ARTICLE IN PRESS

Current Orthopaedics (2004) 18, 97108

www.elsevier.com/locate/cuor

MINI SYMPOSIUM: SHOULDER INSTABILITY

(ii) The classification of shoulder instability:

new light through old windows!
Angus Lewisa, T. Kitamurab, J.I.L. Bayleyc,*
a

2 Bradiston Road, Maida Vale, London, UK

Department of Orthopaedic Surgery, Kumamoto University School of Medicine,
1-1-1 Honjo Kumamoto 860, Japan
c
Royal National Orthopaedic Hospital, Brockley Hill, Stanmore, Middlesex, HA7 4LP, UK
b

KEYWORDS
Shoulder instability;
Classification;
Laxity;
Instability;
Arthroscopy;
Treatment

Summary Shoulder instability is a phenomenon, which has a variety of clinical

presentations. Its complex nature has until recently been poorly understood.
Inadequate understanding of the pathology of instability has been confounded by
confusion over definitions and inadequate classification systems. As a result
treatment failures have been observed in many of the specific pathologies. We
propose a classification system, which challenges previous systems by being all
inclusive and recognises that more than one pathology can occur in an individual
shoulder. The system takes the form of a triangle with polar groups at each corner
and specific subgroups mapped along each axis. It provides a usable framework for
clinicians in the management of what can be complex problems.
& 2004 Published by Elsevier Ltd.

Introduction
Shoulder instability is a long recognised problem.
Papyras reported a case of shoulder dislocation in
30002500 BC. Hippocrates, in 460 BC, described
the reduction of a dislocated shoulder using the
heel in the axilla and application of traction to the
affected arm. He also described the use of a Red
Hot iron inserted into the axilla to cause scarring
in the lower part of the joint to deal with the
recurrent instability, which can follow an acute
dislocation.1
In the first half of the 1900s many non-anatomical
procedures were described for the treatment of the
*Corresponding author. Tel.: 44-208-954-2300.
E-mail address: angusandromney@aol.com (A. Lewis).
0268-0890/$ - see front matter & 2004 Published by Elsevier Ltd.
doi:10.1016/j.cuor.2004.04.002

unstable shoulder, such as bone grafting of the

glenoid, tendon and bone transfers. Unfortunately
these procedures resulted in an unacceptably high
incidence of recurrent instability. It was not until
the work of Putti, Bankart, Platt and Bristow that
the management of shoulder instability became at
all successful or uniform. Limited mobility was
tolerated as a price worth paying in order to
achieve stability.
In the search for mobility with stability, improved
biomechanical studies, imaging techniques and the
introduction of arthroscopy have refocused minds
back to the precise pathologies underlying shoulder
instability. Arthroscopy has clearly demonstrated
the critical importance of the glenohumeral ligaments but has also revealed complex pathologies,
which create a variety of clinical presentations,

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98

requiring a range of management techniques.

Without an adequate classification system to make
sense of all this, management is difficult and the
hope of success is diminished. It is at this point that
the imbroglio starts, since there is still confusion in
the literature and in practice over even quite basic
matters, such as the definition of the commonly
used term multi-directional instability (MDI), the
differentiation of voluntary and involuntary instability; even the differentiation between instability and laxity.

A. Lewis et al.

conditions and allow for critical appraisal of

treatment outcomes. The elements that need to
be encompassed when classifying shoulder instability should include not only an assessment of the
onset of the condition, but also:
(a)
(b)
(c)
(d)

Degree of instability.
Chronicity of instability.
Volition of instability.
Direction of instability.

(a) Degree of instability

Laxity versus instability

Joint laxity implies a degree of translation in the
glenohumeral joint, which falls within a physiological range and which is asymptomatic. Joint
instability is an abnormal symptomatic motion for
that shoulder, which results in pain, subluxation or
dislocation of the shoulder.
Patients with hypermobility syndrome have generalised joint laxity and can present with musculoskeletal complaints. General joint laxity occurs in
only 4.24.6% of the population.2 It is controversial
whether general joint laxity is more common in
males or females. Emery looked at symptomatic
shoulder instability in adolescence and found no
significant difference in the proportions of males
(57%) and females (48%) with general joint laxity.
He found that more than 75% of preadolescents had
shoulder joints that could be asymptomatically
subluxated on examination.3 Even in the athletic
young adult no preponderance was found of males
or females,4 but there is a higher incidence in
females in the African population.5 To date it is still
unclear whether excessive joint laxity is a risk
factor for clinical instability of the shoulder joint.
The evidence to date concludes that general joint
laxity of the shoulder is NOT synonymous with
instability3 and is therefore not a pathological
process and needs to be distinguished from instability.
In this paper we have tried to clarify these issues
by suggesting a method of classification which
unifies the various elements contributing to
shoulder instability.
Classification is the central step in the management of any clinical condition. It provides a basis
for the clinician to guide treatment of the patient
and also provides a means to predict clinical
outcome. An agreed classification system that can
be used universally by different centres will
provide a platform for communication and ultimately improve our understanding of pathological

