Chapter 1
1
2 SECTION 1 Headache and Facial Pain Syndromes
Treatment
Ice pick headache uniformly responds to treatment with indo-
methacin. Failure to respond to indomethacin puts the diagnosis
of ice pick headache in question. A starting dosage of 25 mg daily
for 2 days and titrating to 25 mg three times per day is a reason-
able treatment approach. This dose may be carefully increased
to 150 mg per day. Indomethacin must be used carefully, if at
all, in patients with peptic ulcer disease or impaired renal func-
tion. Anecdotal reports of a positive response to cyclooxygenase-2
(COX-2) inhibitors in the treatment of ice pick headache have
been noted in the headache literature. Underlying sleep distur-
bance and depression are best treated with a tricyclic antidepres-
sant compound, such as nortriptyline, which can be started at a
single bedtime dose of 25 mg.
SUPRAORBITAL NEURALGIA
Testing
Magnetic resonance imaging (MRI) of the brain provides the best
information regarding the cranial vault and its contents. MRI is Figure 2-1 The supraorbital nerve sends fibers all the way to the vertex
highly accurate and helps identify abnormalities that may put the of the scalp and provides sensory innervation to the forehead, upper
patient at risk for neurological disasters secondary to intracranial eyelid, and anterior scalp. n, Nerve.
3
4 SECTION 1 Headache and Facial Pain Syndromes
A B
C
Figure 2-3 Subdural empyema in a patient with sinusitis. A, T2-weighted MRI shows high-signal-intensity extraaxial fluid collection in the right fron-
tal convexity and along the falx on the right side. B and C, Gadolinium-enhanced MRI shows extraaxial fluid collections in the right frontal convexity
and along the falx with intense peripheral enhancement. The signal intensity of the fluid collection is slightly higher than that of cerebrospinal fluid.
(From Haaga JR, Lanzieri CF, Gilkeson RC, editors: CT and MR imaging of the whole body, 4th ed, Philadelphia, 2003, Mosby, p 209.)
6 SECTION 1 Headache and Facial Pain Syndromes
Fixed
semidilated
Hazy corneal reflex pupil
signifying edema
Cataractous
lens
Opaque thickened
edematous cornea
Cataractous lens
Shallow anterior
chamber
Figure 2-4 Acute angle closure resulting from an intumescent cataractous lens. The eye is red with a hazy view of the anterior segment from corneal
edema, with a fixed, irregular, semidilated pupil from iris infarction. The slit image shows the corneal edema and a very shallow anterior chamber.
Some uveitis may be present because of ischemia, and this must be differentiated from the larger accumulations of lens material and macrophages
seen with phacolytic glaucoma. (From Spalton DJ, Hitchings RA, Hunter P: Atlas of clinical ophthalmology, 3rd ed, London, 2005, Mosby, p 225.)
Clinical Pearls
Supraorbital nerve block is especially useful in the diagnosis
and palliation of pain secondary to supraorbital neuralgia.
The first step in the management of this unusual cause of
Supraorbital n.
headache is the correct fitting of swimming goggles that
Supraorbital notch do not compress the supraorbital nerves. Coexistent fron-
tal sinusitis should be ruled out in patients who do not
respond rapidly to a change in swim goggles and a series of
the previously mentioned nerve blocks. Any patient with
headaches severe enough to require neural blockade as part
of the treatment plan should undergo MRI of the head to
rule out unsuspected intracranial pathological conditions.
SUGGESTED READINGS
Levin M: Nerve blocks and nerve stimulation in headache disorders, Tech Reg
Anesth Pain Manage 13:4249, 2009.
Levin M: Nerve blocks in the treatment of headache, Neurotherapeutics 7:197
203, 2010.
Waldman SD: The trigeminal nerve. In Waldman SD, editor: Pain review, Phila-
delphia, 2009, Saunders, pp 1517.
Waldman SD: Swimmers headache. In Waldman SD, editor: Atlas of pain man-
agement injection techniques, Philadelphia, 2007, Saunders, pp 710.
TABLE 3-1
Comparison of Cluster Headache and Chronic
Paroxysmal Hemicrania
Chronic
Cluster Paroxysmal
Comparison Factors Headache Hemicrania
Gender predominance Male Female
Response to indomethacin Negative Positive
Chronobiological pattern Positive Negative
Alcohol trigger Positive Negative
Length of attacks Longer Shorter
Figure 3-1 In contrast to cluster headache, which occurs primarily in
Horners syndrome Present Present men, chronic paroxysmal hemicrania occurs primarily in women.
7
8 SECTION 1 Headache and Facial Pain Syndromes
Treatment
Chronic paroxysmal hemicrania uniformly responds to treatment
with indomethacin. Failure to respond to indomethacin puts the
diagnosis of chronic paroxysmal hemicrania in question. A start-
ing dose of 25 mg daily for 2 days and titrating to 25 mg three
times per day is a reasonable treatment approach. This dose may
be carefully increased up to 150 mg per day. Indomethacin must
be used carefully, if at all, in patients with peptic ulcer disease or
A impaired renal function. Anecdotal reports of a positive response
to cyclooxygenase-2 (COX-2) inhibitors in the treatment of
chronic paroxysmal hemicrania have been noted in the headache
literature. Underlying sleep disturbance and depression are best
treated with a tricyclic antidepressant compound, such as nortrip-
tyline, which can be started at a single bedtime dose of 25 mg.
Clinical Pearls
The diagnosis of chronic paroxysmal hemicrania is made
by obtaining a thorough, targeted headache history.
Between attacks, patients with chronic paroxysmal hemi-
crania should have a normal neurological examination. If
the neurological examination is abnormal between attacks,
the diagnosis of chronic paroxysmal hemicrania should be
B discarded and a careful search for the cause of the patients
neurological findings should be undertaken.
Figure 3-2 Sagittal (A) and semiaxial (B) T2-weighted images of a mas-
sive prolactinoma in a 41-year-old man with chronic daily headache.
