand lifted off the
mid-lumbar area.
We also recommend testing the shoulder internal
rotators with the shoulder at 90° of abduction for
patients unable to assume the Gerger lift-off test
position (Figure 15-16). With this test, there is still a
high level of subscapularis muscle activity coupled with
increased activity in the pectoralis major and latissimus
dorsi muscles compared with the lift-off test.16
Deltoid
Only one muscle test for the deltoid is pictured (Figure
15-17). This muscle test is more specific for the middle
deltoid. Kendall and associates6 described testing for the
446 SECTION IV TREATMENT APPROACHES

Figure 15-15 Manual muscle testing for the subscapularis muscle using
the Gerber lift-off test.

Figure 15-16 Manual muscle testing for the shoulder medial rotator
muscles with the arm in abduction.

anterior and posterior deltoid in the sitting position. The
anterior deltoid is tested with the shoulder in abduction
and slight flexion (POS), with the humerus in slight
lateral rotation. The posterior deltoid is tested with the
shoulder in abduction and slight extension, and the
humerus is in slight medial rotation. With EMG analy-
sis, Brandell and Wilkinson17 found Kendall’s tests for
the anterior and middle deltoid muscles to be quite
selective.
Horizontal abduction of the shoulder with external
rotation also elicits high levels of EMG activity in both
the middle and posterior deltoid muscles.17 Shoulder
hyperextension isolates the posterior deltoid from the
anterior and middle deltoid muscles, but not from the
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 447

Figure 15-17 Muscle test for the deltoid muscle.

Figure 15-18 Muscle test for the sternocostal part of the pectoralis major
muscle.

latissimus dorsi muscle.17 These positions may also be applied. For the clavicular part, the arm is taken toward
considered when testing deltoid strength. the nose and resistance is applied.

Pectoralis Major Latissimus Dorsi, Teres Major, and

Muscle testing of the sternocostal and clavicular parts of Posterior Deltoid
the pectoralis major muscle is pictured in Figures 15-18 The latissimus dorsi, teres major, and posterior deltoid
and 15-19, respectively.6 For the sternocostal part, the muscles can be tested as a unit using a generic shoulder
arm is brought toward the opposite hip and resistance is extension test (Figure 15-20).12
448 SECTION IV TREATMENT APPROACHES

Upper Trapezius
The upper trapezius muscle can be tested with the shoul-
der shrug muscle test (Figure 15-21).6 However, this may
not be a very discriminatory test for the upper trapezius
muscle because there is also a high level of activity in the
levator scapulae muscle during scapular elevation.44
The upper trapezius muscle can also be tested along
with the middle trapezius and lower trapezius muscles
using a horizontal abduction muscle test (Figure 15-22)
or a test with the arm raised above the head in line with
the lower trapezius muscle fibers (Figure 15-23).17 Both
these tests create high levels of EMG activity in all parts
of the trapezius muscle.17

Middle Trapezius
The middle trapezius muscle can be tested with hori-
zontal abduction of the shoulder using lateral rotation
(see Figure 15-22).6 Electromyographic analysis has
demonstrated that this test produces not only maximum
activity in the middle trapezius muscle, but also high
levels of EMG activity in the upper and lower trapezius
muscles.17 Therefore this test allows all parts of the
trapezius muscle to be tested as a unit.

Lower Trapezius
Maximum activation of the lower trapezius muscle is
Figure 15-19 Muscle test for the clavicular part of
achieved through a muscle test with the arm raised over-
the pectoralis major muscle. head in line with the lower trapezius muscle fibers (see

Figure 15-20 Muscle test for the

latissimus dorsi, teres major, and posterior
deltoid muscles.
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 449

Figure 15-23).17 This test also produces high levels of

EMG activity in the upper and middle trapezius
muscles. Therefore it is another test that can be used for
testing all parts of the trapezius muscle.17

Serratus Anterior
We performed an EMG study with 30 subjects and com-
pared the activity in the serratus anterior muscle using a
traditional supine-protraction muscle test with the muscle
test recommended by Kendall and associates6 (Figure 15-
24). There was significantly more EMG activity in the
serratus anterior muscle when the test was performed
with the arm in the plane of the scapula than with the
supine-scapular protraction test. In the shoulder flexion
or plane of the scapula test, the scapula is upwardly
rotated so the examiner tries to de-rotate the scapula from
the upwardly rotated position as flexion is resisted.

Rhomboid Major and Minor

The test we recommend is shown in Figure 15-25.6
There is no EMG evidence to verify whether this is the
optimal test. In this test, the examiner tries to de-rotate
the scapula from a downwardly rotated position.

Muscle Strengthening
In general terms, muscle strength can be defined as the
Figure 15-21 Muscle test for the upper trapezius
ability of the skeletal muscle to develop force to provide
muscle.

Figure 15-22 Muscle test for the middle trapezius muscle.

450 SECTION IV TREATMENT APPROACHES

Figure 15-23 Muscle test for the lower trapezius muscle.

Figure 15-24 Muscle test for the serratus anterior muscle.

stability and mobility for the musculoskeletal system.1 In
more specific terms, muscular strength is the greatest
measurable force that can be exerted by a muscle or
muscle group to overcome resistance during a single,
maximal effort.45,46
Strengthening activities are common components
of comprehensive intervention programs for patients
with shoulder abnormalities.39,47-50 For a muscle to gain
strength, the resistance applied must exceed the meta-
bolic capacity of the muscle.51 The recommended
number of repetitions required to increase strength in an
intervention program is 6 to 12, which is performed in
each of two or three sets of exercise.52-54
Typically, clinicians develop intervention plans for
individuals who require a combination of strength and
endurance to perform activities of daily living (ADL)
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA
Figure 15-25 Muscle test for the rhomboid muscles.
and/or job related functions. Muscular endurance refers
to the ability of a muscle to perform a repetitive activ-
ity (or activities) for a prolonged period against a load
or resistance.55 An example of an endurance activity is
when an assembly line worker repetitively performs an
activity over a long period or is required to hold a static
position for an extended period. In some circumstances,
a worker may perform the same repetitive motions 150
to 200 times or more per day. When designing a reha-
bilitation program for an individual working under these
conditions, endurance activities (high repetition, low
resistance) for the upper limb, and possibly the trunk
musculature, may be a high priority. In this example, as
many as three to five sets of 40 to 50 or more repetitions
might be used employing a low level of resistance.56
In the next section, we describe various strengthen-
ing exercises for the shoulder and discuss the EMG evi-
dence for muscle action that occurs with each exercise.
Shoulder Strengthening Exercises
Military Press. The military press exercise (Figure
15-26) highly activates several shoulder muscles includ-
ing the deltoid, triceps brachii, supraspinatus, trapezius,
and serratus anterior muscles.19,21 Townsend and as-
sociates21 demonstrated high EMG activity in the
supraspinatus muscle during this exercise, with all other
rotator cuff muscles being activated to a lesser degree.
451
Incline Press. The incline press (Figure 15-27) can
be used to permit exercise progression to the full mili-
tary press. As the incline angle increases, the shoulder is
progressively exercised in higher amounts of elevation.
At lower incline angles, the pectoralis major muscle will
work strongly; but as the incline angle increases, the
pectoralis major muscle activity will decrease and the
muscles strengthened by the military press exercise will
be progressively activated.
“Full Can” Exercise. The “full can” exercise is per-
formed in the plane of the scapula with the shoulder
in moderate lateral rotation (thumb up position) (Figure
15-28). It is often used by clinicians for specifically
strengthening the supraspinatus muscle, even though it
highly activates the deltoid muscle as well. Kelly and
associates16 compared the EMG activity during exercise
in the supraspinatus muscle in the plane of the scapula
with the thumb up (“full can” position) and with the
thumb down (“empty can” position) and found no sig-
nificant difference between the two. When comparing
the two exercises, equal activation of the supraspinatus
muscle was also demonstrated when evaluated using
magnetic resonance imaging relaxation time.57 Because
one would expect less subacromial impingement prob-
lems with the shoulder laterally rotated during the exer-
cise, we recommend that the exercise be performed in
452 SECTION IV TREATMENT APPROACHES
Figure 15-26
Figure 15-27
the thumb-up position. Itoi and colleagues42 also found
that patients with supraspinatus tendon tears had
less pain when the exercise was performed in the “full
can” position as compared with the “empty can” position.
The exercise described previously is also excellent for
the serratus anterior muscle when performed at 120° or
above of abduction. We evaluated the EMG activity of
the serratus anterior muscle in 30 subjects during a
Military press exercise.
Incline press exercise.
variety of exercises and found that this exercise produced
maximum activation. This finding agrees with that of
Moseley and associates,19 who demonstrated maximum
activation of the serratus anterior muscle with exercise in
the plane of the scapula from 120° to 150° of elevation.
Shoulder Lateral Rotation Exercises. Shoulder
lateral rotation exercises can be performed in a variety
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 453

Figure 15-28 “Full can” exercise.

Figure 15-29 Shoulder lateral rotation exercise.

of positions including subjects lying on their side prone,
with 0° of shoulder abduction (Figure 15-29) and with
the shoulder abducted to 90° (Figure 15-30) or in
varying degrees of shoulder abduction in a sitting or
standing position (Figure 15-31). Lateral rotation will
activate the posterior deltoid, infraspinatus, teres minor,
and scapular retractor muscles. Basmajian and Bazant58
found that the infraspinatus and teres minor muscles
generally exhibit synchronous firing. So when an exer-
cise is determined to be good for activating the infra-
spinatus muscle, we assume it is also good for
activating the teres minor muscle.
Several researchers have demonstrated that there is
no significant difference in the infraspinatus muscle
454 SECTION IV TREATMENT APPROACHES

Figure 15-30 Shoulder lateral rotation exercise.

Figure 15-31 Shoulder lateral rotation exercise.

activity when lateral rotation is performed at 0° of shoul-
der abduction versus 90° of shoulder abduction.16,20,22
However, as the shoulder is abducted during the exer-
cise, the glenohumeral joint becomes increasingly more
unstable and the deltoid and other rotator cuff muscles
are activated to a greater degree.20 Lateral rotation exer-
cises with shoulder abduction are then considered to be
more advanced exercises for a patient with a shoulder
ailment.
Prone-lateral-rotation exercise performed to the end
range strongly activates the lower trapezius muscle
because the scapula is being maximally depressed (see
Figure 15-30).22 This can be an alternative exercise for
strengthening the lower trapezius muscle.
Shoulder Medial Rotation Exercises. Medial
rotation exercises can be performed in a variety of
positions (Figures 15-32 and 15-33) and will create high
CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 455

Figure 15-32 Shoulder medial rotation exercise.

Figure 15-33 Shoulder medial rotation exercise.

levels of EMG activity in the subscapularis, pectoralis
major, anterior deltoid, latissimus dorsi, and teres
major muscles.20 Kronberg and associates20 found the
greatest amount of EMG activity in the subscapularis,
pectoralis major, and latissimus dorsi muscles when the
shoulder was medially rotated at 0° of abduction.
However, as the shoulder was abducted to 90°, the sub-
scapularis muscle activity remained quite high and a
decrease in activity was seen in the pectoralis major and
latissimus dorsi muscles. The abducted position may
then isolate the exercise more to the subscapularis
muscle.
456 SECTION IV TREATMENT APPROACHES

Because the Gerber lift-off test43 has been shown to

isolate subscapularis weakness,18 we think that an
end-range-active or light-resistive exercise performed in
this position may be an exercise to consider during reha-
bilitation of the rotator cuff (Figure 15-34).

Prone Shoulder Horizontal Abduction Exercise.

Shoulder horizontal abduction exercises are often per-
formed for strengthening the scapular adductor muscles
(Figure 15-35). In a study of 30 subjects in which we
evaluated the EMG activity of the trapezius, we found
that when shoulder horizontal abduction was performed
with lateral rotation there was more trapezius activity
found than with medial rotation. All parts of the trapez-
ius muscle demonstrated high levels of EMG activity, so
this exercise may be good for strengthening the trapez-
ius as a whole. Moseley and associates19 also found high
levels of EMG activity in the trapezius with horizontal
abduction exercises.
When shoulder horizontal abduction is performed in
the medially rotated position, the scapula assumes a
more elevated position. As the trapezius muscle activity
decreases, one can speculate that there is increased activ-
ity in the rhomboid and levator scapulae muscles.
Shoulder horizontal abduction may also be an excel-
lent exercise for strengthening the infraspinatus, teres
minor, and posterior and middle deltoid muscles.21
High levels of EMG activity have been found in the Figure 15-34 Shoulder medial rotation exercise.

Figure 15-35 Shoulder horizontal abduction exercise.

CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 457

Figure 15-36 Prone arm-lift exercise.

above-mentioned muscles with moderate EMG activity

in the supraspinatus and subscapularis muscles, which
work as joint stabilizers during the exercise.21,59

Prone Arm-Lift Exercise. The prone arm-lift

exercise performed at about 135° of abduction, or in line
with the lower trapezius muscle fibers (Figure 15-36),
will activate the same muscles as the shoulder horizon-
tal abduction exercise. In our EMG study of the trapez-
ius, we found that all parts of the trapezius were highly
activated through this exercise.
In addition to the trapezius muscle, the supraspina-
tus also works very strongly. The Blackburn prone posi-
tion for muscle testing the supraspinatus is at about
100° of abduction and has been shown to activate the
supraspinatus to levels that are not significantly differ-
ent when compared with a muscle test at 90° of abduc-
tion in the plane of the scapula.41

Shoulder Shrug. In our EMG study of exercises

for the trapezius muscle, we found that the upper trapez-
ius muscle was maximally activated with the shoulder
shrug exercise (Figure 15-37). Hintermeister and asso-
ciates60 also found that this exercise activated the upper
trapezius very well. However, it also has been shown that
this exercise highly activates the levator scapulae
muscle.19,44 If a clinician wants to work on streng-
thening the upper trapezius muscle in a patient with a Figure 15-37 Shoulder shrug exercise.
458 SECTION IV TREATMENT APPROACHES

downwardly rotated scapula without creating a high

level of activity in the levator scapulae, it may be desir-
able to use an exercise that causes upward rotation of the
scapula. The military press (see Figure 15-26) or wall
slide exercise with the arms overhead (Figure 15-38) as
described by Sahrmann4 would be appropriate for
strengthening the upper trapezius muscle. During the
wall slide exercise, the subject strongly elevates the scapu-
lae as the hands slide up the wall. Dumbbell weights can
be held in the hands to increase the resistance.
When the shoulder shrug meets resistance using
hand-held weights, all the muscles of the rotator cuff are
activated to help prevent inferior subluxation of the
glenohumeral joint.60 The shrug exercise could be con-
sidered a low-level exercise for the rotator cuff.

Rowing Exercise. Rowing is usually performed to

improve the strength of the scapular retractor and shoul-
der extensor muscles. Rowing can either be performed
using a pulley system (Figure 15-39) or can be per-
formed unilaterally in the prone position with the upper
extremity hanging over the side of the table. When
performed with the shoulder in minimal abduction,
the scapula will downwardly rotate as the shoulder is
extended. So one would expect that the rhomboids
would work more in this position as compared with the
trapezius. No datum is available that compares the
EMG activity of the rhomboids during rowing with Figure 15-38 Wall slide with shoulder shrug exercise.

Figure 15-39 Rowing exercise.

CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA
varying degrees of shoulder abduction. In our study of
30 subjects, we found that the trapezius exhibited only
moderate EMG activity with rowing when the shoulder
was minimally abducted. Hintermeister and colleagues60
recommend that the shoulders should be abducted to
90° to increase scapular upward rotation during the
rowing exercise to maximally activate the trapezius.
Therefore it may be possible to selectively strengthen the
rhomboids or the trapezius muscles depending upon the
amount of scapular rotation during the exercise.
Pull-Down Exercise. The pull-down exercise is
performed with either shoulder adduction, extension, or
a combination of both depending upon the position of
the arm during the exercise (Figure 15-40). This exer-
cise is usually performed to strengthen the latissimus
dorsi, pectoralis major, and teres major and the down-
ward rotator muscles of the scapula. McCann and asso-
ciates61 found high levels of EMG activity in the
latissimus dorsi with shoulder extension exercises. If per-
formed with more adduction, the sternocostal part of the
pectoralis major muscle will be activated to a greater
degree.
Press-Up Exercise. Townsend and colleagues21
demonstrated near maximum EMG activity in the
Figure 15-40
459
pectoralis major and minor with the press-up exercise
(Figure 15-41) and a high level of activity in the latis-
simus dorsi muscle. This exercise will also activate all
scapula-stabilizing muscles.
Push-Up Plus Exercise. The push-up plus exer-
cise is performed with full scapular protraction at the
end range of a push-up primarily to exercise the serra-
tus anterior muscle (Figures 15-42 and 15-43). It is not
necessary to perform the full push-up during every rep-
etition, but rather one can perform the scapular pro-
traction repeatedly. We performed an EMG study with
30 subjects and found that this exercise produced near
maximum activity in the serratus anterior muscle. Lear
and Gross62 also demonstrated high levels of activity in
the serratus anterior with this exercise, and even higher
levels of EMG activity if the exercise was performed
with the feet elevated on a stool or chair. We believe
this is an excellent exercise for the serratus anterior
muscle because when evaluating the movement that
occurs, it becomes apparent that the trunk moves on
a fixed scapula, with the thoracic kyphosis increasing
as the ribs move posteriorly. This movement of the
trunk increases the amount of scapular upward rotation,
which helps facilitate serratus anterior muscle activity.
When placing the feet up on a stool or chair, the amount
Pull-down exercise.
460 SECTION IV TREATMENT APPROACHES

of upward rotation of the scapula is increased even

more.

Diagonal Shoulder Exercise With Extension-

Adduction-Medial Rotation. This exercise (Figure
15-44) is excellent for activating the sternocostal part of
the pectoralis major muscle while moderate activity
occurs in the anterior deltoid muscle.63 There is also low-
level EMG activity in the teres major and latissimus
dorsi muscles.63

Diagonal Shoulder Exercise With Flexion-

Adduction-Lateral Rotation. This diagonal pattern
(Figure 15-45) highly activates the anterior and middle
parts of the deltoid and the pectoralis major (clavicular
head) muscles.63 We performed an EMG analysis of the
serratus anterior muscle in 30 subjects and found near
maximum activation when performing this exercise at a
maximum intensity of five repetitions. This exercise
requires maximal protraction with upward rotation of
the scapula. When the scapula is fully protracted, the
trapezius activity tends to decrease during shoulder ele-
vation, transferring the load for upward rotation to the
serratus anterior muscle.

Figure 15-41 Press-up exercise.

Figure 15-42 Push-up exercise without scapular protraction.

CHAPTER 15 MUSCLE LENGTH TESTING AND ELECTROMYOGRAPHIC DATA 461

Figure 15-43 Push-up exercise with scapular protraction.

Figure 15-44 Diagonal shoulder exercise with extension-adduction-

medial rotation.
462 SECTION IV TREATMENT APPROACHES
Figure 15-45 Diagonal shoulder exercise with
flexion-adduction-lateral rotation.
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Myofascial Treatment
T he shoulder is surrounded by an expansive
network of myofascial tissues. This network
extends all the way from the occiput to the base
of the spine.1 These tissues bear the burden of support-
ing the most mobile joint in the body. This excessive
mobility, combined with the sheer volume of tissue,
makes this area very susceptible to dysfunction. The
complexity of the shoulder joint often makes it a diffi-
cult joint for a physical therapist to evaluate and treat.
The biomechanical complexity of the shoulder is a func-
tion of an interrelationship between bony structures and
myofascia. Evaluation and treatment of the shoulder
must therefore address both of these components.
Two highly interrelated approaches to treating the
shoulder are joint manipulation and myofascial manip-
ulation (Figure 16-1). All of the myofascial tissues
including capsule, ligament, and surrounding fascia
are categorized as soft tissue. The question is, when is
one performing joint mobilization and when is one
performing myofascial manipulation? What is the
difference between the two? Both joint mobilization and
myofascial manipulation have their effect on connective
tissue.
Joint manipulation has been defined as “the skilled
passive movement of a joint.”2 This movement is gained
primarily by following the rules of arthrokinematics.
This makes joint mobilization easier to understand and
use. Myofascial mobilization, on the other hand, is
not as clear-cut. Many myofascial lesions do not follow
any arthrokinematic rules. The basis for myofascial
mobilization is more intuitive, relying on palpation
rather than arthrokinematics.
By definition, myofascial manipulation is defined
as “the forceful, passive movement of musculofascial
465
16
Deborah Seidel Cobb
Robert Cantu
elements through its restrictive directions, beginning
with its most superficial layer and progressing into
depth, while taking into account its relationship to the
joints concerned.”1 This definition contains several key
elements:
1. Myofascial manipulation as defined for this chapter
is direct technique. (Find the lesion and treat it in
the direction of the restriction.)
2. Awareness of the three-dimensionality of myofascia
is key to its successful implementation.
3. A strong interrelationship exists between joint
mobilization and myofascial manipulation.
While the primary focus of this chapter is the treatment
of the myofascial tissues significant to the shoulder joint,
other things need to be considered. Treatment of a
patient is not unlike a puzzle. Myofascial manipulation
is only one piece of that puzzle. Other essential pieces
include joint mobilization and exercise. An optimal
treatment outcome cannot be achieved if pieces of the
puzzle are missing (see Figure 16-1). A good clinician
is one who knows how to fit the pieces of the puzzle
together.
Histology of
Connective Tissue
Connective tissue makes up 16% of a person’s body and
stores 23% of the body’s total water content.3 Skin,
muscle, tendon, ligaments, joint capsule, periosteum,
aponeuroses, and blood vessel walls all contain connec-
tive tissue. Bone, cartilage, and adipose tissue can also
histologically be considered connective tissue, but are
not relevant to our discussion of myofascia.1-4 Connec-
tive tissue is composed of cells, ground substance, and
466 SECTION IV TREATMENT APPROACHES
OPTIMAL TREATMENT
Exercise
Joint Myofascial
mobilization manipulation
Figure 16-1 Interrelationship of joint mobilization,
myofascial manipulation, and exercise leading to optimal
patient treatment.
three fiber types: collagen, elastin, and retinaculin (Box
16-1).1,6 As therapists, we are concerned with the
ordinary connective tissue that comprises the superficial
and deep fascia, and the nerve and muscle sheaths,
ligaments, and tendons.
Classification of Connective Tissue
Connective tissue can be divided into three types based
on fiber density and arrangement: dense regular, dense
irregular, and loose regular. Tendons and ligaments are
composed primarily of dense regular connective tissue,
which is characterized by a high proportion of collagen
fibers to ground substance, and a parallel arrangement of
fibers. These characteristics allow for high tensile strength
with low extensibility. Dense regular connective tissue has
poor vascularity because of its compactness. Healing time
is therefore substantially increased after any trauma.
Dense irregular connective tissue is found in joint
capsule, periosteum, dermis of skin, fascial sheaths, and
aponeuroses. A dense multidirectional fiber arrangement
is characteristic of this type of connective tissue. Because
of the structure, it is able to limit forces in a three-
dimensional manner. As compared with dense regular
connective tissue, it possesses a higher proportion of
ground substance as well as increased vascularity.
Loose regular connective tissue is found in the super-
ficial and deep fascia; nerve and muscle sheath; endomy-
sium; and the supportive structure of the lymph system.
This tissue is the most easily mobilized with myofascial
techniques.1,3,4,7
BOX 16-1
Components of Connective Tissue
Collagen: Most tensile of connective tissue fibers
Type I collagen: Ordinary connective tissue (loose
and dense)
Type II collagen: Hyaline cartilage
Type III collagen: Lining of arteries and fetal
dermis
Type IV collagen: Basement membranes
Elastin: More elastic than collagen. Lining of
arteries and ligamentum flavum
Reticulin: Most elastic fiber. Framework of lymph
nodes and glands
Ground substance: Viscous medium in which cells
and connective tissue lie
Mechanical barrier against foreign matter
Medium for nutrient and waste diffusion
Maintains spacing between adjacent collagen
fibers (interfiber distance) to prevent cross-links
Effects of Immobilization
and Mobilization on
Connective Tissue
With an understanding of the normal biomechanics and
histology of the myofascial tissue, it is now important to
see how these tissues are affected by immobilization,
trauma, and remobilization. This is essential to setting
realistic goals in the clinic. It is important to remember
that most of the available information on the effects
of immobilization of connective tissue has come from
research done on animals, most of which were normal
and nontraumatized. This is fundamentally different
from patients typically seen in an orthopedic clinic.2
Videman and associates found that a nontraumatized
joint subjected to immobilization will exhibit changes
within 4 to 10 days. This immobilization begins to limit
mobility.8 Amiel and associates performed extensive
animal studies on the immobilization of connective
tissue during the 1960s and 1970s.10-15 Their studies typ-
ically involved immobilizing a normal animal knee then
analyzing the histologic effects on connective tissue. The
authors found fibrofatty infiltrates, primarily in the areas
of capsular folds. With longer periods of immobiliza-
tion, greater amounts of infiltrate developed and adhe-
sions began to form in the connective tissue.
CHAPTER 16 MYOFASCIAL TREATMENT
Under histologic examination, no significant loss of
collagen was found, only loss of ground substance (gly-
cosaminoglycans and water). With the loss of ground
substance came a decreased fiber distance, leading to
cross-link development between collagen fibers. Immo-
bilization leads to a lack of stress being applied to the
collagen fibers, causing them to align in a haphazard
fashion.15 This alignment leads to a decreased tissue
extensibility.10-15 When immobilization occurs for less
than 12 weeks, the rates of collagen synthesis and degra-
dation are the same. After 12 weeks of immobilization,
collagen degradation exceeds collagen synthesis, result-
ing in a net collagen loss.16
A study by Scholmeier looked at 10 beagle forelimbs
immobilized during a 12-week period. They found there
was a marked decrease in passive range of motion
(PROM) of the glenohumeral joints. Hyperplasia of the
synovial lining was observed along with proliferation of
the capsular wall. After 12 weeks of remobilization, these
changes were completely reversed.17 Another study by
Langenskold looked at healthy male rabbits that were in
casts for 5 to 6 weeks. They found a significant decrease
occurred in knee flexion. They found 90% of joint mobil-
ity could be recovered by simply returning to normal
activity. This changed, however, when the joints were
immobilized for 7 to 8 weeks. It took up to 12 months in
some animals for full joint mobility to return.18
In a study by Evans and associates, it was found that
if rat knees were experimentally immobilized, then
manipulated under high velocity, partial joint mobility
could be restored. If these joints were allowed to move
prior to manipulation, full mobility could then be
restored. This held true for immobilization of less than
30 days. Longer periods of immobilization result in less
optimal return of mobility.15
A more recent study done by Reynolds and associ-
ates looked at rat knees immobilized for 2 to 6 weeks.
This study found mobility was not markedly limited
until after 6 weeks of immobilization. The authors
attribute this finding to discrete adhesions between
tissue folds, which occur between the 2- and 6-week
period.19
Other Physiologic Responses
to Myofascial Manipulation
Soft tissue mobilization and massage are commonly
used interchangeably. Additional effects of massage on
467
the body have been well documented in the literature.
Three secondary effects are on blood flow, the basal
metabolism, and the autonomic system.
Massage has been shown to increase blood flow
to the extremities. Deep massage strokes increase
total blood flow in both animal and human subjects.
Massage causes capillaries to dilate in the region of
the stroking, resulting in increased blood volume and
flow. Of importance is that milder massage does not
produce the same effect. The type and depth of the
myofascial technique may alter the effect produced on
the body.20-22
The autonomic system has also been shown to be
affected by massage. Ebner reported that connective
tissue massage stimulates circulation in a region of the
body, which in turn opens up increased circulatory path-
ways to other body regions. The mechanical friction
created by massage stimulates the mast cells in connec-
tive tissue to produce histamine. Histamine causes
vasodilation, resulting in increased blood flow around
the body.23,24,27
One study of HIV-positive subjects examined the
effects of massage on the human immunodeficiency
system. After 1 month of massage, a significant increase
was noted in the number of natural killer cells. This indi-
cates an enhancement of the immune system with
massage. Further research is warranted.28
Myofascial Evaluation of
the Shoulder
When evaluating the shoulder, the physical therapist is
looking for a correlation of findings that might be indica-
tive of a dysfunction. History, and the results from
visual, movement, and palpatory exams, should be con-
sidered. It is important to remember that connective
tissue changes, in the absence of other objective find-
ings, are not necessarily dysfunctional. Several consistent
findings are a better indicator of a problem. For example,
consider a patient who has a stiff and painful shoulder.
External rotation and abduction are limited most. Phys-
ical evaluation reveals tightness of the internal rotators
and adductors, especially the pectoralis major, latissimus
dorsi, and teres major. Posturally, this patient assumes
a protracted position. This combination of findings
is indicative of a shoulder dysfunction possibly related
to postural abnormalities. The individual findings of
posture or tightness were not significant until they
468 SECTION IV TREATMENT APPROACHES
correlated with pain and loss of motion. Treatment must
then address all the significant components contributing
to the dysfunction.
History
History gives valuable insight into patient conditions
before a hand ever touches them. For example, myofas-
cial pain of nonmechanical origin is usually dull and
nonspecific. Myofascial pain of mechanical origin is
more specific. If a patient reports specific sharp pain that
is easily reproduced, a more specific pathologic condi-
tion may be present. By knowing the behavior of the
patient’s pain, we can begin to isolate the nature of the
problem. We then move on to try to correlate the history
with objective findings.
Postural Evaluation
Body posture can give us clues as to the area of move-
ment disturbance or where the body may have excessive
stress placed upon it. The importance of posture is in
how it relates to function. For the shoulder, we must
consider the trunk and neck positions in sitting and
standing, and the relationship of the scapulae relative to
the trunk. The evaluator should be looking for areas of
muscle or connective tissue asymmetry, and increased
muscle activity. Because fascial planes can be restricted
over large areas of the body, a head-to-foot evaluation
may be needed. If a leg length discrepancy exists, a
patient may develop muscle asymmetry caused by the
prolonged shortening or lengthening of a muscle or
group of muscles.
Vladamir Janda helped demonstrate the effects of
myofascial imbalances on postural imbalances. He
looked extensively at how muscles respond to dysfunc-
tion. Janda observed that changes in muscle function
play an important role in the pathogenesis of many
painful conditions. Janda defined a postural muscle as one
that responds to dysfunction by tightening and a phasic
muscle as one that responds to dysfunction by weaken-
ing. In the upper extremity, we see a typical pattern of
tightening of the upper trapezius, levator scapulae, and
pectoralis with weakening of the deep neck flexors and
lower scapular stabilizers. All of these contribute to the
typical kyphotic, protracted posture often seen in the
clinic (Table 16-1).25,26
Tight muscles tend to act in an inhibitory way on
their antagonist muscles. It does not seem reasonable
to start a strengthening program for the weakened
TABLE 16-1
POSTURAL VERSUS PHASIC MUSCLES OF THE SHOULDER
GIRDLE AND UPPER THORACIC REGION
POSTURAL PHASIC
Upper trapezius Levator scapulae
Pectoralis minor Pectoralis major (upper portion)
Cervical erector spinae Latissimus dorsi
Lower trapezius Middle traps
Rhomboids Anterior cervical musculature
antagonist as the first step in a rehabilitation program.
After stretching of the tightened muscles, the strength
of the inhibited muscles may return without any further
treatment. In the case of a frozen shoulder patient, it
would make sense to first stretch out the shortened
internal rotators and adductors like the subscapularis
before attempting to strengthen the weakened external
rotators and abductors.28,29
Movement Analysis
Active movement testing may provide further informa-
tion with which to correlate postural findings. It is
important to consider what is happening to the entire
body when looking at active shoulder motion. Quality as
well as quantity should be considered. Do limitations in
range correlate with postural findings? For example, if
on postural evaluation the patient was found to have a
forward head position with pectoralis major and minor
shortening, we may expect to see limited forward eleva-
tion of the shoulder.
Passive range of motion should also be for both
quality and quantity of movement and for end feel. Is
the end feel capsular, or is there limitation by soft tissue?
Proper stabilization is necessary to achieve true range of
motion and proper end feel. (See Chapter 3 for a
detailed evaluation sequence.)
Palpatory Examination
Now that posture and movement have been assessed, the
examiner can begin to palpate for the location of the
dysfunction. As previously mentioned, palpatory find-
ings must also correlate with postural and movement
findings to be of any significance. The palpatory exam
includes the myofascial structures by layer and palpation
CHAPTER 16 MYOFASCIAL TREATMENT
of the joint structures. Palpation of the shoulder must
include the scapular, cervical, thoracic, and anterior
chest wall regions.
Superficial palpation is performed on the skin and
superficial connective tissue. The examiner should be
assessing for temperature, moisture, and light touch to
determine the extensibility of the connective tissue.
Tissue rolling is one way to check the extensibility of
these structures. It involves the lifting away of the super-
ficial connective tissue and skin from the underlying
structures.
Deep palpation involves palpation through the layers
of tissue perpendicular to the tissue as well as moving
the perpendicular tissue. The examiner should be able to
palpate the tendons, muscle bellies, muscle sheath,
myotendinous junctions, joint capsule, tenoperiosteal
junctions, and deep periosteal layers of tissue. To assess
mobility of muscle, a technique called transverse muscle
play may be used. This involves bending of the muscle
to assess its transverse flexibility (see Figures 16-4 and
16-5). Palpatory findings will change with treatment, so
it is important to be constantly reassessing them.
Myofascial trigger points are very common in the
shoulder region. They can be either active or latent.
Active trigger points can refer pain to a site far from the
source. They usually prevent full elongation of the host
muscle with active contraction being weak and painful.
They can also refer pain at rest. Latent trigger points
refer pain only upon direct pressure and can reproduce
the patient’s pain upon palpation. If pain is not referred
from the tender area then it is not a latent trigger point.30
Myofascial Techniques for
the Shoulder
The following therapeutic techniques are just a few of
many available treatments for the shoulder. These tech-
niques have been chosen because of their effectiveness
in the clinic as witnessed by the authors. It is important
to remember that any technique can be modified to suit
the patient problem or needs of the clinician.
Positioning of the Patient and Therapist
Maximum effectiveness cannot be achieved if the tech-
nique is not efficiently executed. If a therapist is not
properly positioned, the patient may not be able to relax,
or the therapist may be putting undue stress on the
patient’s body. Remember to avoid needless body
469
Figure 16-2
contact with the patient. A pillow between the patient
and therapist can provide, as needed, a mechanical
barrier.
Joint Protection
Because the hands are the primary tool of the manual
therapist, it is essential to protect them. Here are a few
general suggestions on how a manual therapist can
protect the hands:
1. Avoid hyperflexion or hyperextension of the joints.
This will decrease the problems of hypermobility
and early arthritis.
2. Use elbows, pisiforms, or fists on patients who are
too large to safely use your fingers on. Be creative.
3. During off-hours from work, try to rest your hands
and protect them from excessive strain.
4. Use cold water rinses or short ice massage on your
joints if inflammation occurs from vigorous
treatment of a patient.
Anteroposterior Lateral Elongation of the
Upper Thoracic Region (Figure 16-2)
Rationale. This technique is used for relaxing and
lengthening the myofascia in the upper thoracic region
and the shoulder girdle. This technique is of great value
to patients who have protracted shoulder girdles. It
should be used before trying to teach postural correction
or strengthening.
Patient Position. Supine, with the head in a
neutral position on the treatment table.
Therapist Position. Seated near the patient’s head
at a 45° angle to the shoulder girdle.
470 SECTION IV TREATMENT APPROACHES

Procedure. Begin stroking with the fingertips in a
medial to lateral position. Once the glenohumeral joint
is reached, re-place the hands in the original position
and repeat the stroke. The strokes may become progres-
sively deeper.
Anterior-Posterior Scour (Figure 16-3)
Rationale. Tightening of the pectorals is a com-
mon problem found in shoulder patients, especially those
with the forward head posture. To achieve full shoulder
range of motion and postural correction, the extensibil-
ity of these muscles must be restored. This technique is
used to release and lengthen the pectoral muscles.
Patient Position. Supine, with the head in a
neutral position on the treatment table.
Therapist Position. Seated or standing near the
patient’s head at a 45° angle to the shoulder girdle.
those with the forward head posture. To achieve full
shoulder range of motion and postural correction, the
extensibility of these muscles must be restored.
Patient Position. Supine, with the shoulder
abducted 90° to 120° (less flexion with frozen shoulders).
Therapist Position. Alongside the patient, at a 45°
angle to the shoulder girdle. The patient may rest the
arm on the therapist’s knee to achieve better relaxation.
The thumbs are placed underneath the muscle and the
fingers grasp from above.
Procedure. Gently lift and bend the pectoral
muscle away from the anterior chest wall. Small oscilla-
tions can be performed and a static hold. Be careful to
avoid contact with breast tissue.

Procedure. Tightening of the pectorals is a

common problem found in shoulder patients, especially
those with the forward head posture. To achieve full
shoulder range of motion and postural correction, the
extensibility of these muscles must be restored. Using a
loose fist, the therapist places his or her hand in the in-
fraclavicular region and sweeps medially toward the
axilla. The stroke follows the soft tissue and can pro-
gressively deepen.