Dislocation is defined as complete separation of the

glenohumeral surfaces, whereas subluxation implies a symptomatic separation of the surfaces
without dislocation. In reality the distinction
between the two may not deserve as much
emphasis as has been given in the past, since the
more important distinction is between stability and
instability. Recurrent subluxation may occur with or
without dislocation. A Hill Sachs lesion can occur in
40% of patients with subluxation indicating that at
some point a dislocation may have occurred.
Recurrent subluxation may not present as obvious
instability, but rather as pain or as a dead arm.6

(b) Chronicity of instability

Acute instability results from an acute symptomatic
episode of traumatic shoulder dislocation. The
consequence of this may be either a permanent
glenohumeral disassociation or an intermittent
subluxation/dislocation, which may improve with
time or may progress into recurrent chronically
unstable shoulder. Congenital instability, however,
is a rare cause of chronic instability, which results
from bone deformities, e.g. scapular, humeral or
glenoid.

(c) Volition of instability

Carter Rowe re-introduced this term in 1973.7 Here
the humeral head is displaced as a result of a
deliberate trick movement, whereas adoption of
the term involuntary instability was meant to
differentiate the more common situation in which
there is no muscle-patterning component. However
Kessel and Bayley recognised that cases of apparent
involuntary instability can be due to a progression
from the voluntary into a subclinical involuntary
form. The underlying cause seemed to be an
unbalanced muscle action, which is involuntary
and deeply ingrained.8

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The classification of shoulder instability: new light through old windows!

As a result of these concepts, Kessel and Bayley

proposed the term habitual instability for these
patients, but the use of the term has always been
confusing. One reason is that many clinicians apply
the analogy of habitual instability of the knee to
that of the shoulder. Blumensaat initially presented
a classification system for habitual dislocation of
the patella, however his cases were caused by a
quadriceps contracture, which obliged the patella
to dislocate every time the knee was flexed. A more
accurate term would have been obligatory patella
instability. A similar condition occurs in the
shoulder with localised deltoid fibrosis. This analogy has created much of the confusion with
respect to the shoulder joint. Huber and Gerber
in 1994 presented a study of 25 patients in which
they used the term habitual instability. However, it
was not clear whether this group included those
patients with both voluntary and involuntary use of
abnormal muscle patterns.9 Habitual instability
cannot be used synonymously with voluntary
instability.10 It is important to distinguish between
those who displace their shoulders by a deliberate
active voluntary recruitment of abnormal muscle
couples from those where the displacement is not
deliberate, but caused by an involuntary recruitment of abnormal couples and which usually
present in certain positions of movement, but can
occur with the arm to the side. Voluntary dislocation or subluxation will cease to occur if the patient
is appropriately counselled at an early enough
stage to cease the trick movement. In involuntary
instability retraining of muscle patterning is the
essential component of rehabilitation and some 80%
of shoulders can be stabilised in this way.11
Psychiatric conditions have been said to account
for 30% of patients with voluntary instability,7
but subsequent unpublished work by Fisher and
Bayley found no difference in the incidence of
psychological abnormality between patients with
a muscle patterning instability and structural
instability. Furthermore there was no difference
between these patients and the normal population
distribution.12
To avoid this confusion the term Involuntary
Positional Instability was recently introduced by
Takwale and Calvert 200013. This is defined as
instability, which is involuntary and ingrained
where the subluxation or dislocation occurs every
time the shoulder joint passes through a particular
phase of movement and is caused by a unbalanced
muscle action. In this group there will be a
proportion of patients who have a psychological
abnormality. Therefore, the pathological factor is
the abnormality of muscle patterning not the
psychological abnormality. The problem with the

99

use of this term is that it does not include those

cases in which the shoulder is held permanently
dislocated as a result of a muscle patterning
abnormality. It is the muscle patterning abnormality which is the central matter in all these
different clinical presentations and classification
systems should give full weight to the fact.

(d) Direction of instability

The Bankart lesion (described in 1939) causes
so called unidirectional anterior instability and
has historically been the most common pattern
of instability. In the 1980s Neer et al. introduced the concept of multidirectional instability
(MDI). This is an important entity to recognise,
as the surgical management for unidirectional
instability is not adequate for multidirectional
instability.14 In Neers view, to make the diagnosis
of MDI there must be a component of coexistent inferior instability. However not all
these patients have true global instability: a
proportion can have primarily a unidirectional
instability and it is the addition of an inferior
component that causes them to be described perhaps inappropriately as MDI.10 Therefore
true MDI should have both anterior and posterior instability with an inferior component.
Bi-directional instability on the other hand may
have an inferior component at a certain position of
imbalance, be it anterior or posterior.