(From Benitez-Rosario MA, McDarby G, Doyle R, Fabby G. Chronic cluster-
like headache secondary to prolactinoma: uncommon cephalalgia in asso- SUGGESTED READINGS
ciation with brain tumors, J Pain Symptom Manage 37:271276, 2009. Benitez-Rosario MA, McDarby G, Doyle R, Fabby C: Chronic cluster-like head-
ache secondary to prolactinoma: uncommon cephalalgia in association with
brain tumors, J Pain Symptom Manage 37:271276, 2009.
paroxysmal hemicrania is in question. Intraocular pressure should Benoliel R, Sharav Y: Paroxysmal hemicrania: case studies and review of the lit-
be measured if glaucoma is suspected. erature, Oral Surg Oral Med Oral Pathol Oral Radiol Endodontol 85:285292,
1998.
Camarda C, Camarda R, Monastero R: Chronic paroxysmal hemicrania and
Differential Diagnosis hemicrania continua responding to topiramate: two case reports, Clin Neurol
Neurosurg 110:8891, 2008.
Chronic paroxysmal hemicrania is a clinical diagnosis supported by Klasser GD, Balasubramaniam R: Trigeminal autonomic cephalalgias. II. Par-
a combination of clinical history, abnormal physical examination oxysmal hemicrania, Oral Surg Oral Med Oral Pathol Oral Radiol Endodontol
during attacks, radiography, and MRI. Pain syndromes that may 104:640646, 2007.
Sjaastad O: Chronic paroxysmal hemicrania: clinical aspects and controversies. In
mimic chronic paroxysmal hemicrania include cluster headache, Blau JN, editor: Migraine: clinical, therapeutic, conceptual and research aspects,
trigeminal neuralgia involving the first division of the trigeminal London, 1987, Chapman & Hall, pp 135152.
nerve, demyelinating disease, and ice pick headache. Trigeminal Talvik I, Koch K, Kolk A, Talvik T: Chronic paroxysmal hemicrania in a 3-year,
neuralgia involving the first division of the trigeminal nerve is 10-month-old female, Pediatr Neurol 34:225227, 2006.
Chapter 4
CHARLINS SYNDROME
TABLE 4-1
Comparison of Cluster Headache
and Charlins Syndrome
Cluster Charlins
Comparison Factors Headache Syndrome
Ocular and retroorbital location Yes Yes
Unilateral Yes Yes
Rapid onset to peak Yes Yes
Severe intensity Yes Yes
Attacks occur in paroxysms Yes Yes
Duration of attacks short Yes Yes
Pain free between attacks Yes Yes
Significant rhinorrhea during attacks Yes Yes
Alcohol triggers attacks Yes No
Tactile trigger areas No Yes
Seasonal pattern of attacks Yes No
Figure 4-2 Multiple sclerosis. Fluid-attenuated inversion recovery (FLAIR)
Chronobiological pattern of attacks Yes No parasagittal MR image depicts the extensive demyelinated plaques of
Significant eye inflammation No Yes progressive multiple sclerosis. (From Haaga JR, Lanzieri CF, Gilkeson RC,
editors: CT and MR imaging of the whole body, 4th ed, Philadelphia,
Responds to sphenopalatine Yes No
2003, Mosby, p 466.)
ganglion block
Responds to nasociliary block No Yes
demyelinating disease, which may mimic the clinical presenta-
tion of Charlins syndrome, is overlooked. MRI is indicated in all
patients thought to have Charlins syndrome. Failure to diagnose
glaucoma or temporal arteritis, which also may cause intermittent
ocular pain, may result in permanent loss of sight.
Clinical Pearls
Nasociliary nerve block via the medial orbital approach
is especially useful in the diagnosis and palliation of pain
secondary to Charlins syndrome. Given the uncommon
nature of this headache syndrome and its overlap with the
symptoms of cluster headache and other neurological prob-
lems, including cavernous sinus thrombosis and intracranial
and retroorbital tumors, Charlins syndrome must remain a
diagnosis of exclusion. All patients suspected to have Char-
lins syndrome require MRI of the brain with and without
gadolinium contrast material and thorough ophthalmologi-
cal and neurological evaluation. Nasociliary nerve block via
the medial orbital approach should be performed only by
clinicians familiar with the regional anatomy.
SUGGESTED READINGS
Becker M, Kohler R, Vargas MI, Viallon M, Delavelle J: Pathology of the trigeminal
nerve, Neuroimaging Clin N Am 18:283307, 2008.
Craven J: Anatomy of the cranial nerves, Anaesth Intensive Care Med 11:529534,
2010.
Lewis DW, Gozzo YF, Avner MT: The other primary headaches in children and
adolescents [review], Pediatr Neurol 33:303313, 2005.
Waldman SD: The trigeminal nerve. In Waldman SD, editor: Pain review, Phila-
delphia, 2009, Saunders, pp 1517.
Waldman SD: Charlins syndrome. In Waldman SD, editor: Atlas of pain manage-
Figure 4-1 Patients suffering from Charlins syndrome present with the ment injection techniques, Philadelphia, 2007, Saunders, pp 2024.
complaint of severe paroxysms of ocular or retroorbital pain that radi-
ates into the ipsilateral forehead, nose, and maxillary region. The pain is
associated with voluminous ipsilateral rhinorrhea and congestion of the
nasal mucosa and significant inflammation of the affected eye.
Chapter 5
SEXUAL HEADACHE
11
12 SECTION 1 Headache and Facial Pain Syndromes
COUGH HEADACHE
Herniation of
cerebellar tonsil
Figure 6-1 Symptomatic cough headache is often Spinal cord
associated with structural abnormalities, such as
Arnold-Chiari malformation, and usually occurs in the
third decade of life.