Transverse Muscle Play of the Pectorals

(Figures 16-4 and 16-5) Figure 16-4
Rationale. Tightening of the pectorals is a
common problem found in shoulder patients, especially

Figure 16-3 Figure 16-5

CHAPTER 16 MYOFASCIAL TREATMENT
Subscapularis Techniques
(Figures 16-6 to 16-9)
Rationale. The subscapularis is often found to
have significant restrictions in patients with decreased
shoulder range of motion because of poor posture or
immobilization. When full shoulder motion cannot be
achieved, the therapist should recheck the subscapularis
and the surrounding myofascia for trigger points or
restrictions.
Patient Position. Supine, with the arm abducted
30° to 60°. The arm may rest against the therapist for
relaxation.
Therapist Position. Standing alongside the
patient. One hand is placed from above into the belly of
the subscapularis. The other hand may be used to stabi-
Figure 16-6
Figure 16-7
471
lize the patient’s arm, or it may be used to assist the
upper hand in doing the mobilization. The heel of the
hand may be used if the fingertips are not tolerated as
this diffuses the pressure.
Procedure 1. Small oscillations or sustained pres-
sure can be used as a therapist applies moderate pressure
into the subscapularis. The bottom hand may grasp from
beneath to perform a muscle play technique.
Procedure 2. The patient’s arm is elevated into
flexion and gently distracted. The therapist places the
palm of the hand along the lateral border of the scapula.
Gentle stroking in a caudal direction is applied with the
palm. If more specific fascial restrictions exist, the fin-
gertips may be used to provide a static or oscillatory
pressure.
Figure 16-8
Figure 16-9
472 SECTION IV TREATMENT APPROACHES
Procedure 3. The patient is placed in the side-lying
position. The patient’s arm is elevated into flexion and
gently distracted. The therapist places the palm of
the hand along the lateral border of the scapula.
Gentle stroking in a caudal direction is applied with the
palm. If more specific fascial restrictions exist, the fin-
gertips may be used to provide a static or oscillatory
pressure.
Anterolateral Fascial Elongation
(Figures 16-10 and 16-11)
Rationale. This technique elongates the superficial
anterior fascia, which is often restricted in patients with
a protracted shoulder girdle position.
Patient Position. Supine, with the shoulder ele-
vated 120° to 160° depending on the area of restriction.
Figure 16-10
Figure 16-11
Therapist Position. At the top of the bed, grasp-
ing the patient’s arm and providing a gentle upward dis-
traction. The palm of the upper arm is placed just below
the breast line. Be sure of proper draping and appropri-
ate hand placement when performing this technique.
Procedure. The therapist applies a stronger trac-
tioning force on the flexed arm while the lower arm trac-
tions in the direction of the umbilicus. The direction of
force may be changed to accommodate the existing
restrictions. Lubricants should not be used to prevent
shear. This technique can also be performed with the
patient in slight thoracic rotation.
Rotational Thoracic Laminar Release
(Figure 16-12)
Rationale. To mobilize the paravertebral and
periscapular muscles into rotation. This is a deeper
technique than those already described.
Patient Position. Side-lying, with the head sup-
ported and the upper arm resting on the side of the body.
Therapist Position. Directly facing the patient
with a pillow fit snugly between therapist and patient.
The lower hand is placed along the paravertebral
muscles near the medial border of the scapula. The
upper hand rests on the glenohumeral joint.
Procedure. The fingers of the lower hand apply a
deep pressure in a sweeping downward motion, while
the upper hand retracts the shoulder girdle and applies
a rotational force through the thoracic spine.
Figure 16-12
CHAPTER 16 MYOFASCIAL TREATMENT
Scapular Framing (Figures 16-13 to 16-15)
Rationale. A commonly performed technique that
decreases tone in the periscapular muscles and prepares
the scapulothoracic tissues for aggressive stretching.
Patient Position. Lying on the side facing the
therapist, with a pillow separating the two. The patient’s
arm should be resting comfortably on the pillow.
Therapist Position. Standing facing the patient
with the upper hand placed on the anterior acromion.
Procedure for Medial Border. Lace the fingers of
the lower hand gently along the medial border of the
scapula. Gently retract the shoulder with the upper
hand, and then stroke in a downward direction along the
border of the scapula with the lower hand.
Figure 16-13
Figure 16-14
473
Procedure for Lateral Border. Place the palm of
the lower hand over the acromion to stabilize the joint.
The palm of the upper hand is placed over the lateral
border of the scapula, and then strokes caudally with a
firm pressure down the length of the border.
Procedure for Superior Border. Place the finger-
tips of both hands medial to the cervicothoracic junc-
tion over the upper trapezius. Stroke outward toward the
acromion with a firm pressure. If needed, a gentle stretch
performed with the palm of the hand can be given at
the end of the stroke.
Cervical Techniques/Trapezius Stretches
(Figures 16-16 to 16-18; see also Figure 16-15)
Rationale. Many patients who have shoulder dys-
function will also have associated cervical restrictions.
Figure 16-15
Figure 16-16
474 SECTION IV TREATMENT APPROACHES
Figure 16-17
Figure 16-18
Full shoulder range of motion cannot be achieved
without clearing the neck region as well. These tech-
niques will stretch the posterior structures, levator
scapulae, and trapezius muscles.
Patient Position. The patient is lying supine near
the head of the table.
Therapist Position. Standing/seated directly
behind the patient with the top hand placed on the
anterior shoulder joint.
Procedure 1. One hand cradles the patient’s. The
head can be placed in a combination of sidebend,
forward bend, and rotation based on the restriction and
the tissues that need to be stretched. The other hand is
Figure 16-19
placed on the patient’s shoulder. A firm caudal pressure
is then applied to the shoulder while the upper hand
applies pressure into forward bending, side bending,
and rotation.
Procedure 2. The head can be placed in a combi-
nation of side bend, forward bend, and rotation based
on the restriction and the tissues that need to be
stretched. The therapist can then stand at the patient’s
side, and using both hands, glide the shoulder inferiorly.
The position of the neck serves to increase the stretch
of the trapezius muscle.
Seated Pectoral and Anterior Fascial
Stretches (Figures 16-19 to 16-21)
Rationale. Patients are sometimes better able to
relax in the seated position. These stretches can be used
CHAPTER 16 MYOFASCIAL TREATMENT
Figure 16-20
to elongate the anterior fascia and pectoral muscles to
allow for better posture and improved shoulder range of
motion.
Patient Position. Seated with the hands behind
the head.
Therapist Position. Standing directly behind the
patient with either the knee or hip stabilizing the tho-
racic region. As previously mentioned, a pillow should
be placed between therapist and patient. The therapist
grasps the patient just below the elbows.
Procedure 1. A posterior force towards the
patient’s head is applied while the patient takes deep
breaths to improve anterior elongation. To incorporate
the lateral fascia and muscles, the patient can be asked
to lean or rotate to one side while the same force is
475
Figure 16-21
applied. The patient’s arms may also be fully extended
for this technique.
Procedure 2. The patient may have only one arm
extended upwards, while the therapist places one hand
along the lateral rib cage and the other just below the
elbow. A traction force is then applied in opposite direc-
tions. A rotary component can also be added using the
technique stated earlier.
Seated Forward Bending Laminar Release
(Figure 16-22)
Rationale. This technique is used to elongate the
posterior structures of the cervical and thoracic regions.
It can easily be performed on patients of any size and
the patient can be an active participant.
476 SECTION IV TREATMENT APPROACHES
Figure 16-22
Patient Position. Seated in a chair with his or her
head flexed forward.
Therapist Position. Standing behind the patient
facing his or her back.
Procedure. The patient is asked to forward bend
the cervical/thoracic spine segmentally in order to learn
how to do this. The therapist places each thumb, point-
ing downward, along the erector spinae on each side of
the spine. The elbows are slightly bent. The patient is
then asked to bend segmentally as the therapist strokes
in a downward motion. The motion can be stopped at
the point of restriction whereupon a direct, sustained
pressure can be applied. This can also be done as a
unilateral technique by having the patient forward
bend into a diagonal position. The therapist places
each thumb pointing downward alongside the erector.
Figure 16-23
Because of excessive loading, this technique should be
avoided with discogenic necks and backs.
Cross Friction of Supraspinatus and Biceps
Tendon (Figure 16-23)
Rationale. Cross friction is used to increase local
blood flow to enhance the rate of healing. It is very effec-
tive in treating tendonitis of the biceps or supraspinatus.
Patient Position. Supine, with the arm abducted
30° and the elbow bent.
Therapist Position. At the patient’s side support-
ing the arm with the bottom hand. The thumb of the
top hand is in the bicipital groove.
Procedure. The therapist may alternately laterally
and medially rotate the shoulder to create some gentle
friction. Direct friction over the bicipital groove is
applied with the thumb. The second and third fingers
with slight flexion at the distal interphalangeal joints
may also be used if the patient is less acute. To friction
the supraspinatus, the therapist abducts the shoulder 80°
to 90° and palpates the notch formed by the acromion
spine and the clavicle. The musculotendinous junction
lies here. Use the same technique as described earlier.
Case Study (Fig. 16-24)
GENERAL DEMOGRAPHICS
Mrs. J.M. is a 34-year-old Caucasian, English-
speaking woman who comes to the clinic with an
8-week history of left shoulder pain following a fall.
 CHAPTER 16 MYOFASCIAL TREATMENT 477

SOCIAL HISTORY
Mrs. J.M. is single with no children. She does not
smoke and drinks less than once per week.
EMPLOYMENT
She is a sales representative for a manufacturing
company, which requires some office work and some site
visits.
LIVING ENVIRONMENT
A Mrs. J.M. lives alone in an apartment on the second
floor.
PMH
She has a history of a Bankart repair to the left
shoulder in 1990 after an injury sustained in a motor
vehicle accident.
HISTORY OF CHIEF COMPLAINT
Mrs. J.M. reports falling onto her left side when
stepping out of her car onto a sidewalk 8 weeks ago. The
pain has not subsided and has become constant, causing
her difficulty at work. The pain sometimes wakes her up
at night with shifts in position.
PRIOR TREATMENT FOR THIS CONDITION
The referring physician did not provide her with
exercises, and suggested physical therapy as a conserva-
tive approach before attempting any other treatments.
The orthopedist has ruled out injury to the prior repair
as cause for her pain.
STRUCTURAL EXAMINATION
On evaluation she has atrophy of the rhomboids and
B
lower trapezius. Significant increase in tone is present
in the upper trapezius, levator scapulae, and pectoral
muscles.
RANGE OF MOTION
Cervical range of motion is limited by 25% into rota-
tion and side bending to the right. Left shoulder active
range of motion is 100° of flexion, 90° of abduction, and
45° of external rotation. Passive range of motion is 100°
of flexion, 90° of abduction, and 55° of external rotation
with pain before end range.
TENDERNESS
Figure 16-24 A 34-year-old patient who had an There are multiple tender spots in the upper thoracic,
8-week history of left shoulder pain following a fall. A and scapulothoracic, and anterior chest wall regions. The
B, Presentation of the patient after the first four treatment acromioclavicular joint is painful to palpation and to
sessions.
internal rotation and adduction movements.
REVIEW OF PATIENT PROBLEMS:
1. Increased tone in the upper trapezius
2. Increased tone in the rhomboids
3. Increased tone in the levator scapulae
4. Increased tone in the pectorals
478 SECTION IV TREATMENT APPROACHES
5. Decreased range of motion of the left shoulder
6. Acromioclavicular (AC) joint pain
7. Trigger points in the U/T and scapulothoracic
regions
8. Restrictions in the anterior chest wall myofascia
9. Decreased cervical range of motion
P.T. CLINICAL IMPRESSION: PLAN OF CARE
AND TREATMENT
From a myofascial standpoint, a good way to begin
treatment of this patient would be to address the com-
ponents prior to range of motion or strength. The pre-
viously discussed techniques might be incorporated into
treatment of this patient in the following way.
1. Increased pectoral tone: pectoral muscle play
2. Restricted anterior chest wall: anterior fascial elon-
gation with or without a rotary component
3. Periscapular restrictions: scapular framing, scapular
mobilization, subscapularis release
4. Increased tone in upper thoracic region/upper
trapezius: anterior/posterior lateral elongation of
upper thoracic region
5. Increased tone in paravertebral muscles: rotational
thoracic laminar release
REEXAMINATION
After performing each myofascial technique, reassess
the patient’s range of motion to see what effect the treat-
ment has made. Large increases in range can be achieved
through the performance of myofascial techniques
without ever performing true range of motion or joint
mobilization of the glenohumeral joint.
CONTINUED TREATMENT
Once the myofascial restrictions are eliminated and
the range of motion is improved, begin strengthening
exercises if they are still required. Consider each patient’s
problems individually, continually reassessing the causes
of limitation. Use these findings to guide your choice of
treatment approach. If one approach is not working,
consider a change in technique. Remember that the
aforementioned techniques are only a small sample of
the available treatments.
PROGNOSIS REVIEW
In the case of this patient, myofascial treatment
assisted in the ability to isolate the primary problem. On
initial evaluation, there was too much muscle guarding
and myofascial restriction to identify the cause of this
patient’s pain. After four treatment sessions using the
discussed techniques, this patient’s pain centralized to
the acromioclavicular joint. This problem could not have
been easily identified early on because of the protective
muscular responses of the body. Once those protective
mechanisms were removed, the problem became
obvious. Figure 16-17 shows the presentation of the
patient after the first four treatment sessions. At this
point, the positions of the scapula and clavicle have
moved closer to normal and the prominence of the
acromioclavicular joint has become more obvious. The
patient was referred back to the orthopedist for closer
examination of the AC joint.
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13. Akeson WH, Amial D, Mechanic GL, et al: Collagen cross-
linking alterations in joint contractures, Connective Tissue Res
5:15, 1977.
14. Akeson WH, Amial D: Immobility effects of synovial joints:
the pathomechanics of joint contracture, Biorheology 17:95,
1980.
15. Evans E, Eggers G, Butler JK, et al: Experimental immobi-
lization and mobilization of rat knee joints, J Bone Joint Surg
42A:737, 1960.
16. Amial D, Akeson WH, Woo S, et al: Stress deprivation effect
on metabolic turnover of medial collateral ligament collagen,
Clin Orthop 172:265, 1983.
CHAPTER 16 MYOFASCIAL TREATMENT
17. Schollmeier G, Sarkar K, Fukahara K, et al: Structural and
functional changes in the canine shoulder after cessation of
immobilization, Clin Orthop 323:310-315, 1996.
18. Langenskiold A, Michalsson JE, Videman T: Osteoarthritis
of the knee in rabbit produced by immobilization, Acta Orthop
Scand 50:1-14, 1979.
19. Reynolds CA, Cummings GS, Andrew PD, et al: The effect
of nontraumatic immobilization on ankle dorsiflexion Jos PT
23(13):27-33, 1996.
20. Laban MM: Collagen tissue: implications of its response to
stress in vitro, Arch Phys Med Rehabil 43:461, 1962.
21. Neuberger A, Slack H: The metabolism of collagen from liver,
bones, skin and tendon in normal rats, Biochem J 53:47, 1953.
22. Frankel VH, Nordin M: Basic biomechanics of the skeletal system,
Philadelphia, 1980, Lea and Febiger.
23. Wakim KG: The effects of massage on the circulation of
normal and paralyzed extremities, Arch Phys Med Rehabil
30:135, 1949.
479
24. Wolfson H: Studies on the effect of physical therapeutic pro-
cedures on function and structure, JAMA 96:2020, 1931.
25. Martin GM, Roth GM, Elkins C, et al: Cutaneous temper-
ature of the extremities of normal subjects and patients with
rheumatoid arthritis, Arch Phys Med Rehabil 27:665, 1946.
26. Cuthbertson DP: Effects of massage on metabolism, Glasgow
Med J 2:200, 1933.
27. Ebner M: Connective tissue manipulation, Malabar, Fla., 1985,
Kreiger Publishing.
28. Janda B: Central nervous motor regulation and back prob-
lems. In Korr IM, editor: The neurobiologic mechanisms in
manipulative therapy, New York, 1978, Plenum Press.
29. Donatelli R, Wooden M: Orthopaedic physical therapy, New
York, 1989, Churchill Livingstone.
30. Travell JG: Myofascial pain and dysfunction: the trigger point
manual, Baltimore, 1989, Williams and Wilkins.

Shoulder Instability
T he shoulder is a complex joint, which comprises
the integration of four articulations including
the glenohumeral, scapulothoracic, sternoclav-
icular, and acromioclavicular joints. These articulations
need to work in tandem for proper arm elevation and
function to occur without pain or excessive humeral
head translation. Of these articulations, the gleno-
humeral joint permits a high degree of mobility and
lacks inherent static stability. In fact, the glenohumeral
joint exhibits the greatest amount of motion found in
the body.1 This lack of inherent static stability places a
greater demand on the dynamic stabilizers to help direct
humeral motion in the glenoid and to protect against
aberrant translation of the humeral head, which can pos-
sibly lead to shoulder instability.
Shoulder instability is a vague, nonspecific term that
actually represents a wide spectrum of clinical pathologic
conditions, ranging from gross and occult instability to
symptomatic laxity or subluxation.1,2 Matsen and associ-
ates described shoulder instability as a pathologic con-
dition in which the laxity or the mobility of the joint
increases abnormally.3 In other words, instability is the
inability to maintain the humeral head centered in the
glenoid cavity.3 In all patients with shoulder instability,
some component of the stabilizing matrix has become
dysfunctional.
According to Pagnani and Warren, there typically is
no single “essential lesion” responsible for all cases of
shoulder instability.4 The pathophysiology of the shoul-
der produced may vary with the direction and the extent
of the instability. The glenohumeral joint’s static
restraints include a negative intraarticular pressure
483
17
Michael S. Zazzali
Vijay B. Vad
Joseph Harrera
Michael Lee
Struan H. Coleman
gradient, which induces cohesion and adhesion between
the humeral head and the glenoid fossa. During cadav-
eric sectioning, muscle activity is not required to hold
the shoulder together as long as the capsule is not
vented.5 Speer reported that the magnitude of this pres-
sure is small and is capable of producing an approximate
stabilizing force of only 20 to 30 lb.5 This anatomic neg-
ative intraarticular pressure is often disrupted during
open capsular surgery, leaving a postoperative joint pres-
sure of about 0 mm Hg pressure.5
The glenoid labrum and capsuloligamentous complex
also play an integral part of the static glenohumeral
restraints. The glenoid labrum is a fibrous rim that func-
tions to slightly deepen the glenoid fossa and allows for
attachment of the glenohumeral ligaments (Figure 17-
1). The function of the glenoid labrum is similar to a
“chock-block” or buttress in controlling humeral head
translation.6 Biomechanical studies have indicated that
resection of the labrum can reduce the effectiveness of
the concavity-compression by 20%. Injury to the labrum
is thought to disturb the negative intraarticular pressure
gradient, contributing to shoulder instability.7
The glenohumeral capsule has been reported by
Gohlke and associates to be thickest and strongest at the
anteroinferior region because of its dense organization
of collagen and by the invagination of the inferior gleno-
humeral ligament complex.8 The anterior glenohumeral
joint capsule exhibits three distinct ligaments consisting
of the superior, middle, and inferior glenohumeral liga-
ment complex.9,10 The inferior glenohumeral ligament
complex is the primary restraint at elevated positions
such as in 90° of abduction, whereas the superior
484 SECTION V SURGICAL CONSIDERATIONS

Anterior

Anterior capsule

Humeral head

Anterior labrum

Posterior capsule

Bony glenoid

Posterior labrum

Posterior

Figure 17-1 The glenoid labrum serves to deepen the glenoid and
provides attachment to the glenohumeral capsule. (From Wilkes K, Arrigo C,
Andrews J: Current concepts: the stabilizing structures of the glenohumeral joint, Orthop
Sports Phys Ther 25:364-379, 1997 with permission of the Orthopaedic and Sports
Physical Therapy Sections of the American Physical Therapy Association.)

glenohumeral ligament is taut at 0° of abduction. The
middle glenohumeral ligament tightens more so at the
midrange of elevation when the arm is abducted and
externally rotated.9,10 The inferior glenohumeral liga-
ment consists of an anterior band, which restricts ante-
rior translation of the humeral head, and a posterior
band, which is the primary contributor to posterior
stability of the shoulder when the arm is in 90° of
abduction.9
Proper treatment and management of the shoulder
require an understanding of the pathophysiology of
shoulder instability to direct clinical decision making
with conservative rehabilitation versus surgery. The fol-
lowing section of this chapter will briefly describe the
proposed mechanisms of injury and management guide-
lines for Bankart lesions, SLAP lesions, and rotator cuff
interval injuries, and the latest surgical interventions
suggested for these injuries and those patients with
recurrent instability. The postoperative rehabilitation for
each surgical procedure will be demonstrated in a case
study format.
The operative indications for glenohumeral joint sur-
gical stabilization are: recurrent symptomatic instability,
despite a minimum 3-month trial of a well designed and
supervised rehabilitation program; patients who require
stability for occupational reasons, such as heavy manual
laborers and military cadets; and subgroups, such as ado-
lescents or patients, with connective tissue disorders who
are at high risk for recurrence of instability. In the ado-
lescent subgroup, it is important to rule out a psycho-
logical component through psychological testing before
proceeding with the surgical intervention.
A Bankart lesion typically occurs from a traumatic
anterior dislocation of the shoulder. The lesion itself is
typically identified as a compromise or tear of the
attachment site of the labrum to the glenohumeral lig-
aments. Thus a Bankart lesion is defined as when the
capsular-labral complex is torn from the glenoid rim
(Figure 17-2, A).11 Recent evidence suggests that
patients between the ages of 21 and 30 years who sus-
tained a primary shoulder dislocation and underwent
physical therapy and immobilization did not reduce the
risk of recurrence of dislocating the shoulder.1,2 It is sug-
gested that patients in this age group who participate in
high-risk sports should undergo primary surgical stabi-
lization because of the risk of recurrence. Another
 CHAPTER 17 SHOULDER INSTABILITY
A not respond to nonoperative treatment.15 This procedure
B returned to their preoperative occupation without
Figure 17-2 Plain radiographs demonstrate an ante-
rior glenohumeral dislocation before (A) and after (B) reduc-
tion. Postreduction anteroposterior view (B) demonstrates a
Hill-Sachs lesion of the posterolateral humeral head (arrow-
head) and a typical “bony Bankart” fracture of the anteroinfe-
rior glenoid rim (arrow). (From Stechschulte D, Warren R: Anterior
shoulder instability. In Garrett W, Speer K, Kirkendall D, editors: Princi-
ples & practice of orthopaedic sports medicine, Philadelphia, 2000,
Lippincott Williams & Wilkins.)
485
objective sign of recurrent anterior instability is the
presence of an osseous defect or lesion seen on a
radiograph, commonly noted on the posterolateral
portion of the humeral head, known as a Hill-Sachs
lesion (see Figure 17-2, B).13
The open Bankart surgical stabilization technique for
posttraumatic recurrent anterior stabilization has been
referred as the procedure of choice for patients who do
is based on the premise that anterior instability is caused
by detachment of the anteroinferior labrum from the
glenoid rim.11
Gill and associates16 reported on long-term results
with patients after open stabilization for a Bankart repair
for anterior instability of the shoulder. The study con-
sisted of 60 shoulders on 56 patients that had a
minimum follow-up of eight years after a Bankart pro-
cedure. These individuals had a mean follow-up of 11.9
years and were examined for range of motion, stability,
and strength according to the data form of the Ameri-
can Shoulder and Elbow Surgeons (ASES) for exami-
nation of the shoulder. The mean loss of external
rotation was 12° (range, 0° to 30°). There were no sig-
nificant differences in elevation, abduction, or internal
rotation between the involved shoulder and the con-
tralateral, normal shoulder. Fifty-five of the 56 patients
having to modify their activities. Fifty-two patients
rated the result as good or excellent; three, as fair; and
one, as poor.16 Although this study demonstrated great
patient satisfaction, the average loss of 12° of external
rotation could be disabling for athletes.
Pagnani and Dome reported their open stabilization
procedure on 58 American football players over a 6-year
period and found it to be a predictable method to restore
shoulder stability while maintaining a range of motion
approximating that found after arthroscopic repair.17
The average follow-up was 37 months after surgery and
55 patients reported good or excellent results, and 52 of
the 58 returned to playing football for at least 1 year.17
According to these authors, the open stabilization pro-
cedure offers superior postoperative stability to that
reported after arthroscopic techniques in this patient
population.17 The open Bankart repair as described by
Pagnani and Dome17 involves a vertical tenotomy of the
subscapularis tendon, which is performed with electro-
cautery approximately 1 cm medial to its insertion on the
lesser tuberosity. The interval between the anterior
aspect of the capsule and the subscapularis tendon is
486 SECTION V SURGICAL CONSIDERATIONS
moved with blunt dissection to permit exposure to the
anterior joint and the capsular laxity and quality are
assessed. A transverse capsulotomy is performed to
permit exploration of the Bankart lesion. The glenoid
neck is roughened with an osteotome to provide a bleed-
ing surface. The authors use two or three metallic suture
anchors placed in the anteroinferior aspect of the
glenoid neck near, but not on, the glenoid articular
margin. The capsule and labrum are reattached to the
anterior aspect of the glenoid with slight medial and
superior mobilization of the capsule. The goal of this
surgery is not to reduce external rotation, but to oblit-
erate excess capsular volume to restore the competency
of the inferior glenohumeral ligament at its glenoid
insertion. The authors also propose performing an
anterior capsulorrhaphy to eliminate excess capsular
laxity.17
Case Study 1: Mr. C.M.
REHABILITATION FOLLOWING OPEN BANKART REPAIR
AND STABILIZATION
This case presents a standardized postoperative reha-
bilitation protocol for the athlete after a Bankart repair
based on the latest literature and procedures.17 The
enhancement and the dynamic stabilization or concav-
ity-compression mechanism is not addressed in surgery.
Instead it is neuromuscular exercises and training of
the rotator cuff via a dedicated and essential rehabilita-
tion program that will ultimately optimize functional
recovery of the shoulder following capsulorrhaphy
surgery.5
General Demographics
Mr. C.M. is a 26-year-old professional football
player, who is an offensive lineman. The patient injured
his right (dominant side) shoulder during a blocking
technique while his arm was in a position of abduction
and external rotation. The resultant force stressed his
shoulder quickly into horizontal abduction during the
play and he began feeling a numbness and pain imme-
diately thereafter in the arm. The team physician deter-
mined he was anteriorly dislocated his shoulder, which
was manually relocated on the field and then placed in
a sling. A magnetic resonance imaging (MRI) is taken
in the locker room and displayed a Bankart lesion and
tear of the anterior capsule. The patient underwent an
open Bankart repair 1 week later.
Social History: Mr. C.M. is single with no children.
He does not smoke or drink alcohol.
Employment: He is a professional offensive lineman
in the National Football League.
Living Environment: Mr. C.M. lives with his girl-
friend in a bi-level home.
Growth and Development: He is an extremely muscu-
lar young male, with no external deformities noted.
Patient Medical History (PMH)
He has had right knee arthroscopy 2 years ago for
torn medial meniscus. No complaints over the last year
with respect to his knee.
History of Chief Complaint
Mr. C.M. is unable to resume football at present time
because of weakness, pain, and stiffness in his right
shoulder. He comes to the physical therapy clinic 4
weeks after a right Bankart repair. He reports pain at the
right upper trapezius and anterolateral shoulder, which
wakes him up at night, but he no longer feels numbness
or “dead arm” symptoms. The patient has been immo-
bilized for 4 weeks since surgery and has been taught
only pendulum and elbow range of motion exercises up
to this time.
Prior Treatment for This Condition
None with respect to shoulder stability. Before his
injury the patient was active with a general weight train-
ing program with the team.
Structural Examination
Patient comes to physical therapy with his shoulder
in a sling. Visual inspection reveals a well-healed ante-
rior incision, and the patient is fully intact to light touch
sensation surrounding the surgical incision. There is
mild ecchymosis and swelling noted at the anterior
shoulder region and tenderness along the lesser tuberos-
ity at the insertion of the subscapularis. Mild atrophy
is noted of the right deltoid, pectoralis major, and
infraspinatus when compared with the contralateral
side.
Range of Motion
Active Range of Motion (AROM): Active motion of
the right shoulder is contraindicated at this time because
of the tissue vulnerability from the surgery and pull-out
rate of bioabsorbable tacks for stabilization. Active
motion testing is postponed at this time for the right
shoulder. The left shoulder had full AROM with proper
scapulohumeral rhythm with elevation. Right elbow
flexion and extension, along with wrist flexion and
extension, were full and pain free.
CHAPTER 17 SHOULDER INSTABILITY
Passive Range of Motion (PROM): Initial PROM of
the right shoulder is 95° of flexion, 50° of abduction, 0°
of external rotation in the adducted position, and 45° of
internal rotation. No hypermobility is noted at the con-
tralateral upper extremity at the elbows or metacar-
pophalangeal (MCP) joints.
Accessory Motion Testing of the Glenohumeral Joint:
Moderately tight posterior capsule.
Muscle Testing: No further testing of the right shoul-
der is performed because of the acuteness of the patient’s
symptoms and postoperative timeframe.
Special Tests: The left shoulder does not demonstrate
shoulder laxity in any direction with load and shift
testing. No further special testing is performed at this
time because of the acuteness of the patient’s symptoms
and nature of his postoperative timeframe.
Palpation: Tender to anterior shoulder along the sub-
scapularis tendon insertion and along anterior gleno-
humeral joint.
P.T. Clinical Impression
Based on the patient’s signs and symptoms, and time-
frame out from surgery (4 weeks) the main goal at this
stage of rehabilitation is to begin restoration of passive
and active-assisted shoulder range of motion while still
protecting the surgical site. The main factor to consider
at this stage is using a methodical yet progressive
approach to restore shoulder external rotation while pro-
tecting against overstressing the anterior capsule, infe-
rior glenohumeral ligament complex, and subscapularis
musculotendinous junction. Therefore anterior capsule
joint mobilizations would be contraindicated along with
aggressive pectoral stretching.
Treatment Plan
Initial Treatment: 4 to 8 Weeks
Postoperatively
Initial treatment goals are to reduce and eliminate
inflammation of the anterior shoulder tissues with
modalities as needed and graded manual scar tissue
mobilization. The patient’s external rotation should be
limited to 45°, provided there are no signs or symptoms
of impingement or rotator cuff symptoms. Proximal sta-
bilization for the scapular rotators may begin at this time
for retraction and neuromuscular control exercises. Sub-
maximal isometrics for the internal and external rotators
are performed as tolerated. By the 7th week, the patient
demonstrates 140° of active forward flexion in sitting
with compensatory superior humeral migration and
487
upper trapezius dominance. At this time, a progression
into graded resisted internal/external strengthening
exercises may begin in modified arcs of motion and with
the arm at low abduction angles.
Treatment: 8 to 12 Weeks Postoperatively
At 8 weeks postoperatively, the patient demonstrates
155° of flexion, 120° of abduction, 45° of external rota-
tion, and 62° of internal rotation. At this phase he is
tolerating rhythmic stabilization with the shoulder in
varying degrees of flexion to enhance kinesthetic aware-
ness and dynamic stability. He is emphasizing his infra-
spinatus/teres minor strength, with side-lying external
rotation, using a 3-lb weight. His rotator cuff strength-
ening is advanced by week 10 to Theraband exercises
and his abduction angles are slowly increased during
rotator cuff and deltoid strengthening exercises. The
scapular rotators are strengthened with the following:
press-ups (seated dips), shrugs, horizontal abduction
with modified arc to protect the anterior capsule, and
open can exercises.
Treatment: 12 to 18 Weeks Postoperatively
At this stage of the rehabilitation, the patient demon-
strates 170° of flexion, 160° of abduction, 65° of exter-
nal rotation, and 70° of internal rotation. On manual
muscle testing, he demonstrates: abduction = 4+/5,
flexion = 5/5, external rotation = 4/5 (fatigues with rep-
etition), and internal rotation = 5/5. His scapulohumeral
rhythm is comparable with his contralateral side. He
demonstrates a positive Neer test and mild posterior
capsular tightness relative to the uninvolved side.
During this phase of his rehabilitation, the focus is on
restoration of terminal external rotation and further
enhancement of neuromuscular control of the humeral
head. Uses of proprioceptive neuromuscular facilitation
in dynamic patterns and in sport-specific patterns is ini-
tiated along with plyometric exercises, such as medicine
ball catches and chest passes. Use of Theraband exer-
cises and isokinetics is elevated to the plane of the
scapula and then to 90° of abduction. These are per-
formed in slow and fast speeds to properly prepare the
anterior-posterior stabilizers for quick and prolonged
stress/strain forces to the shoulder.
Assessment of anterior laxity/instability with load
and shift testing is negative, as is apprehension testing.
The end range external rotation in the apprehension
488 SECTION V SURGICAL CONSIDERATIONS
position is 85° by week 18 and pain free. An isokinetic
evaluation to compare strength with the contralateral
shoulder is performed at 17 weeks and demonstrates a
5% and 15% deficit at the external and internal rotators,
respectively.
Treatment: Past 18 Weeks Postoperatively
At this time, the patient demonstrates a negative Neer
test and 174° of flexion, 165° of abduction, 85° of exter-
nal rotation, and 75° of internal rotation. The patient’s
program focuses on closed kinetic chain exercises, which
are more sport specific for his profession as a lineman.
Patient also progresses to a conventional weight-
training program, with education placed on not over-
stressing the anterior capsule with end range dips or
chest presses. The patient is retested at 23 weeks post-
operatively, with a second isokinetic evaluation demon-
strating equal strength at his external rotators and 10%
greater strength of his internal rotators relative to the
contralateral side. At this time the patient is cleared to
progress from field to contact drills with the team.
However, it was suggested by his surgeon that he obtain
an abduction harness initially as protection during
blocking drills. The patient was cleared to return to full
contact football by his physician and physical therapist
by the 25th week postoperatively after demonstrating
good tolerance to contact drills with, and then without,
the abduction brace and after he demonstrated sym-
metrical abduction and external rotation strength on iso-
kinetic and manual muscle testing. Lastly, the patient is
instructed in posterior capsular (cross body) stretching
to maintain tissue extensibility and help reduce the like-
lihood of recurring impingement. The patient was
checked periodically by the team physician for any
recurring signs or symptoms of instability.
SUMMARY OF CASE
The crucial phase of rehabilitation following the
Bankart repair is the initial period of immobilization,
followed by the beginning of ROM restoration. It is vital
that the patients are compliant and understand the need
to permit these anterior structures to heal to permit ade-
quate stabilization. This patient was not seen in physi-
cal therapy until the fourth week, so it was up to his
physician to instill this point. The physical therapist
must also respect the healing nature of the anterior sta-
bilizers by not being too aggressive early on with restor-
ing external rotation. The approach to this case is typical
for a patient post-Bankart repair and emphasizes a safe
progression through rehabilitation. The latter part of the
rehabilitation will be more sport specific and individ-
ualized depending upon the goals of the patient.
However, as in this case when the patient demonstrated
impingement signs, it is important to critically think and
reassess—as the patient progresses—to be able to deter
secondary complications. In this case, it appeared the
patient’s impingement was related to residual posterior
capsular tightness and limited external rotation in the
abducted position, and possibly a concurrent increase in
elevation with his strengthening exercises.
Originally, shoulder instability was corrected prima-
rily through open procedures, current technique now
allows correction of the entire spectrum of instability
patterns via arthroscopic techniques. Speer and associ-
ates18 retrospectively investigated the outcomes of an
arthroscopic technique for anterior stabilization of the
shoulder using a bioabsorbable tack in 52 patients with
shoulder instability. The cause of the instability was a
traumatic injury in 49 of the patients—26 of which were
sustained during participation in a contact sport. Fifty
of the shoulders had a Bankart lesion.
The patients were evaluated at an average follow-up
of 42 months postoperatively. Forty-one (79%) were
asymptomatic and were able to return to their respective
sport without restriction.18 The repair had failed in 11
(21%) of the patients. In four of these patients, the
failure resulted from a single traumatic reinjury during
participation in contact sports, and three of the four were
treated nonoperatively. The remaining seven failures
occurred atraumatically.
The authors reported that the rate of recurrent
instability following this arthroscopic procedure (21%)
greatly exceeded the rates of recurrence of open capsu-
lorrhaphy (up to 5.5%).11,19,20 The authors believed the
wide discrepancy in the rates of the results was due to
this arthroscopic technique does not address the coexis-
tent capsular injury or plastic deformation that has been
reported to occur with Bankart lesions.22 Therefore they
suggest anterior stabilization with a bioabsorbable tack
may be indicated for patients with anterior instability,
but do not need a capsulorrhaphy to reduce joint
volume.18
A prospective study by O’Neill evaluated the results
of an arthroscopic transglenoid suture-stabilization pro-
cedure in athletically active patients who had recurrent
unilateral, unidirectional anterior dislocations of the
CHAPTER 17 SHOULDER INSTABILITY 489