Aetiology of instability
In any classification system it is important to
distinguish traumatic and atraumatic causes. This
distinction is critical in the selection of treatment.
Unfortunately in many classification systems this
distinction is not clear-cut. Rowe reported in 1963
that approximately 96% of patients will present
with a traumatic component and 4% will have an
atraumatic component.15 However these figures
are likely to be different now with the increased
popularity of sport together with the tendency for
athletes to start participation at an earlier age and
to train more intensively.
In an individual with a clear history of trauma the
treatment decision is generally straightforward.
The difficulty comes when the patient is unable to
give a clear-cut history of specific injury. Furthermore patients with lax joints can sustain trivial
injuries which can initiate instability; thus there is
a broad spectrum of presentations. Atraumatic
causes can be confusing to classify and manage.

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Finally there are those patients who have hyperlaxity of all their joints and others, often athletic,
who have laxity of the shoulders only. Some
patients have no laxity, but still present with
atraumatic instability. As our understanding increases it is fair to say that the terms which
describe instability as habitual, voluntary or involuntary become inadequate.
The ideal classification system should satisfy the
following criteria:
*
*
*

*
*

Encompass all clinical presentations.

Simple to implement in the clinical environment.
Account for a shift in pathology with time, i.e. a
dynamic pathology.
Provide a pathway for the treatment.
Provide a prognosis if the patient condition is
correctly classified.
Be easily reproducible between clinicians studying the same pathology.

Concepts of shoulder instability are in a constant

state of evolution and over time many different
classification systems have been proposed.

Rockwood classification
In 1979 Rockwood classified instability on the basis
of the presence or absence of trauma:16
Type I Traumatic subluxation without previous
dislocation.
Type II Traumatic subluxation after previous
dislocation.
Type III Atraumatic voluntary subluxation.
(A) With psychiatric problems.
(B) Without psychiatric problems.
Type IV Atraumatic involuntary subluxation.

A. Lewis et al.

Thomas and Matsen Classification

In 1989 Thomas and Matsen introduced a classification system, which used the acronyms:17
TUBSF Traumatic Unidirectional Bankart Lesion
Treated with Surgery.
AMBRIF Atraumatic Multidirectional Bilateral
Treated with rehabilitation and if surgery is
required an Inferior capsular shift. A second I was
later added to denote closure of the rotator
Interval.
This classification system became popular because it was easy to remember and simple to apply
in the clinic: it also contained within it a management algorithm based on likely pathology.
Based on the Rockwoods original work16 it also
suggested trauma as the single most important
aetiological determinant and the acronyms represent the extremes of a spectrum, therefore tend to
over simplify what we now know to be a very
complex issue. Furthermore the system pushes
voluntary instability to one side and does not
assist the clinician in teasing out the boundary
between the AMBRII and voluntary groups. There is
therefore a real chance of including some patients
with muscle patterning problems in the AMBRII
category and ultimately, wrongly, operate on them.

Schneeberger and Gerber classification

In 1998 Schneeberger and Gerber produced a
system of classification,18 which was a further
refinement of Rockwoods and Thomas and Matsens
concepts.
Degree of Joint Laxity

Degree of Trauma

Multiple traumatic events

Multidirectional Instability

No Laxity
Single traumatic event

Some of the difficulties with this classification arise from trying to define the meaning
of trauma versus no trauma, since there is a
gradation between a severe fall resulting in a
traumatic instability and the absence of injuries in,
for example, the patient who throws a ball and
the arm kept going. The management of
instability which arises as a result of these
intermediate degrees of injury can vary. In these
days of trying to determine, for example, when to
do an arthroscopic repair, classification systems
probably require greater subtlety than can be
obtained in the Rockwood system. Neither does it
allow for mixed pathologies nor shifting pathology
over time.

Direction of instability

Unidirectional Instability
Unidirectional Instability

Generalised Laxity

Minor Traumatic events

Multidirectional Instability

This classification system assumed that in the

absence of joint laxity a single traumatic event
could result in unidirectional instability and that
MDI simply results from repeated traumatic events.
The authors, however, recognised that generalised
joint laxity is not a pathological condition but can
result in instability if the joint is subjected to minor
degrees of repetitive trauma.18 This classification
system also over-simplifies and compartmentalises
patients with instability too readily. The system
assumes that the degree of trauma determines the

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The classification of shoulder instability: new light through old windows!