Differential Diagnosis
Cough headache is a clinical diagnosis supported by a combination
of clinical history, physical examination, radiography, MRI, and
MRA. Pain syndromes that may mimic cough headache include
benign exertional headache, ice pick headache, sexual headache,
trigeminal neuralgia involving the first division of the trigeminal
nerve, demyelinating disease, cluster headache, and chronic par-
oxysmal hemicrania. Trigeminal neuralgia involving the first divi-
sion of the trigeminal nerve is uncommon and is characterized
by trigger areas and tic-like movements. Demyelinating disease
is generally associated with other neurological findings, including
optic neuritis and other motor and sensory abnormalities. The
pain of chronic paroxysmal hemicrania and cluster headache is
associated with redness and watering of the ipsilateral eye, nasal
congestion, and rhinorrhea during the headache. These findings
are absent in all types of cough headache. Migraine headache
may or may not be associated with painless neurological find-
ings known as aura, but the patient almost always reports some
systemic symptoms, such as nausea or photophobia, not typically
associated with cough headache.
Treatment
Indomethacin is the treatment of choice for benign cough head-
ache. A starting dose of 25 mg daily for 2 days and titrating to
Figure 6-2 Low-lying cerebellar tonsils (straight arrows) of a Chiari mal-
formation are shown deforming the medulla (curved arrow) in a sagittal 25 mg three times per day is a reasonable treatment approach.
T1-weighted spin echo image. 4, Fourth ventricle. (From Stark DD, Brad- This dose may be carefully increased up to 150 mg per day. Indo-
ley WG Jr, editors: Magnetic resonance imaging, 3rd ed, St Louis, 1999, methacin must be used carefully, if at all, in patients with peptic
Mosby, p 1841.) ulcer disease or impaired renal function. Headache specialists have
noted anecdotal reports of a positive response to cyclooxygenase-2
(COX-2) inhibitors in the treatment of benign cough headache.
should be included in the evaluation of all patients with cough Underlying sleep disturbance and depression are best treated with
headache. a tricyclic antidepressant compound, such as nortriptyline, which
Screening laboratory tests consisting of complete blood cell can be started at a single bedtime dose of 25 mg.
count, erythrocyte sedimentation rate, and automated blood The only uniformly effective treatment for symptomatic cough
chemistry testing should be performed if the diagnosis of cough headache is surgical decompression of the foramen magnum.
6 Cough Headache 15
This surgery is usually done via suboccipital craniectomy. Surgi- SUGGESTED READINGS
cal decompression prevents the low-lying cerebellar tonsils from Berciano J, Poca M-A, Garca A, Sahuquillo J: Paroxysmal cervicobrachial cough-
obstructing the flow of spinal fluid from the cranium to the spinal induced pain in a patient with syringomyelia extending into spinal cord poste-
subarachnoid space during a Valsalva maneuver. rior gray horns, J Neurol 54:678681, 2007.
Chen YY, Lirng JF, Fuh JL, etal: Primary cough headache is associated with pos-
terior fossa crowdedness: a morphometric MRI study, Cephalalgia 24:694699,
Complications and Pitfalls 2004.
Pascual J: Primary cough headache, Curr Pain Headache Rep 9:272276, 2005.
Failure to diagnose cough headache correctly may put the patient Pascual J, Rubn Martn A, Oterino A: Headaches precipitated by cough, pro-
at risk if intracranial pathology or demyelinating disease (which longed exercise or sexual activity: a prospective etiological and clinical study,
JHeadache Pain 9:259266, 2008.
may mimic the clinical presentation of cough headache) is over- Waldman SD: Arnold Chiari malformation type I. In Waldman SD, Campbell
looked. MRI and MRA are indicated in all patients thought to RS, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 2728.
have cough headache. Failure to diagnose glaucoma, which also Waldman SD: Arnold Chiari malformation type II. In Waldman SD, Campbell
may cause intermittent ocular pain, may result in permanent loss RS, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 2930.
of sight.
Clinical Pearls
Any patient presenting with headaches associated with
exertion or Valsalva maneuver should be taken very seri-
ously. Although statistically most of these headaches ulti-
mately are proved to be of benign cause, a few patients have
potentially life-threatening disease. The diagnosis of cough
headache is made by obtaining a thorough, targeted head-
ache history and performing a careful physical examination.
The clinician must separate patients suffering from benign
cough headache from patients suffering from symptom-
atic cough headache. Patients with benign cough headache
should have a normal neurological examination. If the neu-
rological examination is abnormal, the diagnosis of benign
cough headache should be discarded and a careful search
for the cause of the patients neurological findings should
be undertaken.
Chapter 7
SUDDEN UNILATERAL
NEURALGIFORM CONJUNCTIVAL
INJECTION TEARING HEADACHE
excruciating in intensity (Table 7-3). SUNCT occurs on the right
ICD-9 CODE 350.1 side 70% of the time in a manner analogous to trigeminal neu-
ralgia. Like trigeminal neuralgia, rare cases of bilateral SUNCT
headache have been reported. Also like trigeminal neuralgia, the
ICD-10 CODE G50.0 pain of SUNCT headache rarely switches sides. SUNCT head-
ache occurs slightly more frequently in males. It can occur at any
age, with a peak incidence in the fifth decade.
The Clinical Syndrome
Sudden unilateral neuralgiform conjunctival injection tearing
Testing
(SUNCT) headache is an uncommon primary headache disorder Magnetic resonance imaging (MRI) of the brain provides the cli-
that is one of a group of three headache syndromes known as the nician with the best information regarding the cranial vault and
trigeminal autonomic cephalgias (Table 7-1). Whether SUNCT its contents. MRI is highly accurate and helps identify abnor-
headache is in fact a distinct headache entity or simply a con- malities that may put the patient at risk for neurological disasters
stellation of symptoms that occurs on a continuum along with secondary to intracranial and brainstem pathological conditions,
the other trigeminal autonomic cephalgias is a point of ongoing including tumors and demyelinating disease. Magnetic resonance
debate among headache and pain management specialists (Figure angiography (MRA) also may be useful in helping identify aneu-
7-1). As with most headache syndromes, the exact cause of the rysms, which may be responsible for the patients neurological
pain of SUNCT headache is unknown; however, the pathogenesis findings. In patients who cannot undergo MRI, such as patients
of this uncommon cause of head and face pain is thought to be with pacemakers, computed tomography (CT) is a reasonable sec-
dysfunction of the trigeminal autonomic reflex. ond choice. Radionuclide bone scanning and plain radiography
The pain of SUNCT headache has a rapid onset to peak, with are indicated if fracture or bony abnormality such as metastatic
attacks lasting 5 seconds to 4 minutes and the frequency of attacks disease is considered in the differential diagnosis.