shoulder and an isolated Bankart lesion.21 The mean

duration of follow-up was 52 months, within a range of
Biceps tendon
25 months to 7 years. The patients were evaluated annu- Superior
ally with a physical examination, radiographs, isokinetic glenohumeral
strength-testing, the modified shoulder-rating scale of ligament
12
Rowe and Zarins, and the scoring system of the 1
2
Bankart lesion
ASES.21 3
Glenoid 4
The results of O’Neill’s study determined that 40 5
Labrum
(98%) of the 41 athletes returned to their preoperative Posteroinferior 6 Middle
glenohumeral
sport after surgery. Thirty-nine patients (95%) had no glenohumeral
ligament
additional dislocations or subluxations, and two (5%) ligament
Subscapularis
had a single episode of subluxation. These latter two Anteroinferior tendon
patients were football players. The author concluded glenohumeral ligament
that arthroscopic transglenoid repair of an isolated ante- Figure 17-3 Drawing of the glenoid with numbers
rior labral detachment or Bankart lesion restored stabil- identifying anchor placement. (From Rook R, Savoie F, Field L, et
ity of the shoulder and led to a favorable outcome in 39 al: Arthroscopic treatment of instability attributable to capsular injury or
(95%) of the 41 athletes. The only two patients who suf- laxity, Clin Orthop & Rel Res 390:52-58, 2001.)
fered a postoperative subluxation were the two football
players, who also were the only patients to score less than
matic anterior instability.15 Therefore the choice of
80 points on the ASES scale.2
method for posttraumatic anterior instability must
The arthroscopic Bankart reconstruction, as
still be based on the experience of the surgeon and the
described by Rook and associates,22 uses an anterior
patient’s choice rather than on scientific evidence from
portal to ensure access to the inferior glenoid and to
long-term prospective, randomized studies at the
evaluate the lesion and anterior capsule. The anterior
present time.15
portal is also used for debriding and releasing the cap-
Our preference for surgically treating Bankart lesions
sulolabral complex from the glenoid. The release of the
is primarily arthroscopic. Open repair is reserved for
capsulolabral complex is done inferiorly to the 6 o’clock
patients with gross (3+) instability, gross multidirec-
position of the glenoid. The authors then abrade the
tional instability, large Hill-Sachs lesions, failed thermal
anterior and inferior glenoid to promote a bleeding
capsulorrhaphy, poor capsulolabral tissue observed at the
surface where the suture anchors will be placed at the 5
time of surgery, a history of contralateral shoulder insta-
o’clock, 3 o’clock, and 1 o’clock positions (Figure 17-3).
bility, and failure of arthroscopic repair. Rehabilitation
Recently there is evidence that arthroscopic treat-
following arthroscopic Bankart repair involves 10 to 14
ment for shoulder instability may parallel the gold stan-
days of immobilization versus 4 weeks after open
dard of open surgical techniques.22 However, there are
Bankart repair. Although there is less tissue trauma fol-
studies that may refute this claim and continue to
lowing arthroscopic Bankart repair compared with the
suggest that arthroscopic treatment of shoulder instabil-
open procedure, and patients in general can progress
ity has a greater failure rate comparable to open proce-
faster, the therapist needs to be careful during the initial
dures, especially with athletes that desire to return to
4 to 6 weeks postoperatively and limit the stresses placed
contact sports postoperatively.18,21,23,24 Ultimately, there
on the anterior capsule.
may be a need for longer outcome studies for both
approaches to determine which procedure (open versus
arthroscopic) provides the highest success rate.
Magnusson and associates suggest follow-up studies
Muscle Mechanics:
of up to 7 years and recommend researchers consider
Contribution to Shoulder
incidences of subluxation and recurrent dislocations in
Dislocation and Stability
their success rates. According to Magnusson and asso- Increased understanding of the sequelae and predispo-
ciates, there does not appear to be a “gold standard” for sitions to shoulder dislocation may improve functional
reconstruction in patients with unidirectional, posttrau- results during nonoperative treatment, surgical repair,
490 SECTION V SURGICAL CONSIDERATIONS
and postoperative rehabilitation. McMahon and Lee
developed an in vitro, cadaveric model that investigated
relevant shoulder musculature and its relationship with
glenoid concavity compression for dynamic stability,
and its role in contributing to dislocation.25 The authors’
research integrated work by Matsen and co-workers,26
who defined a muscle’s function as a dynamic restraint
related to a “stability ratio” between the displacing com-
ponent (contributes to instability) of the joint force and
the compressive component (contributes to stability).
Matsen’s model suggests that shoulder muscle dysfunc-
tion on one side of the joint may not only decrease the
compression component, but also increase the displac-
ing component if forces on the other side are
unbalanced.26
McMahon and Lee assessed the alteration in gleno-
humeral joint forces with simulated shoulder muscle
dysfunction.25 The joint was positioned in apprehension
while the rotator cuff and deltoid were simulated and
loaded. While the arm was in the apprehension position
the authors altered the load in the infraspinatus and the
pectoralis major tendons. The conditions were altered
from first removing the load from the infraspinatus
(infraspinatus muscle palsy), then added to the pectoralis
major and then this was repeated simultaneously, remov-
ing the load from the infraspinatus as the load was added
to the pectoralis major.
Compared with the intact condition, the magnitude
of the compression force when the infraspinatus was
unloaded decreased substantially by approximately 31%.
The results also demonstrated a significant increase in
the anterior directed force when the pectoralis major
was loaded with and without infraspinatus muscle
palsy of 143% and 142%, respectively. These simulated
muscle dysfunctions resulted in a significant decrease
in concavity-compression of the humeral head into
the glenoid cavity and a concomitant increase in the
anterior directed force, which could result in joint
instability.25
The authors conclude that the large force developed
in the pectoralis major muscle may be related to its
ideal orientation to effectively lever the humeral head
anteroinferiorly out of the glenoid.25 Additional
improvements in outcome after glenohumeral joint dis-
location warrant improved understanding of the “inter-
play” of the static and dynamic restraints.25 The therapist
should attempt to center the rehabilitation on those
muscles that are found to contribute to concavity-
compression and enhance joint stability while appreci-
ating those that may contribute to dislocation.
Slap Lesions
In 1990, Snyder reported on a lesion that occurred at
the anterosuperior labral-biceps complex, which he
described as a tear located at the superior labrum that
begins posteriorly and extends anteriorly (SLAP).27 This
lesion involves the anchor of the biceps tendon to the
labrum. The cause of SLAP lesions is felt to be second-
ary to a single traumatic event rather than repetitive
stress.28 The two most recent models attempting to
describe the mechanism of SLAP injuries are the
Morgan-Burkhart “peel-back model,”29 which describes
the pathologic lesion at the posterosuperior labrum, and
the Walch-Jobe-Sidles “glenoid impingement upon
rotator cuff model,”30 which centers on anteroinferior
instability as the underlying pathologic mechanism.
It is beyond the scope of this chapter to detail these
hypotheses.
It has also been postulated that SLAP lesions can
result from a compressive force applied directly to the
shoulder from a fall on an outstretched arm, with the
humerus in a position of abduction and slight forward
flexion.28 This type of injury has the potential to drive
the humeral head superiorly, avulsing the biceps or labral
attachment from the glenoid.31 This appears to be the
most common mechanism of SLAP lesions, accounting
for 23% to 31% of injuries.32 Traction injuries have
accounted for 16% to 25% of all SLAP lesions, and dis-
location or subluxation has accounted for up to 19%.31
Bey and associates have made some generalizations as to
the possible causes of SLAP lesions, suggesting Type I,
III, and IV lesions may be the result of a shearing force
between the humeral head and glenoid.33
The presence of a destabilizing SLAP lesion may
have a profound impact on shoulder stability and func-
tion. Rodosky and associates demonstrated that the
presence of superior labrum and biceps anchor injury
diminished the force necessary to translate the humeral
head anteriorly.34 According to Higgins and Warner,31
the rotator cuff may be subject to internal impingement
and lead to tearing secondary to the instability sequelae
of the SLAP lesion. Moreover, SLAP lesions have been
found to occur more commonly in younger patients with
acute rotator cuff tears.35 Snyder27 arthroscopically iden-
tified and classified SLAP lesions into four types of
CHAPTER 17 SHOULDER INSTABILITY
B Higgins and Warner’s technique31 involves three
I
III
SGHL
MGHL
II
IV
IGHL
Figure 17-4 The classification by Snyder and associ-
ates27 of basic superior labral lesions is shown. SGHL = supe-
rior glenohumeral ligament; MGHL = medial glenohumeral
ligament; IGHL = inferior glenohumeral ligament. (From
Snyder S, Karzel R, Del Pizzo W, et al: SLAP lesions of the shoulder,
Arthroscopy 6:274-279, 1990.)
lesions (Figure 17-4). In the Type I lesion, the superior
labrum is markedly frayed, but the attachments of
the labrum and biceps tendon remain intact. The Type
I lesion is regarded by many orthopedic surgeons as
benign, or not pathologic.32,36 The Type II lesion is
similar in appearance to Type I with the exception that
the attachment of the superior labrum is compromised,
resulting in instability of the labral-biceps complex. Type
III lesions consist of a bucket-handle tear of the labrum,
which can be displaced into the joint space. However,
the labral-biceps attachment remains intact. Type IV
lesions are similar to Type III lesions except that the
labral tear extends into the biceps tendon, permitting it
to subluxate into the joint.
Treatment of SLAP Lesions
Higgins and Warner31 describe an arthroscopic tech-
nique for repair of Type II SLAP lesions. Historically,
debridement alone has not provided adequate long-term
results because the underlying instability had not been
addressed.37 Currently, suture anchors are recommended
with an arthroscopic knot-tying technique instead of
bioabsorbable tacks because of the risk of fragmentation
of the tack and further complications.31,35 The authors
also advocate the importance of addressing any associ-
ated disorders at the time of arthroscopy such as Bankart
lesions or instability.
491
portals: a posterior, anterior (under the biceps tendon),
and at the anterolateral acromion to allow for suture
anchors and arthroscopic knots to be tied through this
portal. The superior glenoid is removed of all fibrous
material to prepare for repairing the labrum. The glenoid
is decorticated and the anchors are inserted via the
working cannula. It is critical that at least one anchor be
placed at, or posterior to, the biceps insertion to ensure
solid fixation in this region. The sutures are tied off to
the anchors with a sliding knot and reinforced with
several half stitches.
Type III SLAP lesions are treated similarly to Type
II except that the bucket-handle component of this
lesion is excised and no attempt is made to repair this
lesion. While the patient is under anesthesia the surgeon
should attempt to discern if there is any underlying
instability that predisposed the SLAP tear to occur. Type
IV SLAP lesions that compromise less than one third
of the biceps tendon are debrided. If more than one third
of the biceps tendon is involved, than the torn tendon
is repaired back to the major fragment of the biceps.31
Case Study 2: Mrs. D.M.
REHABILITATION FOLLOWING SLAP LESION REPAIR
This case represents the progression postoperatively
for a patient who underwent repair for a Type II SLAP
lesion. Goals and treatment are based on soft tissue
healing and indications/contraindications postopera-
tively.
General Demographics
The patient is a 27-year-old, English-speaking
woman who comes to the clinic 4 weeks after left SLAP
repair. She is left-hand dominant.
Social History: Mrs. D.M. is married with one child.
She does not smoke and drinks approximately one time
per week.
Employment: She is a compliance officer.
Living Environment: Mrs. D.M. lives with her
husband and child on the second floor.
Growth and Development: She is a muscular lean
female, with hypermobile extremities.
PMH
She has a history of left shoulder pain, which
occurred typically while playing tennis in college. She
treated it successfully in the past with physical therapy.
492 SECTION V SURGICAL CONSIDERATIONS
History of Chief Complaint
Mrs. D.M. fell approximately 4 months ago when she
slipped on ice outside her apartment building and she
recalls landing on her outstretched left arm. She felt a
pop and immediate pain at the front of her shoulder. She
describes her pain as sharp when she tries to carry her
laptop computer to work and when she attempts to
reach overhead. The patient also states she has difficulty
sleeping on the left shoulder at night.
Prior Treatment for This Condition
Her physician ordered a series of x-rays 2 weeks after
the incident occurred, which were negative for fractures
or abnormal deformity/alignment. She was given Cele-
brex and physical therapy was prescribed for 6 weeks.
Her course of physical therapy initially tried to address
her pain and gently initiate rotator cuff and scapular
strengthening. On her third visit she complains of more
pain and a feeling of clicking with movements above 90°.
On reexamination, she demonstrates a positive result on
O’Brien’s test, crank test, and apprehension and reloca-
tion tests. She is sent back to the referring physician,
who is given the above findings. A magnetic resonance
imaging (MRI) is ordered and a type II SLAP lesion is
found. She is then scheduled for surgical repair.
Structural Examination
The patient is seen 2 weeks postoperatively and visual
inspection shows mild swelling along the anterior suture
lines, but the sutures are intact and healing well. Left
scapula is elevated relative to the right side.
Range of Motion
Shoulder ROM: This is not assessed because of the
acuteness of her symptoms and contraindications of the
surgery. Elbow and wrist ROM are within normal
limits.
Accessory Motion Testing of the Glenohumeral Joint:
This is not assessed until 4 weeks postoperatively.
Muscle Testing: No resisted testing is permitted at this
time except for wrist motions and hand/finger motions,
which are 5/5 grossly throughout.
Special Tests: No testing is done at this time.
Tenderness: Patient displays focal tenderness along
the anterosuperior glenohumeral joint.
Palpation: Tenderness found along the proximal
biceps tendon.
P.T. Clinical Impression
The patient underwent a Type II SLAP repair
because of a compression injury from a fall. She may
have had some underlying attrition in this region
because of her history of anterior shoulder pain while
playing tennis back in college. The main factors to con-
sider in the early postoperative period are to permit
proper soft tissue healing and to protect the biceps-
superior labral complex from tensile stress. This involves
avoiding elbow flexion exercises early on, which are typ-
ically permitted after most shoulder procedures. Post-
SLAP lesion repairs also require a longer period before
stressing the shoulder motion with external rotation in
the abducted position. This is due to the biceps acting
as a secondary anterior stabilizer in this position.37
Treatment Plan
The following is an overview of this patient’s post-
operative rehabilitation program. The patient is
instructed on continued use of the sling for an additional
2 weeks to protect her biceps-labral complex and told
not to lift or hold objects with her left arm. She is
instructed to ice her shoulder three times a day for 10
to 15 minutes to alleviate local inflammation and
swelling, and to work on maintaining AROM of the
elbow, wrist, and hand. She is instructed in middle and
lower trapezius isometrics in the supine position to facil-
itate neuromuscular control at her scapular region. This
is reinforced during verbal and tactile cues instructing
her to squeeze her shoulder blades down and in, gently
and slowly, while holding for 5 seconds. The patient’s
ROM is strictly passive at this time. She avoids pain and
limits external rotation to 45° initially in the adducted
position.
At 4 weeks postoperatively the sling is removed and
active ROM is initiated in pain-free arcs. The patient’s
initial AROM at this time is shoulder flexion = 85°,
abduction = 60°, external rotation = 25°, and internal
rotation = 50°. The initial phase of rehabilitation is to
restore ROM and pay particular attention to regaining
proper length to the posterior capsule. When the poste-
rior capsule is taut there is a tendency for the humeral
head to shift anterosuperiorly, increasing the potential
for augmenting compressive loading and shear at the
biceps-labral complex. Modalities are used as needed to
quell local postoperative inflammation and prevent
manifestation of biceps or rotator cuff tendonitis.
At 6 weeks postoperatively, strengthening of the
rotator cuff and periscapular musculature is initiated
beginning first with isometrics and progressing to iso-
tonic resisted training as tolerated in a pain-free arc of
motion and in the adducted position. At this time Mrs.
D.M.’s manual muscle testing demonstrates: shoulder
CHAPTER 17 SHOULDER INSTABILITY
flexion = 3+/5, abduction = 4-/5, external rotation =
3-/5, internal rotation = 4/5. Biceps curls and resisted
shoulder flexion is held for an additional 2 weeks time.
At 8 to 12 weeks postoperatively, the patient pro-
gresses to light biceps curls and she is instructed to begin
shoulder flexion with 1-lb weights and progress in 1-lb
increments after she can perform three sets of 12 repe-
titions without altering the mechanics of the lift. Once
she can perform external rotation with a 3-lb weight
while side lying, she progresses to Theraband tubing
beginning in the adducted position. Once she can tol-
erate Theraband scapular strengthening with rows and
shoulder extensions, she progresses to prone scapular
rotator exercises. The patient is instructed to avoid
lifting her arm beyond her torso in the prone position
to avoid overstressing her anterior shoulder.
At 12 weeks after surgery, she demonstrates full
restoration of AROM with the exception of external
rotation in abduction, which is 78°. This motion is not
stressed actively or with resisted exercises until 6 months
postoperatively to avoid possibly overstressing the supe-
rior labral-biceps attachment. On manual muscle testing
she demonstrates forward flexion = 4+/5, abduction =
5/5, external rotation = 4+/5, internal rotation = 5/5. At
this time she is discharged and given a home exercise
program. She is instructed to avoid overstressing her
shoulder with throwing activities or tennis until she
comes back in 4 weeks for a follow-up assessment.
SUMMARY OF CASE
The patient continued her home program for a
month and returned for a follow-up assessment that
demonstrated 5/5 strength throughout her rotator mus-
culature and full AROM. One of the keys with her expe-
ditious rehabilitation was the definitive diagnosis that
was made when she was suspected of having an alterna-
tive cause for her shoulder symptoms other than shoul-
der impingement. Work by Liu and associates has
demonstrated the validity and accuracy of using a cluster
of special tests, which have proven to be more accurate
in predicting glenoid labral tears than MRI.38 The tests
recommended by Liu and associates include the appre-
hension, relocation, load and shift, inferior sulcus sign,
and crank tests.38 We also recommend the use of the
“active compression test” as proposed by O’Brien and
colleagues to more precisely diagnose the possibility of
a SLAP lesion on exam.39 Several authors believe
patients are predisposed to SLAP lesions when shoul-
der instability is present.28,29,31 This is typically checked
493
on physical examination and confirmed when the
patient is under anesthesia. This patient did not demon-
strate any signs of instability, therefore her surgical pro-
cedure did not warrant any capsulorrhaphy and did not
require further soft tissue healing time.
For the athlete following SLAP repair surgery, he
typically is permitted to participate in sports at 3 to 4
months after surgery unless his sport involves throw-
ing.31 According to Higgins and Warner, throwing short
distances and at low velocity commences at approxi-
mately 4 months with emphasis on proper mechanics.
Pitchers are permitted to practice low velocity pitches
from the mound at 6 months and unrestricted throwing
is held until at least 7 months postoperatively.
Rotator Interval Capsule
Recent evidence suggests that the rotator interval region
of the glenohumeral joint plays an integral role in the
pathomechanics and intervention of patients with
shoulder instability.40-42 The term rotator interval has
two distinct meanings when referring to the anterior-
superior aspect of the shoulder. According to Gartsman
and associates, when it is used in conjunction with repair
of the rotator cuff, it is referring to the tendinous con-
nection between the supraspinatus and subscapularis.42
When the rotator interval is in reference to shoulder
instability, it is defined as a triangular space bordered
superiorly by the anterior margin of the supraspinatus
tendon and inferiorly by the superior border of the sub-
scapularis tendon (Figure 17-5).41,42 This triangular
interval is bridged by capsular tissue and is reinforced
superficially by the coracohumeral ligament and in
its deepest segment by the superior glenohumeral
ligament.42-44
Harryman and associates were some of the first to
investigate the role of the rotator interval in gleno-
humeral stability with a cadaveric model.43 They deter-
mined that through operative sectioning of the rotator
interval there was a resultant increase in anterior, poste-
rior, and inferior humeral head translation. Conversely,
imbricating the rotator interval decreased inferior and
posterior translation compared with the intact state of
the shoulder.43 The studies by Harryman and colleagues,
and Rowe and Zarins, suggest that the presence of
defects in the rotator interval may be an important
anatomic factor in shoulder instability.20,43
494 SECTION V SURGICAL CONSIDERATIONS
Supraspinatus
ri
thl
Subscapularis
Figure 17-5 The rotator interval is bordered above
by the supraspinatus tendon and below by the subscapularis
tendon. Its medial margin is the coracoid process and the apex
of this triangle-shaped interval ends laterally at the transverse
humeral ligament. (From Field L, Warren R, O’Brien S, et al: Isolated
closure of rotator interval defects for shoulder instability, Am J Sports Med
23:557-563, 1995.)
More recently, Fields and associates have retrospec-
tively reported on an operative approach for patients
with recurrent instability symptoms involving isolated
closure of the rotator interval.41 The authors determined
clinically a relationship between a 2+ or more positive
sulcus sign for inferior instability and rotator interval
defects that influenced shoulder instability. These
authors also examined the shoulders for direction of
instability while the patient was under anesthesia. They
determined that in all patients the humeral head could
be subluxated anteriorly either grade 2+ (11 cases) or 1+
(4 cases), posterior translation had an average grade of
1+, and a positive sulcus sign was present in all patients.
In our experience, the rotator interval defects are asso-
ciated with a large sulcus sign combined with anterior
instability. Both issues need to be addressed if found
during the surgical repair.
Typically, before arthroscopic closure of the rotator
interval, a supervised physical therapy regimen is imple-
mented to attempt dynamic stabilization via a specific
rotator cuff– and scapular rotator–strengthening
program. These exercises should be designed to enhance
the concavity-compression effect of the rotator cuff at
the glenohumeral joint without further compromising
the static restraints of the shoulder. The physical therapy
trial typically lasts 5 to 6 months before considering sur-
gical intervention.
The surgical technique for isolated closure of the
rotator interval defect as described by Field and associ-
ates41 involves an anterior arthroscopic technique, which
necessitates release of the lateral 30% of the conjoined
tendon insertion to permit access to the anterior capsule.
The subscapularis tendon is released approximately 1 cm
medial to its insertion on the lesser tuberosity, which
also enhances visualization of the rotator interval. After
delineation of the rotator interval, the defect edges are
then approximated—typically with the patient’s arm
placed in 45° of abduction and external rotation. Imbri-
cation is done in a “pants-over-vest” fashion. The closure
of the rotator interval defects reduces the anterior and
inferior capsular redundancy. If necessary to further
reduce inferior translation, imbrication of a lax superior
glenohumeral ligament is performed by overlapping and
suturing the ends with nonabsorbable sutures. Finally,
the subscapularis tendon is reapproximated to its inser-
tion with nonabsorbable sutures.
Case Study 3: Mr. S.Y.
REHABILITATION FOLLOWING ROTATOR INTERVAL REPAIR
This case represents the progression postoperatively
for a patient who underwent isolated closure of a rotator
interval defect that induced shoulder instability.
General Demographics
The patient is a 30-year-old, English-speaking,
Asian male who comes to physical therapy 4 weeks after
rotator interval closure. He is right-hand dominant.
Social History: Mr. S.Y. is single and lives alone. He
does not smoke and drinks approximately twice per
week.
Employment and Environment: He is a director of a
nonprofit company who plays squash and tennis.
Living Environment: Mr. S.Y. lives alone on the fifth
floor.
PMH
He has a history of right shoulder pain and “dead
arm” symptoms, which occurred typically while playing
recreational squash.
History of Chief Complaint
Mr. S.Y. reports his chief complaint is a recurrent
feeling of instability and clicking at the right shoulder,
CHAPTER 17 SHOULDER INSTABILITY
which occurs with tennis and squash, and pain that
began approximately 4 months ago. He has ceased these
activities secondary to exacerbation of his symptoms.
Prior Treatment for This Condition
The patient was seen by his respective orthopedic
surgeon, who determined his symptoms to be associated
with anterior instability based on his history and a pos-
itive apprehension test, positive sulcus test, and 2+ load
and shift test for anterior instability grading. Standard
radiographs of the affected shoulder showed no Bankart
lesions or Hill-Sachs deformities. An MRI was taken,
which did not demonstrate the presence of capsular
irregularities. The patient underwent arthroscopic
exploratory surgery and was found to have a 2.75 cm in
medial-to-lateral width and 2.1 cm in superior-to-infe-
rior height defect at the rotator interval capsule. The
patient underwent arthroscopy to close this defect and
reduce anterior and inferior capsular redundancy.
Structural Examination
The patient is seen 7 days postoperatively wearing a
sling. Visual inspection reveals modest swelling along
the anterior suture lines and ecchymosis, but the sutures
are intact, clean, and dry. His right scapula is elevated
relative to the right side.
Range of Motion
Shoulder AROM: Not assessed because of the acute-
ness of his symptoms and contraindications relative to
the postoperative time period. His PROM was assessed
as follows: shoulder flexion = 85°, abduction = 70°,
external rotation = 0°, and internal rotation = 50°. Elbow
and wrist ROM are within normal limits.
Accessory Motion Testing of the Glenohumeral Joint:
Not assessed because of the acuteness of symptoms and
timeframe from surgery.
Muscle Testing: No resisted testing is permitted at this
time except for elbow, wrist, and hand/finger motions,
which were within normal limits.
Special Tests: No testing is done at this time.
Tenderness: The patient had focal tenderness along
the anterosuperior glenohumeral joint.
Palpation: Tenderness noted along the subscapularis
tendon insertion.
P.T. Clinical Impression
The patient arrives for physical therapy for rehabili-
tation 1 week after a right arthroscopy for isolated
closure of the rotator interval. This surgical procedure is
suggested to help reduce anteroinferior instability.41 The
patient’s ROM will need to be restored with priority to
495
achieve a minimum of 35° of external rotation before
advancing elevation beyond 90° to prevent impinge-
ment.45 However, external rotation will initially be
limited to 0° for the first 4 weeks to permit adequate fix-
ation of the rotator interval region. Care will also need
to be taken to avoid joint mobilization to the anterior or
inferior capsules to prevent overstressing the rotator
interval.
Treatment Plan
The following is an overview for this patient’s post-
operative rehabilitation program.
Pendulum exercises are started immediately postop-
eratively. The patient is instructed on continued use of
the sling for an additional 3 weeks to protect the rotator
interval when he is not in physical therapy or perform-
ing ROM exercises independently. Active-assisted
external rotation exercises are initially limited to 0° for
the first 4 weeks. He is instructed to ice his shoulder two
to three times a day for 10 to 15 minutes to alleviate
local inflammation and swelling, and work on main-
taining AROM of the elbow, wrist, and hand.
After the fourth postoperative week, the sling is
removed and forward flexion and external rotation exer-
cises for ROM and motor control are progressing. The
patient’s initial AROM at this time is shoulder flexion
= 105°, abduction = 65°, external rotation = 10°, and
internal rotation = 50°. The initial phase of rehabilita-
tion is to restore ROM with graded physiologic stretch-
ing coupled with soft tissue mobilization to address
periarticular fibrosis secondary to immobilization.
Aggressive joint mobilizations are contraindicated at
this time because of the possible risk of interfering with
capsular length tension. Modalities are used as needed
to quell local postoperative inflammation and to prevent
manifestation of secondary rotator cuff tendonitis.
At 8 weeks postoperatively, he demonstrates: full
forward flexion = 170°, abduction = 165°, internal rota-
tion = 70°, and external rotation = 85°. At this time a
graduated strengthening program for the rotator cuff
and periscapular musculature is initiated, beginning first
with isometrics and progressing to isotonic-resisted
training as tolerated in a pain-free arc of motion and in
the adducted position. At this time, Mr. S.Y.’s manual
muscle testing demonstrates: shoulder flexion = 4/5,
abduction = 4-/5, external rotation = 3+/5, internal
rotation = 4-/5.
At 12 weeks postoperatively, the patient progresses to
Theraband rotator cuff exercises and prone scapular
496 SECTION V SURGICAL CONSIDERATIONS
rotator exercises to address the middle and lower trapez-
ius musculature. The patient is instructed to avoid lifting
his arm beyond his torso in the prone position and to
avoid overstressing the anterior shoulder. The rotator
cuff exercises are gradually progressing to more provoca-
tive positions of elevated abduction for more sport-
specific and functional patterns of motion.
By 16 to 20 weeks postoperatively, the patient
demonstrates 5/5 strength throughout his right shoul-
der musculature on manual testing. He does not show
any signs of laxity or symptoms of instability and is pro-
gressing to sport-specific exercises to prepare his arm for
tennis and squash. Plyometric training is also instituted
for proprioception and kinesthetic awareness with use of
a medicine ball and quick Theraband repetitions in ele-
vated positions of abduction for the internal rotators.
The patient is permitted to return playing squash and
tennis slowly by the sixth month postoperatively.
SUMMARY OF CASE
The true incidence of rotator interval defects is
unknown at the present time, but there is recent evi-
dence these biologic insufficiencies may be congenital in
origin.40 The aforementioned patient was treated solely
for surgical closure of a rotator interval defect. The
surgeon determined via arthroscopic examination that
there was not any comorbidity to the labrum or anterior
or posterior capsules. It is critical that the therapist is in
communication with the referring surgeon to appreciate
exactly which tissue was involved during the surgical
procedure. Once the initial period of healing is permit-
ted and a pragmatic approach is instituted, with the chief
concern not to be aggressive with joint mobilization
techniques (especially anteriorly and inferiorly before 6
weeks postoperatively), the patient progresses pre-
dictably with respect to strength and return to function.
Open Inferior Capsular Shift
In 1980, Neer and Foster were among the first to em-
phasize the importance of distinguishing between uni-
directional and multidirectional instability because the
standard repairs designed to correct unidirectional insta-
bility would fail when performed on a multidirectional
unstable shoulder.46,47 Neer and Foster describe the infe-
rior capsular shift procedure for treating patients with
symptomatic multidirectional instability of the shoulder
who had failed to respond to nonoperative manage-
ment.46 The inferior capsular shift is still considered the
gold standard for multidirectional instability.46-48
Operative Technique
The operative approach is based on the predominant
direction of instability in each case. This is determined
by the preoperative symptoms and physical findings, and
verified at time of surgery while the patient is under
anesthesia. The anterior approach will be described as
the following per Pollock and associates.47
Once the superficial fascia is removed the subscapu-
laris tendon is incised 1 cm medial to its insertion on
the lesser tuberosity. The incision proceeds from the
superior rotator interval to the inferior border of the
subscapularis tendon. The muscular portion of the sub-
scapularis is also separated from the capsule. The capsule
is then incised starting superiorly in the region of the
capsular cleft between the superior and middle gleno-
humeral ligaments and proceeds inferiorly around the
anatomic neck of the humerus. The dissection of the
capsule proceeds inferiorly until the redundant inferior
pouch can be sufficiently reduced by pulling up on the
traction sutures placed in the capsule and thus extrud-
ing the surgeon’s index finger from the redundant
inferior pouch. The surgeon must anchor the capsule
medially to the glenoid with either nonabsorbable
sutures or suture anchors. The capsule is then split in a
T-fashion just above the superior border of the inferior
glenohumeral ligament (Figure 17-6, A). The patient’s
arm is now placed in 20° of abduction and external rota-
tion. The inferior flap is pulled superiorly, thereby reduc-
ing the inferior capsular pouch and is sutured to the
lateral capsular remnant (see Figure 17-6, B). The cap-
sular cleft between the superior and middle gleno-
humeral ligaments is closed, and this entire superior flap
is then shifted inferiorly over the inferior flap in a cru-
ciate fashion to reinforce the capsule anteriorly (see
Figure 17-6, B). Finally, the subscapularis is repaired
back to the lesser tuberosity and the deltopectoral inter-
val and skin are closed.
Case Study 4: Mr. E.P.
REHABILITATION FOLLOWING INFERIOR CAPSULAR
SHIFT PROCEDURE
This case represents the progression postoperatively
for a patient who underwent an inferior capsular shift
CHAPTER 17 SHOULDER INSTABILITY 497

A B

Figure 17-6 A, T-shaped incision in the glenohumeral joint capsule and synovial lining. B, Superior shift of
the inferior flap and inferior shift of the superior capsular flap. (From Jobe F, Giangarra C, Kvitne R, et al: Anterior capsulobral
reconstruction of the shoulder in athletes in overhand sports, Am J Sports Med 19:428, 1991.)