type of instability that results and that all

instability does have a traumatic aetiology. This
we know not to be the case, as true voluntary
instability is a real phenomenon. The classification
does assume that generalised joint laxity is not a
pathological condition, which we do know to be
true, but the classification does not adequately
address the issue that there is no doubt that
generalised joint laxity does play a role in the
clinical presentation of shoulder instability.
A major and common problem with these systems
is that they ignore the possibility that instability
can be a dynamic process involving mixed pathologies, which can change over time. A patient may
initially present as traumatic instability but with
neglect develop a secondary muscle patterning
disorder. Conversely a patient who initially presents
with a purely muscle patterning disorder can later
develop a structural problem. Kuroda et al. observed this phenomenon. They reviewed 573
shoulders presenting with atraumatic shoulder
instability over a mean time period of 4 years.
They observed in 8.7% a shift in their defined
shoulder instability: loose shoulder, voluntary
dislocation, habitual dislocation and sustained
subluxation over time. Although their definitions
of the types of instability were not clear it does
confirm the idea of a dynamic pathology. Furthermore, those with a mean age of 14 years were
statistically more likely to experience a shift in
their type of instability than those with a mean age
of 19 years.19
We have for some years utilised a system of
classification, which challenges many of our perceived inadequacies of previous classification systems. Our system sought to include all types or
aetiology within a simple clinically useable framework. This system keeps all types of cases in the
minds eye. It encompasses the different types of
instability, from pure muscle patterning problems
to uncomplicated traumatic instability. It accounts
for anterior and posterior directional instability,
which may be subluxing or dislocating.

Stanmore classification
Patients are classified into three polar groups: Type
I (True TUBS), Type II (True AMBRI), or Type III
(Muscle patterning disorders/Habitual non-structural). In using this system over the years we
became aware that there is a continuum between
these polar groups with some patients falling in
between. We found that the best model in which to
capture these cases is in the form of a triangle with
the polar groups at each corner (Fig. 1).

101

Polar Type I
Traumatic
Structural

Polar Type III

Muscle patterning
Non-structural

Reducing
Muscle
Patterning

Polar Type II
Atraumatic
Structural

Reducing Trauma
Figure 1 Stanmore classification: the triangle model,
which demonstrates the polar group concept.

The system therefore:

*

Takes into account the shifting nature of the

pathology in shoulder instability.
Allows patients to be positioned between the
poles.
Incorporates a gradation from traumatic to
atraumatic causes.
Incorporates a gradation from muscle patterning
to purely structural causes.

A summary of the characteristics of the Polar

groups is seen in Table 1.
The system has been in use in our referral
shoulder service for many years and has recently
been tested with a retrospective survey of 223
patients (Fig. 2).
Using our classification system approximately
one-third of the patients were classified into the
polar groups and two-thirds of the patients were
classified into the more challenging subgroups.
Limitations of the previous classification systems
would mean that two-thirds of the patients would
be classified incorrectly and subsequently mismanaged. A summary of the characteristics of the
Subgroups is seen in Table 2.
Along each axis there are two subgroups. In
subgroup I (II) the patients all sustained an injury,
not requiring formal reduction and developed clear
episodes of subsequent instability. At arthroscopic
assessment there was clear structural damage to
the articular surfaces with either attenuation of
the glenoid rim or the humeral head (Broca
defect).20
In subgroup II (I) the patients sustained a much
less severe injury than polar group I, or subgroup I

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A. Lewis et al.

Table 1

Demonstrates the characteristics of the polar groups.

Pathology

Group I

Group II

Group III

Trauma
Articular surface damage
Capsular problem
Laxity
Muscle patterning

Yes
Yes
Bankart lesion
Unilateral
Normal

No
Yes
Dysfunctional
Uni/bilateral
Normal

No
No
Dysfunctional
Often bilateral
Abnormal

Polar Type I
Traumatic

Reducing
Muscle
Patterning

43

I(II)47

I(III)21
III(I)27

II(I)30

subgroup II (III) where the muscle patterning

disorder was only apparent on functional EMG
studies. In the absence of functional EMG testing
patients in this group require a high index
of suspicion to differentiate them from polar
group III.21
We feel the benefits of this system are:
*

24
Polar Type III
Muscle patterning
Non-structural

III(II)11

II(III) 4

16

Polar Type II
Atraumatic
Structural

Reducing Trauma

Figure 2 Stanmore classification: the triangle model,

which demonstrates the subgroup classification, n 223:

(II). They gave a history of a mechanical event, but

no documented complete dislocation. They went
on to complain of pain and, like subgroup I (II),
there was clear-cut evidence of a structural
instability with glenohumeral rim attenuation
and/or a humeral head defect. At no time did any
of these patients on this axis demonstrate any
abnormal muscle patterning.
In subgroup I (III) the patients described a
definite traumatic episode, as with subgroup I (II),
and at arthroscopic assessment there was evidence
of structural damage. What was important about
these patients, however, is that they all demonstrated a muscle patterning disorder. In subgroup III
(I) there was less trauma and arthroscopy proved
normal, in contrast to subgroup II (I). The patients
all demonstrated a muscle patterning component.
Subgroups III (II) and II (III) were the most difficult
to identify and correctly classify. These patients
showed some evidence of articular surface damage,
which could vary from a Broca defect to early
erosion of the articular surface with associated
damage to the glenoid labrum. With patients in
subgroup III (II) there was a clinically apparent
muscle patterning disorder, but this was not so in

The triangle system does provide a means of

classifying all presentations of shoulder instability with a unifying system.
It allows for a shift in the pattern of instability
with time.
It is a simple system to implement and easy to
remember.
It provides a route for treatment of all the
varieties of instability.