ranging from 20 to 200 attacks per day. In some patients, these Screening laboratory tests consisting of complete blood cell
attacks can be triggered by sensory stimulation of the affected count, erythrocyte sedimentation rate, and automated blood
areas, such as when washing the face, brushing the teeth, and so chemistry testing should be performed if the diagnosis of SUNCT
forth. Although in many ways similar to cluster headache (e.g.,
unilateral, periorbital and frontal location of pain, sclera injec-
tion, rapid onset to peak, short duration of attacks, and pain-free TABLE 7-1
periods between attacks), SUNCT exhibits many dissimilarities as Trigeminal Autonomic Cephalgias
well. In contrast to cluster headache, alcohol consumption does
not seem to trigger attacks of SUNCT headache, and there do not Cluster headache
seem to be the seasonal and chronobiological patterns so charac- Chronic paroxysm hemicrania
teristic of cluster headache, although SUNCT headache occurs SUNCT headache
most frequently in the morning and afternoon (Table 7-2). SUNCT, Sudden unilateral neuralgiform conjunctival injection tearing.
Blockade of the sphenopalatine ganglion, which is so effec-
tive in the treatment of cluster headache, is of little value in the
treatment of SUNCT headache. Patients suffering from SUNCT Paroxysmal Cluster
headache may respond to daily trigeminal nerve blocks with local SUNCT hemicrania headache
anesthetic, as described subsequently.
5 s4 min 230 min 15180 min Time
Signs and Symptoms
Overlap Overlap
Patients with SUNCT headache present with the complaint of between duration between duration
severe paroxysms of ocular or periorbital pain that radiate into
Figure 7-1 Overlap between attack duration in trigeminal autonomic
the ipsilateral temple, forehead, nose, cheek, throat, and maxillary cephalalgias. SUNCT, Sudden unilateral neuralgiform conjunctival
region. This pain is associated with significant inflammation of the injection tearing. (From Leone M, Bussone G: Pathophysiology of trigemi-
affected eye (Figure 7-2). The pain is neuralgiform and severe to nal autonomic cephalalgias, Lancet Neurol 8:755774, 2009.)
16
7 Sudden Unilateral Neuralgiform Conjunctival Injection Tearing Headache 17
headache is in question. Intraocular pressure should be measured involving the first division of the trigeminal nerve, demyelinating
if glaucoma is suspected. disease, primary stabbing headache, hypnic headache, and chronic
paroxysmal hemicranias, although because of the overlapping fea-
tures of all headache and facial pain syndromes, SUNCT head-
Differential Diagnosis ache can be easily mistaken for another type of headache or facial
SUNCT headache is a clinical diagnosis supported by a combina- pain (Figure 7-3; Table 7-4). Trigeminal neuralgia involving the
tion of clinical history, normal physical examination, radiography, first division of the trigeminal nerve is uncommon and is charac-
and MRI. Pain syndromes that may mimic SUNCT headache terized by trigger areas and tic-like movements. Demyelinating
include cluster headache, temporal arteritis, trigeminal neuralgia disease is generally associated with other neurological findings,
including optic neuritis and other motor and sensory abnormali-
ties. The pain of chronic paroxysmal hemicrania lasts much longer
TABLE 7-2 than the pain of SUNCT headache.
Comparison of Cluster Headache and Sudden Unilateral
Neuralgiform Conjunctival Injection Tearing Headache Treatment
Comparison Factors Cluster SUNCT
Headache Headache The treatment of SUNCT headache is analogous to the treatment
Ocular and retroorbital location Yes Yes
of trigeminal neuralgia, although the pharmacological manage-
ment of this uncommon headache disorder is disappointing. The
Unilateral Yes Yes use of anticonvulsants such as lamotrigine and gabapentin repre-
Rapid onset to peak Yes Yes sents a reasonable starting point. High-dose steroids tapered over
Severe intensity Yes Yes 10 days also have been anecdotally reported to provide relief. For
Attacks occur in paroxysms Yes Yes patients who do not respond to the previously mentioned treat-
Duration of attacks short Yes Yes
ments, daily trigeminal nerve block with a local anesthetic and
steroid is a reasonable next step.
Pain free between attacks Yes Yes Occasionally, retrogasserian injection of glycerol, balloon com-
Significant rhinorrhea during attacks Yes No pression of the Gasserian ganglion, and microvascular decompres-
Alcohol triggers attacks Yes No sion of the trigeminal nerve root are required to provide palliation
Tactile trigger areas No Yes of pain. Underlying sleep disturbance and depression associated
Seasonal pattern of attacks Yes No
with the pain of SUNCT headache are best treated with a tricy-
clic antidepressant compound, such as nortriptyline, which can be
Chronobiological pattern of attacks Yes No started at a single bedtime dose of 25 mg.
Significant eye inflammation No Yes
Responds to sphenopalatine ganglion
block
Yes No
Complications and Pitfalls
Responds to trigeminal nerve block No Yes Failure to diagnose SUNCT headache correctly may put the
SUNCT, Sudden unilateral neuralgiform conjunctival injection tearing. patient at risk if an intracranial pathological condition or demy-
elinating disease, which may mimic the clinical presentation of
SUNCT headache, is overlooked. MRI is indicated in all patients
thought to have SUNCT headache. Failure to diagnose glaucoma
or temporal arteritis, which also may cause intermittent ocular
pain, may result in permanent loss of sight.
TABLE 7-3
Descriptors of Pain Associated with Sudden Unilateral
Neuralgiform Conjunctival Injection Tearing Headache
Stabbing
Shooting
Lancinating
Shocklike
Sharp
Piercing
Pricking
Staccato-like
Figure 7-2 Patients with SUNCT headache present with severe parox-
ysms of ocular or periorbital pain that radiates into the ipsilateral temple,
forehead, nose, cheek, throat, and maxillary region that is associated
with significant inflammation of the affected eye.