procedure to address anteroinferior instability of the
shoulder.
General Demographics
The patient is a 29-year-old, English-speaking,
Greek man who comes to physical therapy 4 weeks after
inferior capsular shift of his right shoulder. He is right-
hand dominant.
Social History: Mr. E.P. is single and lives alone. He
does not smoke and drinks approximately twice per
week.
Employment and Environment: He is a professor at a
local university.
Living Environment: Mr. E.P. lives alone in a second
floor apartment.
PMH
He has a history of right shoulder pain and “dead
arm” symptoms, which occurred after his first shoulder
dislocation while playing recreational basketball. Over
the course of a 3-year period, the patient dislocated his
shoulder 8 to 10 times with an increase in the ease of
dislocation and subsequently greater difficulty leave the
original way: with reduction of the shoulder. The patient
reports intermittent paresthesia after each dislocation,
which would typically abate readily after relocation.
History of Chief Complaint
Mr. E.P. reports his chief complaint is a recurrent
feeling of instability and clicking at the right shoulder,
which occurs during basketball and overhead weight
training. The patient reports that the pain and instabil-
ity symptoms are more frequent and recently began to
occur during sleep. His goal is to function with activi-
ties of daily living (ADL) without shoulder pain and
instability, and return to recreational basketball after
surgery.
Prior Treatment for This Condition
The patient is seen for physical therapy at another
clinic to attempt dynamic stabilization of his shoulder,
with a regimented and progressive exercise program
addressing the rotator cuff and scapular rotators. He is
seen for 4 months, which helps decrease his pain con-
498 SECTION V SURGICAL CONSIDERATIONS
siderably with ADL. However, he still has frequent
episodes of subluxation/dislocation with his right shoul-
der during sleep. He also is not able to resume basket-
ball because of residual signs and symptoms of instability
with overhead quick movements.
Structural Examination
The patient is seen 14 days postoperatively wearing
a sling. Visual inspection reveals a well-healed anterior
incision, which is intact to light touch. Moderate
atrophy of the infraspinatus and supraspinatus is noted
relative to the uninvolved side. His scapula is elevated
on the right side when his arms rest at his side in the
standing position.
Range of Motion
Shoulder AROM is not assessed at this time because
of the acuteness of his symptoms related to the early
postoperative time period. His PROM is assessed as
follows: shoulder flexion = 90°, abduction = 60°, external
rotation = -10°, and internal rotation = 50°. Elbow and
wrist ROM were within normal limits.
Accessory Motion Testing of the Glenohumeral Joint:
Not assessed because of the acuteness of symptoms and
time frame from surgery.
Muscle Testing: No resisted testing is permitted at this
time except for elbow, wrist, and hand/finger motions,
which are of normal strength.
Special Tests: The load and shift test is performed for
the left shoulder demonstrating 1° of anterior and infe-
rior translation. Hypermobility is also noted in the left
and right elbows and MCP joints.
Tenderness: The patients displays focal tenderness
along the anterior glenohumeral joint and through the
belly of the right upper trapezius muscle and subscapu-
laris tendon insertion.
P.T. Clinical Impression
Given the patient’s long history of instability it is
important to communicate with the referring surgeon
regarding the patient’s chief directions of instability at
the time of the surgery. The surgeon reports using an
anterior approach after determining, while the patient
was under anesthesia, that his chief direction of insta-
bility was anteroinferiorly. Furthermore, the surgeon
states the patient’s posterior capsule is tight, possibly
augmenting the anterior capsular redundancy. Therefore
it was felt posterior capsular mobilization techniques are
indicated to reduce the stress at the anteroinferior region
of the shoulder and would not threaten posterior stabil-
ity. The initial course of physical therapy is focused on
addressing the impairments related to connective tissue
dysfunction from immobilization and the surgical
procedure.
Treatment Plan
Initial Treatment: Weeks 2 to 4
The patient is instructed on continued use of the sling
for an additional 2 weeks to protect the anterior shoul-
der when he is not in physical therapy or performing
ROM exercises independently. External rotation is
limited to 30° for the first 6 weeks after repair. Sub-
maximal isometrics for the rotator cuff are started at
3 weeks after surgery along with manual resistance to
the biceps, triceps, forearm, and wrist musculature.
Manual resistance is also applied to the scapular retrac-
tors with care to support and protect the glenohumeral
joint.
Weeks 4 to 6
At the fourth postoperative week, the sling is removed
and forward flexion and external rotation exercises for
ROM and motor control are begun, but external rota-
tion is still progressing slowly to prevent stretching out
the repair. Soft tissue mobilization and scapulothoracic
mobilization are initiated along with glenohumeral
posterior capsular mobilizations. The anterior and infe-
rior joint glides are avoided to protect the healing
anteroinferior capsule. Rhythmic stabilization with the
involved shoulder in varying planes of motion is initi-
ated to promote proprioception, co-contraction, and
kinesthetic awareness of the rotator cuff and scapular
musculature.
Weeks 6 to 12
The patient’s initial AROM at this time is shoulder
flexion = 140°, abduction = 125°, external rotation = 40°,
and internal rotation = 60°. At this time isotonic
strengthening exercises are initiated for the rotator cuff,
scapular rotators, and deltoid. A low resistance and high
repetitions format is used to promote the circulatory
phase of healing and build endurance of the surround-
ing dynamic stabilizers. The goal at this phase is to con-
tinue progressing ROM to gradually attain end range
motion. Continued passive stretching and posterior
capsule joint mobilization techniques, and now caudal
glides to restore flexion and internal rotation, are
CHAPTER 17 SHOULDER INSTABILITY
coupled with progressive strength training while moni-
toring the patient’s signs and symptoms of tendonitis or
instability.
Weeks 12 to 20
Active range of motion by 12 weeks postoperatively is
170° of flexion, 165° of abduction, 75° of external rota-
tion in 90° of abduction, and 70° of internal rotation.
His manual muscle tests were as follows: forward flexion
= 4+/5, abduction = 4+/5, external rotation = 4/5, inter-
nal rotation = 4+/5, and prone horizontal abduction-
thumb up (middle trapezius) = 4/5. At this time the
patient’s strengthening program is advanced to plyo-
metric exercises initially using therapeutic balls, includ-
ing a basketball for chest passes and then progressing to
a 5-lb medicine ball for chest and overhead passes. The
patient is using Theraband tubing with progressive
resistance in the plane of the scapula to work his exter-
nal rotators and in 90° of abduction to work his inter-
nal rotators. Proprioceptive neuromuscular facilitation
patterns are initiated to promote functional and syner-
gistic patterning of his scapulohumeral rotators with the
deltoid. The initiation of isokinetic exercise for the
internal and external rotator cuff in the “modified base
position” is recommended at this time. The criterion for
isokinetic progression is the tolerance of a 3-lb isotonic
rotator cuff exercise in side lying and standing external
rotation, with at least blue Theraband resistance and full
range of motion within the training zones of motion.
The isokinetic test on this patient is performed 16 weeks
postoperatively and shows external rotation strength to
be 10% weaker on the involved side and internal rota-
tion strength to be 10% stronger on the involved side
relative to the uninvolved, nondominant side.
Weeks 20 to 28
At week 20 postoperatively, the patient demonstrates
full forward flexion of 175°, abduction of 170°, external
rotation of 90°, and internal rotation of 70°. He does not
show any signs of laxity or symptoms of instability and
is progressing to sport-specific exercises to prepare for
return to basketball. At 24 weeks postoperatively, a
second isokinetic test shows equal external rotation
strength at 60°, 180°, and 240°/sec and 20% greater
internal rotation strength on the involved, dominant
side. At this time he progresses with closed chain exer-
cises for his home program, including modified arc
499
push-ups with a plus to protect the anterior capsule,
seated press-ups, and Swiss ball wall circles.
SUMMARY OF CASE
The inferior capsular shift procedure that this patient
underwent was specific for anterior and, to a lesser
degree, inferior instability. The surgical approach is most
often related to the primary direction of instability to
permit adequate visualization and stabilization. Ade-
quate communication between the surgeon and the
therapist is essential to avoid overstressing the repaired
capsular component with directed joint mobilization
techniques. This procedure is also used for multidirec-
tional instability, which would preclude the use of
posterior capsular mobilizations early on in the rehabil-
itation process. This patient has a long history of dislo-
cations and needs adequate surgical fixation and
postoperative rehabilitation to permit a safe return to
sports without jeopardizing his glenohumeral stability
and to perform ADL pain-free.
Thermal Capsulorraphy
Thermal capsulorraphy was first introduced in 1944, yet
it is considered a new treatment intervention for shoul-
der instability because it has gained popularity among
orthopedic surgeons in recent years.49 Thermal capsu-
lorraphy involves the application of thermal energy to
the joint’s pericapsular tissue via arthroscopy to produce
tissue temperatures of approximately 70° to 80°C
without exceeding 100°C. The immediate thermal effect
causes shrinkage and thickening of the tissue, which
helps abolish the capsular redundancy common to
shoulder instability.49 The use of thermal shrinkage may
help in eliminating the need for open capsular shifts,
which necessitates an open procedure and involves
greater surgical morbidity. However, there is a paucity
of long-term clinical follow-up studies of thermal
capsulorrhaphy of the shoulder and uncertainty remains
at the present time as to the clinical reliability, applica-
tions, safety, and longevity of the effect of collagen
shrinkage.
Experimental studies have described the various
effects of thermal energy on joint capsular tissue.50,51
These studies discovered that tissue modification or
shrinkage is predominantly caused by thermal denatu-
ration of collagen, a major constituent of joint capsular
tissue. Thus when collagen is heated it loses its highly
500 SECTION V SURGICAL CONSIDERATIONS
organized structure and shrinks. More recently, shrink-
age of collagen was proposed to be secondary to unwind-
ing of the triple helix by disruption of the hydrogen
bonds between alpha chains of collagen molecules.49,52
The complications involved with thermal shrinkage
of the glenohumeral capsule include recurrent instabil-
ity, capsule ablation, axillary nerve damage, and postop-
erative adhesive capsulitis.53 Anderson and associates
performed a retrospective review of 106 patients treated
with monopolar radiofrequency thermal capsulorrhaphy
to identify preoperative risk factors for early failure.54
They determined that a history of prior stabilization
procedures and multiple dislocations were both statisti-
cally significant predictors of early clinical failure. Post-
operative factors were specifically related to patient
noncompliance with immobilization, placing thermally
treated tissue at risk for recurrent stretching before bio-
logic repair and restoration of mechanical strength. Our
experience suggests that thermal capsulorrhaphy has
inconsistent long-term results especially in overhead
throwing athletes, with our institutional data showing a
35% failure rate at 2 years postoperatively. This subgroup
is currently treated with a capsular shift followed by
precise rehabilitation. Thermal shrinkage is used cur-
rently for our overhead athletes who have internal
impingement or multidirectional instability as proposed
by Andrews and Dugas.55
Case Study 5: Mr. P.Z.
REHABILITATION FOLLOWING ARTHROSCOPIC ANTERIOR
THERMAL CAPSULORRHAPHY
This case represents the progression postoperatively
for a patient who underwent thermal capsulorrhaphy for
anterior instability of the shoulder.
General Demographics
The patient is a 20-year-old, English-speaking man
who comes to physical therapy 14 days after laser
capsulorrhaphy of his left shoulder. He is left-hand
dominant.
Social History: Mr. P.Z. is single and lives alone. He
does not smoke and drinks approximately once per
week.
Employment and Environment: He is a college base-
ball player.
Living Environment: Mr. P.Z. lives alone in a second
floor apartment.
PMH
He reports a 1-year history of anterior instability of
his left shoulder. He initially experienced his left-
shoulder dislocation that required reduction after diving
headfirst for a ball in center field. Since then, he com-
plains of an intermittent feeling of subluxation and
instability with overhead throws from center field to
home plate. He received nonoperative physical therapy
in the off-season for 5 months, but it did not reduce his
feelings of shoulder instability. He underwent an arthro-
scopic anterior stabilization using Suretacbioabsorbable
tacks and thermal capsulorrhaphy using monopolar
radiofrequency.
History of Chief Complaint
Mr. P.Z. reports his chief complaint is a recurrent
feeling of left shoulder instability and pain, which occurs
with throwing a baseball and overhead weight training.
His goal is to be ready to play baseball on his college
team by the spring season of next year.
Prior Treatment for This Condition
The patient is seen for physical therapy for 5 months
to attempt dynamic stabilization of his shoulder, with a
regimented and progressive exercise program addressing
the rotator cuff and scapular rotators. After 5 months of
physical therapy, he is still unable to throw a baseball
consistently because of residual symptoms of instability
and pain.
Structural Examination
The patient is seen 14 days postoperatively wearing
a sling. Visual inspection reveals a well-healed anterior
incision, which was intact to light touch. Moderate
atrophy of the infraspinatus is noted as is winging of the
inferior angle of the scapula. The patient demonstrates
bilateral 15° hyperextension of right elbow and hyper-
extension of MCP joints in both hands, indicating
general physiologic laxity of both upper extremities.
Range of Motion
Shoulder AROM is not assessed at this time because
of the acuteness of his symptoms related to the early
postoperative time period. His PROM is assessed as
follows: shoulder flexion = 98°, abduction = 65°, external
rotation = 10°, and internal rotation = 50°. Elbow and
wrist ROM were within normal limits. The patient is
instructed to continue wearing the sling for an addi-
tional 2 weeks to protect the anterior capsule and respec-
tive collagen healing. He is instructed to begin elbow,
wrist, and hand ROM exercises along with resisted putty
exercises for grip strength.
CHAPTER 17 SHOULDER INSTABILITY
Accessory Motion Testing of the Glenohumeral Joint:
Not assessed because of the acuteness of symptoms and
time from surgery.
Muscle Testing: No resisted testing is permitted at
this time except for the elbow, wrist, and hand/finger
motions, which demonstrate 5/5 strength.
Special Tests: The load and shift test is performed
for the left shoulder demonstrating 2° of anterior
translation.
Tenderness: Palpation yields focal tenderness along
the anterior glenohumeral joint and through the belly of
the right subscapularis tendon insertion.
P.T. Clinical Impression
The patient displays typical postsurgical stiffness
from a period of immobilization and acute discomfort
anteriorly at the primary surgical site. The initial plan of
care is to protect the shoulder as the covalent bonds of
the collagen fibers are still in a weak state because of col-
lagen denaturation and cell necrosis from the thermal
treatment. Because Mr. P.Z. demonstrates generalized
hypermobility, it is recommended that he progress more
slowly with restoration of ROM in all planes to permit
further tightening of the capsular restraints.56
Treatment Plan
Initial Treatment: Weeks 4 to 6
The patient is instructed to discontinue use of the sling
at this time, but is taught the importance of protecting
the anterior shoulder as ROM is restored. Active-
assisted and passive glenohumeral joint motion is initi-
ated along with scapular mobilization techniques.
Passive range of motion is initially limited in a safe spec-
trum of 100° to 120° of flexion, abduction, and scapular
plane elevation. External rotation and internal rotation
are initially limited to 45° for the first 6 weeks after
repair.56 Avoid the use of accessory motion techniques
or joint mobilization that stress the anterior capsule.
However, posterior glides to the humeral head can be
used to restore full, unrestricted internal rotation by
judiciously stressing the posterior capsule. Submaximal
isometrics for the rotator cuff are started at 4 weeks after
surgery along with manual resistance to the biceps,
triceps, forearm, and wrist musculature. Manual resist-
ance is also applied to the scapular retractors with care
to support and protect the glenohumeral joint. Rhyth-
mic stabilization with the involved shoulder in varying
planes of motion is initiated to promote proprioception,
501
co-contraction, and kinesthetic awareness of the rotator
cuff and scapular musculature. Modalities such as elec-
tric stimulation and ice/heat are used to facilitate ROM
and control postsurgical inflammation.
Weeks 6 to 10
Passive ROM progresses to terminal ranges of motion
in flexion and abduction with external rotation slowly
progressing to 90°. Continued emphasis is placed on
maintaining posterior capsule mobility, with posterior
glides and capsular stretching encouraged to restore
internal rotation and to balance the center or rotation
at the humeral head.43,56 The upper body ergometer is
used to promote total arm and scapular motion, and to
increase circulation. Rotator cuff– and scapular rotator–
strengthening exercises progress to isotonics in a safe
range of motion. Closed kinetic chain exercises are also
initiated at this stage to encourage scapular and rotator
cuff co-activation of the anteroposterior stabilizers using
Swiss balls and modified wall push-ups to protect the
anterior capsule. By the eighth postoperative week, the
patient’s AROM is shoulder flexion = 165°, abduction =
140°, external rotation = 60°, and internal rotation = 50°.
Weeks 12 to 16
Mr. P.Z.’s active range of motion by 12 weeks postop-
eratively is 170° of flexion; 165° of abduction; and 85° of
external rotation and 70° of internal rotation, both in 90°
of abduction. His manual muscle tests are as follows:
forward flexion = 4+/5, abduction = 4+/5, external rota-
tion = 4/5, internal rotation = 4+/5, and prone horizon-
tal abduction-thumb up (middle trapezius) = 4-/5.
Theraband is implemented for glenohumeral internal
and external rotation at first in the adducted position
and then progressing to 90° of abduction, and in the
plane of the scapula for a more functional motion. These
elevated positions progress slowly and with caution to
make certain not to overstress the anterior capsule of
the shoulder or induce symptoms of instability. The
strengthening program is advanced to plyometric exer-
cises initially using therapeutic balls. This includes chest
passes, using a 3 lb and progressing to a 5-lb medicine
ball, to challenge the patient’s dynamic stability and
motor control. Proprioceptive neuromuscular facilitation
patterns are used to promote functional and synergistic
patterning of his scapulohumeral rotators with the
deltoid in diagonal and sport-specific directions. Isoki-
502 SECTION V SURGICAL CONSIDERATIONS
netic exercise for the internal and external rotator cuff
in the “modified base position” is started at this time.
The criterion for isokinetic progression is the tolerance
of 3-lb isotonic rotator cuff exercise weights in a side-
lying position. The criteria also include standing exter-
nal rotation with at least blue Theraband resistance and
full ROM within the training zones of motion. The iso-
kinetic test on this patient is performed 16 weeks post-
operatively and shows external rotation strength to be
10% weaker on the involved side and internal rotation
strength to be 10% stronger on the involved side rela-
tive to the uninvolved, nondominant side.
Weeks 16 to 20
At 16 weeks postoperatively, he demonstrates full
forward flexion of 175°, abduction of 170°, external rota-
tion of 90°, and internal rotation = 70° in 90° of abduc-
tion without signs of instability on examination or
symptomatic complaints of pain or laxity. At this time
he progresses to sport-specific exercises to prepare for a
return to baseball. His isotonic and isokinetic exercises
are elevated into more functional positions, including
the plane of the scapula and in 90° of abduction to better
simulate the demands of throwing on the scapulo-
humeral rotators. At 20 weeks postoperatively, his iso-
kinetic test indicates equal external rotation strength at
90°, 210°, and 300°/sec and 20% greater internal rota-
tion strength on the involved, dominant side. He is
instructed to begin throwing at three-quarter arcs of
motion, first at 60 feet from his teammate for the first
week and progressing to 90 feet for the next 2 to 3 weeks
without throwing overhead. He is cleared to begin
throwing overhead with a gradual progression in inten-
sity, duration, and distance, with the caution to always
warm up properly and stretch his posterior capsule
before, during, and after practices and games.
SUMMARY OF CASE
Mr. P.Z. was followed up 4 weeks after his last visit
or approximately 24 weeks postoperatively and reported
80% of his throwing strength had returned. He also
believed his accuracy was more consistent. He did not
have any complaints of pain or feeling of instability with
throwing at this time.
The importance was reinforced again to continue to
strengthen his rotator cuff and scapular rotators on a
maintenance basis and, as his season progressed, to
properly stretch his posterior capsule. Some of the crit-
ical parameters that guided his rehabilitation were ini-
tially to protect the capsule from early and aggressive
stretching. One of the possible causes of failure after
thermal capsulorrhaphy may be premature stretching of
the anterior shoulder because of the vulnerability of the
collagen early after surgery. Hayashi and associates
suggest limiting ROM for the first 6 to 12 weeks after
thermal capsulorrhaphy because of the deleterious effect
on the mechanical properties of the collagen.49
The patient’s progression with his strength phases
was based on a continuum of treatment, which required
progression to elevated and functional or sport-specific
exercises only if they were pain free. The criterion for
advancing to plyometric training was based on the
patient demonstrating a minimum of 4/5 strength
throughout the rotator cuff.56 Finally, he was not cleared
to resume a throwing program until he could demon-
strate functional and full ROM, negative impingement
tests, and negative muscle-tendon provocation tests, and
objectively document isokinetic strength within 10% of
the contralateral extremity for internal and external rota-
tion.56 It has been recommended that external rota-
tion/internal rotation strength ratios for patients with
rotator cuff and labral pathologic conditions equal 66%
or greater to help bias the extremity towards greater
external rotation strength and to help possibly induce a
posterior drawer of the humeral head.56-58
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Matsen F, editors: The shoulder, Philadelphia, 1990, WB
Saunders.
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45. Browne A, Hoffmeyer P, Tananka S, et al: Glenohumeral ele-
vation studied in three dimensions, J Bone Joint Surg Br
72B:843-845, 1990.
46. Neer C, Foster C: Inferior capsular shift for involuntary infe-
rior and multidirectional instability of the shoulder: a prelim-
inary report, J Bone Joint Surg 62A:897-908, 1980.
47. Pollock R, Owens J, Flatow E, et al: Operative results of the
inferior capsular shift procedure for multidirectional instabil-
ity of the shoulder, J Bone Joint Surg 82A:919-928, 2000.
48. Altchek D, Warren R, Skyhar M, et al: T-Plasty modification
of the Bankart procedure for multidirectional instability of the
anterior and inferior types, J Bone Joint Surg 73:105-112,
1991.
49. Hayashi K, Markel M: Thermal capsulorrhaphy treatment
of shoulder instability: basic science, Clin Orthop & Rel Res
390:59-72, 2001.
50. Hecht P, Hayashi K, et al: Monopolar radiofrequency energy
effects on joint capsular tissue: an in vivo mechanical, mor-
phological, and biochemical study using an ovine model, Am
J Sports Med 27:761-771, 1999.
51. Hayashi K, Hecht P, et al: The biological response to laser
thermal modification in an in vivo sheep model, Clin Orthop
& Rel Res 373:265-276, 2000.
52. Allain J, Le Lous M, Cohen-Solal L, et al: Isometric tension
developed during thermal swelling of rat skin, Connect Tiss Res
7:127-133, 1980.
53. Ritzman T, Parker R: Thermal capsulorrhaphy of the shoul-
der, Curr Opin Orthop 13:288-291, 2002.
54. Anderson K, Warren R, Altchek D, et al: Risk factors for early
failure after thermal capsulorrhaphy, Am J Sports Med 10:231-
235, 2002.
55. Andrews J, Dugas J: Diagnosis and treatment of shoulder
injuries in the throwing athlete: the role of thermal-assisted
capsular shrinkage, Instr Course Lect 50:17-21, 2001.
56. Ellenbecker T, Mattalino A: Glenohumeral joint range of
motion and rotator cuff strength following arthroscopic sta-
bilization with thermal capsulorraphy, J Orthop Sports Phys
Ther 29:160-167, 1999.
57. Kibler W, Livingston B, Bruce R: Current concepts in shoul-
der rehabilitation, Advances in Operative Orthopaedics 3:249-
300, 1995.
58. Warner J, Micheli L, Arslanian L, et al: Patterns of flexibil-
ity, laxity, and strength in normal shoulders and shoulders
with instability and impingement, Am J Sports Med 18:366-
375, 1990.

Rotator Cuff Repairs
T he causes of rotator cuff tears vary and depend
on the age of the patient and on the precipi-
tating activity. Rotator cuff tears may be trau-
matic or degenerative. Because of their locations, the
supraspinatus, primarily, and the infraspinatus, second-
arily, are the most frequently torn muscles of the rotator
cuff (Figure 18-1).
Etiology
The relationship between the impingement syndrome
and rotator cuff disorders, including tears, is well
known.1 Impingement occurs when the coracoacromial
arch causes mechanical irritation of the tendon because
of the narrowing of the subacromial bursal space from
either bony encroachment, such as from spur formation
or abnormalities of the acromion, or from enlargement
of the tendon, such as from tendonitis and inflamma-
tion (Figure 18-2).2,3
Impingement is not the only cause of rotator cuff
tears. Eccentric overload of the rotator cuff muscles,
resulting in overuse and fatigue, can cause failure of the
tendon fibers of the rotator cuff and is probably the most
common cause of tears in young, athletic patients.4 Fiber
failure can also result from chronic tendonitis—includ-
ing eccentric overload patterns of the rotator cuff that
cause tears of the undersurface of the cuff by creating
repetitive deceleration stresses (Figure 18-3). Injuries to
the rotator cuff interval or the superior aspect of the
capsule and the coracohumeral ligament add strain to
the rotator cuff and can precipitate fiber failure.5,6
Another cause of rotator cuff lesions is shoulder dislo-
cation. Primary anterior shoulder dislocation is the cause
of rotator cuff tears in up to 60% of patients, and gleno-
humeral instability can cause fraying of either the upper
505
18
Joseph S. Wilkes
or lower surface of the cuff depending on whether
impingement, known as secondary impingement, or
overload-type forces are placed on the rotator cuff.7-13
Acute tears of the rotator cuff can occur from extrin-
sic overload, such as when a great force is applied to the
abducted arm while the rotator cuff is active. Another
example of extrinsic overload would be a situation in
which a person was forced to catch himself during a fall
by reaching overhead and placing a large distraction
force on the arm. These mechanisms can injure the
capsule and other muscles of the shoulder.
Internal impingement in abduction activities can injure
the supraspinatus and subscapularis.14,15 Additionally,
coracoid impingement syndrome may result from rotator
interval lesions and cause rotator cuff and biceps fraying.16
Other causes of rotator cuff tears are calcific
tendonitis (Figure 18-4),17 tumors,18 and degenerative
changes of the acromioclavicular joint that produce infe-
rior spurs (Figure 18-5).19 Tears in older patients pri-
marily result from coracoacromial arch abrasion.20-22
How the rotator cuff tear develops depends on the
pattern of the abnormal forces applied to the rotator
cuff. Patients with primary impingement have fraying of
the upper surface of the rotator cuff that subsequently
leads to rotator cuff tears and tendon ruptures (Figure
18-6). The subscapularis also can be involved in the
impingement syndrome, and its integrity should be eval-
uated.23 In a reconstruction procedure, the subscapularis
should be used cautiously because secondary impinge-
ment causes the same type of wear pattern.
Diagnosis
The diagnosis of a rotator cuff tear can be difficult
because the signs and symptoms are similar to those of
506 SECTION V SURGICAL CONSIDERATIONS

Clavicle
Coracoid process
Acromion
Coracoacromial ligament
Supraspinatus m.
Coracohumeral ligament
Infraspinatus m.

Subscapularis m.

Biceps tendon

Figure 18-1 Anterosuperior view of the shoulder shows the relationship of the
osseous structures to the rotator cuff and the coracoacromial arch.

Figure 18-3 Arthroscopic view of the inferior surface

of the rotator cuff shows fraying of the undersurface.

Figure 18-2 The pain of impingement is reproduced

with the arm in the fully abducted and flexed position.
CHAPTER 18 ROTATOR CUFF REPAIRS
Figure 18-4 Calcific deposit within the supraspina-
tus tendon.
Figure 18-5 Osteoarthritis of the acromioclavicular
(AC) joint. An inferior spur is impinging on the rotator cuff.
acute rotator cuff tendonitis. The clinical history and
physical examination are the most important compo-
nents in making the diagnosis.24 As part of the initial
examination of a patient with a shoulder problem, plain
radiographs frequently show sclerotic or cystic changes
in the area of the greater tuberosity—a finding that may
indicate advanced rotator cuff disease. If symptoms
persist after a trial of nonoperative treatment, further
507
Figure 18-6 Arthroscopic subacromial view shows
fraying of the rotator cuff (grade II).
Figure 18-7 Arthrogram of the shoulder with dye
extravasation into the subacromial bursa indicates a tear of the
rotator cuff.
noninvasive evaluation should be undertaken to deter-
mine the status of the rotator cuff.
Diagnostic Imaging Techniques
In addition to plain radiography, there are two main
imaging methods for confirming the presence, location,
and size of a defect in the rotator cuff. For many years,
the arthrogram was the standard for documenting a
rotator cuff tear (Figure 18-7).25 An arthrogram is pro-
duced by using radiography after radiographic dye is
injected into the glenohumeral joint. Extravasation of
508 SECTION V SURGICAL CONSIDERATIONS
dye into the area of the subacromial bursa suggests a
rupture. Arthrograms are extremely sensitive for full-
thickness rotator cuff tears, with greater than 90%
sensitivity and specificity,26,27 an accuracy of 98% to
99%, and an 8% incidence of false-negative results.28
However, arthrograms usually cannot provide informa-
tion about incomplete tears, tears on the superior
surface, or advanced rotator cuff tendon disease. Ultra-
sonography is noninvasive and has approximately the
same accuracy as the arthrogram.29
Recently, magnetic resonance imaging (MRI) has
become well established in the evaluation of the rotator
cuff tear. With this newer technology, the sensitivity and
specificity are greater than 90% for all tears in most
studies.29 MRI can detect not only the presence of full-
thickness tears, but also the presence of partial tears,
their size, and their location with a high degree of accu-
racy (Figure 18-8).28,30
Arthroscopic Evaluation
When exercise methods do not relieve a patient’s symp-
toms, surgery may be helpful.31,32 Arthroscopy also can
play an important role in evaluating the rotator cuff for
tears. Both the inferior and superior surfaces of the
rotator cuff along with the biceps tendon can be seen
arthroscopically. The rotator cuff can be palpated with
arthroscopic instruments to determine its integrity
(Figure 18-9) and to differentiate partial-thickness
and full-thickness tears from chronic tendonitis.
Arthroscopy also can help detect instabilities that may
Figure 18-8 MRI of the supraspinatus showing the
compact space under the coracoacromial area and an abnormal
signal in the supraspinatus tendon indicating a tear.
be associated with rotator cuff disorders. During the
arthroscopic examination, the integrity of the anterior
labrum and inferior glenohumeral ligament should be
assessed, and the shoulder joint should be examined for
instability. SLAP lesions of the labrum—that is, supe-
rior labrum anterior and posterior tears—can indicate
glenohumeral dysfunction.33
Treatment
Nonoperative Treatment
Initially, a trial of nonoperative treatment should be pre-
scribed for most rotator cuff problems. Reduction or
elimination of the precipitating activities or modifica-
tion of technique in athletes may alleviate pain and allow
healing. Steroid injections may help to reduce inflam-
mation and allow the patient to begin an exercise
program. However, these injections should be given
infrequently and should not be given to patients with
complete rotator cuff tears. Nonsteroidal antiinflamma-
tory medications should be used judiciously and under
the supervision of a physician.
Exercises to reduce inflammation and restore range
of motion of the shoulder should be prescribed for each
patient on an individual basis. The communication
between the patient and those who are treating him or
her is extremely important during any exercise program
for rotator cuff disease.
Figure 18-9 Arthroscopic view of the glenohumeral
joint shows the undersurface of the supraspinatus portion of
the rotator cuff.
CHAPTER 18 ROTATOR CUFF REPAIRS
Operative Treatment
The indication for surgical treatment is a documented
partial- or full-thickness rotator cuff tear that has not
responded to nonoperative treatment and produces
symptoms that interfere with the patient’s normal func-
tioning. However, acute, symptomatic tears in relatively
young people probably should be repaired early.34,35
Arthroscopic evaluation of the rotator cuff can be
combined with the surgical treatment of most tears. The
partial-thickness tear with fraying on either the inferior
or superior surface can be treated with debridement of
the involved portion of the tendon (Figure 18-10).36,37
The debridement allows for freshening of the injured
portion of the rotator cuff, thus stimulating a healing
response. The remaining fibers hold the cuff in position
to heal. Certainly, a patient with a more advanced
partial-thickness tear (i.e., more torn fibers) of this type
should proceed cautiously in the postoperative period
with regard to activities. For a superior lesion, a cora-
coacromial decompression procedure can also be per-
formed. The rehabilitation is similar to that after open
repair of the rotator cuff, but the program is slightly
accelerated. The rehabilitation period in these patients
can be shortened because they have intact fibers remain-
ing to protect the integrity of the rotator cuff. The results
with this method are initially very good, but long-term
results vary.38,39
During the arthroscopic evaluation, the intraarticu-
lar portion of the biceps tendon should be examined for
Figure 18-10 Arthroscopic view of the gleno-
humeral joint with an arthroscopic motorized blade trimming
the frayed rotator cuff ends.
509
injuries associated with rotator cuff lesions. Frequently,
debridement or tenodesis of the long head of the biceps
muscle is indicated when there is a rotator cuff tear.
Instability and labral abnormalities also can be evaluated
at this time.
Some partial-thickness tears should be repaired to
prevent progression,40 and repair should be considered
for all small full-thickness tears.41 An arthroscopically
assisted method has been developed for the repair of
most rotator cuff tears. The same principles of repair are
used in the arthroscopically assisted method as in an
open repair. Under arthroscopic visualization, the greater
tuberosity in the area of the involved tendon is burred
down to a bleeding bony trough. Next, using an intraar-
ticular suturing technique, sutures are passed through
suture anchors in the greater tuberosity, and the rotator
cuff is attached to the bone by tightening the suture.
Side-to-side suture repair is used for larger tears
(Figure 18-11).42-44
Some lesions must be repaired by an open technique.
Muscle retraction, poor tissue quality, and weak bones
are indications for using open repair. Tears are repaired
through a superior-lateral incision of the surgeon’s
choice (Figure 18-12, A).
Exposure of the rotator cuff tear is facilitated by cora-
coacromial decompression. Small tears can generally be
debrided and advanced to the bony bed without prob-
lems (see Figure 18-12, B,C). Medium and large tears
frequently need moderate mobilization of the muscle
bellies by tension to obtain good repair to the bony bed,
or a V-Y repair can be done (Figure 18-13). Massive
rotator cuff repairs require extensive mobilization of the
muscle bellies and perhaps of the surrounding muscles,
particularly of the subscapularis or infraspinatus, to
allow coverage of the humeral head. In these patients,
the biceps tendon usually is damaged severely or rup-
tured, and a tenodesis can be performed at the bicipital
groove (Figure 18-14).19,45-47
Results
The results of rotator cuff repair are variable and seem
to have a direct relationship to the patient’s age and the
severity of the tear.48,49 Although it has been shown that
repair of rotator cuff tears results in a significant increase
in function for all patients, the degree of patient satis-
faction with the repair depends on the size of the tear,
associated pathologic conditions, and the age of the
 510 SECTION V SURGICAL CONSIDERATIONS

Acromion
Supraspinatus m.

A
B

C Supraspinatus m. D

Exposed bone of
humeral head

E F
Suture anchor
Suture

Humeral head

Supraspinatus tendon
Figure 18-11 A, Arthroscopically assisted repair of
a rotator cuff tear. The arthroscopic portal is in the subacro-
mial bursa. B, Arthroscopic view from the subacromial bursa
Greater tubercle of a tear of the rotator cuff. C, Rupture of the tendinous inser-
G of humeral head tion of the supraspinatus at its attachment to the humeral
head. D, Arthroscopic view of the greater tuberosity after
preparation for rotator cuff repair. E, Sutures are passed
through suture anchors in the greater tuberosity. F, Arthro-
scopic view of the repaired rotator cuff. G, Supraspinatus
tendon is sutured to the humeral head.
 CHAPTER 18 ROTATOR CUFF REPAIRS 511

patient. Patients older than 65 years have a less favor-
able outcome than those younger than 65 years of age,
although symptomatic patients of any age with complete
rotator cuff tears have at least partial relief of their symp-
toms after a successful rotator cuff repair.50-58
Recurring tears of the rotator cuff, especially in the
elderly, are complex and can require extensive recon-
struction if symptomatic. Mobilization of the infra-
spinatus and subscapularis muscles, along with muscle
transfers, has been described.59-61 Rotator cuff arthropa-
thy has been reported in association with long-term
rotator cuff dysfunction.62

Supraspinatus

Articular surface
of humeral head A

B
Tear is trimmed
C to V shape

Figure 18-12 A, The acromion and clavicle are out-

lined for the intended superior-lateral incision. B, Small tear Figure 18-13 A, Medium to large tear with
exposed with the open technique. C, Small tear repaired by supraspinatus muscle retraction. B, Tear is trimmed and cut
open technique. into a V shape. Continued
 512 SECTION V SURGICAL CONSIDERATIONS
Sutured V cut
creates Y
effect
Trough
Edges of supraspinatus
sutured into trough
Figure 18-13, cont’d. C, V-Y closure of tear. The
edges of the V cut are reopposed along the direction of the
muscle fibers. The edges of the supraspinatus are buried in a
bony trough in the humeral head.
Case Study 1
A 46-year-old woman is a volleyball coach for a local
college. She has participated in volleyball as an athlete
and a coach for more than 20 years. She noted increas-
ing pain and discomfort in her right shoulder. She was
treated with nonsteroidal antiinflammatory medications
and physical therapy without relief. An MRI was per-
formed for continued symptoms, which showed an
abnormal supraspinatus tendon with probable rotator
cuff tear. During the initial examination by the ortho-
pedic surgeon, the patient had full range-of-shoulder-
motion; but she had a positive impingement sign and
some weakness on abduction at 90°. She had no insta-
bility and her neurovascular examination was intact.
Infraspinatus
mobilized
Subscapularis
mobilized
Humeral head A
Trough
Supraspinatus m.
Subscapularis m.
Infraspinatus m.
B
Figure 18-14 A, Massive tear of the rotator cuff
with the “bald head” appearance of the humeral head. Mobi-
lization of the infraspinatus and subscapularis and elevation
of the supraspinatus muscle body to repair the rotator cuff.
B, Repaired massive tear after muscle mobilization.
Radiographic examination showed normal bony struc-
tures and joint spaces. A review of the MRI scan showed
a grossly abnormal tendon and a probable tear in the
supraspinatus muscle of the rotator cuff. She was sched-
uled for arthroscopic examination of the shoulder.
At surgery, the diagnostic arthroscopy showed an
intact biceps tendon and articular surfaces. She had a
separation of the anterior-superior labrum, but the infe-
rior labrum was intact with no evidence of instability.
CHAPTER 18 ROTATOR CUFF REPAIRS
Figure 18-15 Arthroscopic view of the inferior
surface of the rotator cuff tear in Case Study 1.
When its inferior surface was viewed, the rotator cuff
tendon was found to be abnormal and to have a tear
(Figure 18-15). It was abnormal over a fairly large area,
and it was thought that open repair was necessary.
Therefore an open incision in the anterolateral aspect of
the shoulder was made to expose the rotator cuff, and a
2-cm superior tear was identified with some retraction
of the tendon. The area was freshened, and the rotator
cuff was repaired to a bony bed with advancement of the
tendon back to the bone (Figure 18-16). After surgery,
she started pendulum and passive range-of-motion exer-
cises, which she continued for the first 4 weeks after
surgery. At that time, she had flexion to 90° and abduc-
tion to 60°, but minimal external rotation. She began a
structured program of physical therapy at 4 weeks after
surgery and progressed satisfactorily over the next 6 to
8 weeks to full range of motion and full strength. At that
point, 3 months after surgery, she was allowed to resume
her normal activities.
Case Study 2
A 48-year-old man was seen in the orthopedic surgeon’s
office with insidious right shoulder pain without a
known precipitating injury. He had pain in the 60° to
120° arc of motion and some pain on forced abduction
at 90°. However, he had good strength, no instability,
and full range of motion. He began a trial of physical
therapy and nonsteroidal antiinflammatory medications,
which allowed him to improve slightly.
513
B
Figure 18-16 A, Appearance of the rotator cuff tear
in Case Study 1 after exposure by open technique. B, Repaired
rotator cuff in Case Study 1.
He returned in 6 months with recurrent pain in
the shoulder. His physical examination was essentially
unchanged at that time. An MRI scan showed a prob-
able rotator cuff tear. The patient underwent arthro-
scopic evaluation and was found to have no evidence of
instability and an intact labrum. However, he had
fraying of the undersurface of the rotator cuff and some
fraying of the articular side of the subscapularis on the
superior aspect (Figure 18-17, A). Examination with the
arthroscope in the subacromial bursa showed a 1-cm tear
of the rotator cuff without retraction. The tear extended
through approximately 80% of the supraspinatus tendon
(see Figure 18-17, B), which was slightly pulled away
from the bone. After subacromial decompression, the
bony bed on the greater tuberosity was freshened with a
motorized arthroscopic blade through a third portal
lateral to the acromion. Two sutures were placed through
514 SECTION V SURGICAL CONSIDERATIONS
A After surgery, the patient was started on full passive
B treatments, Phys Sportsmed 16:129, 1988.
Figure 18-17 A, Arthroscopic view of the under-
surface of the rotator cuff in Case Study 2. B, Arthroscopic
subacromial view of the superior surface of the rotator cuff
showing an incomplete tear of the rotator cuff in Case
Study 2.
Figure 18-18 Arthroscopic subacromial view of the
repaired rotator cuff in Case Study 2.
the supraspinatus tendon, and after drilling two holes in
the greater tuberosity, the sutures were anchored into the
bone with plastic suture anchors. With the shoulder in
the abducted position, the sutures were tied digitally,
pulling the rotator cuff tendon back down to the bony
bed (Figure 18-18).
range-of-motion exercises. By 6 weeks, he had achieved
full range of motion and had started strengthening exer-
cises. By 10 weeks, he had excellent range of motion and
was gaining strength with relief of postoperative pain.
He was started on an increased exercise program.
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37. Budoff JE, Nirschl RP, Guidi EJ: Debridement of partial
thickness tears of the rotator cuff without acromioplasty:
long-term follow-up and review of the literature, J Bone Joint
Surg Am 80A(5):733-748, 1998.
38. Hyvonen P, Lohi S, Jalovaara P: Open acromioplasty does not
prevent the progression of an impingement syndrome to a
tear: nine-year follow-up of 96 cases, J Bone Joint Surg Br
80B(5):813-816, 1998.
39. Hoe-Hansen CE, Palm L, Norlin R: The influence of cuff
pathology on shoulder function after arthroscopic subacro-
mial decompression: a 3- and 6-year follow-up study, J Shoul-
der Elbow Surg 8(6):585-589, 1999.
40. Weber SC: Arthroscopic debridement and acromioplasty
versus mini-open repair in the treatment of significant partial-
thickness rotator cuff tears, Arthroscopy 15(2):126-131, 1999.
41. Gartsman GM: Arthroscopic rotator cuff repair, Clin Orthop
390:95-106, 2001.
42. Yamaguchi K, Ball CM, Galatz LM: Arthroscopic rotator cuff
repair: transition from mini-open to all-arthroscopic, Clin
Orthop 390:83-94, 2001.
43. Gartsman GM: All arthroscopic rotator cuff repairs, Orthop
Clin North Am 32(3):501-510, 2001.
44. Burkhart SS: Arthroscopic treatment of massive rotator cuff
tears, Clin Orthop 390:107-118, 2001.
45. Ellman H, Hanker G, Bayer M: Repair of the rotator cuff:
end-result study of factors influencing reconstruction, J Bone
Joint Surg Am 68(8):1136-1144, 1986.
46. Neviaser JS, Neviaser RJ, Neviaser TJ: The repair of chronic
massive ruptures of the rotator cuff of the shoulder by use of
a freeze-dried rotator cuff, J Bone Joint Surg Am 60A(5):681-
684, 1978.
47. Packer NP, Calvert PT, Bayley JI, et al: Operative treatment
of chronic ruptures of the rotator cuff of the shoulder, J Bone
Joint Surg Br 65B(2):171-175, 1983.
48. Hattrup SJ: Rotator cuff repair: relevance of patient age,
J Shoulder Elbow Surg 4(2):95-100, 1995.
49. Burkhart SS, Danaceau SM, Pearce CE: Arthroscopic rotator
cuff repair: analysis of results by tear size and by repair tech-
nique; margin convergence versus direct tendon-to-bone
repair, Arthroscopy 17(9):905-912, 2001.
50. Adamson GJ, Tibone JE: Ten-year assessment of primary
rotator cuff repairs, J Shoulder Elbow Surg 2:57, 1993.
516 SECTION V SURGICAL CONSIDERATIONS
51. Wilson F, Hinov V, Adams G: Arthroscopic repair of full-
thickness tears of the rotator cuff: 2-14-year follow-up,
Arthroscopy 18(2):136-144, 2002.
52. Habernek H, Schmid L, Frauenschuh E: Five year results of
rotator cuff repair, Br J Sports Med 33(6):430-433, 1999.
53. Gerber C, Fuchs B, Hodler J: The results of repair of massive
tears of the rotator cuff, J Bone Joint Surg Am 82-A(4):505-
515, 2000.
54. Rokito AS, Cuomo F, Gallagher MA, et al: Long-term func-
tional outcome of repair of large and massive chronic tears of
the rotator cuff, J Bone Joint Surg Am 81A(7):991-997, 1999.
55. Worland RL, Arredondo J, Angles F, et al: Repair of massive
rotator cuff tears in patients older than 70 years, J Shoulder
Elbow Surg 8(1):26-30, 1999.
56. Grondel RJ, Savoie FH 3rd, Field LD: Rotator cuff repairs in
patients 62 years of age or older, J Shoulder Elbow Surg
10(2):97-99, 2001.
57. Yel M, Shankwiler JA, Noonan JE, et al: Results of decom-
pression and rotator cuff repair in patients 65 years old and
older: 6- to 14-year follow-up, Am J Orthop 30(4):347-352,
2001.
58. Galatz LM, Griggs S, Cameron BD, et al: Prospective longi-
tudinal analysis of postoperative shoulder function: a ten-year
follow-up study of full-thickness rotator cuff tears, J Bone Joint
Surg Am 83A(7):1052-1056, 2001.
59. Djurasovic M, Marra G, Arroyo JS, et al: Revision rotator cuff
repair: factors influencing results, J Bone Joint Surg Am
83A(12):1849-1855, 2001.
60. Warner JJP, Parsons IM 4th: Latissimus dorsi tendon trans-
fer: a comparative analysis of primary and salvage reconstruc-
tion of massive, irreparable rotator cuff tears, J Shoulder Elbow
Surg 10(6):514-521, 2001.
61. Schoierer O, Herzberg G, Berthonnaud E, et al: Anatomical
basis of latissimus dorsi and teres major transfers in rotator
cuff tear surgery with particular reference to the neurovascu-
lar pedicles, Surg Radiol Anat 23(2):75-80, 2001.
62. Jensen KL, Williams GR, Russell IJ, et al: Rotator cuff tear
arthropathy, J Bone Joint Surg Am 81A(9):1312-1324, 1999.