Patients are placed within the classification on

the basis of:
J History
J Clinical examination
J Investigations
Examination under anaesthetic
Imaging
Arthroscopy
Functional EMG analysis.

History
Taking an adequate history and performing an
accurate and thorough examination remains the
bedrock in assessing patients with instability. It is
possible, in 90% of cases, to arrive at a correct
diagnosis.10,22
When taking a history from these patients it is
important to identify precisely the part which
trauma played in the onset of the condition. A
documented anterior dislocation associated with
significant trauma, that later develops into a
recurrent problem, is a straightforward management problem (Type I instability). Fortunately

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The classification of shoulder instability: new light through old windows!

Table 2

103

Demonstrates the characteristics of the subgroups.

Pathology

Group I (II) Group II (I) Group I(III) Group III(I) Group II(III) Group III(II)

Trauma

Articular surface damage

Yes
(Humeral head and/or gleniod rim)
Muscle patterning
No

Yes

Yes

/
No

/
Yes

/
Yes

No

Yes

Yes

Yesn

Yes

BUT apparent on functional EMGs.

these account for the majority of cases. What is

more of a challenge is the group of patients who
present with a non-specific, or even no, history of
trauma. In these patients it is important to elicit an
accurate description of the initial event from which
the ongoing symptoms have developed. Generally
most patients (84%)9 with true voluntary instability
present with no history of pain. However pain is an
important issue where there is no documented
history of trauma, as it can imply shoulder
subluxation. Rowe described Dead Arm Syndrome
in patients with voluntary instability.7
Age is another important factor. Most patients
with atraumatic instability (Type II and III instability) tend to be adolescent and almost always below
the age of 25 years. Associated rotator cuff injuries
are much less common in this age group, but
beware of the older patient presenting with
impingement secondary to instability caused by
an associated cuff tear.
Documentation of previous treatment cannot be
underestimated. Many of the patients referred to
our unit have had some form of treatment. Many
patients have had some form of physiotherapy. It is
important to know what form of physiotherapy was
undertaken. If the incorrect type of physiotherapy
is given to certain types of instability the condition
can be made worse. For example, if a patient with
a pure muscle patterning problem (Type III) is given
a physiotherapy regimen which concentrates on
muscle strengthening it is possible to re-enforce
the abnormal muscle pattern. If the patient is given
a Biofeedback physiotherapy regimen to correct
the muscle-patterning problem and improve core
stability of the trunk muscles and shoulder girdle
then the instability related to the muscle patterning can improve. Conversely it would be wrong to
implement a standard biofeedback regimen to a
Type I or Type II patient, as their problem is not one
of muscle patterning, but one of muscle imbalance
secondary to selective weakness.
If patients have had previous surgery for shoulder
instability it important to know what operation was
performed. There are essentially three main causes
of recurrent instability following surgery: (a) wrong

operation (b) inadequate operation (c) wrong

diagnosis.23 If a patient has had a previous Putti
Platt24 or a Magnuson Stack25 procedure for what
was thought to be a traumatic anterior instability
and the Bankart lesion was not addressed then the
operation was inadequate and is more likely to fail.
Furthermore patients can present with recurrent
posterior instability having previously been surgically treated for anterior instability. This may not
necessarily represent unrecognised muscle patterning/atraumatic instability, but could be a true
structural instability secondary to over-tightening
of the anterior capsular structures.
It is important to know and document any
abnormal psychosocial disturbance which, if present, will be important in future management.
However, we are strongly of the view that those
factors have been overemphasised as a cause of
instability. A comparison of the incidence of
psychological conditions between groups of muscle
patterning versus structural instability did not
reveal any difference in incidence.12

Examination
General examination in recurrent instability is
important. It is also important to specifically look
at the contour of the shoulder. Look for any muscle
wasting of the shoulder girdle including the rotator
cuff. It is important to assess general posture, since
poor posture can be one of the predisposing factors
to a muscle patterning disorder, as can a general
tendency to poor joint position sense and balancing
mechanisms.
There are specific tests for laxity of the shoulder,
for example the Sulcus sign (which tests inferior
laxity) and the anterior and posterior drawer tests.
It is important however to realise that these
demonstrate laxity and are not tests of instability.
To test for instability there are both anterior and
posterior apprehension tests. The anterior apprehension tests tend to be more valuable.10 It is
important to assess for impingement and secondary
rotator cuff damage.