18 SECTION 1 Headache and Facial Pain Syndromes
Cluster headache Figure 7-3 Pain location in the trigeminal autonomic cephalgias (TACs)
and neurovascular orofacial pain. The TACs are characterized by orbital
and periorbital pain. In paroxysmal hemicrania and hemicrania conti-
nua, large adjacent areas are affected. Migraine is largely unilateral but
may be bilateral in up to 30% of cases (this has been marked by a lighter
shaded area contralaterally). Neurovascular orofacial pain is character-
ized by its location in the lower two thirds of the face with intraoral and
perioral areas frequently involved as primary sites. Two-headed arrow
above diagram indicates the side shift that occurs in specific headache.
NVOP, Neurovascular orofacial pain. (Modified from Benoliel R, Sharav Y:
Neck The trigeminal autonomic cephalgias (TACs). In: Sharav Y, editor: Orofacial
Paroxysmal hemicrania pain and headache, Edinburgh, 2008, Elsevier, pp 225254.)
TABLE 7-4
Differential Diagnosis: Sudden Unilateral Neuralgiform
Conjunctival Injection Tearing Headache
Shoulder, Cluster headache
neck, arm Temporal arteritis
SUNCT Trigeminal neuralgia
Demyelinating disease
Primary stabbing headache
Hypnic headache
Chronic paroxysmal hemicrania
Clinical Pearls
Hemicrania continua Trigeminal nerve block with local anesthetic is especially
useful in the diagnosis and palliation of pain secondary to
SUNCT headache. Given the uncommon nature of this
headache syndrome and its overlap with the symptoms of
cluster headache and other neurological problems, includ-
ing cavernous sinus thrombosis and intracranial and retroor-
bital tumors, SUNCT headache must remain a diagnosis of
exclusion. All patients suspected to have SUNCT headache
require MRI of the brain with and without gadolinium con-
Migraine trast material and thorough ophthalmological and neurolog-
ical evaluation. Trigeminal nerve block should be performed
only by clinicians familiar with the regional anatomy.
SUGGESTED READINGS
Leone M, Bussone G: Pathophysiology of trigeminal autonomic cephalalgias, Lan-
cet Neurol 8:755774, 2009.
Levin M: Nerve blocks and nerve stimulation in headache disorders, Tech Reg
Anesth Pain Manage 13:4249, 2009.
Levin M: Nerve blocks in the treatment of headache, Neurotherapeutics 7:197
NVOP 203, 2010.
Klasser GD, Balasubramaniam R: Trigeminal autonomic cephalalgias. III. Short-
lasting unilateral neuralgiform headache attacks with conjunctival injection and
tearing, Oral Surg Oral Med Oral Pathol Oral Radiol Endodontol 104: 773771.
2007.
Rozen TD: Trigeminal autonomic cephalalgias, Neurol Clin 27:537557, 2009.
Waldman SD: The trigeminal nerve. In Waldman SD, editor: Pain Review, Phila-
delphia, 2009, Saunders, pp 1517.
Waldman SD: Gasserian ganglion block. In Waldman SD, editor: Atlas of inter-
ventional pain management, ed 3, Philadelphia, 2009, Saunders, pp 3238.
Waldman SD: Gasserian ganglion block: balloon compression technique. In
Waldman SD, editor: Atlas of interventional pain management, ed 3, Philadel-
phia, 2009, Saunders, pp 4347.
Waldman SD: Trigeminal nerve block: coronoid approach. In Waldman SD, edi-
tor: Atlas of interventional pain management, ed 3, Philadelphia, 2009, Saunders,
pp 4750.
Williams MH, Broadley SA: SUNCT and SUNA: clinical features and medical
treatment, J Clin Neurosci 15:527534, 2008.
Chapter 8
PRIMARY THUNDERCLAP
HEADACHE
19
20 SECTION 1 Headache and Facial Pain Syndromes
TABLE 8-2
Comparison of Primary Thunderclap Headache and
Subarachnoid Hemorrhage
Primary Thunderclap Subarachnoid
Comparison Factors Headache Hemorrhage
Severe headache Yes Yes
Nausea and vomiting Yes Yes
Focal neurological signs No Yes
Nuchal rigidity No Yes
Photophobia No Yes A
Vertigo No Yes
Neck and back pain No Yes
TABLE 8-3
Diseases That May Mimic Primary Thunderclap
Headache
Hemorrhagic
Ischemic
Neoplasm
Infection B
Meningitis
Encephalitis
Abscess
Parasitic
Hypertensive crisis
Loss of spinal fluid
Postdural puncture headache
Spontaneous spinal fluid leak
Collagen-vascular disease
Lupus cerebritis
C
Vasculitis
Polymyositis Figure 8-1 Computed tomography scan showing subarachnoid hem-
Headache orrhage (SAH). Right middle cerebral artery aneurysm in a 58-year-old
man with SAH and intracranial hematoma (IH). A, Volume rendering
Cluster headache image from computed tomography angiography (CTA) clearly displays
Primary exertional headache the relationship of the aneurysm to bone structures, adjacent branch
vessels, and aneurysmal neck (arrow). B, Maximum intensity projec-
Primary cough headache tion (MIP) image from CTA clearly demonstrates the relationship of the
Migraine aneurysm (arrow). C, Thin-MIP image from CTA shows the relationship
of the aneurysm to IH (arrowhead), and the ruptured aneurysm has a
Ice pick headache small nipple (arrow). (From Chen W, Yang Y, Xing W, etal: Applications
Primary sexual headache of multislice CT angiography in the surgical clipping and endovascular coil-
ing of intracranial aneurysms, J Biomed Res 24:467473, 2010.)
(Figure 8-1). Modern multidetector CT scanners have a diagnos- should be performed in patients with subarachnoid hemorrhage.
tic accuracy approaching 100% for subarachnoid hemorrhage if Blood typing and crossmatching should be considered in any
CT angiography of the cerebral vessels is part of the scanning patient in whom surgery is being contemplated or who has pre-
protocol. Cerebral angiography may also be required if surgical existing anemia. Careful serial ophthalmological examination
intervention is being considered and the site of bleeding cannot should be performed on all patients with subarachnoid hemor-
be accurately identified. rhage to chart the course of papilledema.