Shoulder Girdle Fractures
F ractures of the shoulder girdle present the phys-
ical therapist with many issues. Rehabilitation is
often oriented toward the complications caused
by immobilization rather than the fracture itself.
Shoulder pain, stiffness, and weakness after fractures are
common problems presented to the orthopedic physical
therapist. Fractures are always accompanied to some
degree by soft tissue injury, leaving serious implications
for rehabilitation well after the fracture has healed. Even
if the fracture itself heals solidly, it is the soft tissue
recovery that will determine the ultimate outcome of
function.1
This chapter presents a brief overview of some of the
more common types of fractures, fracture healing, the
effects of immobilization on soft tissue, and most impor-
tantly rehabilitation of shoulder girdle fractures. Each
type of shoulder girdle fracture will be reviewed and fol-
lowed by important guidelines regarding rehabilitation.
Types of Fractures
In the simplest of terms fractures can be divided into
two categories, complete and incomplete. Subunits of each
category are further divided and become more compli-
cated. A complete fracture can be described as one in
which the entire surface of the bone is disrupted. An
incomplete fracture does not penetrate the entire surface
of the bone. Complete fractures can be either closed or
open, also called simple or complex, respectively. Open
fractures occur when some portion of the bone pene-
trates the protection of the skin, and complications
caused by infection are common. Complete fractures can
also be described as being displaced or undisplaced, which
517
19
Michael J. Wooden
Jacob P. Irwin
David J. Conaway
describes the relative apposition of the ends of the bones.
Undisplaced fractures occur when all fragments remain
perfectly aligned in normal anatomic positions.
Fractures can be further disseminated based on the
direction of the fracture with reference to the shaft of
the bone. Regarding tubular bone, four terms to describe
direction are regularly found in the literature: transverse,
oblique, oblique-transverse, and spiral. The direction of
the fracture depends on the type of force conferred onto
the bone, that is, a torsion force causes a spiral fracture.
The last types of complete fractures are comminuted and
impacted. Both require a great deal of force. Commin-
uted fractures include any break resulting in more than
two pieces of bone. Impacted fractures occur when one
bone becomes imbedded in another, that is, the humerus
being displaced into the glenoid fossa of the scapula—
usually resulting in fractures of both bones. These frac-
tures require more intensive interventions and there-
fore usually require a greater time and intensity of
rehabilitation.
Another descriptor of fractures is based on the angle
of the bone fragments to one another; this is known as
the alignment of the fracture. The distal portion is gen-
erally described in relation to the proximal portion in the
literature and is described as medial or lateral, dorsal or
ventral.2 The latter of these descriptors are also some-
times referred to as having an anterior or posterior angu-
lation. Fractures of tubular bone—such as the clavicle
and the humerus—can be described by the location of
the fracture, which is, by convention broken into thirds:
proximal, middle, and distal. The exception is a fracture
that is relatively equal in distance from either end, which
is known as a midshaft fracture.2
518 SECTION V SURGICAL CONSIDERATIONS
Stages of Fracture Healing
As in any other body region, displaced fractures of the
shoulder girdle must be immobilized to allow the frac-
ture to progress through the stages of healing. Three
stages of fracture healing are acknowledged in the
literature. The first is the acute, inflammatory stage3 of
hematoma formation, which accounts for approximately
10% of the healing time for a normal fracture.2 During
this phase, the fragment ends and nearby soft tissue
experience a great deal of bleeding, and a hematoma
forms, which leads to the development of a clot. In this
stage of vasodilation and serous exudation, inflammatory
cells are brought to the area to remove necrotic soft
tissue and bone from the ends of the fragments. As the
hematoma becomes more organized at the start of the
reparative stage,3 which encompasses approximately 40%
of the healing time,2 a “fibrin scaffold” is provided for
the reparative cells, which differentiate and begin to
produce collagen, cartilage, and bone. These cells, pri-
marily osteoblasts, invade the hematoma through capil-
lary formation to form a callus of immature bone, which
covers the fragment ends and leads to increased stabil-
ity of the fracture.2 Meanwhile, osteoclast cells resorb
necrotic bone from the ends of the fragments. In the
final remodeling stage,3 which may account for as much
as 70% of the healing time,2 resorption and new bone
formation continue as trabecular bone patterns are laid
down in response to the stress applied (Wolff ’s law). By
this time the immobilization period should be ending so
that the necessary “stress” is provided by remobilization
of the limb.
The length of time required for each healing stage is
influenced by many factors.3 Some of these include the
severity of the trauma, how much bone is lost, the pres-
ence of infection, which bone is fractured, how effective
the immobilization is, and the patient’s age, general
health, and level of activity.
Effects of Immobilization on
Soft Tissue
The combination of trauma to soft tissue and subse-
quent immobilization needed for bone healing con-
tributes to stiffness of periarticular connective tissue
structures and weakness of the surrounding muscula-
ture.4 Much has been researched and written about
changes in histologic, biochemical, and mechanical
properties. To summarize, the most significant motion-
limiting effects are as follows:
1. Loss of extensibility of capsule, ligaments, tendons,
and fascia. Immobilization results in a decrease in
water and glycosaminoglycan content. This
contributes to an increase in aberrant cross-linking
and a loss of movement between fibers.5–7
2. Deposition of fibrofatty infiltrates between joint
structures acting as intraarticular “glue.8”
3. Breakdown of hyaline articular cartilage.9
4. Atrophy and adaptive length changes in muscle.10,11
The factors of immobilization time, fiber type, and
muscle specificity need to be considered when rehabili-
tating the patient who has been immobilized in a cast,
or had their upper extremity suspended in a sling. It has
been shown in animal and human models that casting
and limb suspension will result in decreases in muscle
and bone mass. Atrophy progresses quickly because
of the lack of voluntary contraction, especially when
casting is combined with suspension. This combination
has been shown to result in a 4% decrease of forearm
cross-sectional area (CSA) with only 9 days of immobi-
lization.12 The data collected among human subjects
suggest that much of this loss is found among the fast-
twitch muscle fiber group13 and that extensor muscle
groups incur greater loss than do the flexors.14 Muscle
mass is not all that is lost with decreased use of a limb.
Decreases in muscle strength are also related to
decreased ability to activate motor units at the neuro-
muscular level.15 Also, the duration of casting and/or
limb suspension directly affects the amount of loss.12,16
It has been shown that movement tends to prevent or
reduce the above changes in connective tissue5,22 and
muscle.10,11 It has also been proved that the decreases in
neuromuscular activity caused by 5 weeks of casting can
be reversed entirely with 18 weeks of strength training.15
The problem for us, as clinicians, is knowing when to
begin passive motion and when to progress to active
exercise. This necessitates close communication with the
physician and an understanding of the stages of soft
tissue healing. Evaluation of the direction of restriction,
pain, and reactivity is essential in determining the readi-
ness of movement.23
Clavicle Fractures
Clavicle fractures (Figure 19-1) most commonly occur
from a fall on the lateral aspect of the shoulder or, less
CHAPTER 19 SHOULDER GIRDLE FRACTURES 519

commonly, onto the outstretched arm.24 The clavicle
typically fractures at the juncture of the middle one third
(82%) and distal one third (12%) (Figure 19-2) and less
often in the medial one third (6%) (Figure 19-3). The
ligaments may cause up to a 40% rotation of the frac-
tures that occur in the middle one third of the clavicle.25
Fractures across the distal third can be categorized into
three distinct types. Type I fractures are minimally
displaced and the coracoclavicular ligaments remain
attached to the medial bone fragment. A type II frac-
ture is displaced and includes a functional detachment
of the coracoclavicular ligaments from the medial frag-
ment. Finally, type III fractures include disruption of the
articular surface of the lateral fragment.25
The shoulder is immobilized for 14 to 21 days, either
in a clavicle (or figure eight) brace or in an arm sling.
However, there is no difference in the speed of recovery
between these two treatments.25 Badly comminuted,
delayed union, or surgically repaired fractures will
require more immobilization.

Rehabilitation
Figure 19-1 Clavicle fractures at the (1) juncture of Active range of motion (AROM) exercises should begin
the middle and distal thirds and the (2) middle one third. within 14 to 21 days. Exercises should involve the

Figure 19-2 Radiograph of clavicle fracture at the juncture of the

middle and distal thirds (A) before reduction and (B) after reduction.
520 SECTION V SURGICAL CONSIDERATIONS

Figure 19-3 Radiograph of clavicle fracture in the middle one third

(A) before reduction and (B) after reduction.

shoulder girdle (elevation, depression, protraction, and
retraction) and the shoulder joint (pendulum and wand
exercises). In most cases, a home program is sufficient.
In unusual cases of prolonged immobilization and exces-
sive stiffness, passive mobilization may be necessary.
Evaluation and treatment should include accessory and
physiologic movements of the sternoclavicular, acromio-
clavicular, glenohumeral, and scapulothoracic joints. The
latter is often overlooked, but may be particularly impor-
tant when immobilization occurs in a retracted position.
Prolonged immobilization can also result in muscle
weakness and even in visible atrophy. Resistive exercises
can begin when the fracture appears solidly healed and
when pain with movement is reduced.
Scapula Fractures
Scapula fractures are usually the result of a direct blow.24
Most are nondisplaced. Therefore little or no immobi-
lization is required.
Neck of the Scapula
The fracture line extends from the suprascapular
notch to the lateral border (Figure 19-4, 1). Downward
CHAPTER 19 SHOULDER GIRDLE FRACTURES 521

Figure 19.4 Scapular fractures of the (1) neck,

(2) body, (3) coracoid process, and (4) acromion process.

displacement of the glenoid fragment is not usually

severe.

Body of the Scapula

Fragments are well protected by layers of muscle, even
if comminuted (see Figure 19-4, 2).

Coracoid Process
The fracture is usually not displaced, but occasionally is
displaced downward (see Figure 19-4, 3).

Acromion Process Figure 19-5 Fractures of the upper humerus in the

Again, this is not often displaced. If the fracture is com-
minuted or badly displaced, fragments can be removed
surgically (see Figure 19-4, 4).
Rehabilitation
In most cases, AROM exercises can begin within the
first few days and a home program will suffice. However,
occasional prolonged immobilization because of severe
displacement or surgical treatment may necessitate
passive mobilization and muscle strengthening. All
joints in the shoulder girdle complex should be evalu-
ated, with particular emphasis on the scapulothoracic
and its related musculature. If a direct blow to the
(1) greater tuberosity, (2) neck, and (3) shaft.
scapula was the cause of injury, evaluation of the tho-
racic spine and rib mechanics should be included.
Fractures of The Humerus
Fractures of the upper humerus can involve the greater
tuberosity, neck, or shaft (Figure 19-5). The Neer clas-
sification describes proximal humeral fractures as dis-
placed if there is greater than 1 cm of displacement or
greater than 45° of angulation. Mechanisms of injury are
varied, as are the needs for immobilization and surgery.
522 SECTION V SURGICAL CONSIDERATIONS
Figure 19-6 Radiograph of nondisplaced greater tuberosity
fracture.
The effects of trauma and immobilization on gleno-
humeral joint soft tissue have especially significant
implications for rehabilitation.
Lesser Tuberosity
Lesser tuberosity fractures are rare and are usually asso-
ciated with a posterior dislocation of the glenohumeral
joint. Treatment may include closed reduction if found
within 2 to 3 weeks of the injury, and if there is minimal
articular involvement.
Greater Tuberosity
Fractures of the greater tuberosity are usually the result
of a fall on the shoulder, most commonly in elderly indi-
viduals.24 Fractures are generally retracted posteriorly
and superiorly, making closed reduction very difficult.
These fractures can be associated with an anterior dis-
location, in which a closed reduction of the gleno-
humeral dislocation may reduce the fracture of the
greater tuberosity. Greater tuberosity fractures that
become displaced superiorly or medially may result in a
longitudinal tear of the rotator cuff. In nondisplaced
fractures (Figure 19-6), splinting should be avoided so
that active exercise can begin soon. An avulsed and dis-
placed fragment must be reduced to prevent impinge-
ment with the acromion or coracoacromial ligament,
which will result in painful, limited abduction.20,24 These
are often treated surgically with a fixation screw.
Additional clearance acromioplasty or removal of the
acromion may be necessary. Postoperative immobiliza-
tion is generally from 14 to 21 days.
Neck of the Humerus
Humeral neck fractures are caused by a fall on the out-
stretched arm or the elbow, often in elderly, osteoporotic
women. If the fracture is through the surgical neck of
the humerus, it can be classified in three distinct cate-
gories; unimpacted, angulated impacted, and commin-
uted. In older patients, hemiarthroplasty is often
required, especially if there is more than 45° of anterior
angulation of the fracture. With this type of fracture, the
shaft of the humerus is often pulled medially by the pec-
toralis major. Fractures of the anatomic neck of the
humerus are rare and require open reduction internal fix-
ation (ORIF). If these occur in older patients, a primary
prosthesis is the treatment of choice and it allows early
motion for a rapid recovery.
Because shoulder joint stiffness is a common com-
plication of humeral neck fractures, early movement is
desirable. The immobilization required depends on the
severity of the displacement. In impacted and nondis-
placed fractures (Figure 19-7), the arm can come out of
the sling frequently for exercise. If the fragments are
displaced (Figure 19-8), the arm may need to be
CHAPTER 19 SHOULDER GIRDLE FRACTURES 523

Figure 19-7 Radiograph of impacted humeral neck fracture.

immobilized in a sling held tightly to the chest for 14

to 21 days. Occasionally, an abduction splint is needed
for as much as 4 weeks. Immobilization will vary in cases
of open reduction, internal fixation with plates, or intra-
medullary rods.

Shaft of the Humerus

Humeral shaft fractures usually involve the middle one
third, resulting from a direct blow or a twisting force,
which causes a spiral fracture (Figure 19-9). As in other
upper humerus fractures, early joint motion is desirable.
However, immobilization is greatly variable, depending
on the stability and whether casting or surgical fixation
is used. Surgical intervention is indicated for open frac-
tures, poor closed reduction, segmental fractures, float-
ing elbows, polytrauma, bilateral humeral fractures,
vascular injury, pathologic fractures, and radial nerve
injury following closed reduction, which is associated
with up to 18% of humeral shaft fractures.26 However,
90% of these palsies will resolve within 3 to 4 months
without intervention.26

Rehabilitation
The glenohumeral joint is particularly susceptible to
Figure 19-8 Radiograph of displaced humeral neck stiffness, therefore early remobilization, when safe, is
fracture. essential. Even while the arm is in a sling or cast, the
524 SECTION V SURGICAL CONSIDERATIONS

patient should be taught careful active exercises or be

seen frequently for active assistance-providing exercises.
As the immobilization period ends, the exercises should
be increased gradually in range and vigor.
Once the fracture is stable and reactivity is reduced
at least to moderate (pain and end range resistance
are simultaneous21,23), careful passive mobilization can
begin. Each movement should be tested for reactivity
before mobilizing because some structures may be more
inflamed and painful than others. For example, immo-
A bilizing the arm in a sling, or in a position of adduction
and internal rotation, can result in a “capsular pattern”
limitation.22 In this capsular pattern, all movements at
the glenohumeral joint—especially external rotation and
abduction—will be restricted.23 Therefore mobilization
should emphasize stretching the anterior and inferior
portions of the capsule. During mobilization, pain
should always be respected. When reactivity is moder-
ate to high, grade I and II accessory mobilizations are
used to reduce pain and promote relaxation. When reac-
tivity is low to moderate, grade III and IV accessory and
physiologic mobilizations are used to increase ROM.24
Although most effort will be concentrated at the gleno-
humeral joint, other joints in the shoulder girdle should
be assessed after prolonged immobilization. The reader
is referred to Chapter 14 for a detailed summary of
shoulder joint and girdle mobilization techniques.
Immobilizing the shoulder girdle can result in sig-
nificant muscle weakness. Muscles commonly involved
are the upper and middle trapezius, the pectorals, and
all muscles of the rotator cuff. To minimize weakness
and atrophy, specific isometric exercises should be given
B early. After immobilization—if the fracture is stable,
reactivity is not high, and ROM is at least 50%—sub-
maximal effort progressive resistive exercises can begin,
with progression to maximal effort as tolerated. Isoki-
netic devices are preferred because “stops” can be used
to protect the joint and because resistance can be applied
to all planes of movement, including functional diago-
nals. Chapter 15 outlines the use of shoulder
isokinetics.

Figure 19-9 Radiographs of spiral/oblique humeral
shaft fracture (A) before surgical reduction and (B) after open
reduction, internal fixation.
Fracture-Dislocations
These types of injuries occur in three major classifica-
tions. Two-part fracture-dislocations require closed
reduction of the dislocation and internal fixation of the
displaced fractures. Three-part fracture-dislocations
CHAPTER 19 SHOULDER GIRDLE FRACTURES
require ORIF or use of a prosthetic device. Finally, four-
part fracture-dislocations require hemiarthroplasty, with
tuberosity or rotator cuff reconstruction; or ORIF in
younger patients with quality bone remaining. Rehabil-
itation depends on fracture stability and the treatment
needed to reduce the fracture.
Epiphyseal Fractures
Fractures in adolescents, unlike adults, often occur at or
through the epiphyseal, or growth, plate, resulting in a
greater risk of serious injury and disability. Fractures
result in this region because the plate itself can be up to
five times weaker than the surrounding joint capsule and
ligaments.27 Approximately 80% of growth plate injuries
are caused by shearing or avulsive forces to the bone. The
remaining 20% are caused by splitting and compressive
forces.27 The only commonly injured growth plate in the
shoulder girdle is at the proximal humerus. However,
clavicular epiphyseal injuries are possible.
The types of epiphyseal injuries are most commonly
described by the Salter-Harris classification system. This
system describes five distinct types of epiphyseal frac-
ture. A type I fracture accounts for approximately 6% of
all growth plate fractures, and is characterized by a pure
epiphyseal plate separation and includes no fractured
bone.28 These are caused by shearing across the plate and
are common in very young children (under 5 years old).28
The proximal humerus is a common site for this type of
fracture, but the prognosis is very good for normal
healing with proper immobilization.28 The most
common epiphyseal injury (75%) is a type II Salter-
Harris fracture, which is an epiphyseal separation com-
bined with a fracture of the metaphyseal bone—leaving
a small fragment of bone attached to the growth plate.28
While this injury is the most common type of epiphy-
seal fracture, it is found most often in the lower extrem-
ity and is usually an ulnar fracture if occurring in the
upper extremity.28 Type III and V fractures occur in the
lower extremity and therefore will not be discussed here.
Type IV fractures commonly occur in the distal humerus
and consists of a vertical fracture splitting the metaph-
ysis, growth plate, and epiphysis.28 These fractures occur
about 10% of the time, and may require open reduction
for proper healing.28 Further disseminations of these
injuries have been described and many more types of
fractures across the epiphyseal plate do occur, but are
beyond the scope of this discussion.
525
Summary
Fractures of the shoulder girdle are common and,
because of soft tissue trauma and immobilization, often
result in stiffness—especially at the glenohumeral joint.
When possible, early movement is essential. After a
period of immobilization, all joints of the shoulder
complex should be assessed regardless of the location of
the fracture.
Case Study
GENERAL DEMOGRAPHICS
Patient O.C. is a 58-year-old white, English-
speaking woman whose main complaint is a right shoul-
der fracture-dislocation.
SOCIAL HISTORY
Mrs. O.C. is married and has one child who has
moved away for graduate school. She does not smoke
and drinks occasionally. She walks 1 mile every morning
with her friends.
EMPLOYMENT AND ENVIRONMENT
The patient has been retired for 10 years, but is
responsible for all of the house and yard work including
cleaning, lifting laundry, and tending to outdoor plants.
GROWTH AND DEVELOPMENT
She has no abnormalities and is right-hand
dominant.
LIVING ENVIRONMENT
Mrs. O.C. lives in a two-story home with her
husband.
PAST MEDICAL HISTORY
The patient has no significant history of shoulder or
neck injuries and claims no medical conditions.
HISTORY OF CHIEF COMPLAINT
Mrs. O.C. slipped and fell onto her right shoulder on
June 11, 1994, sustaining a comminuted fracture of
the proximal humerus, with anterior dislocation of the
glenohumeral joint (Figure 19-10, A). This combined
injury required open reduction to relocate the shoulder
joint and internal fixation of the fracture with an
intramedullary rod (see Figure 19-10, B). To facilitate
shoulder joint ROM as the patient began physical
therapy, the rod was removed 1 month later on July 11,
1994. This kept the rod from impinging in the area of
the supraspinatus. There was radiographic evidence of
delayed healing, but the fracture was stable enough for
the patient to begin physical therapy. The patient was
 526 SECTION V SURGICAL CONSIDERATIONS

referred for physical therapy 6 weeks after the injury on

July 25, 1994.
FUNCTIONAL STATUS AND ACTIVITY LEVEL
She complained of severe shoulder pain (7 on a scale
of 10), stiffness, and disability, indicating that she
needed her husband’s assistance with almost all activi-
ties of daily living (ADL), including dressing, bathing,
going to the toilet, and getting in and out of bed. She
reported having been unable to move the upper extrem-
ity because of the pain.
MEDICATIONS
The patient reports that she is taking a pain reliever
prescribed by the referring physician, but cannot recall
A
the name of the drug at the time of evaluation.
HYPOTHESIS DIFFERENTIAL—PATHOLOGY/IMPAIRMENT
Proximal humeral fracture with anterior dislocation—
decreased ROM and increased pain
Rotator cuff tear—impingement with increased ROM
Adhesive capsulitis—capsular pattern to decreased ROM
TESTS AND MEASURES
Because of pain and high reactivity, range of motion
(ROM) and accessory motions could not be assessed on
the initial visit. Muscle strength was grossly 2/5, at best.
PT CLINICAL IMPRESSION: PROGNOSIS AND PLAN
OF CARE

The patient is unable to tolerate most tests and meas-

ures, therefore the primary concern for the initial treat-
ment will be pain reduction to allow further testing and
progress treatment options. The patient tolerated moist
heat and grades 1 and 2 oscillations to reduce pain and
was instructed in gentle pendulum exercises to be done
at home.

Weeks 1 and 2
B Combinations of moist heat, narrow pulse electrical
stimulation, and oscillations were used to reduce pain
and reactivity, and to promote relaxation. During this
time the patient tolerated AAROM exercise. By the end
of the second week, PROM and muscle strength were
as follows.

PROM Reactivity Strength

Flexion 60° Moderate 2+/5

Figure 19-10 A, Patient O.C., comminuted fracture
Abduction 42° High 2+/5
of the right humerus, with anterior dislocation of the gleno-
External rot. 10° High 2+/5
humeral joint. B, After reduction, with the intramedullary rod
Internal rot. 30° Moderate 3+/5
in place.
CHAPTER 19 SHOULDER GIRDLE FRACTURES 527

Weeks 3 to 6

The patient reported gradually decreased pain. She was

better able to dress herself and was able to get com-
fortable at night. During this time joint reactivity con-
tinued to decline and the patient was more tolerant
to passive glenohumeral ROM and mobilization tech-
niques. To improve decreased scapulothoracic mobility,
passive scapular distraction, elevation/depression,
and protraction/retraction were begun. Glenohumeral
and scapular proprioceptive neuromuscular facilitation
(PNF) was begun to increase functional muscle strength.
The patient’s home exercise program (HEP) included
pendulum and wand exercises in all planes, and low-
resistance Theraband strengthening exercises for shoul-
der elevation, abduction, adduction, and internal and
external rotation. At the end of the sixth week, findings
were as follows.

PROM Reactivity Strength

Flexion 120° Low 3+/5

Abduction 98° Moderate 3+/5
External rot. 42° Moderate 3+/5
Internal rot. 64° Low 3+/5
Figure 19-11 Patient O.C., 7 months post injury.

Weeks 7 to 10

By this time physical therapy frequency had been PROM Reactivity Strength
reduced to twice weekly because ROM and function
continued to improve. The passive mobilization Flexion 175° No pain 4+/5
program now included grades 4 to 6 physiologic and Abduction 155° No pain 4+/5
accessory movements with excellent tolerance. Progres- External rot. 90° Low 4+/5
Internal rot. 85° No pain 5/5
sive resistive exercises (PREs) included pull downs,
military presses, and elbow curls. To promote further
scapular strength and mobility, closed kinetic chain exer-
cises included wall pushups, modified prone pushups on She was advised to continue her HEP indefinitely
4-inch foam rolls, and the upper extremity ergometer and to return for reevaluation if any problems arose. The
with resistance to tolerance. Isokinetic internal and patient was seen for a follow-up visit by the surgeon on
external rotation in the plane of the scapula at maximal Jan. 24, 1995. Radiographs revealed that some align-
effort was employed during the last 3 weeks of therapy. ment was lost, but that overall position and healing were
DISCHARGE AND FOLLOW-UP satisfactory (Figure 19-11).
On Oct. 31, 1994—after 10 weeks of therapy and 14
weeks after surgery—the patient reported only minimal, REFERENCES
occasional pain. She was fully independent in her ADL, 1. Gradisar IA: Fracture stabilization and healing. In Davies G,
although overhead activities were still somewhat diffi- Gould J, editors: Orthopaedic and sports physical therapy, St.
cult. ROM and strength findings were as follows. Louis, 1985, CV Mosby.
528 SECTION V SURGICAL CONSIDERATIONS
2. Resnick D: Physical injury: concepts and terminology. In
Resnick D, editor: Diagnosis of bone and joint disorders, ed 3,
Philadelphia, 1995, WB Saunders.
3. Cruess RL: Healing of bone, tendon and ligament. In Rock-
wood CA, Green DP, editors: Fractures in adults, Philadelphia,
1984, JB Lippincott.
4. Engles M: Tissue response. In Donatelli R, Wooden MJ,
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5. Akeson WH, Amiel D, Woo S: Immobility effects on syn-
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6. Woo S, Matthews JV, Akeson WH, et al: Connective tissue
response to immobility: an accelerated aging response, Exp
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7. La Vigne A, Watkins R: Preliminary results on immobiliza-
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8. Enneking W, Horowitz M: The intraarticular effects of
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9. Ham A, Cormack D: Histology, ed 8, Philadelphia, 1979, JB
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10. Tabary JC, Tabary C, Tardieu S, et al: Physiological and struc-
tural changes in cat soleus muscle due to immobilization at
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11. Cooper R: Alterations during immobilization and regenera-
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12. Miles MP, Clarkson PM, Bean M, et al: Muscle function at
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metabolic characteristics of human skeletal muscle following
30 days of simulated microgravity, Aviat Space Environ Med
60:664–670, 1989.
14. Bloomfield SA: Changes in musculoskeletal structure and
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15. Sale DG, McComas AJ, MacDougall JD, et al: Neuromus-
cular adaptation in human thenar muscles following strength
training and immobilization, J Appl Physiol 53:419–424, 1982.
16. MacDougall JD, Elder GC, Sale DG, et al: Effects of strength
training and immobilization on human muscle fibers, Eur J
Appl Physiol 43:25–34, 1980.
17. Akeson WH, Amiel D, Mechanic GL, et al: Collagen cross-
linking alteration in joint contractures: changes in reducible
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18. Wooden MJ: Mobilization of the upper extremity. In
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London, 1994, Churchill Livingstone.
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Philadelphia, 1980, JB Lippincott.
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1980, Institute Press.
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Adams JC, Hamblen DL: Outline of fractures including joint
injuries, Philadelphia, 1999, Churchill Livingstone.
Bucholz RW, Heckman JD, editors: Rockwood and Green’s fractures
in adults, ed 5, Philadelphia, 2001, Lippincott Williams and
Wilkins.
Connolly JF: Fractures and dislocations: closed management,
Philadelphia, 1993, WB Saunders.
Craig EV: Shoulder fractures in the athlete. In Pettrone FA,
editor: Athletic injuries of the shoulder, New York, 1995,
McGraw-Hill.
Crenshaw AH, editor: Campbell’s operative orthopaedics, Philadel-
phia, 1970, WB Saunders.
DePalma AF: Surgery of the shoulder, Philadelphia, 1983, JB
Lippincott.
Gustillo RB, Kyle RF, Templeman DC, editors: Fractures and dis-
locations, St. Louis, 1993, CV Mosby.
Mueller KH: Intramedullary nailing and other intramedullary
osteosyntheses, Philadelphia, 1986, WB Saunders.
Park WH, Hughes SPF, editors: Orthopaedic radiology, London,
1987, Blackwell Scientific Publications.
Rockwood CA, Wilkens KE, Beaty JH, editors: Fractures in chil-
dren, Philadelphia, 1996, Lippincott-Raven.
Rockwood CA, Matsen FA: The shoulder, Philadelphia, 1991, WB
Saunders.
Rowe CR: The shoulder, New York, 1988, Churchill Livingstone.

Total Shoulder
Replacements
S houlder arthroplasty can often result in seem-
ingly miraculous improvement in both pain and
function for the patient with glenohumeral
joint arthritis.1,2 The earliest reported arthroplasty of the
shoulder was performed in 18923 by a French surgeon,
J.E. Pean, who inserted a shoulder replacement made of
platinum and rubber into a young man afflicted with
tuberculous arthritis.3 This prosthesis unfortunately
required removal for sepsis in the early postoperative
period. The modern era of shoulder arthroplasty was
pioneered by Dr. Charles S. Neer II, who initially devel-
oped a shoulder hemiarthroplasty for the treatment of
severe proximal humeral fractures in the early 1950s.4
Neer’s shoulder prosthesis was redesigned in 1973 and
has remained the prototype for all subsequent success-
ful variations in shoulder arthroplasty design (Figure
20-1, A,B).5 In contrast to arthoplasty of the hip and
knee, shoulder replacement remains a more rarely per-
formed procedure, with the average shoulder specialist
performing this operation approximately 40 times per
year and the average general orthopedic surgeon per-
forming this procedure only once per year. Recent
advances in our knowledge of shoulder anatomy and
kinematics and a clearer understanding of shoulder
injuries have led to notable improvements in the design
of the latest generation of shoulder prostheses. Improve-
ments in modularity and design have improved the
surgeon’s ability to more closely duplicate the patient’s
native anatomy and perform complex reconstructions for
arthritic conditions.
529
20
Xavier A. Duralde
This chapter discusses the clinical evaluation of
patients afflicted with arthritis of the glenohumeral joint
and the distinguishing features of each of the various
arthritic processes along with their respective implica-
tions in terms of surgical technique, postoperative
rehabilitation, and overall prognosis. Although gleno-
humeral joint arthroplasty is very reliable in terms of
pain relief, the functional outcome is related to the diag-
nosis. Modification in postoperative rehabilitation is
required depending not only on the bony anatomy but
also on the condition of the surrounding soft tissue.
The indications for shoulder arthroplasty have been
expanding steadily since its first use in proximal humerus
fractures.6 Currently, the most common indications for
shoulder arthroplasty are osteoarthritis,1,5,7-11 rheuma-
toid arthritis,4,12-15 arthritis of dislocation,4,16,17 avascular
necrosis,18,19 cuff tear arthropathy,20-24 acute frac-
tures,4,25,26 and posttraumatic arthritis.4,27
Clinical Considerations
History
Patients who are candidates for shoulder arthroplasty
must undergo a thorough evaluation before considera-
tion of surgery.28,29 This evaluation should include a
history of the onset and progression of shoulder pain,
a detailed medical history, physical examination, and
radiographic evaluation. From a medical standpoint,
the patient’s condition must be adequate to tolerate
530 SECTION V SURGICAL CONSIDERATIONS

Figure 20-1 (A) Anteroposterior and (B) axillary radiographic views of glenohumeral joint osteoarthritis. Notice the
hypertrophic osteophytes on the humeral head, bone on bone contact between the head and glenoid, and posterior subluxation
of the humeral head on the glenoid.

anesthesia and surgery. Certain medical conditions, such
as rheumatoid arthritis, affect not only the bones but
also the soft tissue around the glenohumeral joint and
will affect the surgical technique and rehabilitation.
Patients with osteonecrosis and humeral head collapse
are often on high doses of steroids, which can also have
substantial detrimental effects on the surrounding soft
tissue of the shoulder. Careful evaluation of other body
systems including the heart, lungs, and immune system
is a critical part of the patient evaluation before shoul-
der arthroplasty.
Other important historical considerations include the
patient’s age, hand dominance, work and recreational
activities, socioeconomic and educational background,
and family history. The patient’s ability to participate in
postoperative rehabilitation in terms both of motiva-
tional level and understanding is crucial to the success
of this procedure.
The primary indication for prosthetic replacement of
the glenohumeral joint is pain.4 This is true with pros-
thetic replacement of any joint in the body. Commonly
patients report progression of pain over several years.
Typical complaints include night pain, pain at rest,
and pain provoked by activities of daily living (ADL),
work, or recreational sports. Shoulder pain can have
multiple causes. Other causes of shoulder pain—includ-
ing neurologic, cervical, thoracic, and abdominal
sources—should all be investigated and excluded.
In addition, multiple structures surrounding the
glenohumeral joint, including the rotator cuff and
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS
acromioclavicular joint, can be sources of pain, especially
in the rheumatoid population. They should be excluded
before the consideration of shoulder arthroplasty.15 Pain
characteristics, such as location, character, frequency,
duration, and radiation, are important to evaluate before
surgery.
Limitation of shoulder function and motion should
be considered only secondarily as an indication for shoul-
der replacement. It is highly unusual to recommend and
perform a shoulder arthroplasty in the absence of severe
pain. Although most patients do note a significant
improvement in range of motion (ROM) and function,
the primary indication for shoulder arthroplasty remains
pain. Improvement in function and ROM is more
limited in cases of associated soft tissue injury, severe
bone loss, scarring, or nerve or muscle injury. In patients
with severe damage to surrounding soft tissue, a “limited
goals”4 rehabilitation program is recommended post-
operatively—with the primary goal of pain relief with-
out significant expected improvements in function.
Physical Examination
Following a careful general physical examination, a thor-
ough evaluation of both shoulders is required to include
active range of motion (AROM) and passive range of
motion (PROM), strength, tenderness, and crepitus.
ROM is generally restricted both actively and passively,
and active elevation is characterized by substitution and
exaggerated scapulothoracic motion. Limitation of
external rotation is very sensitive in determining the
degree of glenohumeral restriction in an arthritic shoul-
der.4 Glenohumeral arthritis is differentiated from adhe-
sive capsulitis radiographically, with the latter typically
demonstrating normal radiographs. Patients with severe
weakness, such as those with massive rotator cuff tears,
have limitation in active motion but not passive motion.
Tenderness can be elicited in the arthritic shoulder
by palpation of the posterior joint line. The tuberosity is
typically not tender in the absence of rotator cuff disease.
Pain may be elicited throughout the ROM. Crepitation
in the glenohumeral joint can be elicited with both
AROM and PROM of the shoulder, and often a ratch-
eting motion is visible during active motion of the
glenohumeral joint.
A patient’s strength postoperatively will be critical in
terms of functional improvement following shoulder
arthroplasty. A standardized five-point muscle grading
system allows the surgeon to compare preoperative and
531
postoperative strength.29 Patients with long-standing
glenohumeral arthritis typically display muscle atrophy
and weakness, and pain inhibition to resistive testing.
Nerve injury and rotator cuff disruption must be iden-
tified preoperatively because these will impact both
operative technique and postoperative rehabilitation.
Strength is usually tested by resisted forward elevation
(anterior deltoid and supraspinatus), external rotation
(infraspinatus and teres minor), and abdominal com-
pression testing (subscapularis).
Osteoarthritis
Osteoarthritis of the glenohumeral joint is the most
common indication for total shoulder arthroplasty.4
Although it occurs only one tenth as often as
osteoarthritis of the hip and knee, glenohumeral joint
osteoarthritis usually affects patients approximately 10
years earlier and total shoulder arthroplasty is commonly
performed on patients in their early 50s. Pathologically,
signs of osteoarthritis include loss of the glenohumeral
articular space, large rimming osteophytes of the
humeral neck, and peripheral glenoid spurring (Figure
20-2, A,B). Posterior glenoid erosion with posterior sub-
luxation is common, and loose bodies are typically seen.
Anterior capsular contractures, combined with posterior
capsular stretching, often result in an appearance of
anterior flattening of the shoulder on clinical examina-
tion. The rotator cuff is intact in 90% to 95% of cases.4,11
Biceps tears, when they do occur, are secondary to osteo-
phytes in the proximal humerus. Bone quality in gleno-
humeral osteoarthritis is excellent and typically supports
both humeral and glenoid prostheses well.
Surgical technique in the placement of a total shoul-
der arthroplasty in an osteoarthritic patient begins with
excision of the rimming osteophytes around the humeral
head. This decreases the quantity of bony tissue within
the capsule and aids in the recuperation of motion fol-
lowing surgery. Resection of these osteophytes can be
challenging at the time of surgery because the demarca-
tion between normal bone and osteophyte is not as
clear-cut as one would expect based on preoperative
radiographs. Glenoid version must also be restored to
recenter the humeral head. This can be achieved either
through contouring of the anterior glenoid rim or, more
rarely, bone grafting posteriorly.4 Failure to do this may
lead to posterior instability of the shoulder. Successful
total shoulder arthroplasty depends not only on restora-
tion of the articular surfaces, but also an soft tissue bal-
532 SECTION V SURGICAL CONSIDERATIONS

ancing. Anterior soft tissue contractures, including the
subscapularis, must be released and the posterior capsule
may require plication to restore posterior stability.
Reestablishment of proper resting tension for both the
rotator cuff and deltoid myofascial sleeves is critical to
the restoration of strength following surgery. These two
elements are determined by proper size selection and
orientation of the humeral and glenoid components.30
There is a growing trend among shoulder specialists to
tenodese the biceps tendon during total shoulder
replacement to prevent future complications with this
structure following surgery. In rare cases of concomitant
impingement syndrome, acromioplasty may be desir-
able. In general, the results of total shoulder arthroplasty
have been superior to those of humeral head replace-
ment alone for osteoarthritis—in terms of both motion
and pain.31,32 Patients who undergo humeral head
replacement alone for osteoarthritis do not realize the
full benefit of the procedure for approximately 1 year fol-
lowing surgery, whereas patients with total shoulder
arthroplasty often report that the arthritic-type pain has
disappeared by the first postoperative day. The most
common intraoperative complication of a total shoulder
replacement in osteoarthritis remains fracture of the
humerus, which has been reported in up to 5% of cases.6
This typically requires some type of internal fixation at
the time of initial surgery and may result in increased
blood loss and inflammation postoperatively.