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Investigations
Imaging
Basic investigations, such as a simple plain X-ray,
still have an important place. A true AP projection
perpendicular to the glenohumeral joint has its
limitations, as many of the radiographic features
that are likely to be present are obscured by
projection overlap of the glenoid fossa and the
back of the humeral head. If the arm is internally
rotated to throw the back of the humeral head into
profile it may be possible to define a posterior
Broca cleavage defect,20 subsequently called a Hill
Sachs defect.26 An axial view is useful in diagnosing
acute dislocation, but in the case of recurrent
instability a Stryker Notch View is of greater value
to identify a Broca defect, which is pathognomonic
of a structural anterior instability.27 More sophisticated investigations to assess instability have been
introduced, such as CT and MRI scanning. Certainly
CT-scanning is useful in assessing bone architecture, especially in cases where there is instability
secondary to glenoid dysplasia or traumatic fractures. CT arthrography is also effective at identifying labral tears and ligamentous laxity. MRI and MR
arthrography have probably superseded CT, MRI
being most useful for identifying associated rotator
cuff damage, but is less useful for identifying labral
lesions. Recent reports of sensitivities and specificities of 88% and 93%, respectively, have been
reported. Other reports are not so impressive. MR
arthrography certainly is an encouraging alternative.28
Examination under anaesthetic
This forms an essential part of assessing instability.29 Both shoulders need to be examined. Reports
have demonstrated sensitivities and specificities of
100% and 93%, respectively.3032 However this
investigation is only sufficient by itself in a few
cases. Usually it cannot confidently distinguish
between laxity and instability without the benefit
of additional techniques such as arthroscopy.
Arthroscopy
Although this is invasive it is the only way to
accurately assess structural damage in the
shoulder. It enables the clinician to assess both
the static and dynamic processes in the shoulder
joint. It allows identification of the subtle humeral
head defects and scuffing of the labrum, which can
be the clinching evidence in difficult cases. A Hill
Sachs (Broca) lesion can occur in 80% of patients
with recurrent instability at arthroscopy compared
to only 47% of Hill Sachs lesion26 and only 13% of

A. Lewis et al.

reverse Hill Sachs lesions diagnosed radiologically.32

The drive through sign described by Pagnani
1993 has been postulated to indicate instability.33 A
recent study of 234 patients has shown this sign to
be a non-specific sign for instability with sensitivities and specificities of 92% and 37.6%, respectively.34 It may simply be a feature of shoulder
laxity.
Arthroscopy is fundamental to the differentiation
of atraumatic structural (Polar Group II) and muscle
patterning non-structural (Polar Group III) cases.
Additional damage to the glenoid rim and/or the
humeral head implies a structural instability,
whereas in the absence of visible damage it is our
firm belief that such an instability should be
classified as due to a muscle patterning disorder
until proven otherwise. The absence of apparent
deficiency of the middle and/ or inferior glenohumeral ligaments is in itself not a discriminator
between Polar Group II and III. In our study of 223
patients the incidence of glenohumeral ligament
abnormality in these two groups differed from the
normal stable population, but was the same
between the two groups

Electromyography
Electromyography (EMG) studies are not essential
for the classic traumatic unidirectional instability
(Type I). However its contribution to the atraumatic
complex instability (Type II and III) can be invaluable. It is well known that normal scapulothoracic rhythm depends on the normal co-ordinated
muscle coupling activity to enable smooth placement of the upper limb in space, whilst maintaining dynamic constraint to glenohumeral joint
displacement. Despite this knowledge, scapulothoracic dysfunction is grossly underestimated
with respect to shoulder instability. EMG analysis
can help to validate this clinical observation and to
reveal dysfunction, which is not clinically apparent.
Rowe observed this phenomenon in patients with
voluntary instability where the instability was
caused by certain muscles becoming abnormally
suppressed while others were abnormally recruited, the direction of instability varying with
the precise patterns of uncoupling.7 Over-activity
of the rotator cuff muscles has been observed in
patients with generalised joint laxity.35 We use
functional EMG analysis with flexible wire electrodes in all patients in whom we suspect a muscle
patterning disorder, either on clinical or arthroscopic grounds. We have come to recognise a
number of patterns (Fig. 1).

ARTICLE IN PRESS
The classification of shoulder instability: new light through old windows!

Principles of treatment
Using this classification system we can suggest some
principles of treatment, which can be summarised
by the statements:
*

Surgical stabilisation is indicated if there is a

purely structural instability whether traumatic
or atraumatic, or in between; anterior, posterior
or multidirectional; subluxing or fully dislocating-when the instability repeatedly compromises
shoulder function despite a trial of physiotherapy.
Non-operative management is the correct treatment for patients with muscle patterning, nonstructural instability, whether anterior, posterior
or multidirectional; subluxing, dislocating or
permanently dislocated and failure of conservative treatment is not an indication for surgery.
Non-operative management is the correct first
line treatment for patients with mixed muscle
patterning and structural instability, whether
traumatic or atraumatic; anterior, posterior or
multidirectional; subluxing or dislocating and
surgery is only permitted if the muscle patterning component can be corrected and the underlying structural instability remains a problem.
Operative treatment in these patients is contraindicated if the muscle patterning component
cannot be corrected.