Magnetic resonance imaging (MRI) of the brain and magnetic Lumbar puncture is useful in revealing the presence or absence
resonance angiography may be useful if an aneurysm is not identi- of blood in the spinal fluid, but its utility may be limited by the
fied on CT studies and may be more accurate in the diagnosis of presence of increased intracranial pressure, making lumbar punc-
arteriovenous malformations (Figure 8-2). Screening laboratory ture too dangerous. Electrocardiographic abnormalities are com-
tests, including an erythrocyte sedimentation rate, complete blood mon in patients with subarachnoid hemorrhage and are thought
count, coagulation studies, and automated blood chemistry, to be due to abnormally high levels of circulating catecholamines
8 Primary Thunderclap Headache 21
A B C
D E F
Figure 8-2 Magnetic resonance imaging showing arteriovenous malformation. Patient with aneurysm-related false aneurysm (FA) in right parietal
region. Preangiographic T1-weighted magnetic resonance axial image (A) and T2-weighted magnetic resonance coronal image (B) show round lesion
(arrow) with flow void and mixed signal in the center and mixed signal on the periphery. Fluid attenuated inversion recovery image (C) reveals small
area of surrounding edema (arrow). D, Flow in the center of FA (arrow) on two-dimensional time-of-flight magnetic resonance angiography. E, Preem-
bolization digital subtraction angiography image. F, Residual inflow to FA (arrow) on postembolization DSA image. (From Brzozowski K, Frankowska E,
Piasecki P, etal. The use of routine imaging data in diagnosis of cerebral pseudoaneurysm prior to angiography, Eur J Radiol. 80:e401e409, 2011.)
and hypothalamic dysfunction; however, they are rarely present in does not have a stroke or brain tumor is indicated. In general,
patients with primary thunderclap headache. drugs used to treat headaches whose primary mechanism of action
is vasoconstriction (e.g., ergots, triptans) should be avoided. Anec-
Differential Diagnosis dotal reports indicate that intravenous nimodipine may help abort
acute attacks and prevent recurrent headache episodes. Gabapen-
The differential diagnosis of primary thunderclap headache gen- tin also has been advocated as a reasonable treatment for primary
erally can be thought of as the diagnosis of the lesser of two evils thunderclap headache and given its favorable risk-to-benefit ratio
because most of the diseases that mimic primary thunderclap may be a reasonable therapeutic option.
headache are also associated with significant mortality and mor-
bidity. Table 8-3 lists diseases that may be mistaken for primary
thunderclap headache. Prominent among them is subarachnoid
Complications and Pitfalls
hemorrhage, stroke, collagen-vascular disease, infection, neo- Complications and pitfalls in the diagnosis and treatment of pri-
plasm, hypertensive crisis, spinal fluid leaks, and a variety of more mary thunderclap headache generally fall into three categories.
benign causes of headache. The first category involves the failure to recognize a sentinel bleed
associated with subarachnoid hemorrhage and evaluate and treat
the patient before significant morbidity or mortality occurs. The
Treatment second category involves misdiagnosis that results in unnecessary
Although no generally accepted treatment for primary thunder- testing, in particular, cerebral angiography, which itself is associ-
clap headache has been defined, the following guidelines may be ated with significant morbidity and rarely death. The third cat-
useful for the clinician when faced with a patient thought to have egory involves iatrogenic morbidity and rarely mortality from the
this uncommon headache syndrome. First and foremost, if test use of medications to treat primary thunderclap headache (e.g.,
results reveal no evidence of intracranial pathology or other seri- triptans, ergots) that not only do not treat this primary headache
ous, life-threatening diseases, constant reassurance that the patient syndrome but also have significant side effects.
22 SECTION 1 Headache and Facial Pain Syndromes
HYPNIC HEADACHE
23
24 SECTION 1 Headache and Facial Pain Syndromes
suspected even if blood is not present on MRI or CT. Plain radio- Lithium carbonate is used in the same manner as in the treatment
graphs of the cervical spine also may be useful in the evaluation of cluster headache and has its basis in use in its proven efficacy in
of Arnold-Chiari malformations and should be included in the the treatment of other diseases thought to have a chronobiological
evaluation of all patients with hypnic headache. basis, such as cluster headache and bipolar disorders. However,
Screening laboratory tests consisting of complete blood cell the therapeutic window of lithium carbonate is small and this
count, erythrocyte sedimentation rate, and automated blood drug should be used with caution. A starting dose of 300 mg at
chemistry testing should be performed if the diagnosis of hypnic bedtime may be increased after 48 hours to 300 mg twice per
headache is in question. Intraocular pressure should be measured day. If no side effects are noted after 48 hours, the dose may be
if glaucoma is suspected. increased again to 300 mg three times per day. Anecdotal reports
exist that gabapentin and pregabalin also may be useful in decreas-
Differential Diagnosis ing the frequency and intensity of attacks of hypnic headache.
Unlike with cluster headache, oxygen inhalation has been ineffec-
Hypnic headache is a clinical diagnosis supported by a combina- tive in aborting attacks of hypnic headache once the patient has
tion of clinical history, physical examination, radiography, MRI, been awakened by the pain.
and MRA. Pain syndromes that may mimic hypnic headache
include the uncommon primary headaches benign exertional
headache, ice pick headache, and sexual headache, although the
Complications and Pitfalls
unique same-time nocturnal occurrence should help the clinician Failure to diagnose hypnic headache correctly may put the
easily identify the patients symptoms as hypnic headache. The patient at risk if an intracranial pathological condition or demye-
clinician must consider other types of headache that occur more linating disease (which may rarely mimic the clinical presentation
frequently at night, including cluster headache and headaches of hypnic headache) is overlooked. MRI and MRA are indicated
associated with sleep apnea, nocturnal arterial hypertension, anal- in all patients thought to have hypnic headache. Failure to diag-
gesic rebound, and increased intracranial pressure (Table 9-1). nose glaucoma, which also may cause intermittent ocular pain,
Less commonly, hypnic headache may be confused with trigem- may result in permanent loss of sight.