Figure 20-2 (A) Anteroposterior and (B) scapular lateral radiographs of rheumatoid arthritis of the glenohumeral
joint. Note the severe bone loss, erosions in the humeral head, and centralization because of loss of glenoid bone stock.
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS 533

These special surgical considerations in the treatment The wet and resorptive forms are characterized by severe
of osteoarthritis by total shoulder arthroplasty have bone loss, bone erosion secondary to pannus formation,
implications with regards to postoperative rehabilita- and central glenoid wear with medial migration of
tion. The only muscle released during this procedure is the humeral head (Figure 20-3, A,B). These patients
the subscapularis, which will require protection post- often have a marked synovial hypertrophy in both the
operatively by limiting passive external rotation and
avoiding resisted internal rotation for at least 6 weeks
until this muscle has healed. Active elevation, however,
can be started on the first day after the operation. Cap-
sular releases will require the immediate institution of
stretching exercises in the midrange to maintain flexi-
bility. Patients with severe posterior wear and capsular
stretching may have a tendency towards posterior sub-
luxation in the early postoperative period. In this situa-
tion, the surgeon may request exercises be done in
the upright position and the arm be elevated more in the
plane of abduction than flexion to prevent stress on the
posterior shoulder capsule in the early postoperative
period until adequate scarring has occurred.
Patients with glenohumeral joint osteoarthritis are A
ideal candidates for total shoulder arthroplasty and have
the best prognosis of all patients who undergo this pro-
cedure. Good to excellent results are typically found in
more than 90% of patients.1,4,8-11 Active forward eleva-
tion ranges on average between 130° and 145° in
reported series and external rotation typically averages
approximately 40°.5,7,8 Significant improvement in ADL
and shoulder function is reported routinely from multi-
ple centers around the world.1,2,10

Rheumatoid Arthritis
Rheumatoid arthritis is a progressive, systemic disease
that affects not only the joint surfaces but also the
muscles, ligaments, tendons, and bone itself. Approxi-
mately 80% of patients with rheumatoid arthritis have
involvement of their shoulder joint and treatment of
rheumatoid arthritis of the shoulder is often hampered
by associated upper extremity involvement of the elbow, B
wrist, and fingers.13 Rheumatoid arthritis occurs in a
variety of fashions. Dr. Neer has described three clinical
varieties of rheumatoid arthritis involving the shoulder:
the dry, wet, and resorptive forms.4 The dry form resem-
bles osteoarthritis with sclerosis, rimming osteophytes,
and loss of the joint space. This is sometimes referred to
as a “mixed arthritis.” Contractures may be noted in this Figure 20-3 (A) Anteroposterior and (B) axillary
form of rheumatoid arthritis, but are rare in all other lateral radiographs of a patient with avascular necrosis of the
forms. In the dry form, bone quality is typically good humeral head. Notice the subchondral collapse and crescent
although severe erosion is noted at the articular surfaces. sign indicative of subchondral fracture.
534 SECTION V SURGICAL CONSIDERATIONS
glenohumeral joint and subdeltoid bursa, which will
require excision at the time of surgery. Rotator cuff tears
are present in approximately 30% to 40% of patients
with rheumatoid arthritis in marked contrast to
osteoarthritis.15 Bone destruction and osteoporosis are
also much more common with rheumatoid arthritis.
Medical treatment for rheumatoid patients often
includes high-dose steroid treatment, which also affects
soft tissue surrounding the joints.
During surgery, great care must be taken to avoid
fracture to the bone, which is much more osteoporotic
than in osteoarthritis. In some cases, rotator cuff repair
will be possible and can be performed simultaneously
with shoulder arthroplasty. A glenoid prosthesis is
placed only when adequate bone stock is available and
an intact or easily repairable rotator cuff is found at the
time of surgery. Soft tissue contractures, which are so
typical of osteoarthritis, are rarely a problem with
rheumatoid arthritis, and balancing of soft tissue does
not play as important a role as it does in osteoarthritis.
Occasionally in cases of large rotator cuff tears, a
humeral head replacement alone is preferred to prevent
early glenoid loosening because of superior migration of
the humerus and subsequent eccentric loading of the
superior glenoid. (Note: The superior migration happens
anyway. If the glenoid prosthesis is left out, it cannot get
loose). This eccentric glenoid loading has been referred
to as the “rocking horse glenoid” in the orthopedic
literature.33 In cases of severe bone loss, erosion, and
centralization of the humeral head, arthroplasty is still
indicated for pain relief although functional improve-
ment will be much more limited in these patients.
Postoperatively, rehabilitation for arthroplasty in the
rheumatoid patient will progress at a much slower pace.
Therapy must be modified to protect the rotator cuff
repair in these cases. In cases of severe tissue loss, a
“limited goals” program may be instituted to regain
function from “eyes to the thighs.4” Patients who have a
humeral head replacement alone may have more pain in
the early postoperative period than that seen following
total shoulder arthroplasty. Excessive force should be
avoided during stretching exercises. Rheumatoid
patients may be weaker overall with more limited goals
obtained in function and AROM. Non-ambulatory
patients should be restricted from active transfers for
approximately 4 to 6 months after this surgery. It is crit-
ical to avoid aggravation of other affected joints in both
the upper and lower extremity during rehabilitation of
the shoulder.
Pain relief following shoulder arthroplasty in
rheumatoid arthritis is reported in more than 90% of
patients.14,15,4 Functional results are more limited and are
more dependent on the quality of the bone and soft
tissue surrounding the shoulder joint. Most cases obtain
a good or acceptable functional result, but deterioration
of results is noted with time because of progression of
the disease in the soft tissue.13 Average active forward
elevation has been reported postoperatively between 75°
and 100°, with external rotation averaging between 30°
and 45°.9,13 Average function postoperatively is approx-
imately 70% of normal for an age-matched group.9
Glenoid loosening has been reported postoperatively in
more than 40% of patients.13
Arthritis of Dislocation
Arthritis of dislocation refers to glenohumeral joint
arthritis after instability repair. This is characterized by
altered joint anatomy and biomechanics typically result-
ing from an internal rotation contracture following
instability repair. This form of arthritis is most com-
monly seen following nonanatomic repairs and is usually
seen in younger patients below the age of 45.4,16,17 Con-
tracture of the anterior structures, including the
subscapularis and anterior capsule, is typically encoun-
tered. Hardware may also complicate the surgical
approach. This problem can follow unidirectional repairs
in patients with multidirectional instability. Patients may
have posterior subluxation of the shoulder as seen in
osteoarthritis, with internal rotation contractures and
progressive posterior glenoid wear. The pathoanatomy in
this process is similar to that of osteoarthritis, but is
complicated by postoperative anterior contractures,
hardware, and the high demands of this patient group
because of their young age.
At surgery, special attention is directed toward release
of anterior capsular contractures. The subscapularis may
require lengthening and soft tissue must be balanced
with anterior capsular releases and posterior capsular
imbrication. Hardware is usually removed if it is in the
way of prosthetic placement, and glenoid version must
be corrected similar to osteoarthritis. Because this
arthritis typically occurs in younger age groups, a
humeral head replacement may be selected by the
surgeon to prevent progressive glenoid loosening
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS 535

because of high demands placed on the shoulder. This

may result in less complete pain relief than is seen with
total shoulder replacement, especially in the early post-
operative period.31
Postoperative rehabilitation must be modified to
protect the subscapularis repair, and passive external
rotation may be limited more than that allowed follow-
ing arthroplasty for other diagnoses. The subscapularis
may be weak from previous damage and must be
protected early. Residual instability, especially posterior,
may be a problem following arthroplasty, for this diag-
nosis again necessitates elevation be performed more in
the plane of abduction than flexion with stretching exer-
cises performed in the upright position. In cases of pre-
vious deltoid damage, the deltoid will require protection A
postoperatively, and active elevation may not be allowed
in the immediate postoperative period.
The results of arthroplasty for arthritis of dislocation
are inferior to those of arthroplasty for osteoarthritis.16,17
Average forward elevation following this procedure is
approximately 120°, with external rotation of approxi-
mately 40°. Patients in some series have regained only
60% of normal shoulder function following arthroplasty
for arthritis of dislocation.9

Avascular Necrosis
Avascular necrosis of the humeral head occurs second-
ary to an acute vascular insult to the proximal humerus.
It results in collapse and irregularity of the humeral
head, with subsequent loss of bony support for the artic-
ular cartilage (Figure 20-4, A,B).18,19 The articular carti-
lage is not primarily affected but becomes disrupted
following collapse of the bone of the humeral head. If
allowed to progress, the glenoid becomes secondarily
arthritic by articulating against this irregular humeral B
head. Avascular necrosis has been separated into four
stages.18 Stage III is defined by collapse of the humeral
head. Stage IV occurs when the glenoid becomes
involved. Arthroplasty is indicated for these last two
stages. The most common identified cause for avascular
necrosis of the humeral head is corticosteroid use. Other Figure 20-4 (A) Anteroposterior and (B) axillary
causes include trauma, sickle cell anemia, Gaucher’s lateral radiographs of a total shoulder replacement. The normal
disease, alcohol abuse, and Caisson disease. Some cases anatomic relationships have been reestablished by the humeral
can be idiopathic. The rotator cuff is usually normal in head and glenoid prostheses. The variety of stem sizes and
these patients. Stage IV avascular necrosis is also noted humeral head sizes in third-generation prostheses allows the
by capsular contractures, which are typically not present surgeon to customize the prosthesis to each individual patient.
during Stage III.
536 SECTION V SURGICAL CONSIDERATIONS
The surgical management of Stage III avascular
necrosis includes humeral head replacement alone. By
definition, the glenoid is normal at this stage and does
not require replacement. Capsular contractures tend to
be minimal. Once the avascular necrosis has progressed
to Stage IV, a total shoulder replacement in indicated.
Capsular releases are typically required at this stage.
Postoperatively, physical therapy can progress in a
relatively aggressive fashion. These patients are often
younger with good soft tissue quality and can tolerate
rapid progress. Patients must be examined for systemic
disease, which may affect other joints and soft tissue.
Other musculoskeletal structures may be involved,
which will require modification of the rehabilitation
program.
Overall prognosis in this patient group is good, with
average forward elevation of approximately 130° and
external rotation of 80°. These patients tend to regain
approximately 75% of normal shoulder function.4,9
Cuff Tear Arthropathy
Cuff tear arthropathy is a challenging problem for both
surgeon and physical therapist.20 It is characterized by
severe destruction of the glenohumeral joint, with
humeral head collapse and a massive rotator cuff tear in
the absence of other known etiologic factors. This has
been described both in the rheumatologic and orthope-
dic literature with various proposed pathophysiologic
causes. This process typically affects older patients in
their early 70s and is more common in women than
among men. In 1983, Neer described both mechanical
and nutritional causes for the progressive development
of cuff tear arthropathy.20 Fortunately, this problem
occurs in only approximately 4% of patients with rotator
cuff tears. In the rheumatologic literature, McCarty has
called this “Milwaukee shoulder” and has described
active agents in the joint fluid of these patients, includ-
ing hydroxyapatite crystals, neutral proteases, and active
collagenases, which may contribute to the progression of
joint destruction.34 Patients display a high-riding
humeral head and weakness of external rotation associ-
ated with a massive rotator cuff tear. The humeral head
becomes medialized and the proximal scapula wears into
the form of a large cavity between the glenoid and the
undersurface of the acromion. This process has been
called “acetabularization.” The greater tuberosity pro-
gressively wears away from the proximal humerus,
leading to rounding of the humeral head in a process
that has similarly been described as “femoralization.”
Patients have gross instability of the shoulder because of
the massive rotator cuff tear, a large effusion, and severe
weakness.
Historically, constrained prostheses were used to
compensate for rotator cuff deficiency. This was com-
plicated by painful early loosening of the glenoid com-
ponent, which required revision surgery.4 Total shoulder
arthroplasty similarly has been associated with a high
degree of glenoid loosening, and currently humeral head
replacement alone is favored in the treatment of this
complex problem. A bipolar type prosthesis has been
used in some centers, but results to date have been infe-
rior to those seen with standard humeral head replace-
ment.6 A reverse ball-and-socket type of prosthesis, in
which a glenosphere is fixed to the glenoid and a cup-
type stem is placed in the humerus, is currently being
used in Europe. However, it is not approved for use in
the United States as of this writing. This may be an
option for these patients in the future.
In surgery, a humeral head replacement—which is
anatomically sized for the patient—is recommended to
prevent overstuffing of the joint.21 A glenoid prosthesis
is typically not inserted, but contouring of the glenoid
improves stability and can be performed with a reamer.
The subscapularis is often advanced superiorly and
repaired to the greater and lesser tuberosities to improve
stability. Patients who have had a previous decompres-
sion with acromioplasty and release of the coracoacro-
mial ligament are at high risk for the development of
anterosuperior instability following arthroplasty, and
shoulder arthroplasty may be contraindicated in these
patients. Newer techniques, including a fascial arthro-
plasty over the glenoid, may improve results in terms of
pain relief—and early data with this technique has been
encouraging.
Postoperatively, these patients display extreme weak-
ness and require an extremely slow advancement in reha-
bilitation. The rotator cuff repair must be protected with
PROM exercises for 6 weeks and the institution
of a “limited goals” therapy program. The goal of use of
the arm between “eyes and thighs” is realistic in this
severely affected patient group. Because of severe
involvement of the rotator cuff, rehabilitation of the
deltoid muscle is critical for successful management of
these patients.
Humeral head replacement for cuff tear arthropathy
is successful in 90% of cases using “limited goals”
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS
criteria, excluding patients with a prior subacromial
decompression.20-22 Adequate pain relief has been
achieved in 80% to 90% of patients in most series, but
average active forward elevation ranges postoperatively
between 90° and 120°.22-24 External rotation averages
between 30° and 45°.
Acute Fractures
Shoulder arthroplasty is indicated in four-part fractures,
humeral head split fractures, and three-part fractures in
older patients.4,25,26 The greater and lesser tuberosities
are typically displaced from the shaft and humeral head.
At the time of surgery, hemorrhage and inflammation
from trauma are present, and these fractures may also be
further complicated by axillary nerve damage or damage
to other nerves surrounding the shoulder. Proximal
humeral fractures most commonly occur in older
patients and are associated with osteoporosis.
The surgeon is challenged by loss of the normal
anatomic relationships between the tuberosities and
shaft, making placement of the humeral head extremely
difficult at its proper height and version. Some pros-
thetic systems do offer a jig, which may be of some assis-
tance. In addition, the tuberosities and attached rotator
cuff tendons must be repaired back to each other and
the humeral shaft, usually with heavy sutures.
Postoperatively, rehabilitation of these patients pro-
ceeds in a fashion very similar to rehabilitation follow-
ing repair of a massive rotator cuff tear. Active elevation
of the arm is avoided for 6 weeks to protect the tuberosi-
ties, and passive stretching is used to regain flexibility.
Posttraumatic inflammation and scarring more com-
monly lead to tightness of the shoulder following arthro-
plasty for fracture than in other diagnoses. A greater
emphasis on stretching is required. Careful evaluation of
the neurologic structures, especially the axillary nerve, is
critical postoperatively because this structure cannot be
adequately assessed before surgery because of pain and
swelling.
The results of arthroplasty for acute fracture are by
far superior to nonoperative management of these same
fractures.4,26,27 Typically, pain relief is excellent in more
than 80% of cases although function is variable. The
average patient will regain active forward elevation of
approximately 90° to 100° and regain the ability to
perform only approximately 50% of their ADL. Results
are better in patients above the age of 65, primarily
because of lower demands.26
537
Posttraumatic Arthritis
Posttraumatic glenohumeral joint arthritis is related to
previous fractures or fracture/dislocations and is associ-
ated with extensive soft tissue scarring, bone loss, retrac-
tion of the tuberosities, bony malunion, and even
nonunion. If previous attempts have occurred for open
reduction and internal fixation, retained hardware is
found and may complicate matters further. Nerve
injuries may be associated with the initial trauma or sub-
sequent surgery, and there is a higher risk of infection in
these patients because of the previous surgery. In addi-
tion, the rotator cuff may have been injured by the initial
trauma as well.
In surgery, rotator cuff injuries—in the form both of
scarring and tearing—must be addressed with attempts
at mobilization and repair of the rotator cuff. Osteotomy
of the tuberosities is avoided, if this is required, because
results are clearly inferior in cases in which this is per-
formed. The deltoid myofascial resting length must be
restored by placement of the prosthesis at the proper
height and version in the face of altered anatomy.
Modular prostheses currently in use have improved the
surgeon’s ability to modify the fit of the prosthesis to
bony distortion of the proximal humerus following old
fractures.
Postoperative rehabilitation must be individualized
because this is a very heterogeneous group. Early
PROM exercises are critical because this group has a
greater tendency towards stiffness following surgery.
Instability following arthroplasty is of greatest risk in
this patient group and must be prevented by modifica-
tion of the rehabilitation program, depending on the
areas of potential instability. These patients often require
1 full year of rehabilitation to maximize the results of
surgery.
The results of arthroplasty for posttraumatic arthri-
tis are inferior to those seen in acute trauma.4,27 Active
forward elevation has been reported to average approx-
imately 60°, with external rotation of approximately 20°.
Pain relief is also inferior to arthroplasty following early
trauma.
Rehabilitation
The overall goals for postoperative rehabilitation fol-
lowing arthroplasty include pain relief and improvement
in function. Specifically, physical therapy must focus on
538 SECTION V SURGICAL CONSIDERATIONS
limiting postoperative contractures following arthro-
plasty and increasing the strength of the rotator cuff and
deltoid muscles to maximize functional improvement.
Early in the course of physical therapy, the subscapularis
and any other repaired structure must be protected and
patient comfort must be maintained at reasonable levels.
As time progresses more emphasis on strengthening and
functional improvement is critical. Careful communica-
tion with the surgeon and teamwork between the
patient, therapist, and surgeon are critical to a success-
ful outcome following shoulder arthroplasty.
Categories of Rehabilitation Following
Shoulder Arthroplasty
The steps of rehabilitation and overall goals following
shoulder arthroplasty will vary according to the diagno-
sis. Patients fall into three general categories for reha-
bilitation: (A) Programs for patients with a good rotator
cuff and deltoid; (B) programs for patients with a poor
or repaired rotator cuff and deltoid; and (C) “limited
goals” programs.35 Patients in category “A” generally
include those with osteoarthritis, rheumatoid arthritis
with a good cuff, arthritis of dislocation, or avascular
necrosis. Patients in category “B” generally include
rheumatoids with a repaired cuff, acute fracture patients,
and some patients with posttraumatic arthritis. Patients
in the limited goals category include rheumatoids with
an irreparable cuff, patients with previously failed cuff
surgery, cuff tear arthropathy, patients with neurologic
problems, and those with a previously failed shoulder
arthroplasty.
The following protocols can serve as a guide in the
progression of rehabilitation after shoulder arthroplasty
for the variety of diagnoses outlined previously. Careful
communication with the surgeon and patient is a pre-
requisite for safe and tolerable progression. The time
lines specified are general recommendations and must be
adjusted individually based on feedback from the patient
and demonstration of functional improvement.
Patients in the limited goals category are placed there
by the surgeon based on encountered pathologic condi-
tions at the time of surgery. The goals in this patient
group are reasonable pain relief and adequate function
from “eyes to thighs.”
Critical Points and Technique
Because of the variety of pathologic conditions encoun-
tered during shoulder arthroplasty, clear communica-
tion—either written or oral—between the therapist and
surgeon is critical. The therapist must know whether the
rotator cuff was repaired at surgery as this will require 6
weeks of passive elevation rather than the usual active-
assisted exercises. If posterior instability is a concern,
supine exercises may be dangerous. If the quality of the
subscapularis was poor because of prior surgery, external
rotation may require further limitations.
Initiating Treatment
The first step towards achieving a cooperative relation-
ship in postoperative therapy is for the surgeon and ther-
apist to gain the patient’s trust and confidence. The
session in which the arm is moved passively for the first
time sets the stage for the rest of the program and must
be accomplished with confidence and compassion. It is
more important to gain the patient’s trust than achieve
a specific goal of motion in that first session. Confidence
on the part of the therapist comes from a clear under-
standing of that patient’s particular pathologic condition
and its implications on the postoperative rehabilitation
program.
Arm elevation is most comfortably obtained in the
plane of the scapula with the patient’s back and scapula
well supported, either in the supine or sitting position.
A more proximal and certainly firm grasp of the patient’s
arm allows better control by the therapist and results
in better relaxation on the part of the patient (Figure
20-5).
To comfortably externally rotate the patient’s arm,
first make sure that the arm is not in extension because
this will place further stress on the anterior suture line.
If the patient is supine, bolstering under the elbow is
helpful. Slight abduction (~30°) is also beneficial in
unlocking the greater tuberosity from underneath the
acromion (Figure 20-6).
The volume and intensity of daily exercises given to
the patient should be kept at a reasonable level. Shoul-
der arthroplasty patients tend to be elderly and may have
associated medical problems or arthritic processes
involving other joints. Exercises can be performed in
repetitions of 5 to 10 at a frequency of 2 to 3 times per
day. As a group, these patients tend to be motivated and
at times must be cautioned to avoid excessive stress on
their replacement shoulder. Irritation of the rotator cuff
can occur at transitions in the exercise program, espe-
cially when initiating resistive exercises. The exercise
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS 539

Figure 20-5 Passive forward elevation in the plane of

the scapula with the assistance of a therapist or family member.

Figure 20-6 Passive external rotation of the shoulder

using a stick with the arm supported by a bolster.

program can be modified individually based on response
to exercises and levels of pain.
The progression to resistive exercises is allowed when
muscle tendon units, such as the subscapularis, have
safely healed to bone. These exercises are orchestrated
to gradually lead the patient from light muscle reeduca-
tion to full activities. The usual program progresses from
light isometrics (Figure 20-7) to gravity eliminated
(Figure 20-8) and active-assisted ROM exercises
(Figures 20-9 and 20-10). At this point, the patient is
allowed to begin eccentric lowering following active-
assisted elevation (Figure 20-11) and then active ROM
exercises (Figure 20-12). This is followed by light resis-
tive exercises with elastic bands (Figure 20-13) and
dumbbells (Figures 20-14 and 20-15; see also Figure 20-
12). Modified and then full activities follow.
Progression from one level to another is allowed
when a patient can demonstrate the exercises comfort-
ably and in a biomechanically correct fashion. Depend-
ing on the amount of atrophy and associated pathologic
540 SECTION V SURGICAL CONSIDERATIONS

A C

Figure 20-7 Five-way isometric exercises for the glenohumeral

joint with the elbow fixed at 90°. A, Flexion. B, Extension. C, Abduc-
tion. D, Internal and external rotation.
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS 541

Figure 20-8 Gravity eliminated elevation on a table

top.

conditions in the shoulder, each patient will progress at

a different rate.

Summary
Successful outcome following shoulder arthroplasty
requires meticulous surgical technique and a well-
orchestrated and safe rehabilitation program. This
chapter outlines the variety of pathologic conditions
encountered in arthritic processes involving the shoul-
der and details special surgical techniques required with
each diagnosis. Understanding the implications of these
techniques on postoperative rehabilitation and the
overall prognosis with each of the various diagnoses
leading to glenohumeral joint arthritis will assist the
therapist in organizing a safe rehabilitation program
with realistic and reachable goals. Communication
between the therapist, physician, and patient is critical Figure 20-9 Active-assisted elevation of the arm in
to the successful management of these patients. the plane of the scapula using a pulley system.
542 SECTION V SURGICAL CONSIDERATIONS

Figure 20-11 Prone horizontal abduction to

strengthen the supraspinatus.

Figure 20-10 Active-assisted elevation with a stick

in the plane of the scapula.

Figure 20-12 Active elevation of the arm in the

plane of the scapula (scaption).
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS 543

Figure 20-13 Theraband resistive exercises for the rotator cuff and deltoid. A, Flexion. B, Extension. C, Abduction.
D, Internal rotation. E, External rotation.
544 SECTION V SURGICAL CONSIDERATIONS

Figure 20-14 Passive elevation with a stick followed
by active eccentric lowering as tolerated.
Figure 20-15 External rotation exercises with a
dumbbell lying on the contralateral side.
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3. Pean JE, Bick EM (translated): The classic on prosthetic
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4. Neer CS: Glenohumeral arthroplasty: shoulder reconstruction,
Philadelphia, 1990, WB Saunders Co.
5. Neer CS: Replacement arthroplasty for glenohumeral
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7. Sperling JW, Cofield RH, Rowland CM: Neer hemiarthro-
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8. Godeneche A, Boileau P, Favard L, et al: Prosthetic replace-
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13. Sojbjerg JO, Frich LH, Johannsen HV, et al: Late results of
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14. Barrett WP, Franklin JL, Jackins SE, et al: Total shoulder
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17. Biglaini LU, Weinstein DM, Glasgow MT, et al: Gleno-
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18. Ficat P, Arlet J: Necrosis of the femoral head, Ischemia and
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20. Neer CS, Craig EV, Fakuda H: Cuff-tear arthropathy, J Bone
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in total shoulder arthroplasty: association with rotator cuff
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apatite crystals: active collagenase, and neutral protease with
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35. McCluskey GM, Uhl T: Total shoulder replacement, physical
therapy of the shoulder, ed 3, New York, 1997, Churchill
Livingston.

Rehabilitation Programs
Following Total Shoulder
Arthroplasty
Category A: Postoperative
Rehabilitation Program for Total
Shoulder Arthroplasty: Good Rotator
Cuff and Deltoid
Day 1 Arm in sling at rest
Out of bed as tolerated
Elbow, wrist, and finger active exercises
Passive external rotation with stick to
pain tolerance but less than 30° (see
Figure 20-6)
Pendulum exercises (Figure 20-16)
Light use of arm for eating
Days 2-3 Family instructed in passive elevation
exercises
Passive elevation in the plane of the
scapula (see Figure 20-5)
Patient may begin using pulley when
120° of elevation is reached and arm
control adequate (see Figure 20-9)
Instruct in ADL use
Discharge from hospital
Appendix
20-1
Home Program
Weeks 1-2 Protection and use:
—Sling for outdoor use
—Patient may be more comfortable
out of sling when indoors
—May bring hand to mouth for
eating or washing
—May place hand pointing straight
ahead as on armrest of chair
—May use hand for writing
—May begin gentle active use as
tolerated
Modalities:
—Cold pack
—Ultrasound to scapular muscles
—TENS for pain if needed
—Advance to hot packs after sutures
removed
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS
Figure 20-16 Pendulum exercises allow early passive
motion following shoulder arthroplasty.
Exercises:
—PRECAUTION: Avoid excessive
resistance
—Gentle elbow ROM exercises
—Codman’s pendulum exercises
(see Figure 20-16)
—Full passive forward elevation as
tolerated (see Figure 20-5)
—External rotation as tolerated (see
Figure 20-6)
—Light isometrics for muscle re-
education (see Figure 20-7)
(avoid internal rotation isometric)
—Pulley exercises as tolerated (see
Figure 20-9)
—No extension exercises
—Avoid scapular substitution
—May begin scapular stabilizing
exercises (Figure 20-17)
Weeks 2-4 Protection and use: same
Modalities: same
Exercise:
—Goals are full ROM as tolerated
—Add overhead training as
tolerated
—Supine elevation with a stick
advancing to standing elevation
with a stick (see Figure 20-10)
—Continue pulley (see Figure 20-9)
547
Figure 20-17 Scapular stabilizing exercises of retrac-
tion and elevation.
Weeks 4-6 Protection and use: same
Modalities: same
Exercises:
—Begin gravity eliminated elevation
on table top (Figure 20-18)
—Begin wall stretches for full ROM
(Figure 20-19)
—May begin internal rotation and
extension stretches (see Figures
20-18 and 20-19)
Weeks 6-12 Protection and use:
—Discontinue sling
—Advance use in ADLs as strength
and pain allow
Modalities: same as needed
Exercises:
—Add isometric exercises for
strengthening of rotator cuff and
deltoid (see Figure 20-7)
—Advance to resistive exercises as
tolerated (see Figs. 20-11 to 20-
13 and 20-15)
548 SECTION V SURGICAL CONSIDERATIONS

Figure 20-18 Extension exercises with a stick.

Figure 20-19 Internal rotation exercises using a

stick.
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS 549

Figure 20-21 Corner or doorway stretch for termi-

nal external rotation in abduction.

Weeks 12-16 Exercises:

—May add isokinetics when patient
obtains 85% of normal AROM
and at least 4/5 strength for ante-
rior deltoid, and internal and
external rotators. Modified sports
are allowed; short irons and
putting in golf, and ground
strokes in tennis.
4+ Months Progressive return to sports allowed
Progress stretching and strengthening
Figure 20-20 Wall slides for terminal elevation.

—Avoid excessive resistance in

internal rotation to protect sub-
scapularis
—Advance passive stretching exer-
cises to full PROM (Figures 20-
20 and 20-21)
550 SECTION V SURGICAL CONSIDERATIONS
Category B: Postoperative
Rehabilitation Program for Total
Shoulder Arthroplasty—Poor or
Repaired Rotator Cuff and Deltoid
Days 1-3 Arm in sling or abduction pillow
In Hospital Out of bed ambulating
Elbow, wrist, and finger AROM
exercises
Passive pendulum exercises with thera-
pist to tolerance (see Figure 20-16)
Family member instructed in passive
forward elevation within limits set at
surgery (see Figure 20-5)
Home Program
Weeks 1-6 Protection and use:
—Wear sling outdoors and to sleep
—Patient may or may not have
abduction pillow and exercises
may be performed from pillow
—May take arm out of sling indoors
but should protect arm at all
times; do not take shoulder below
position it was in while on pillow
—Patient may bring hand to mouth
for eating or washing while main-
taining elbow at their side
—May place hand pointing straight
ahead, as on armrest of chair
No active elevation Modalities:
—Cold pack
—Ultrasound to scapular muscles
—TENS for pain if needed
—May advance to hot packs after
sutures removed
Exercises:
—Goal in ROM determined at time
of surgery
—Passive elevation to limit set at
surgery (see Figure 20-5)
—Passive external rotation to
limit set at surgery (see Figure
20-6)
—Codman’s pendulum exercises
(see Figure 20-16)
—No pulleys
—No active-assisted exercises
including supine arm elevation
with stick
—Begin scapular stabilizing exer-
cises at week 4 (see Figure 20-17)
Weeks 6-8 Protection and use:
—Discontinue sling or abduction
pillow
—May begin active elevation as tol-
erated beginning with weight of
the arm
Modalities: same
Exercises:
—GOAL: Full passive elevation and
external rotation
—Begin active-assisted supine ele-
vation with stick, advancing to
standing elevation with stick (see
Figure 20-10)
—Start table or thigh level slides
before wall slides (see Figure 20-
8)
—Begin internal rotation and exten-
sion exercises (see Figures 20-18
and 20-20)
—Light isometrics for muscle re-
education (see Figure 20-7)
—Begin pulley (see Figure 20-9)
CHAPTER 20 TOTAL SHOULDER REPLACEMENTS 551

—Advance to assisted wall slides Weeks 10-12 Exercises:

and external rotation in doorway
(see Figures 20-20 to 20-21)
—Begin passive elevation with
active eccentric arm lowering (see
Figure 20-14)
Weeks 8-10 Protection and use: same
Modalities: same
Exercises:
—Begin isometric exercises for
strengthening of deltoid and
rotator cuff as tolerated (see
Figure 20-7)
—Begin terminal stretching for ele-
vation and external rotation (see
Figures 20-20 and 20-21)
—Advance to resistive exercises as
tolerated with elastic bands or
dumbbells (see Figures 20-11 to
20-13, and 20-15)
—Minimize pain avoiding recurrent
impingement problems
12+ Weeks Exercises:
—Advance to isokinetic exercises
—Focus on correct scapulothoracic
rhythm with AROM exercises

Category C: Limited Goals Program

In Hospital Arm in sling Begin passive external rotation to

Elbow, wrist, and finger AROM 20° (see Figure 20-6)
exercises
Week 12 —Begin isometric strengthening
May or may not begin limited
(see Figure 20-7)
passive
—Begin gravity eliminated activi-
ROM exercises of the shoulder
ties within pain tolerance (see
No use of arm with ADL
Figures 20-8 to 20-10)
Pendulum exercises (see Figure
20-16) Month 4 —Begin light elastic resistive exer-
cises (see Figures 20-11, 20-13,
Weeks 2-3 —May begin limited passive ele-
and 20-15)
vation exercises with family
member (see Figure 20-5) Expected Results —Active elevation to 120°
—Active external rotation to 30°
Week 6 —Gradually wean from sling
—Pain free use of arm below shoul-
—Begin scapular stabilizing
der level (“eyes to thighs”)
exercises to pain tolerance (see
Figure 20-17)
Index
A Acetabularization, 536
Abdomen, palpation of, 361
Abducted scapula, 437f, 440f
Abduction external rotation test
(AER), 223
Abduction of shoulder, 55f, 136. See
also Elevation of shoulder
depression, 55f
dynamic ballistic horizontal
abduction exercise, 312f
elevation/depression, 53
in exercise program for throwing
injuries of shoulder, 53-54, 53f,
55f, 56, 60f-61f
in isokinetic exercise with
extension/internal rotation
movements, 350, 351f
ninety degrees/frontal plane with
internal rotation
prone, 48
ninety degrees/scapular plane with
internal rotation
supine, 47
protraction/retraction, 51-53
retraction, 53f
in scapular plane, 13f
in strengthening exercises, 299t
testing of, 55f, 300f
Abscess, perinephric, 374-375
Acceleration, 30-31
Accelerators in overhand throwers,
41
Accessory motion with passive range
of motion (PROM), 100
Note: Page numbers followed by “f ” refer to illustrations; page numbers followed by “t” refer to tables; page numbers followed by “b”
refer to boxes.
Acromioclavicular joint, 12f, 20
anterior glide of, 424, 424f
degenerative changes of, 505
gapping of, 424, 424f
limitation at, 96
mobilization techniques for, 422-424
osteoarthritis of, 507f
palpation of, 106t
synovitis of, 371
Acromioclavicular ligament, 20
Acromiodeltoid muscle, 18
Acromion, 19, 292f
anterior, decompression of, 338-339
architecture of, 338
fracture of, 521, 521f
impingement of humeral greater
tuberosity in hemiplegia, 293,
293f, 295f
palpation of, 106t
superior-lateral incision, 511f
types of, 297, 297f
Action Research Arm Test, 275
Active-assisted elevation
of arm, 541f
with pulley, 541f
with stick, 542f
Active Compression Test, 34, 35
Active compression test-O’Briens, 110,
112f
Active movement
dysfunction of, 191-192
evaluating nervous system sensitivity,
219, 220t
553
Active movement (Continued)
in frozen shoulder, 332-333
subjective evaluation of, 276
Active pump massage of trapezius
muscle, 175f
Active range of motion (AROM), 94-
96, 124, 531
cardinal planes, 94
limitation of, 199f
plane of scapula, 94-96
Activities of daily living (ADL), 136,
137f
in brachial plexus injuries, 251-252
in cumulative trauma disorder
(CTD), 216
interneuron pool electrical activity,
147
Acute fractures, 537
Acute rotator cuff tears with SLAP
lesion, 490-491
Adduction of scapula, 437f
Adduction of shoulder
in active range of motion (AROM)
assessment, 95f
in passive range of motion (PROM)
assessment, 124
Adductor pollicis, 217
Adhesive capsulitis, 19, 99, 136, 159,
319
case study of, 412-416
ADL. See Activities of daily living
(ADL)
Administrative assistants, 141f
Administrators, 141f
554 INDEX
Adolescents, epiphyseal fractures in,
525
Adson’s test, 223
AER, 223
Aerobic walking, 229-230
Afferent nerve, cardiopulmonary, 370f
Afferent nerve fiber, 364f, 366f
Alcohol abuse, 535
Allodynia, mechanical, 145
Altered sensation, 265-266
Alternate supraspinatus test, 118f
Amateur baseball pitcher vs.
professional baseball pitcher, 31
American Physical Therapy
Association
Guide to Physical Therapist Practice,
3-9
content of, 4-9
origins of, 3-4
purpose of, 4
American Shoulder and Elbow
Surgeons (ASES), 485, 489
Anatomy of brachial plexus, 239-243
nerve trunks, 241-242
relationships to, 241
superficial, 239-241
Anatomy of shoulder complex, 15-22
acromioclavicular joint in, 29
brachial plexus in, 234-243
glenohumeral joint in, 15-20
scapulothoracic joint in, 21-22
sternoclavicular joint in, 20, 20f
thoracic outlet, 207-212
Anesthesia
facet joints, 158
local, physical therapy with, 326-
327, 326t
Aneurysm, referring pain to shoulder,
371
Angina pectoris, 372
case study of, 385-390
referring pain to shoulder complex,
90t
Angiography, contrast, 372
Angular joint replication testing, 104
Anterior acromion, decompression of,
338-339
Anterior deltoid muscle, strengthening
exercises for, 299t
Anterior glenohumeral joint
capsule of, 483
dislocation of, radiograph of, 485f
Anterior glenohumeral joint
(Continued)
impingement of, 295-296
subluxation of, 270f, 273f
Anterior/posterior glenohumeral joint,
subluxation of, 270-272
Anterior-posterior scour, 470, 470f
Anterior rami, 144, 211
Anterior release test, 107-109, 108f
Anterior-superior labrum, tears, 33
Anterior tubercles of transverse
processes, palpation of, 105t
Anterior view of posture, 92
Anterolateral fascial elongation, 472,
472f
Anteroposterior lateral elongation of
upper thoracic region, 469-470,
469f
Anxiety, 145, 167
Aortic aneurysm referring pain to
shoulder, 371
Appendix, perforated, 366
Apprehension test, 105, 107f, 126
Arachidonic acid, 178
Arm
active-assisted elevation of, 541f,
542f
active assistive movement of, 287f-
288f
dead, 34
elevation of, 138f, 293, 293f
in planes, 11
flail, 216
hyperabduction of, 223
outstretched, fall on, 490
AROM. See Active range of motion
(AROM)
Arterial obstruction
referring pain to shoulder, 371-
372
with thoracic outlet syndrome
(TOS), 217
Arterial pulses, palpation of, 361
Arthritis, 537
of acromioclavicular joint, 507f
after dislocations, 534-535
of glenohumeral joint, 531-532
radiography of, 530f
of knee, 97
osteoarthritis, 97, 507f, 531-532
radiography of, 530f
posttraumatic, 537
Arthrography
of frozen shoulder, 327-328, 328t
of rotator cuff tears, 507-508
Arthrokinematic movement, 13-14,
14f, 293
definition of, 13
of glenohumeral joint, 14f
restoration of normal, 348-349
Arthroscopy
of anterior thermal capsulorrhaphy
rehabilitation following, 500-
502
of frozen shoulder, 328-332, 329t-
330t
of rotator cuff tears, 507f
case study of, 353-354
of shoulder instability, 489
SLAP lesion in throwing athlete,
86-88
Articular cartilage, 139
Articulatory techniques, definition of,
405
ASES, 485, 489
Assembly line work, 216
Assessment. See Evaluation
Assisted movement, subjective
evaluation of, 276
Asthma, 211
Asymmetric scapular malposition, 35-
36
Athletes. See also specific sport
rotator cuff tears in, 302-315, 505
classification of, 302
instability-impingement complex,
304
instability-subluxation-
impingement-rotator cuff
tear, 304
neuromuscular retraining, 311-312
open and closed chain exercise,
307-315
posterior impingement, 304-305
primary tensile overload, 302-
303
rehabilitation, 305-306
scapula role in, 306-307
secondary tensile overload, 303-
304
throwing injuries in, 86-88
Atypical reach, 265
Autonomic nervous systems, normal
protective reflex of, 212