Looking at specific groups

Polar group I (traumatic structural instability)
Anterior structural instability is the most common
clinical presentation and it affects up to 2% of the
population.36 Studies have reported instability
rates following acute dislocation between 88% and
95% in patients under the age of 20.3739 The
recurrence rate decreases to 14% over the age of 40
years.39
Surgical stabilisation for recurrent instability
may be divided into anatomical repairs (Bankart
repair)40 and non-anatomical repairs (Putti-Platt,24
Magnuson-Stack,25 Bristow,41 etc.). The latter
procedures now have a limited role in the management of shoulder instability as they do not address
the causative pathology, which will only result in
failure to stabilise the shoulder. They are also
associated with an unacceptable loss of movement
and therefore function. Reports of recurrent
instability of 20%, loss of external rotation of 10
301 and late onset degenerative joint disease are
common.4247 The gold standard procedure for
traumatic anterior instability due to a Bankart
lesion is the Bankart repair, first described in 1939.

105

The primary goal in this technique is to restore the

detached labrum to the anterior glenoid (Bankart
Lesion),40 thereby reattaching the Inferior glenohumeral Ligament (IGHL). Failure to do so will
result in recurrent instability. It was originally
described as an open repair, but the introduction
of arthroscopy has resulted in the development of a
closed technique to achieve the same.
Early studies of arthroscopic repair revealed
recurrence rates of 1525%.4042 Poor patient
selection was certainly one problem. The other
was failure of the early anchors used to repair and
reconstitute the GHL. Caspari introduced the
transglenoid suture capsulorraphy procedure in
1991.43 Initial results were favourable, with an 8%
recurrence rate at 2 years. Unfortunately at 4 years
this rate increased to 16%.44 Other authors have
reported higher recurrence rates of 4060%.4547
When comparing this arthroscopic technique with
the open repair Geiger reported a 50% recurrence
rate with arthroscopy compared to 17% with the
open operation.48 Other bioabsorbable anchoring
devices have been introduced, such as Suretacs,
but, recurrence rates of more than 20% over 26
years have been reported.49,50 Non-absorbable
anchors, were initially no more successful. However when Weber et al compared the use of open
versus arthroscopic stabilisation with suture anchors, unusually low rates of recurrence were
reported at 2% and 8%, respectively. Interestingly
the patients were allowed to request either open or
arthroscopic technique.51 There is no doubt that
the arthroscope has improved our understanding of
instability. A better application of this understanding will allow us to define those cases that are
amenable to arthroscopic repair and to clarify the
refinements in arthroscopic techniques needed to
widen their application.
In addition to correcting the Bankart lesion some
authors believe in the concept of plastic deformation of the IGHL as a contributing factor in
recurrence.52 It is unclear whether this occurs prior
to the Bankart lesion, but it has lead to the
development of a number of procedures, which
address this problem by capsular imbrication
procedures, either open or arthroscopic.
Rockwood initially advocated capsular imbrication in 1978 for patients with recurrent anterior
instability. Initial results were encouraging with
97% stability at 5 years and an average loss of 71 of
external rotation.48 Many modifications of this
original procedure have been proposed. Neer and
Foster in 1980 described a lateral-based capsular
shift procedure.14 Jobe, in 1989, described an
alternative capsular shift via a subscapularis split,
where a horizontal incision is made in the capsule

ARTICLE IN PRESS
106

and the inferior flap of the capsule is shifted

superomedially.49 The advantage of this procedure
was less scarring and shortening of the soft tissues.
In 1991 Altcheck proposed a medial capsular shift
procedure. The T-plasty was the reverse of that
proposed by Neer and the inferior flap was
advanced superomedially and the Bankart lesion
repaired simultaneously.50 These operations were
initially described for multidirectional instability of
the shoulder, not for traumatic anterior instability.
However the principle of the capsular shift has
been adopted for unidirectional traumatic instability to cope with the secondary capsular stretching
which occurs after multiple dislocations. It was only
a matter of time before these capsular procedures
were performed using a minimally invasive approach, but it is not yet clear whether in this type
of instability arthroscopic techniques can yet
reliably reproduce the results of open procedures,
although a recent study by Levy and Copeland has
shown this might be the case.51

Polar groups II and III (atraumatic structural

and non-structural muscle-patterning
instability)
This type of instability is less common than Polar
Group I traumatic unidirectional instability. The
management is complex and traditionally there
have been difficulties over an agreed treatment
plan suitable for all the patients. In the majority of
cases the treatment involves a multidisciplinary
approach. These patients may either require
surgery, or a non-surgical approach, or both. The
problem is that they tend to be lumped together as
MDI. Some authors argue that true MDI does not
exist, others label patients as MDI, but define it as
instability in at least two directions, i.e. a bidirectional instability.52 This makes treatment very
difficult to standardise and compare between
different units.
The matter is simplified by defining whether the
problem is structural or non-structural and therefore due to abnormal muscle patterns. Using these
factors as the determinant it does not then matter
whether the instability is anterior or posterior or
multidirectional. Indeed these terms indicate a
symptom rather than a diagnosis since, in the same
way that one can encounter anterior structural and
anterior muscle patterning disorders, so one can
encounter the same variation in the multidirectional displacements. Armed with this knowledge
one can recognise a variety of situations in a
multidirectional lax shoulder. For example a structural anteriorly unstable shoulder with posterior