inal neuralgia involving the first division of the trigeminal nerve or
demyelinating disease. Trigeminal neuralgia involving the first divi-
sion of the trigeminal nerve is uncommon and is characterized by Clinical Pearls
trigger areas and tic-like movements. Demyelinating disease is gen- Any patient presenting with nocturnal headaches should
erally associated with other neurological findings, including optic be taken very seriously. Although statistically most of these
neuritis and other motor and sensory abnormalities. The pain of headaches ultimately are proved to be of benign cause, a
chronic paroxysmal hemicrania and cluster headache is associated few patients have potentially life-threatening disease. The
with redness and watering of the ipsilateral eye, nasal congestion, diagnosis of hypnic headache is made by obtaining a thor-
and rhinorrhea during the headache. These findings are absent in ough, targeted headache history and performing a careful
hypnic headache. Migraine headache may or may not be associ- physical examination. The clinician must separate patients
ated with painless neurological findings known as aura, but patients with hypnic headache from patients with headaches caused
almost always report some systemic symptoms, such as nausea or by an intracranial pathological condition such as tumors
photophobia, not typically associated with hypnic headache. or systemic disease such as nocturnal arterial hyperten-
sion. Patients with hypnic headache should have a normal
Treatment neurological examination. If the neurological examina-
tion is abnormal, the diagnosis of benign hypnic headache
Indomethacin and lithium carbonate are the treatments of choice should be discarded and a careful search for the cause of the
for hypnic headache, with indomethacin being slightly more patients neurological findings should be undertaken.
effective for the unilateral form of the syndrome. Indomethacin
at a starting dose of 25 mg daily for 2 days and titrating to 25 mg
three times per day is a reasonable treatment approach. This dose
may be carefully increased up to 150 mg per day. Indometha- SUGGESTED READINGS
cin must be used carefully, if at all, in patients with peptic ulcer Alberti A: Headache and sleep, Sleep Med Rev 10:431437, 2006.
disease or impaired renal function. Headache specialists have Berciano J, Poca M-A, Garca A, Sahuquillo J: Paroxysmal cervicobrachial hypnic-
induced pain in a patient with syringomyelia extending into spinal cord poste-
noted anecdotal reports of a positive response to cyclooxygenase-2 rior gray horns, J Neurol 254:678681, 2007.
(COX-2) inhibitors in the treatment of benign hypnic headache. Chen Y-Y, Lirng J-F, Fuh J-L, etal: Primary hypnic headache is associated with
posterior fossa crowdedness: a morphometric MRI study, Cephalalgia 24:
694699, 2004.
Fowler MV, Capobianco DJ, Dodick DW: Headache in the elderly, Semin Pain
TABLE 9-1
Med 2:123128, 2004.
Nocturnal Headaches That May Be Confused with Manni R, Ghiotto N: In Aminoff M, editor: Handbook of clinical neurology, New
Hypnic Headache York, 2010, Elsevier, pp 469472.
Pascual J: Primary hypnic headache, Curr Pain Headache Rep 9:272276, 2005.
Cluster headache Pascual J, Gonzlez-Mandly A, Martn R, Oterino A: Headaches precipitated by
cough, prolonged exercise or sexual activity: a prospective etiological and clini-
Headache associated with sleep apnea
cal study, J Headache Pain 9:259266, 2008.
Headache associated with nocturnal arterial hypertension Waldman SD: Arnold Chiari malformation type I. In Waldman SD, Campbell
Headache associated with increased intracranial pressure RS, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 2728.
Waldman SD: Arnold Chiari malformation type II. In Waldman SD, Campbell
Analgesic rebound headache RS, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 2930.
Chapter 10
NUMMULAR HEADACHE
Testing
Magnetic resonance imaging (MRI) of the brain provides the best
information regarding the cranial vault and its contents. MRI is
highly accurate and helps identify abnormalities that may put the
patient at risk for neurological disasters secondary to intracranial
and brainstem pathological conditions, including tumors and
calvarial lesions (Figure 10-2). Magnetic resonance angiography
(MRA) also may be useful in helping identify aneurysms, which
may be responsible for the patients pain. In patients who can- Figure 10-1 Patients suffering from nummular headache complain of
not undergo MRI, such as patients with pacemakers, computed unifocal area of pain and scalp sensitivity.
25
26 SECTION 1 Headache and Facial Pain Syndromes
A B
Figure 10-2 Calvarial metastases. A, Abnormal enhancement (arrows) is present within the diplo on this gadolinium-enhanced T1-weighted image.
Expansion of the left parietal bone occurs, affecting the inner table more than the outer table. B, Heterogeneous hyperintensity (arrows) persists within
the calvaria on this T2-weighted image. The right parietal lesion is no longer imaged on this more superior section. (From Edelman RR, Hesselink JR,
Zlatkin MB, Crues JV III, editors: Clinical magnetic resonance imaging, 3rd ed, Philadelphia, 2005, Saunders.)
HEADACHE ASSOCIATED
WITHTEMPORAL ARTERITIS
Temporal artery
External
carotid artery
Ophthalmic
artery
Figure 11-1 A, Temporal arteritis is a disease of the sixth decade that occurs almost exclusively in whites, with a predilection of 3:1 for women.
B, The sine qua non of temporal arteritis is jaw claudication.
27
28 SECTION 1 Headache and Facial Pain Syndromes
In addition to the signs and symptoms mentioned previously, neurological symptoms. In patients who cannot undergo MRI,
patients with temporal arteritis experience myalgia and morning such as patients with pacemakers, computed tomography (CT)
stiffness. Muscle weakness associated with inflammatory muscle is a reasonable second choice. If intracranial hemorrhage is sus-
disease and many other collagen-vascular diseases is absent in tem- pected, lumbar puncture should be performed, even if blood is
poral arteritis, unless the patient has been treated with prolonged not present on MRI or CT. Intraocular pressure should be mea-
doses of corticosteroids for other systemic disease, such as poly- sured if glaucoma is suspected.
myalgia rheumatica. The patient also may experience nonspecific
systemic symptoms, including malaise, weight loss, night sweats,
and depression.