Avascular necrosis, 535-536
of humeral head, 533f
Axial compression of cervical spine,
151f, 153f
Axillary nerve, 145
lesions of, 246
Axillary support, 288, 290f
Axiohumeral muscle, 18. See also
Latissimus dorsi; Pectoralis major
length assessment of, 438-440
response to dysfunction, 101t
Axioscapular muscle, 18. See also
Levator scapulae muscle;
Pectoralis minor; Rhomboid(s);
Serratus anterior muscle;
Trapezius muscle
length assessment of, 436-438
response to dysfunction, 101t
B relationships to, 241
Back. See also Lower back
exercises for, 59-72
Bacterial endocarditis, 371
case study of, 390-395
referring pain to shoulder, 371
Bankart lesion, 484, 491
Bankart reconstruction, 489
Bankart surgical stabilization, 485
Baseball pitchers, 96
amateur vs. professional, 31
internal rotation, 39
shoulder range of motion, 39
SLAP, 34
subscapularis muscle of, 18
Baseball players
internal rotation, 38
range of motion, 38
Basketball players, mobilization for,
407-412
Bench press plus, 60
Biceps load test, 112, 114f
Biceps long head tendon, 341
Biceps muscle, 19
Biceps tendon
cross friction of, 476
intraarticular portion of, 509
long head of, 18f
Biceps tendon superior labral complex,
33-35, 39
Bicipital groove tenderness test, 34
Bicipital tendinitis, 140
Bilateral lunge, 65-66
INDEX 555
Biofeedback, electromyographic, 286 Brachial plexus provocation test
Bioflavonoids, 178 (BPPT), 219-221
Biomechanics, functional, 22-26 Brain reacting to injury, 167-168
Blocks Breaking balls, 29
injection, facet joints, 158 Breathing, diaphragmatic, 226-228,
interscalene, physical therapy with, 226f-229f
326-327, 326t Breathing pattern
Blood flow, 467 paradoxical, 212-213
Blood vessels of thoracic outlet, 211- thoracic outlet syndrome (TOS),
212 222-223
Body mechanics in joint mobilization, Breathing techniques, 167
417 Burner syndrome, 247
Bones of thoracic outlet, 207-209 Bursitis, 159
Bone spurs in impingement, 338 Byl, Nancy, 224
Bony Bankart fracture, 485f
BPPT, 219-221 C
Brachial plexus, 144, 211, 239-260 Caffeinated drinks, 178
anatomy of, 239-243 Caisson disease, 535
nerve trunks, 241-242 Calcific tendonitis, 505
Canal of Guyon, 209f
superficial, 239-241 Cancer
protection of, 242 pain with, 360
provocation test for, 219-221 referred pain from
Brachial plexus injuries gallbladder, 374
activities of daily living (ADL), 251- kidney, 374
252 liver, 373
case studies of, 254-259 lung, 368
classification of, 243-246 pancreas, 90t
axillary nerve lesions, 246 spine, 368
infraclavicular lesions, 245 stomach, 375
lateral cord lesions, 245 Cane, grasping with wrist extension,
long thoracic nerve lesions, 245- 281f-282f
246 Capsule, 16, 32-33
medial cord lesions, 245 of anterior glenohumeral joint, 483
peripheral nerve lesions, 245 mobility testing, 346
supraclavicular lesions, 243-244 Capsuloligamentous complex, 483
trunk lesions, 244-245 Capsulorrhaphy, arthroscopic anterior
of construction workers, 258-259 thermal, rehabilitation following,
etiologic classification of, 244b 500-502
history of, 249-250 Cardinal planes, active range of motion
laboratory evaluation of, 253 (AROM), 94
musculoskeletal, 247-248 Cardiopulmonary afferent nerve, 370f
nerve conduction studies of, 253- Cardiovascular conditioning, 229-230
254 Carpal tunnel, 209f, 210f
pathophysiology of, 248 pressure gradients in, 214, 214f
patient management, 248-249 Carpal tunnel syndrome (CTS), 217
physical examination chart for Carpenters, 141f
recording, 249f with brachial plexus injuries, 254-
rehabilitation prognosis and 258
intervention, 254 Cartilage, articular, 139
tests and measures for, 250-251 Cashiers, 142
traumatic, 246-247, 246f Cash register work, 216
556 INDEX
CELF, 166f
Central muscle weakness, 262-263
Central sensitization, 145-148, 146f,
168
Cervical disk disease, magnetic
resonance imaging (MRI), 151
Cervical disks
computed tomography of, 151
herniated, 153
intervertebral, 143
referring pain, 150-151, 150f
Cervical facet joints, 139, 144
computed tomography of, 158
degenerative joint disease of, 153f
irritation of, 155-160
magnetic resonance imaging (MRI),
158
osteophytosis of, 153f
palpation of, 105t
referred pain patterns from, 158f
Cervical fascia
deep, 134
posttraumatic scarring along, 211
Cervical lateral glide, 196-197
Cervical muscle, response to
dysfunction, 101t
Cervical plexus, 144
Cervical quadrant test in extension,
155f, 161
Cervical radiculopathy
causing referred pain, 91
EMG responses to, 195-196, 200,
200f
incidence of, 187-188
Cervical Rotation Lateral Flexion
(CRLF), 166f
Cervical screening, 123-124
differential soft tissue diagnosis, 91
Cervical spinal cord, facilitated
segment of, 146f
Cervical spine
axial compression of, 151f
axial compression testing of, 153f
muscles of, 156f-157f
negative tests, 171
nerves of, 143
neurologic screening of, 92t
positive tests, 171
Cervical techniques/trapezius stretches,
473-474, 474f
Cervical ventral rami, 144
Cervicobrachial disorder, 187
Cervicobrachial pain syndrome, 187-
188
C fibers, 215
Cholecystitis
case study of, 395-400
referring pain to shoulder complex,
90t
Cholelithiasis, 374
Chondroitin sulfate, 178
Chronic obstructive pulmonary disease
(COPD), 211
Chronic pain and neuroplasticity,
215
Chronic tendonitis, 505
Circle theory, 16
Clavicle, 135
axes of motion of, 21f
fractures of, 518-519, 519f, 520f
inferior, 427-429, 428f
palpation of, 105t
rotation of, 20
for superior-lateral incision, 511f
Clavipectoral fascia, 135
Closed chain exercise, 308-309
Closed fractures, 517
Closed manipulation for frozen
shoulder, 328-332, 329t-330t
Clubbing, fingernail, 371
Clunk test, 110, 111f
Cocking, 30
Co-contraction, 265
Coffee, 178
Cold applications. See Cryotherapy
Collagen, 466b
Colon referring pain to shoulder, 375-
376
Comminuted fractures, 517
of humerus, 526f
Complete fractures, 517
Complex fractures, 517
Compressive cuff disease, 291-302. See
also Impingement syndrome
case studies of, 301-302
pathology of, 292-297
extrinsic factors, 292-296
intrinsic factors, 296-297
Computed tomography (CT)
of cervical disk disease, 151
of cervical joints, 158
of thoracic facet disease, 163f
of thoracic outlet syndrome, 218
of thoracic spine, 161
Computer keyboard operators, 143
Computer screens, 218
Connective tissue
classification of, 466
histology of, 465-466
immobilization effects on, 466-467
Constrained prostheses, 536
Construction workers with brachial
plexus injuries, 258-259
Contralateral flexion, 197
Contrast angiography, 372
Coordination in brachial plexus
injuries, 251
COPD, 211
Coracoacromial arch, related to rotator
cuff, 506f
Coracoacromial ligament, 292f
palpation of, 106t
Coracoclavicular ligament, palpation
of, 106t
Coracohumeral ligament, 16, 20
Coracohumeral space, 291-292
Coracoid impingement syndrome, 505
Coracoid process, 292f
fracture of, 521, 521f
palpation of, 106t
Coronary artery insufficiency, 191
Corticosteroids, 535
Costoclavicular syndrome, 247
Costocoracoid ligament, 135
Costocoracoid membrane, 135
Costosternal joint, 12f
Costovertebral joint, 12f
Crank test, 110, 111f
Cross friction of supraspinatus and
biceps tendon, 476, 476f
Cryotherapy for frozen shoulder, 332
CT. See Computed tomography (CT)
CTDS. See Cumulative trauma
disorder (CTD)
CTS, 217
Cubital tunnel, 209f, 210f
Cumulative trauma disorder (CTD),
140
activities of daily living (ADL),
216
ergonomic solutions to, 143
fluid dynamics, 213-216
pathophysiology of, 212-217
dysfunctional reflexes affecting
tunnel diameter, 212-213
fluid dynamics, 213-216

Cumulative trauma disorder (CTD)
(Continued)
gender issues, 216-217
occupational and ADL issues, 216
Cutaneous tissue, hyperalgesic
responses to palpation, 195
Cyriax’s sequence of pain and
resistance, 97
D cervical screening, 123-124
Daily living. See Activities of daily
living (ADL)
Dead arm, 34
Deep cervical fascia, 134
posttraumatic scarring along, 211
Deep vein thrombosis (DVT), 367-368
Degenerative disease
of acromioclavicular joint, 505
of disks, 361
of left cervical facet, 153f
of uncovertebral joint, 153f
Dejerine Klumpke paralysis, 245
Deltoid muscle, 19, 24f
anterior, strengthening exercises for,
299t
EMG activity of, 23
force couple of, 24f
mid and posterior heads of, 19
resistive tests, 101t
response to dysfunction, 101t
rotator cuff force couple, 347f
splitting of, 339, 351-352
case study of, 354-355
strengthening exercises for, 299t
strength testing of, 445-447, 447f,
448f
Depression, 145
Dermatomes, 154f
Desensitization, 147
Diabetic neuropathy, painful, 195
Diagnosis, 6, 7f
Diagonal pull, 65
Diagonal shoulder exercise
with extension-adduction-medial
rotation, 460, 461f
with flexion-adduction-lateral
rotation, 460, 462f
Diaphragm
inflammation of, case study of, 376-
377
referring pain to shoulder, 190, 365-
366
Diaphragmatic breathing, 226-228,
226f-229f
Differential soft tissue diagnosis, 89-
127
case study of, 120-127
accessory motion, 125
active range of motion (AROM),
123
assessment, 126
isokinetic testing, 125
manual muscle testing, 125
midline resisted tests, 125
mobility, 125
musculotendinous strength
testing, 125-126
observation, 123
palpation, 126
passive range of motion (PROM),
123-124
patient history, 121-123
scapular position, 123
scapular stability testing, 125
treatment, 126, 127t
cervical screening, 91
mobility, 94-100
musculotendinous strength, 100-102
observation, 91-94
palpation, 104-105
patient history, 89-90
patient interview, 89-91
proprioception and kinesthesia, 102-
104
special tests, 105-126
glenohumeral stability, 105-110
impingement, 112-119
labral integrity, 110-112
musculotendinous unit tests, 115-
119
rotator cuff rupture, 120
transverse humeral ligament tests,
119-120
Dimethyl sulfoxide (DMSO) for
frozen shoulder, 323
Direct oscillations, 425b
Dislocations, 247
of anterior glenohumeral joint
radiograph, 485f
arthritis of, 534-535
Displaced fractures, 517
Distension arthrography for frozen
shoulder, 327-328, 328t
INDEX 557
Distraction, definition of, 406
Disuse, learned, 266
Diverticulitis, 376
DMSO for frozen shoulder, 323
Dorsal nerve root, 143
anatomy of, 143f
Dorsal (posterior) rami, 144
Dorsal root ganglia, 144
Dorsal scapular nerve, 145
Double crush syndrome, 217
Droopy shoulder syndrome, 149
Drop arm test, 117f. See also
Supraspinatus test
Drop sign-infraspinatus, 120, 122f
D rotation, 46f
Duchenne-Erb paralysis, 244, 250
Dura mater, 243
DVT, 367-368
Dynamic ballistic shoulder external
rotation, 313f
Dysesthetic pain, 189
E
Early cocking, 30
EAST, 223
Eccentric overload, 505
Edema
in brachial plexus injuries, 251
in impingement, 338
Edgelow Protocol, 224
Education, 167
Elastin, 466b
Elbow
extension with lateral reach, 281f-
282f
injury to, 29
Elderly, 361, 371
Electricians, 141f, 216
Electrodiagnostic tests for thoracic
outlet syndrome (TOS), 218
Electromyography (EMG), 18, 302-
303, 443
biofeedback, 286
of brachial plexus injuries, 253
of deltoid muscle, 23
in open and closed chain exercise,
310
Electronic digital inclinometer, 104
Elevated arm stress test (EAST),
223
Elevation of arm, 541f, 542f
Elevation of first rib, 216
558 INDEX
Elevation of shoulder, 55f. See also
Abduction of shoulder
in AROM assessment, 95
exercises involving, 64, 64f
final phase of [140 to 180 degrees],
25
initial phase of [0 to 60 degrees],
22-23
middle phase of [60 to 100 degrees],
23-25
Elongated transverse process with
thoracic outlet syndrome (TOS),
218
EMG. See Electromyography (EMG)
Emphysema predisposing to thoracic
outlet syndrome (TOS), 216
End-feel, passive range of motion
(PROM), 97-99
Epiphyseal fractures, 525
Erbs palsy, 244
Ergonomics for cumulative trauma
disorder (CTD), 143
ERLS (external rotation lag sign), 120,
121f
Erythrocyte sedimentation rate (ESR),
371
Esophagus referring pain to shoulder,
369
ESR, 371
Essential-essential lesion, 40
Evaluation, 6, 7f
of active movement, 219, 220t, 276
of assisted movement, 276
of impingement syndrome
rehabilitation, 305-306
of movement control, 276
myofascial, 467-468, 467-469
of nervous system, 219-221
of nonprotective injury, 412
of pain, 190-195
of protective injuries, 408
of rotator cuff injury, 342-346
of soft tissue, 126
of thoracic outlet syndrome (TOS),
217-224
Exaggerated military position, 223
Examination. See Physical examination
Exercise. See also Strengthening
exercises; individual exercises
for back, 59-72
dynamic stabilization, 312
equipment used in Impulse Inertial
Exercise System (IES), 311
Exercise. See also Strengthening
exercises; individual exercises
(Continued)
for fractures
of clavicle, 519-520
of humerus, 523-524
of scapula, 521
for frozen shoulder, 332
related to joint mobilization, 466f
for rotator cuff tear, 350, 508
for scapular elevation, 41
for scapula retraction, 41, 51
for shoulder instability, 486-489
for thoracic outlet syndrome (TOS),
235-236
for throwing injuries of shoulder,
53-54, 53f, 55f, 56, 60f-61f
for total shoulder replacement, 537-
541
for unstable shoulder, 305
Exercise protocol
for off-season upper extremity
conditioning, 79-84
for SLAP repair rehabilitation, 86-
88
Extension
cervical quadrant test in, 155f, 161
of elbow with lateral reach, 281f-
282f
of glenohumerus, 99f
mobilization of facet joints, 178f
of trunk, 98f
of wrist, grasping cane with, 281f-
282f
External rotation, 15, 60
exercises, 544f
horizontal abduction in, 310f
External rotation lag sign (ERLS),
120, 121f
External rotator muscle, 12
Extrinsic overload, 505
F 486-489
Facet joints. See also Cervical facet
joints
anesthesia, 158
bilateral distraction of, 175f, 177f
compression of, 140f
extension mobilization of, 178f
injection blocks, 158
meniscoid, 139
referred pain, 155-156, 159f
unilateral distraction of, 176f
Facilitated segment. See Central
sensitization
Fall on outstretched arm, 490
Fascia
anterolateral elongation of, 472,
472f
clavipectoral, 135
deep cervical, 134
posttraumatic scarring along,
211
directly related to rib cage, 135
elongation of, 475
Fear, 145, 167
Femoralization, 536
FES, 281-282
Fibrosis in impingement, 338
Fingernail clubbing, 371
First rib
disorders of, referring pain to
shoulder, 164
elevated, 216
mobility testing of, 164f
palpation of, 105t
test of, 166f
Five-way isometric exercises for
glenohumeral joint, 540f
Flail arm, 216
Flexion, 13. See also Forward flexion
of elbow with lateral reach, 281f-
282f
Flexion withdrawal reflex, 212
Flexor carpi ulnaris, 217
Flexor pollicis brevis, 217
Fluid dynamics, 206, 213-216, 213t
cumulative trauma disorder (CTD),
213-216
Focal hand dystonia, 224
Follow-through in overhand throwing,
31
Football players
open stabilization of, 485
with shoulder instability case study,
Force couple
definition of, 293
of deltoid muscle, 24f
scapula, 293-294
Forced-use protocol, 281
Force production
impairment of, 262-263, 264f, 265
measurement of, 275-276
interventions for, 277-281
Forebrain, modulating pain, 146-147

Forward flexion, 40
side lying
ninety degrees with internal
rotation, 48
one hundred ten degrees with
internal rotation, 49
seventy degrees with internal
rotation, 48
side lying and roll over, ninety
degrees with internal rotation,
49-50
supine with internal rotation, 47
Forward head posture, 92, 140, 140f,
296
Forward lunge, 65
Forward rotation, 46f
Fracture-dislocations, 524-525
Fractures, 247
of acromion, 521
acute, 537
alignment of, 517
case studies of, 525-527
of clavicle, 518-519, 519f, 520f
comminuted, 517
of humerus, 526f
of coracoid process, 521, 521f
displaced, 517
epiphyseal, 525
greater tuberosity, 522
of humeral neck, 522-523, 523f
of humeral shaft, 523, 524f
of humerus, 521-522, 521f
impacted, 517
incomplete, 517
lesser tuberosity, 522
oblique, 517
oblique-transverse, 517
open, 517
of scapula, 520-521, 521f
stages of healing, 518
types of, 517
Frenchay Arm Test, 275
Frozen shoulder, 99, 319-334, 468
active movement in, 332-333
arthrogram of, 18
case study of, 377-385
clinical presentation of, 320
definition of, 320
dimethyl sulfoxide (DMSO) for,
323
epidemiology of, 320
historical review of, 319-320
primary, 320-321
Frozen shoulder (Continued)
research, 321-332
closed-manipulation arthroscopic
release, 328-332, 329t-330t
distension arthrography, 327-328,
328t
physical therapy, 323-327, 323t-
324t, 326t
steroid injections, 321-323, 322t
secondary, 321
treatment objectives for, 332-333
Frustration, 207
Fugl-Meyer Assessment Scale, 276
Full can exercise, 451-452, 453f
Functional abilities, focusing on, 168
Functional anatomy and mechanics,
11-26
Functional arc of elevation of arm,
293, 293f
Functional biomechanics, 22-26
Functional electrical stimulation
(FES), 281-282
Funiculi, 243f
G normal alignment of, 270f
Gallbladder, referring pain to shoulder,
374
Gallstones
case study of, 395-400
referring pain to shoulder, 90t
Gapping of acromioclavicular joint,
424, 424f
Gastritis, 375
Gaucher’s disease, 535
Gender and cumulative trauma
disorder (CTD), 216-217
Gerber lift off test, 119, 119f, 444,
446f, 456
Gilcrest sign, 115-117, 116f, 126
Glenohumeral capsule, 483
restriction of, 96
thermal shrinkage of, 500
Glenohumeral extension, substitution
for glenohumeral internal rotation
in posterior capsule restriction,
99f
Glenohumeral external rotation
in ninety degrees of abduction in
frontal plane supine, 42
in ninety degrees of abduction in
scapular plane supine, 43
in ninety degrees of forward flexion
side lying, 44
INDEX 559
Glenohumeral force couple, 295f
Glenohumeral internal rotation
deficit, 36-40
in ninety degrees of abduction in
frontal plane
prone, 44
supine, 42
in ninety degrees of abduction in
scapular plane supine, 42-43
in ninety degrees of forward flexion
side lying, 43
Glenohumeral joint, 11, 12f, 29
anterior capsule, 483
anterior dislocation of, radiograph
of, 485f
capsule of, incision of, 497f
dynamic stabilizers of, 18-20
five-way isometric exercises for, 540f
frayed, 509f
indications for replacement, 530
manual therapy techniques, 418-423
mobilization techniques, 418-423
humerus glide, 418-422
humerus rotation, 422
operative indications for, 484
osteoarthritis of, 531-532, 533
radiography of, 530f
primary instability of, 294-295
range of motion, measurement of,
344-345
rotator cuff tear effect on, 341
static stabilizers of, 15-18
subluxation, 269-270
subluxation of, 269-272, 270f, 271f,
273f
Glenohumeral ligament, 16
inferior, 16, 17, 483
posterior band of, 32
Glenohumeral ligaments, 484
anatomy of, 16-17
tight, 99
Glenohumeral load and shift test, 109,
109f
Glenohumeral muscle, imbalance of,
293-294
Glenohumeral stability tests, 105-110
anterior release test, 107-109, 108f
apprehension test, 105, 107f
glenohumeral load and shift test,
109, 109f
Jobe relocation test, 107, 108f
Jobe subluxation test, 105-107, 107f
560 INDEX
Glenohumeral stability tests
(Continued)
sulcus sign, 109-110, 109f
sulcus sign at ninety degrees, 109-
110, 110f
Glenoid
anchor placement, 489f
erosion of, 531
impingement of, 295-296
anterior, 295-296
schematic representation of, 340f
Glenoid fossa, 16
Glenoid labrum, 483, 484f
Glide, 22
Gliding, 13, 14f
Global supine incline, 66-68
Globe, dynamic hug front, 75f
Glucosamine sulfate, 178
Glycosaminoglycans, 416
Golf, 96
Gravity eliminated elevation on table
top, 541f
Greater tuberosity fractures, 522
Ground substance, 466b
Guided movements, 278f-279f
Guide to Physical Therapist Practice. See
American Physical Therapy
Association
Guyen canal, 210f
H complex, 90t
Hands
behind back, 96
behind neck, 96
focal dystonia, 224
to opposite shoulder, 96
position in joint mobilization, 416-
417
protection of, 469
treatment techniques for, 425b
Hawkins and Kennedy impingement
test, 114-115, 115f, 126, 346
Headaches, 139
Health-related quality of life,
relationship to Nagi model of
disablement, 6f
Heart
referring pain to shoulder, 369-370
in thoracic outlet, 214
in visceral referred pain, 190-191
Heart murmur, 371
Heat for frozen shoulder, 332
Hemiplegia, 262-291, 264f, 272f, 273f
clinical decision making, 276-277
grasping objects, 278f-279f
intervention for, 277-281
EMG biofeedback, 286
functional electrical stimulation,
281-282
increasing force production and
control, 277-281
musculoskeletal impairments,
286-291
lifting arm forward, 280f
musculoskeletal impairments, 267-
275
interventions for, 286-291
pain, 273-275
soft tissue tightness and
contracture, 268
subluxation, 268-272
neuromuscular impairments, 262-
267
altered sensation, 265-266
central weakness, 262-263
muscle activation deficits, 264-265
spasticity and hypertonicity, 266-
267
physical examination of, 275-276
weight bearing positions in, 289f
Hemorrhage in impingement, 338
Hepatitis referring pain to shoulder
Hernia, 361
Hiatal hernia referring pain to
shoulder complex, 90t
Higgins and Warner’s technique, 491
Hill-Sachs lesions, 485
Histamine, blood flow, 467
History, 6, 468
History taking. See Patient history
HIV, massage, 467
Home exercises
for frozen shoulder, 333
for thoracic outlet syndrome (TOS),
235-236
Horizontal abduction, 60
Horizontal adduction, supine, 42, 46
Horner’s syndrome, 241, 245, 250, 368
Human immunodeficiency syndrome
(HIV), massage, 467
Humerus
abduction of, 422, 422f
in anterior subluxations, 271-272
Humerus (Continued)
comminuted fracture of, 526f
external rotation of, 17f, 20f, 422,
422f
fractures of, 521-524, 521f
gliding motion of
anterior, 420-421, 420f
anterior/posterior, 421-422, 421f
inferior, 418-419, 418f, 422, 422f
posterior, 419-420, 419f, 420f
head of, 15
anteriorly displaced, 92
avascular necrosis of, 533f
excursion of, 24
fulcrum affect on neural tissue,
193f
palpation of, 106t
replacement of, 536-537
lateral distraction of, 420, 420f
neck fractures of, 522-523, 523f
partial separation from glenoid
fossa, 268
retroversion of, 15, 15f
rotation of, 14-15
shaft fractures of, 523, 524f
in superior subluxations, 272
Hyperabduction of arms, 223
Hyperalgesia, 145, 360
Hypertonicity, 266-267
I
ICLC, 221, 222f
ICR, scapula, 23
IES, 311
Immobilization
connective tissue, 466-467
effects on connective tissue, 466-467
effects on soft tissue, 518
length of, following rotator cuff
repair, 352
passive range of motion (PROM),
467
of protective injuries, 408
Impacted fractures, 517
Impingement, 304-305, 505
of anterior glenohumeral joint, 295-
296
fibrosis in, 338
instability-related, case study of,
313-315
internal rotation range of motion,
38

Impingement (Continued)
magnetic resonance imaging (MRI),
340
pain of, 506f
rotator cuff tears in, 304-305
Impingement-instability complex, Jobe
classification of, 302
Impingement syndrome. See also
Compressive cuff disease
coracoid, 505
instability-related, case study of,
313-315
primary, 297-302
case study of, 301-302
secondary, 302-315
classification of, 302
instability-impingement complex,
304
instability-subluxation-
impingement-rotator cuff
tear, 304
neuromuscular retraining, 311-312
open and closed chain exercise,
307-311
posterior impingement, 304-305
primary tensile overload, 302-303
rehabilitation, 305-306
scapula role, 306-307
secondary tensile overload, 303-
304
subscapularis in, 505
treatment of, 297-302
primary, 301-302
stage I, 298-299
stage II, 299-300
stage III, 300
Impingement tests, 112-119, 346
Hawkins and Kennedy impingement
test, 114-115, 115f
locking tests, 112-114, 114f
Neer and Welsh impingement test,
114, 115f
Yocum’s test for impingement, 115,
116f
Impulse Inertial Exercise System
(IES), 311
Incline press, 451, 452f
Inclinometer, electronic digital, 104
Incomplete fractures, 517
Inferior angle of scapula
dysfunction of, 343f
palpation of, 106t
Inferior capsular shift procedure,
rehabilitation following, case
study of, 495-499
Inferior clavicle, 427-429, 428f
Inferior glenohumeral joint,
subluxation, 269-270, 270f
Inferior glenohumeral ligament, 16,
17, 483
posterior band of, 32
Inferior recess, 18
Infraclavicular, 209f
Infraclavicular lesions, 245
Infrahyoid muscle
palpation of, 105t
response to dysfunction, 101t
Infraspinatus muscle, 19, 30
length assessment of, 441-442, 442f
palpation of, 106t
resistive tests, 101t
response to dysfunction, 101t
strengthening exercises for, 299t
strength testing of, 444, 445f
Injection blocks, facet joints, 158
Injured thrower, EMG activity in, 31-
32
Instability-impingement complex, 304
Instability-related impingement, case
study of, 313-315
Instability-subluxation-impingement-
rotator cuff tear, 304
Instantaneous center of rotation (ICR),
scapula, 23
Internal rotation
baseball pitchers, 39
lag sign-subscapularis, 120, 123f
passive testing for, 124f
professional baseball players, 38
range of motion
goniometric measurement of,
344f
impingement, 38
scaption in, 307f
Internal rotators, exercising, 179f
Interrater reliability with scapular
measurements, 94
Interscalene block, physical therapy
with, 326-327, 326t
Interstitial rotator cuff tear, 342
Intervention, 7f
Intervertebral disks, 139-140
cervical, 143
Intervertebral foramina, 209f, 210f
INDEX 561
Intrarater reliability with scapular
measurements, 93-94
Intratendinous rotator cuff tear, 342
Irritability level, 89, 91, 123
passive range of motion (PROM),
96-97
Irritable bowel syndrome, 123, 375-
376
Isokinetic internal/external rotation,
351f
Isokinetic testing, 125
Isometric contraction of longus colli
(ICLC), 221, 222f
Isometric exercises
for glenohumeral joint, 540f
for rotator cuff rehabilitation, 350
J
Janeway lesions, 371
JAS, 333, 334f
Jaundice, 373
Jobe
classification of impingement-
instability complex, 302
horizontal abduction, 60f
relocation test, 34, 35, 107, 108f
subluxation test, 105-107, 107f
Joint active systems ( JAS), 333, 334f
Joint arthrokinematics, restoration of
normal, 348-349
Joint manipulation, definition of, 465
Joint mobilization
biomechanical effect of, 416
body mechanics in, 417
related to myofascial manipulation
and exercise, 466f
techniques for, 416-418
Joint pain in hemiplegia, 273
Jull and Janda classification system of
skeletal muscle, 100
K
Kabat, Herman, 217, 222f
Kabat sign, 217, 221-222, 225, 232,
235
Keyboarding, 216
Kibler scapular classification system,
343
Kibler scapular slide test, 342
Kidneys, referring pain to shoulder,
374-375
Kidney stones, 375
562 INDEX
Kinesthesia
definition of, 102
differential soft tissue diagnosis,
102-104
Kinesthetic awareness, 311
Kinesthetic model of sequencing and
distal initiation, 278f-279f
Knee osteoarthritis, Cyriax’s sequence
of pain and resistance, 97
L Lippman test, 119-120, 120f
Labral integrity tests, 110-112
active compression test-O’Briens,
110, 112f
biceps load test, 112, 114f
clunk test, 110, 111f
crank test, 110, 111f
new pain provocation, 110-112, 112f
superior labrum anteroposterior
(SLAP) lesion test-Speeds test,
112, 112f
Labrum, 16, 17
anterior-superior tears, 33
Lachman test, 347
Lag signs, 120
Large intestine referring pain to
shoulder, 375-376
Late cocking, 30
Lateral bulge of right scapula during
passive range of motion (PROM)
testing, 97f
Lateral glide, cervical, 196-197
Lateral lunge, 64-65
Lateral reach, shoulder flexion and
elbow extension with, 281f-282f
Lateral slide test, 94, 102, 102f-103f,
294
Lateral view of posture, 92
Latissimus dorsi, 12, 19, 31, 165
length assessment of, 439-440, 441f
origin of, 134
resistive tests, 101t
restriction of, 96
strength testing of, 447, 448f
Learned disuse, 266
Learned non-use, 281
Left hemiplegia, 264f, 273f
weight bearing positions in, 289f
Lesser tuberosity fractures, 522
Levator scapulae muscle
insertion of, 134
scapula, 106t
Levator scapulae muscle (Continued)
length assessment of, 436
origin of, 134
response to dysfunction, 101t
strengthening exercises for, 474
tightness of, 96
Levator scapulae syndrome, 149
LHB. See Long head of the biceps
(LHB)
Ligaments, connective tissue in, 466
Liver referring pain, 190-191, 373
LLPS. See Low-load prolonged stretch
(LLPS)
Loading conditions, 333f
Local anesthesia, physical therapy
with, 326-327, 326t
Local pain, 188
Locking tests, 112-114, 114f, 126
Long head of the biceps (LHB), 15,
17, 19, 34, 291, 292f
debridement of, 509
palpation of, 106t
tears, 33
tenodesis of, 509
Long thoracic nerve lesions, 245-246
Longus capitus muscle, response to
dysfunction, 101t
Longus colli muscle
palpation of, 105t
response to dysfunction, 101t
Lordosis, lumbar, 136, 139
Lower back
injuries of, 165
pain of, 371
Lower subscapular nerve, 145
Lower trapezius muscle
muscle test for, 450f
strengthening exercises for, 299t
strength testing of, 448-449
Low-load prolonged stretch (LLPS),
417, 417f, 418f
Ludington’s test, 117, 117f
Lumbar lordosis, 136, 139
Lumbar spine referring pain to
shoulder, 165
Lung
cancer of, 368
referring pain to shoulder, 367-368
Lunge
bilateral lunge rear, 72f, 73f
forward, 65
Lunge (Continued)
forward lunge start side, 68f
forward middle side, 68f
lateral left front, 67f
lateral start front, 67f
lawn mower lunge end front, 69f
lawn mower lunge start front, 69f
same side lunge, 70f, 72f
Lymph nodes, palpation of, 361
M
Macrotrauma, 89
tendon failure, 339
Magnesium, 178
Magnetic resonance imaging (MRI)
of brachial plexus injuries, 253
of cervical disk disease, 151
of cervical joints, 158
of posterior impingement, 340
of rotator cuff tears, 508, 508f
of thoracic facet disease, 163f
of thoracic outlet syndrome (TOS),
218
of thoracic spine, 161
Maitland irritability level
establishment during passive
range of motion (PROM) testing,
97
Manipulation
closed for frozen shoulder, 328-332,
329t-330t
definition of, 406, 465
myofascial
definition of, 465
physiologic responses to, 467
related to joint mobilization, 466f
Manual muscle testing, 125, 275-276,
443
musculotendinous strength, 100-102
Manual strength testing, 435-462
Manual therapy
definition of, 405
techniques, 405-431
case study of, 197-202
cervical lateral glide, 196-197
definitions of, 405-406
evidence-based practice, 406-407
glenohumeral joint, 418-423
of neural tissue, 196-202
passive movement, 407-416
randomized clinical trials, 406-407
shoulder girdle oscillation, 197

MAS, 276
Massage
blood flow, 467
HIV, 467
Mass movement patterns, 64-72
Matsen model, 490
Maximum manual muscle test
(MMT), 302-303
McMillan, Mary, 3
Mechanical allodynia, 145
Mechanics, 142f
Mechanism of injury, determination of,
89
Mechanoreceptors, 147
Medial border scapular dysfunction,
343f
Medial rotator muscle, strength testing
of, 446f
Medial tilting angle, 11-12
Medical exercise therapy (MET),
176
Medicine balls, 350
Meister and Andrews classification,
302
Meniscus, upper and lower
attachments of, 20f
MET, 176
Metacarpophalangeal extension splint,
252f
Metacarpophalangeal joint, synovitis
of, 371
Microtrauma, 89, 123, 126
muscle imbalances in, 100
Middle glenohumeral ligament, 16
Middle subscapular nerve, 145
Middle trapezius muscle
strengthening exercises for, 299t
strength testing of, 448, 449f
Midline resisted test, 125
Military position, exaggerated, 223
Military press, 451, 452f
Milwaukee shoulder, 536
Mini-open approach, 339
Mixed spinal nerve, 143
pathway of, 143f
MMT, 302-303
Mobility, 125
active range of motion, 94-96
differential soft tissue diagnosis, 94-
100
passive range of motion (PROM),
96-100
Mobility (Continued)
testing of
capsule, 346
first rib, 164f
Mobilization
biomechanical effect of, 416
body mechanics in, 417
case study of, 407-416
contraindications for, 416
definition of, 406
effects on connective tissue, 466-467
of facet joints, 178f
indications and contraindications
for, 407-416
related to myofascial manipulation
and exercise, 466f
role of, 416-417
of scapula, 44-46
techniques for, 416-418
techniques for acromioclavicular
joint, 422-424
Modified pushups, 309f
Morgan-Burkhart peel-back model,
490
Motor Assessment Scale (MAS), 276
Motor strength, in brachial plexus
injuries, 250-251
Motor vehicle accidents associated
with thoracic outlet syndrome
(TOS), 218
Movement
analysis of, 468
assisted, subjective evaluation of, 276
control, subjective evaluation of, 276
guided, 278f-279f
mass patterns of, 64-72
reeducation of, 278f-279f
MRI. See Magnetic resonance imaging
(MRI)
Multiple crush, 217
Muscles, 156f-157f. See also specific
muscle
activation deficits of, 264-265, 276
belly of, pain in, 100
in brachial plexus injuries, 247-248
central weakness of, 262-263
endurance of, promotion of, 349-
351
function of, definition of, 490
of glenohumeral joint, imbalance of,
293-294
in hemiplegia, 267-275
INDEX 563
Muscles (Continued)
length of, 435-442
axiohumeral, 438-440
axioscapular, 436-438
scapulohumeral, 440-442
testing of, 435-462
memory of, loss of, 266
pain of in hemiplegia, 273-274
reeducation of, 409
segmental motor innervation of,
240f, 241f
strength balance of, promotion of,
349-351
strengthening exercises for, 41, 449-
456
strength testing of, 345-346, 443-
449
of thoracic outlet, 209-211
timing and sequencing problems,
265
Muscle testing. See Manual muscle
testing
Musculocutaneous nerve, 244
Musculoskeletal impairments
hemiplegia, 267-275
interventions for, 286-291
Musculoskeletal syndromes, 148-150
droopy shoulder syndrome, 149
levator scapulae syndrome, 149
omohyoid syndrome, 148
snapping scapula syndrome, 149-
150
Musculoskeletal tumor, case study of,
376-377
Musculotendinous strength
manual muscle testing, 100-102
resistive tests, 100
scapular stability tests, 102
testing, 125-126
Musculotendinous unit tests, 115-
119
alternate supraspinatus test, 117,
118f
drop arm test, 117f
Gerber’s lift off test, 119, 119f
Gilcrest sign, 115-117, 116f
Ludington’s test, 117, 117f
Patte’s test for infraspinatus and
teres minor, 119, 119f
supraspinatus test, 117, 118f
Yergason’s test, 115, 116f
Musicians, 142f
564 INDEX
Myelography
of brachial plexus injuries, 253
of cervical disk disease, 151
of thoracic spine, 161
Myocardial infarction referring pain to
shoulder complex, 90t
Myocardial ischemia, case study of,
385-390
Myofascial evaluation of shoulder, 467-
468
Myofascial manipulation
definition of, 465
physiologic responses to, 467
related to joint mobilization, 466f
Myofascial pain, 468
Myofascial techniques, 469-476
anterior-posterior scour, 470
anterolateral fascial elongation, 472
anteroposterior lateral elongation of
upper thoracic region, 469-470
case studies of, 476-478
cervical techniques/trapezius
stretches, 473-474
cross friction of supraspinatus and
biceps tendon, 476f
patient positioning for, 469
rotational thoracic laminar release,
472
scapular framing, 473
seated forward bending laminar
release, 475-476
seated pectoral and anterior fascial
stretches, 474-475
subscapularis techniques, 471f
transverse muscle play of pectorals,
470
Myofascial treatment, 465-478
Myofascial trigger points, 469
Myotomes, 154
N Nonprotective injuries
Nagi model of disablement, 4-5, 4t
relationship to quality of life, 6f
Neer, Charles S., 529
Neer and Welsh impingement test,
114, 115f, 126
Neer impingement test, 293, 294f, 346
Neer’s classification, 302
Neer stages of impingement, 298t
Nerves
compression of, 140f
conduction studies of with brachial
plexus injuries, 253-254
Nerves (Continued)
displacement of, 243f
referring pain, 151-155
roots referring pain, 154-155
of thoracic outlet, 211
Nerve trunks
anatomy of, 241-243
non-noxious mechanical stimulation
EMG responses to, 195-196
pain, 189
palpation, hyperalgesic responses to,
194-195
protecting from physical deformation
and injury, 242-243
structural features of, 242f
Nervous system, evaluation of, 219-
221
Neural tissue, 187-202
adverse responses to provocation
tests, 193-194
evaluation of, 190-195
extensibility and sensitivity of, 221
manual therapy treatment of, 196-
202
physical signs of involvement, 190
provocation test, 199f
treatment technique, 201f
Neuromuscular impairments,
hemiplegia, 262-267
Neuromuscular retraining, rotator cuff
tears in, 311-312
Neuropathic referred pain, 188
Neuroplasticity and chronic pain, 215
New pain provocation, 110-112, 113f
Nine-level rehabilitation throwing
program, 85, 85t
Nitroglycerin, 370, 390
Nociceptors, 359-360, 365, 416
Nondisplaced greater tuberosity
fracture, 522f
case study of, 412-416
range of motion measurements,
413t
rehabilitation, 415t
Nonsteroidal antiinflammatory drugs
(NSAID), 167, 178
for rotator cuff tear, 508
Nutrition, 178-179
O Osteophytosis
Oblique fractures, 517
Oblique-transverse fractures, 517
OBPL, 247-248
O’Brien’s cross arm test (Active
Compression Test), 34, 35
O’Briens’ test, 110
Observation, 124
in differential soft tissue diagnosis,
91-94
of mobility, 94-100
of posture, 92-94
of symmetry, 91-92
in thoracic outlet syndrome (TOS),
219
Obstetric brachial plexus lesions
(OBPL), 247-248
Occupations and cumulative trauma
disorder (CTD), 216
Office work, 216
Off-season upper extremity
conditioning protocol, guidelines
for, 79-84, 80t-84t
Omega-3 fatty acids, 178
Omohyoid muscle, 134
Omohyoid syndrome, 148
Open and closed chain exercise, 307-
315
EMG in, 310
rotator cuff tears in, 307-315
Open Bankart repair and stabilization,
rehabilitation following, case
study of, 486-489
Open fractures, 517
Open inferior capsular shift, shoulder
instability, 495-499
Open release for frozen shoulder, 328-
332, 329t-330t
Open rotator cuff repair, case study of,
354-355
Orthopedic evaluation detecting
visceral disease, 360
Orthopedic sling, 290f
Oscillations, direct, 425b
Oscillatory techniques, definition of, 406
Osteoarthritis, 361
of AC joint, 507f
of glenohumeral joint, 531-532
of knee, 97
total shoulder replacement, 531-533
Osteokinematic movement, 11-13
Osteonecrosis, 530
Osteophytes, 153
of left cervical facet, 153f
of uncovertebral joint, 153f