A. Lewis et al.

muscle patterning instability and vice versa; a truly

anterior and posterior structurally unstable
shoulder; a truly anterior and posterior muscle
patterning instability.
The initial step when treating atraumatic instability is to assess the muscle patterning/function
and the direction of instability. The presence of a
muscle-patterning component to the instability
would place the patient on the II/III axis of the
triangle. The more dominant the muscle-patterning
problem, the more the patient migrates towards
the Type III polar group. We often investigate such
patients with functional EMG analysis. If this
confirms inappropriate muscle recruitment then
that is addressed before any surgery is considered.
Management requires careful explanation to the
patient. This is of prime importance to maintain
compliance and can only be achieved through
proper counselling. Patients with a muscle patterning disorder do not have a problem with muscle
strength, but have a muscle co-ordination problem
and this is the basis of the biofeedback exercises.
This exercise programme concentrates on improving joint position sense and relearning correct
muscle movement patterns. One can utilise mirrors, or closed circuit television, or even electronic
biofeedback devices. All these exercises aim to
improve scapulothoracic and glenohumeral muscle
patterns. There is little published on the subject of
non-operative management of atraumatic MDI. Kiss
followed up 62 patients with atraumatic MDI at
3.7 yr. All patients were entered into a biofeedback-retraining programme and ultimately 61% had
no symptoms of instability.52 Tibone reported 70%
satisfaction with a 6-month rehabilitation programme in athletes with atraumatic posterior
subluxation.53 Although published results can be
variable, it is generally accepted that patients with
a muscle patterning problem and an associated
psychological component, equally those with a
work-related injury and those who have had
previous surgery have a poor outcome with rehabilitation.52
Surgery should only be considered in patients
along the IIIII axis if there is a demonstrable
structural component to the instability, i.e. bone,
cartilage or labral abnormalities, which can best be
identified at arthroscopy and the underlying muscle
patterning abnormality has been shown to have
been corrected. If a structural problem is identified
and any muscle-patterning problem corrected then
a number of operations are open to the clinician,
depending on the problem. Neer initially described
the capsular shift procedure for MDI in 1980.14 He
initially described a laterally based capsular shift,
which can reduce capsular volume by as much as

ARTICLE IN PRESS
The classification of shoulder instability: new light through old windows!
57%.54 This procedure was described for both
anterior and posterior instability, but recurrence
rates from 20% to 30% have been reported.5557
Variations on the original technique have been
using a medially based shift with similar
results.58,59
In addition to capsular shift procedures, arthroscopic techniques have diversified. Laser assisted
and radio frequency capsulorraphy have been
introduced to shrink the capsule, but the exact
role of these procedures has not yet been defined.
Lyons reported encouraging results with laserassisted capsulorraphy (LASC) in 26 patients,
achieving stability in 96%,60 but the minimum
follow-up was only 2 years. Another recent study
compared LASC with radio frequency capsulorraphy
in 56 patients with MDI and at 18 months follow-up
there was still a 2030% failure rate with both
treatments. However these results were comparable with an open inferior capsular shift procedure,
with the added advantage of being minimally
invasive.51
In addition to soft tissue procedures the literature contains descriptions of bony procedures, the
goals of which are the same as those for the soft
tissue techniques. These operations are less frequently performed these days, but on the glenoid
side an osteotomy of the glenoid neck can be
performed for posterior instability if there is
excessive retroversion or flattening of the glenoid
surface. Scott originally described this procedure in
1967.61 In patients with unidirectional posterior
instability with no other structural abnormality one
can expect a 12% recurrence rate at 5 years.62 Auto
graft bone blocks have been used to treat Broca
defects of less than 50% of the surface of the
humeral head, again with varying success. Defects
greater than 50% really require prosthetic replacement.63 Other bone block procedures have been
described for posterior instability to augment
stability of the humeral head within the glenoid
fossa with reasonable results. They are more
applicable to recurrent instability where previous
soft tissue surgery has failed.

Conclusion
There are many different treatment regimens
available to treat the complicated and diverse
pathologies which contribute to shoulder instability. It is difficult to decide which to use in specific
cases and many failures of treatment come about
as a result of an inadequate understanding of the
precise pathologies active in each case. We feel

107

that the Stanmore Triangle is a valuable tool, which

provides the clinician with a clear method to
classify cases and thereby to advise a sensible
management plan.

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