Outcomes, 7f
Outstretched arm, fall on, 490
Overhand throwers
accelerators, 41
posterior capsular restriction
measurement, 41-42
SLAP, 39
Overhand throwing, 29-32. See also
Throwing injuries
follow-through in, 31
range of motion changes in, 36-37
SLAP, 34, 35
Overhand throwing athletes,
preventive protocol, 40
Overload
eccentric, 505
extrinsic, 505
reduction of, 348
Overuse, 296
P Pancoast’s tumor, 367
Packers, 216
PAG, 145, 146
Pain
from altered sensitivity in
hemiplegia, 274
in brachial plexus injuries, 249-
250
chronic and neuroplasticity, 215
Cyriax’s sequence of, 97
definition of, 359
dysesthetic, 189
in hemiplegia, 273-275
identification of, 166
of impingement, 506f
indicating glenohumeral joint
replacement, 530
interventions for, 288-290
local, 188
of low back, 371
medical conditions referring pain to
shoulder complex, 90t
modulation by forebrain, 146-147
during muscle contraction, 100
muscle in hemiplegia, 273-274
myofascial, 468
prolongation of, 145
in soft tissue injuries, 90-91
with thoracic outlet syndrome
(TOS), 217
Painful diabetic neuropathy, 195
Painters, 216
Palmar erythema, 373
Palpation, 126, 221, 361, 468-469
of brachial plexus injuries, 251
of clavicle, 105t
of coracoacromial ligament, 106t
of coracoclavicular ligament, 106t
of coracoid process, 106t
of cutaneous tissue, hyperalgesic
responses to, 195
differential soft tissue diagnosis,
104-105
of first rib, 105t
of humeral head, 106t
of infrahyoid muscle, 105t
of infraspinatus muscle, 106t
of levator scapulae muscle, 106t
of long head of the biceps (LHB),
106t
of nerve trunks, hyperalgesic
responses to, 194-195
of soft tissue, 126
case study of, 377-385
referring pain to shoulder, 368-369
Pancreas referring pain to shoulder,
373-374
Pancreatic carcinoma referring pain to
shoulder complex, 90t
Pancreatitis, 366, 373-374
referring pain to shoulder complex, 90t
Paradoxical breathing pattern, 212-213
Parallel mobilization, 425b
Paralysis
Dejerine Klumpke, 245
Duchenne-Erb, 244, 250
Parascapular muscle resisted posterior
scapular depression for, 299, 299f
Paravertebral muscle, mobilization of,
472
Passive elevation with stick, 544f
Passive external rotation, 539f
Passive forward elevation, 539f
Passive movement
dysfunction, 192-193
effects on scar tissue, 407-416
evaluating nervous system sensitivity,
219-221, 220t
manual therapy techniques, 407-416
Passive pump massage of trapezius
muscle, 175f
Passive range of motion (PROM), 96-
100, 124-125, 531
accessory motion, 100
in brachial plexus injuries, 250
INDEX 565
Passive range of motion (PROM)
(Continued)
end-feel, 97-99
excessive extension of trunk, 98f
immobilization, 467
irritability level, 96-97
lateral bulge of right scapula, 97f
Maitland irritability level
establishment testing, 97
for nonprotective injuries, 413
for protective injuries, 409, 411
restriction patterns, 99-100
Passive testing for internal rotation,
124f
Patient empowerment, 206
Patient history, 8f
in brachial plexus injuries, 249-250
differential soft tissue diagnosis, 89-90
in differential soft tissue diagnosis,
89-90, 121-123
with differential soft tissue
diagnosis, 121-123
for thoracic outlet syndrome (TOS),
218
total shoulder replacement, 529-531
for total shoulder replacements, 529-
531
Patient interview, differential soft
tissue diagnosis, 89-91
Patient management, 7f
Patient management system, 6
Patient positioning for myofascial
techniques, 469
Patient questionnaire self-
administered, 361, 362f-363f
Patient understanding, 206
Patte’s test for infraspinatus and teres
minor, 119, 119f
Pean, J.E., 529
Pectoralis major, 12, 31, 490
assessment of, 440f
deltoid and clavicular head of, 19
length assessment of, 438-439
origin of, 134-135
palpation of, 106t
resistive tests, 101t
response to dysfunction, 101t
restriction of, 96
strength testing of, 447, 447f, 448f
Pectoralis minor, 209f, 210, 426, 427f
flexibility of, 439f
length assessment of, 437-438
origin of, 135
566 INDEX
Pectoralis minor (Continued)
palpation of, 106t
response to dysfunction, 101t
shortening of, 438f, 439f
stretch, 45f
Pectoralis minor/conjoined tendon
stretch
supine, 44
Pectoral muscle
elongation of, 475
exercises for, 470
transverse muscle play of, 470, 470f
Pelvis referring pain to shoulder, 165
Pendulum exercises, 495
Peptic ulcer, 366
Perforated appendix, 366
Periaqueductal grey (PAG), 145, 146
Periarthritis scapulohumeral, 319
Pericardial friction rub, 370
Pericarditis referring pain to shoulder,
370
Perinephric abscess, 374-375
Peripheral nerves
blood supply within, 213-214
lesions, 245
structural features of, 242f
Periscapular muscle, mobilization of,
472, 473
Perpendicular mobilization, 425b
Perpendicular (transverse) strumming,
425b
Phalen’s test, 217
Phasic muscle, 468
vs. postural muscle, 468t
Physical examination, 6, 7f
of brachial plexus injuries, chart for
recording, 249f
of total shoulder replacement, 531
Physical therapists, practice of, 5, 5f
Physical therapy
diagnoses, 3
for frozen shoulder, 323-326, 323t-
324t
Physical Therapy Journal, 5
Pillow squeezes, 59
Pitchers, 29, 96
internal rotation, 39
vs. professional baseball pitcher, 31
range of motion, 38
rotator cuff injury in, 306
SLAP, 34
Pitching, supraspinatus activity in, 303
Plane of scapula, 11-12
abduction in, 13f
active range of motion (AROM),
94-96
elevation in, 12f
Plan of care, 9
Platysma, 135
Plexus, 241
Pneumoperitoneum, 367f
referring pain to shoulder, 366-
367
PNF, 221, 311, 413f
Poor posture, 139
Postcapsule stretch, 419f
Posterior capsular restriction, overhand
throwers measurement, 41-42
Posterior capsular syndrome, 36-40
Posterior capsule
restriction of substitution of
glenohumeral extension for
glenohumeral internal rotation,
99f
tight, 99
Posterior deltoid muscle
strengthening exercises for, 299t
strength testing of, 447, 448f
Posterior glenoid
erosion of, 531
impingement of, 295-296
Posterior impingement, 304-305
magnetic resonance imaging (MRI),
340
rotator cuff tears in, 304-305
Posterior inferior capsule stretching,
46-50
Posterior rami, 144
Posterior shoulder, 38, 39
Posterior tilting stretch, 45-46
Posterior triangle, 241
Posterior tubercles of transverse
processes, palpation of, 105t
Posterior view of posture, 92
Posterosuperior glenoid impingement
schematic representation, 340f
Posttraumatic arthritis, 537
Postural muscle, 468
vs. phasic muscle, 468t
Posture, 124. See also Forward head
posture
in brachial plexus injuries, 250
evaluation of, 468
in impingement syndrome, 296
Posture (Continued)
observation of, 92-94
in standing, 138f
Practice patterns, 6
Pregnancy, 366
Press ups, 308, 308f, 459, 460f
seated dips, 62
Pressure gradients in carpal tunnel,
214, 214f
Primary compressive disease, 338-339
Primary tensile overload, 302-303
Professional baseball pitcher, 96
vs. amateur baseball pitcher, 31
shoulder range of motion, 39
subscapularis muscle of, 18
Professional baseball players, 38
Prognosis, 7f, 9
Projected pain. See Radicular pain
PROM. See Passive range of motion
(PROM)
Prone
arm-lift exercise, 457, 457f
100 degree shoulder abduction with
thumbs forward, 57
100 degree shoulder abduction with
thumbs up (external rotation),
57
exercises, 54-58
horizontal abduction, 542f
ninety degree shoulder abduction
with ninety degree elbow
flexion, 57
ninety degree shoulder abduction
with thumbs forward (neutral
rotation), 54-56
ninety degree shoulder abduction
with thumbs up (external
rotation), 57
rowing, 60
shoulder extension, 57
shoulder horizontal abduction
exercise, 456-457
thoracic P/A glides, 161f
Proprioception
definition of, 102
differential soft tissue diagnosis,
102-104
exercises facilitating, 311
Proprioceptive neuromuscular
facilitation (PNF), 221, 311, 413f
Proprioceptive training, cognitive role
in, 311

Prostheses, constrained, 536
Protective injuries, case study of, range
of motion measurements in, 408t
Protective injuries, rehabilitation
phases for, 410t
Protracted shoulder girdles, 469
Protraction, stretch, 45f
Protraction/retraction stretch, side
lying, 45
Provocation tests
for brachial plexus, 219
neural tissue adverse responses to,
193-194
Pull-down exercise, 459, 459f
Pulmonary infarction, 367
Pulses, arterial, palpation of, 361
Pulsus paradoxus, 370
Pump massage of trapezius muscle,
175f
Purdue pegboard test, 251
Pushups, 308, 308f, 309f, 460f, 461f
Pushups plus, 60-61, 459-460
Q neuropathic, 188
Quadrangular space palpation, 106t
Quality of life, relationship to Nagi
model of disablement, 6f
Questionnaire self-administered by
patient, 361, 362f-363f
R from spine, 368
Radicular pain, 189-190, 189f
Radicular referred pain, 188
Radiculopathy, 187
Radiological studies for thoracic outlet
syndrome (TOS), 218
Range of motion
internal rotation, impingement, 38
loss of in hemiplegia, 290-291
measurements of
in nonprotective injury, 413t
in protective injury case study,
408t
professional baseball players, 38
Rapid ballistic movements, 311
Reach, atypical, 265
Recurrent meningeal nerve, 144, 150
pathway of, 143f
Referred pain, 90t, 150-160, 188, 365-
376
from angina pectoris, 90t
from bacterial endocarditis, 371
Referred pain (Continued)
from cancer, 367-376
case study of, 165-179, 197-202
from cervical disks, 150-151, 150f
from cervical facet joints, 158f
from cervical intervertebral disks,
150f
from cervical radiculopathy, 91
from colon and large intestine, 375-
376
definition of, 364
from diaphragm, 365-366
from disk, 150-151, 160-161
from esophagus, 369
from facet joints, 155-160, 159f
from gallbladder, 374
from heart, 369-370
from kidney, 374-375
from liver, 373
from lumbar spine, 165
from lung, 367-369, 368
from nerves, 151-155, 161-163
in neurologic conditions, 188-189
from pancreas, 90t, 373-374
from pelvis, 165
from pericarditis, 370
from pneumoperitoneum, 366-367
radicular, 189-190
from rib injuries, 164-165
from stomach, 375
vascular, 371-373
Reflex arch, 18
Reflexive patterning, 311
Reflex testing, 223
Rehabilitation
of anterior thermal capsulorrhaphy
arthroscopy, 500-502
of brachial plexus injuries, 254
following arthroscopic anterior
thermal capsulorrhaphy, 500-
502
following inferior capsular shift
procedure, 496-499
following rotator interval repair,
495-496
following SLAP lesion repair, 491-
495
of humeral fractures, 523-524
of impingement syndrome, 305-306
of nonprotective injuries, 415t
INDEX 567
Rehabilitation (Continued)
of nonprotective shoulder injuries,
415t
of protective shoulder injuries, 410t
of rotator cuff tears, 305-306
of scapular fractures, 521
of shoulder girdle fractures, 519-520
of total shoulder replacement, 537-
541
Rehabilitation protocol, 86-88
Rehabilitative exercises for unstable
shoulder, 305
Relaxation techniques, 167
Relocation test, 126
Repetitive motion jobs, 140-142, 141f
Replication testing of angular joint,
104
Resistance, Cyriax’s sequence of, 97
Resisted posterior scapular depression
for parascapular muscles, 299,
299f
Resistive exercises, 539
for rotator cuff rehabilitation, 350
Resistive tests
deltoid muscle, 101t
diagnosis based on, 100t
muscle/tendon lesions, 101t
musculotendinous strength, 100, 100t
Resistive tubing, 312, 312f
Resting hand splint, 252f
Restriction patterns, 99
Reticulin, 466b
Retraction, stretch, 45f
Retroversion (posterior tilting) stretch,
45-46
Reversible hand weakness, thinking
position for, 225
Rheumatoid arthritis, 530, 533-534
radiography of, 532f
Rhomboid(s), 134-136
atrophy of, case study of, 476-477,
477f
length assessment of, 436-437
muscle test for, 451f
strengthening exercises for, 299t
strength testing of, 449
Rhomboid major
biomechanical relationship, 136
evaluation of, 102
origin of, 134
palpation of, 106t
response to dysfunction, 101t
568 INDEX
Rhomboid minor, 134
biomechanical relationship, 136
evaluation of, 102
palpation of, 106t
response to dysfunction, 101t
Rib. See also First rib
injuries referring pain to shoulder,
164-165
mobility of, 136
mobility testing of, 165f
musculoskeletal syndromes
involving, 148-150
negative tests, 172
positive tests, 172
Rib cage
shoulder bones directly related to,
135-136
shoulder fascia directly related to,
135
shoulder muscles directly related to,
134-135
Right arm, active assistive movement
of, 287f-288f
Right hemiplegia, 272f
grasping objects, 278f-279f
lifting arm forward, 280f
Right inferior glenohumeral
subluxation, 271f
Right scapula, lateral bulge of during
passive range of motion (PROM)
testing, 97f
Rocking horse glenoid, 534
Rolling, 13, 14f, 22
Rolyan hemi-arm sling, 288, 290f
Rostral ventromedial medulla (RVM),
145-146
Rotation, 13, 14f
of clavicle, 20
forward, 46f
Rotational thoracic laminar release,
472, 472f
Rotational unity rule, 39
Rotation of shoulder, 15, 60
dynamic ballistic shoulder external
rotation, 313f
horizontal abduction in, 310f
Rotator cuff
arthroscopic subacromial view of,
507f
in athlete, 302-315
classification of, 302
instability-impingement complex,
304
Rotator cuff (Continued)
instability-subluxation-
impingement-rotator cuff
tear, 304
neuromuscular retraining, 311-
312
open and closed chain exercise,
307-315
posterior impingement, 304-
305
primary tensile overload, 302-
303
rehabilitation, 305-306
scapula role in, 306-307
secondary tensile overload, 303-
304
exercises for, 350f
force couple, deltoid muscle, 347f
interval, 16, 494f
capsule, 493-494
repair, rehabilitation following,
494-496
muscles, 14, 18, 19
eccentric overload of, 505
external, 12
force couple of, 24f
imbalance of, 100-102
strength testing of, 446f
weakness of, 96
pathologic conditions, etiology and
evaluation of, 337-356
related to coracoacromial arch,
506f
rupture of, clinical tests for, 120
tear, 507f
tendons of, 291
degeneration of, 296-297
undersurface fraying, 506f
vascularity of, 340-341
Rotator cuff injury
clinical evaluation of, 342-346
etiology and classification of, 337-
341
macrotraumatic tendon failure,
339
posterior “undersurface”
impingement, 340
primary compressive disease, 338-
339
secondary compressive disease,
339
tensile overload, 339
evaluation for, 342-346
Rotator cuff injury (Continued)
glenohumeral joint range of motion
measurement, 344-345
muscular strength testing, 345-
346
scapular examination, 342-344
rehabilitation of, 348-351
biomechanical concepts of, 347-
348
factors influencing, 351-353
muscular endurance, 349-351
muscular strength balance, 349-
351
normal joint arthrokinematics
restoration, 348-349
overload reduction, 348
total arm rehabilitation, 348
scapular examination, 342-344
special tests for, 346-347
Rotator cuff tears, 505-514, 512f,
514f
acute with SLAP lesion, 490-491
anatomic description of, 341-342
and arthropathy, 536-537
arthroscopy, 508
in athletes, 505
case study of, 512-514
classification of, 300t
diagnosis of, 505-508
etiology of, 505
imaging techniques, 507-508
inferior surface of, 513f
interstitial, 342
intratendinous, 342
magnetic resonance imaging (MRI),
508, 508f
repair of, 510f
treatment of, 508-511
Rotators, internal, exercising, 179f
Roth’s spots, 371
Rounded shoulder, 296
Rowing, 307f
prone, 60
Rowing exercise, 458-459, 458f
RVM, 145-146
S
Salter-Harris classification system, 525
Same side pull, 65
Scalene muscle, 209f, 211, 212
block, 219
palpation of, 105t
response to dysfunction, 101t
 INDEX 569

Scalenus anticus, 210 Scapula (Continued) Scapula (Continued)

Scalenus medius, 210 measurements of intrarater winging of, 92
Scaption reliability, 93-94 serratus anterior muscle weakness,
in external rotation, 60 medial border dysfunction of, 343f wall push-up, 104f
in internal rotation, 59-60, 307f mobilization of, 44-46 sitting press-up, 104f
Scaption-abduction, 11-12 movement of, weight shift with, thoracic nerve palsy, sitting press-
Scapula, 21, 135-136 50 up, 104f
abducted, 437f, 440f pain, 36 Scapula infera coracoid dyskinesis
adducted, 437f plane of, 11-12 (SICK) scapula, 36, 37f
asymmetric malposition of, 35-36 active range of motion (AROM), Scapular muscle, weakness of, 96
circles, 59 94-96 Scapular nerve, dorsal, 145
depression of, 52f elevation in, 12f Scapular plane and active range of
bilateral, 64 glenohumeral external rotation in motion (AROM), 94-96
exercise for, 41 ninety degrees of abduction Scapulohumeral movement, patterns
seated, 51 in, 43 of, 25
unilateral, 64 glenohumeral internal rotation in Scapulohumeral muscle, 18. See also
differential soft tissue diagnosis, case ninety degrees of abduction Infraspinatus muscle;
study of, 123 in, 42-43 Subscapularis muscle; Teres major
distraction of, 429, 429f plane with internal rotation, muscle; Teres minor muscle
posterior approach, 429, 429f abduction ninety degrees, 47 length assessment of, 440-442
prone, 431f position of, 124 response to dysfunction, 101t
dysfunction of, superior angle, clinical measurement of, 92-94 Scapulothoracic joint, 12f, 21-22
343f protraction measurements vs. Scapulothoracic release techniques,
elevation of, 41, 52f radiograph measurements, 94 424-431
exercise for, 41 protraction of, 92 inferior clavicle, 427-429
and internal rotation of, 50 exercise for, 41 pectoralis minor, 426
seated, 51 push-up, 460f, 461f scapular distraction, 429, 431
unilateral, 64 seated, 51 scapular external rotation, 429-430
examination of in rotator cuff injury, sidelying manual, 349f serratus anterior-lower portion, 426-
342-344 resisted posterior depression of, 427
excessive left adduction of during 299 serratus anterior-upper portion, 426
active range of motion restricted upward rotation of, 438f sidelying subscapularis, 425-426
(AROM) testing, 95f retraction of, 180f subscapularis, 425
external rotation of, 429-431, 430f exercise for, 41 subscapularis arc stretch, 425
force, 21f seated, 51 Scar tissue, passive movement effects
force couple, 293-294 retroversion, prone, 47f on, 407-416
fractures of, 520-521, 521f role of, 35 Sciatic nerve, 242
framing of, 473, 473f in rotator cuff tears, 306-307 Scientific therapeutic exercise
myofascial techniques, 473 rotators of, 21-22 progressions (STEP), 176
imbalance of, 293-294 force couple of, 22f SCM, origin of, 134
inferior angle of shrug, 59f Scoliosis, 140
dysfunction of, 343f side lying, 46f Seated
palpation of, 106t spine of, palpation of, 106t forward bending laminar release,
instability of, 96 stability tests of, 102, 125 475-476, 476f
instantaneous center of rotation case study of, 125 pectoral and anterior fascial
(ICR), 23 lateral slide test, 102, 102f-103f stretches, 474-475, 474f-475f
Kibler classification system, 343 musculotendinous strength, 102 protraction, 51f
Kibler slide test of, 342 scapular winging functional test, retraction, 51f
lateral bulge during passive range of 102 scapular depression/elevation, 51
motion (PROM) testing, 97f stretch retroversion, side lying, 46f scapular protraction/retraction, 51
lateral slide test of, 294 supine rowing, 60 Secondary tensile overload, 303-304
levator scapulae insertion on, width of, 92, 93f Second rib disorders referring pain to
palpation of, 106t winging functional test of, 102 shoulder, 164
570 INDEX
Self-administered patient
questionnaire, 361, 362f-363f
Self-cervical traction, 217
Self-discipline, 206-207
Self-mobilization exercises for thoracic
spine, 179f
Sensation
altered, 265-266
in brachial plexus injuries, 251
Sensitization, central, 145-148, 146f, 168
Sensory deficits, 265-266
Sensory testing, 224
Serratus anterior-lower portion, 426-
427, 428f
Serratus anterior muscle, 31
biomechanical relationship, 136
evaluation of, 102
length assessment of, 437
muscle test for, 450f
origin of, 135
response to dysfunction, 101t
scapular winging wall push-up, 104f
strengthening exercises for, 299t
strength testing of, 449
weakness of, 96
Serratus anterior-upper portion, 426,
427f
SHB, 17
Shear test, 153f
Short head of the biceps (SHB), 17
Shoulder
adduction protraction, 53f
adduction test, 101t
arthrosis of, 334f
dislocation of, 505
external rotation test, 101t
flexion, 310f
depression, 54f
elevation, 54f
elevation/depression, 53
with lateral reach, 281f-282f
protraction, 52f
protraction/retraction, 51
retraction, 52f
girdle
fractures of, 517-527
oscillation of, 197
manual therapy techniques, 197
protraction of, 469-470
horizontal abduction exercise, 456f
injuries of, scapular patterns related
to, 40
Shoulder (Continued)
instability of, 483-502
arthroscopic treatment of, 489
case study of, 486-489
in football players, 486-489
muscle mechanics of, 489-491
open inferior capsular shift, 495-
499
rotator interval capsule, 493-494
SLAP lesions, 490-491
thermal capsulorraphy, 499-500
internal rotation test, 101t
lateral rotation exercise, 452-454,
453f, 454f
medial rotation exercise, 454-456,
455f, 456f
muscles of, 156f-157f
myofascial evaluation of, 467-469
pain of risk factors, 29
passive elevation of, 38f
range of motion, professional
baseball pitcher, 39
rotation, 53-54
saddle sling, 288, 290f
shrug, 59, 457-458, 457f
wall slide with, 458
strain, case study of, 395-400
strengthening exercises, 299t, 451-
456
subluxation supports, 287-288
tightness of, 39
volleyball attackers, 38
Shoulder (positive tests), 172
Shoulder complex, components of, 12f
Shoulder-hand syndrome, 275
Sickle cell anemia, 535
SICK scapula, 36, 37f
Sidelying manual scapular protraction,
349f
Sidelying subscapularis, 425-426, 426f
Simple fractures, 517
Sitting postures, 139, 139f
Sitting press-up, thoracic nerve palsy,
scapular winging, 104f
Six back, 54-58, 56f, 57f, 58f
Skeletal muscle, Jull and Janda
classification system of, 100
SLAP. See Superior labrum anterior to
posterior (SLAP)
Sleeping postures predisposing to
thoracic outlet syndrome (TOS),
216
Slide test. See also Lateral slide test
Kibler scapular, 342
SLR, 217
Smokers, 369
Smoking, 178
Snapping scapula syndrome, 149-150
Snow angel self-assessment, 228-229
SNS, 148
Soft tissue. See also Differential soft
tissue diagnosis
immobilization effects on, 518
mobilization of, 424-431
tightness and contracture in
hemiplegia, 268
Soft tissue mobilization (STM), 174
definition of, 406
Somatic afferent nerve, 365f, 370f
Somatic fibers, 143
Somatic nervous systems, normal
protective reflex of, 212
Somatic pain, 360
Somatic referred pain, 188-189, 189f
Space, movements in, 277-279
Spasticity, 266-267, 276
Speed’s test, 34, 35
Spider angiomas, 373
Spin, 22
Spinal cord
anatomy of, 143
cervical, facilitated segment of, 146f
Spinal cord lesions, 245
Spinal nerve, 143
Spine. See also Cervical spine
cancer of, 368
exercises integrating efforts with
spine, 180f
lumbar, referring pain to shoulder,
165
mobility of, 136
musculoskeletal syndromes
involving, 148-150
of scapula, palpation of, 106t
shoulder muscles directly related to,
133-134
Spine-rib cage-shoulder
biomechanical relationship, 136-138
musculoskeletal relationship, 133-
136
neurologic relationship, 143-145
occupational relationship, 140-143
postural relationship, 138-140
Spiral fractures, 517

Splenic rupture, 366
Splinting in brachial plexus injuries,
252
Spondylosis, 361
Stability ball
dynamic hug, 72
mass movements, 72
prone exercise pattern of
movements, 72
Stability tests, 126. See also
Glenohumeral stability tests
Standing, normal postural alignment
in, 138f
Standing postures, 139
Stenosis, 206
STEP, 176
Sternoclavicular joints, 12f, 20
inferior/posterior glide of, 423-424,
423f
limitation at, 96
mobilization techniques, 422-424
palpation of, 106t
superior glide of, 422-423, 423f
synovitis of, 371
upper and lower ligaments of, 20f
Sternocleidomastoid muscle (SCM)
origin of, 134
palpation of, 105t
response to dysfunction, 101t
Steroids for frozen shoulder, 321-323,
322t
Stiff painful shoulder syndrome, 191
STM, 174
definition of, 406
Stomach, 375
Stomatognathic muscle, response to
dysfunction, 101t
Straight leg raising (SLR), 217
Strain, identification of, 166-167
Strengthening exercises, 41, 451-461
for anterior deltoid muscle, 299t
for deltoid muscle, 299t
diagonal shoulder with extension-
adduction-medial rotation, 460
diagonal shoulder with flexion-
adduction-lateral rotation, 460,
462f
full can exercise, 451-452
incline press, 451
for infraspinatus muscle, 299t
military press, 451
press-up exercise, 459
Strengthening exercises (Continued)
prone arm-lift exercise, 457
prone shoulder horizontal abduction
exercises, 456-457
pull-down exercise, 459
push-up plus exercise, 459-460
rowing exercise, 458-459
shoulder lateral rotation exercises,
452-464
shoulder medial rotation exercises,
454-456
shoulder shrug, 457-458
Strength testing, 221-224, 443-449
breathing pattern, 222-223
of deltoid muscles, 445-4497
of infraspinatus muscle, 444, 445f
of infraspinatus muscles, 444
Kabat sign, 221-222
of latissimus dorsi muscles, 447
of lower trapezius muscles, 448-
449
manual, 435-462
of middle trapezius muscles, 448
of pectoralis major, 447
of posterior deltoid muscles, 447
reflex, 223
of rhomboid muscles, 449
sensory, 224
of serratus anterior muscles, 449
of subscapularis muscles, 444-445
of supraspinatus muscles, 443-444
temperature, 223-224
of teres major muscles, 447
of teres minor muscles, 444
of upper trapezius muscles, 448
vestibular, 224
Stress test, elevated arm, 223
Stretch pectoralis minor, 45f
Stretch protraction, 45f
Stretch retraction, 45f
Stretch retroversion, scapula, 46f
Subacromial decompression, pain
following, 168-179, 169f
Subacromial distance, 291
Subacromial pain, 36
Subacromial space, 291, 292f
Subacromial structures, impingement
of, 96
Subacromial-subdeltoid bursa, 291
Subclavian artery, 211
Subclavian vein, 210f, 211
thrombosis of, 372f
INDEX 571
Subclavian vessel aneurysm referring
pain to shoulder, 371
Subclavius muscle, origin of, 135
Subcoracoid bursa, 292
Subdeltoid joint, 12f
Subluxation
of anterior glenohumeral joint, 270f,
273f
of anterior/posterior glenohumeral
joint, 270-272
in hemiplegia, 268-269
interventions for, 286-288
Suboccipital muscle, response to
dysfunction, 101t
Subscapularis arc stretch, 425f, 426f
Subscapularis bursa, 292
Subscapularis muscle, 18, 19, 31, 425f
exercises for, 471-472, 471f
in impingement syndrome, 505
length assessment of, 440-441, 441f
palpation of, 106t
of professional baseball pitcher, 18
resistive tests, 101t
response to dysfunction, 101t
restriction of, 96
strengthening exercises for, 299t
strength testing of, 444-445, 446f
tight, 99
Subscapularis tendon, 292
Subscapular nerve, 145
Sulcus sign, 109-110, 109f, 110f
Superior angle scapular dysfunction,
343f
Superior glenohumeral joint,
subluxation, 270f, 272-273
Superior glenohumeral ligament, 16
Superior labrum anterior to posterior
(SLAP) lesions, 34-35, 484, 490-
491
with acute rotator cuff tears, 490-
491
arthroscopic repair of in throwing
athlete, 86-88
case studies of, 491-493
classification of, 491f
overhand throwers, 39
repair of, rehabilitation following,
491-493
Superior labrum anteroposterior
(SLAP) lesion test-Speeds test,
112, 113f
Superior nuchal line, 133
572 INDEX
Superior recess, 18
Supine scapular rowing, 60
Supraclavicular lesions, 243-244
Suprahumeral space, 291
Suprahyoid muscle, 134
palpation of, 105t
response to dysfunction, 101t
Suprascapular nerve, 145
Suprascapular notch, palpation of, 106t
Supraspinatus, 18
magnetic resonance imaging of, 508f
Supraspinatus MMT position, 345f
Supraspinatus muscle, 30
EMG activity of, 23
palpation of, 106t
resistive tests, 101t
response to dysfunction, 101t
retraction of, 511f-512f
strengthening exercises for, 299t
strength testing of, 443-444, 444f
Supraspinatus outlet, 291
Supraspinatus tendinitis, 140
Supraspinatus tendon
calcific deposit within, 507f
cross friction of, 476
Supraspinatus test, 117, 118f, 126, 300,
300f
Suspensory ligament of axilla, 135
Sustained pressure, 425b
Suture anchors for SLAP lesions, 491
Swimmers exercise, 180f
Symmetry, 124
observation of, 91-92
Sympathetic nervous system (SNS),
148
Synovial bursa, 18
Synovial capsule, 139
Synovitis, 371
T Thoracic kyphosis, 139, 140
Table top, gravity eliminated elevation
on, 541f
Table top exercises, 50-51
Tachycardia, 372
Tea, 178
Temperature testing, 223-224
Tendinitis, 159
bicipital, 140
Tendon, pain in, 100
Tendonitis
calcific, 505
chronic, 505
Tendonitis (Continued)
exercises for, 476
in impingement, 338
Tendons
connective tissue in, 466
rupture of in impingement, 338
Tennis, 96
Teres major muscle, 19
length assessment of, 442
resistive tests, 101t
strength testing of, 447, 448f
Teres major stretch, 425-426, 426f
Teres minor muscle, 19, 30
length assessment of, 441-442,
442f
palpation of, 106t
resistive tests, 101t
response to dysfunction, 101t
strengthening exercises for, 299t
strength testing of, 444, 445f
Tests and measures, 5
for brachial plexus injuries, 250-251
Theraband resistive exercises, 543f
Therapeutic Swiss balls, 350
Thermal capsulorraphy, 499-500
case study of, 500-502
Thermography for thoracic outlet
syndrome (TOS), 218-219
Thinking position exercise, 225-227
Third rib disorders, referring pain to
shoulder, 164
Thoracic disk referring pain to
shoulder, 160-161
Thoracic facet disease
computed tomography of, 163f
magnetic resonance imaging (MRI),
163f
Thoracic facet joints referring pain to
shoulder, 163-164, 163f
Thoracic lordosis, 216
Thoracic nerve lesions, 245-246
Thoracic nerve palsy, scapular winging,
sitting press-up, 104f
Thoracic nerves referring pain to
shoulder, 161-163
Thoracic outlet
anatomy of, 207-212, 208f
blood vessels of, 211-212
bones of, 207-209
muscles of, 209-211
nerves of, 211
Thoracic outlet syndrome (TOS), 205-
236, 372
breathing pattern, 222-223
case study of, 230-236
active movements, 231, 234
pain patterns, 231, 233
passive neural testing, 232, 234
posture, 231, 234
computed tomography of, 218
differential diagnosis of, 217
examination findings in, 217-224
by physical therapist, 219
strength testing, 221-224
subjective symptoms, 217-218
tests and measures for, 218-219
functional profile of, 218
history of, 218
home exercises for, 235-236
magnetic resonance imaging (MRI),
218
nervous system sensitivity
evaluation, 219-221
potential risk factors, 212
prevention of, 230
symptom patterns for, 217
tests and measures for, 218-219
treating whole person, 206-207
treatment of, 224-236
core methods, 225-230
Edgelow protocol, 224
patient-guided, 224-225
physical components, 225
Thoracic spine
computed tomography of, 161
magnetic resonance imaging (MRI),
161
referring pain to shoulder, 160-164
self-mobilization exercises for, 179f
Thoracic spine (negative tests), 172
Thoracic spine (positive tests), 172
Thoracodorsal nerve, 145
Thrombophlebitis referring pain to
shoulder, 372-373
Thrower, injured, EMG activity in,
31-32
Throwing athlete, arthroscopic repair
of SLAP lesion, 86-88
Throwing injuries, 29-76
asymmetric scapular malposition,
35-36
biceps tendon superior labral
complex, 33-35

Throwing injuries (Continued)
capsule, 32-33
essential-essential lesion, 40
exercise protocol, 50-76
measurements, 41-42
overhand throwing, 30-32
posterior capsular syndrome, 36-40
posterior inferior capsule stretching,
46-50
preventive protocol, 40-44
scapula mobilization, 44-46
scapula mobilization of, 44-46
Thumbometer, 222f, 225
Thumbtack in shoulder flexion, 55f
Thumbtack shoulder, 56f
Tinel’s sign, 217, 221
in brachial plexus injuries, 251
T-1 nerve stretch test, 162f
Tobacco, 178
TOS. See Thoracic outlet syndrome
(TOS)
Total arm rehabilitation, 348
Total shoulder arthroplasty
rehabilitation programs following,
546-551
with good rotator cuff and
deltoid, 546-549
with limited goals, 551
with poor rotator cuff and deltoid,
550-551
Total shoulder replacement, 529-
544
acute fractures, 537
arthritis of dislocation, 534-535
avascular necrosis, 535
clinical considerations, 529-531
cuff tear arthropathy, 536-537
osteoarthritis, 531-533
patient history, 529-531
physical examination of, 531
posttraumatic arthritis, 537
radiography of, 535f
rehabilitation of, 537-541
Transverse capsulotomy, 486
Transverse fractures, 517
Transverse humeral ligament tests,
119-120, 120f
Transverse muscle play of pectorals,
470, 470f
Transverse processes, anterior tubercles
palpation of, 105t
Transverse strumming, 425b
INDEX 573
Trapezius muscle. See also Lower Upper trapezius muscle
trapezius muscle strengthening exercises for, 299t
active pump massage of, 175f strength testing of, 448, 449f
atrophy of, case study of, 476-478, Upper trunk lesions, 244
477f Upper trunk rotation, 180f
biomechanical relationship, 136 Upward/downward rotation stretch
evaluation of, 102 side lying, 45
insertion of, 133
length assessment of, 436 V
lengthened, 437f Vascular thoracic outlet syndrome
origin of, 133 (TOS), 218
palpation of, 106t Vasoconstriction, 212-213
pump massage of, 175f Venous stasis, scenario of, 215f
response to dysfunction, 101t Ventral nerve root, anatomy of, 143f
strengthening exercises for, 299t, Ventral (anterior) rami, 144, 211
474 Ventral root, 143
strength testing of, 448, 449f Vertebral canal, 209f
weakness of, 96 Vestibular testing, 224
Triangle, 241 Vibrating tools, 216
Triceps brachii, 31 Visceral afferent nerve, 365f
Trigger points, myofascial, 469 Visceral disease
Trunk in elderly, 361
excessive extension of during passive orthopedic evaluation for, 360-361
range of motion (PROM), 98f referred pain to shoulder, 188, 190,
importance to limbs, 264 359-400
T4 syndrome, 217 case studies of, 376-400
Tubercle humerus, palpation of, 106t causes of, 364
Tubercles of transverse processes theories on, 364-365
palpation, 105t sites of referred pain to shoulder,
Tunnels, 210f 365-376
dysfunctional reflexes affecting bacterial endocarditis, 371
diameter of, 212-213 colon and large intestine, 375-376
diaphragm, 365-366
U esophagus, 369
Ulcerative colitis, 375-376 gallbladder, 374
Ulcers, 375 heart, 369-370
Ulnar nerve, 242 kidney, 374-375
compression of, 217 liver, 373
Uncovertebral joint, 143 lung, 367-369
degenerative joint disease of, 153f pancreas, 373-374
osteophytosis of, 153f pericarditis, 370
Undisplaced fractures, 517 pneumoperitoneum, 366-367
Unstable shoulder, rehabilitative stomach, 375
exercises for, 305 vascular, 371-373
Upper extremities warning signs of, 361
conditioning protocol, off-season, Visceral referred pain
79-84 description of, 359
muscles of, 156f-157f diaphragm, 190
Upper quarter pain, 188-189 heart, 190-191
Upper subscapular nerve, 145 liver, 190-191
Upper thoracic region, anteroposterior Visual display terminal, sitting postures
lateral elongation of, 469-470, 469f at, 139f
574 INDEX

Visual imaging exercises, 167 Wall slide with shoulder shrug Windup, 30
Volleyball attackers, 38 exercise, 458 Wolf Motor Function Test, 275
Volumetric, 251 Wand exercises, 327 Women’s Physiotherapy Association,
Warning signs of visceral disease, 3
W 361 Workstation, sitting postures at,
Walch-Jobe-Sidles glenoid Weight 139f
impingement upon rotator cuff shift left, 51f Wringing out phenomenon, 341
model, 490 shift right, 51f Wrist extension, grasping cane with,
Walking, aerobic, 229-230 shift start, 50f 281f-282f
Wall exercises, 51-54, 52f, 53f, 54f, shift with scapular movement, 50
55f, 56f Weight bearing Y
Wall pushups, 309f movements in, 279-280 Yergason’s test, 115
Wall pushups, serratus anterior muscle positions in left hemiplegia, 289f Yocum’s test for impingement, 115,
weakness, scapular winging, 104f reaching activities, 309f 116f