Differential Diagnosis
On physical examination, a swollen, indurated, nodular tem- Headache associated with temporal arteritis is a clinical diagnosis
poral artery is present. Diminished pulses are often noted, as is supported by a combination of clinical history, abnormal find-
tenderness to palpation. Scalp tenderness to palpation is often ings on physical examination of the temporal artery, normal radi-
seen. Funduscopic examination may reveal a pale, edematous ography, MRI findings, an elevated erythrocyte sedimentation
optic disc. The patient with temporal arteritis often appears rate, and a positive temporal artery biopsy result. Pain syndromes
chronically ill, depressed, or both. that may mimic temporal arteritis include tension type of head-
ache, brain tumor, other forms of arteritis, trigeminal neuralgia
involving the first division of the trigeminal nerve, demyelinating
Testing disease, migraine headache, cluster headache, and chronic parox-
Erythrocyte sedimentation rate should be obtained in all patients ysmal hemicrania. Trigeminal neuralgia involving the first division
suspected to have temporal arteritis. In temporal arteritis, the of the trigeminal nerve is uncommon and is characterized by trig-
erythrocyte sedimentation rate is greater than 50 mm/hr in more ger areas and tic-like movements. Demyelinating disease is gener-
than 90% of patients. Less than 2% of patients with biopsy-proved ally associated with other neurological findings, including optic
temporal arteritis have normal erythrocyte sedimentation rates. neuritis and other motor and sensory abnormalities. The pain of
Ideally, the blood for the erythrocyte sedimentation rate should chronic paroxysmal hemicrania and cluster headache is associated
be obtained before beginning corticosteroid therapy because the with redness and watering of the ipsilateral eye, nasal congestion,
initial level of elevation of this test is useful not only to help diag- and rhinorrhea during the headache. These findings are absent in
nose the disease but also as a mechanism to establish the efficacy of all types of sexual headache. Migraine headache may or may not
therapy. The erythrocyte sedimentation rate is a nonspecific test, be associated with painless neurological findings known as aura,
and other diseases that may manifest clinically in a manner similar but the patient almost always reports some systemic symptoms,
to that of temporal arteritis, such as malignancy or infection, also such as nausea or photophobia, not typically associated with the
may markedly elevate the erythrocyte sedimentation rate. Con- headache of temporal arteritis.
firmation of the clinical diagnosis of temporal arteritis requires a
temporal artery biopsy.
Given the simplicity and safety of temporal artery biopsy, it
Treatment
probably should be performed on all patients suspected of hav- The mainstay of treatment for temporal arteritis and its associ-
ing temporal arteritis. The presence of an inflammatory infiltrate ated headaches and other systemic symptoms is the immediate use
with giant cells in the biopsied artery is characteristic of the dis- of corticosteroids. If visual symptoms are present, an initial dose
ease. Edema of the intima and disruption of the internal elastic of 80 mg of prednisone is indicated. This dose should be con-
lamina strengthen the diagnosis. A small percentage of patients tinued until the symptoms of temporal arteritis have completely
with clinical signs and symptoms strongly suggestive of tempo- abated. At this point, the dose may be decreased by 5 mg/wk as
ral arteritis who also exhibit a significantly elevated erythrocyte long as the symptoms remain quiescent and the erythrocyte sedi-
sedimentation rate have a negative temporal artery biopsy result. mentation rate does not increase. Cytoprotection of the stomach
As mentioned, in the presence of a strong clinical impression that mucosa should be considered because ulceration and gastrointes-
the patient has temporal arteritis, an immediate blood sample for tinal bleeding are possible. If the patient cannot tolerate cortico-
erythrocyte sedimentation rate testing should be obtained and the steroids, or the maintenance dose of steroids remains so high as to
patient started on corticosteroids. Complete blood cell count and produce adverse effects, azathioprine is a reasonable next choice.
automated chemistries, including thyroid testing, are indicated in
all patients with suspected temporal arteritis to help rule out other Complications and Pitfalls
systemic disease that may mimic the clinical presentation of tem-
poral arteritis. Failure to recognize, diagnose, and treat temporal arteritis
If the diagnosis of temporal arteritis is in doubt, magnetic reso- promptly may result in the permanent loss of vision. Failure to
nance imaging (MRI) of the brain provides the best information diagnose the headache associated with temporal arteritis correctly
regarding the cranial vault and its contents. MRI is highly accurate may put the patient at risk if an intracranial pathological con-
and helps identify abnormalities that may put the patient at risk dition or demyelinating disease (which may mimic the clinical
for neurological disasters secondary to intracranial and brainstem presentation of temporal arteritis) is overlooked. MRI of the brain
pathological conditions, including tumors and demyelinating dis- is indicated in all patients thought to have headaches associated
ease. More important, MRI helps identify bleeding associated with with temporal arteritis. Failure to diagnose glaucoma, which also
leaking intracranial aneurysms. Magnetic resonance angiography may cause intermittent ocular pain, may result in permanent loss
(MRA) may be useful to help identify aneurysms responsible for of sight.
11 Headache Associated with Temporal Arteritis 29
POSTDURAL PUNCTURE
HEADACHE
from the horizontal to the upright position and then abates when
ICD-9 CODE 349.0 the patient resumes a horizontal position is the sine qua non of
postdural puncture headache (Figure 12-1). A history of inten-
tional dural puncture, such as lumbar puncture, spinal anesthe-
ICD-10 CODE G97.1 sia, or myelography, or accidental dural puncture, such as failed
epidural block or dural injury during spinal surgery, strongly
points to the diagnosis of postdural puncture headache. As men-
tioned, a spontaneous postural headache that manifests identically
The Clinical Syndrome to headache after dural puncture can occur after bouts of heavy
When the dura is intentionally or accidentally punctured, the sneezing or coughing and is thought to be due to traumatic rents
potential for headache exists. The clinical presentation of post in the dura. In this setting, a diagnosis of postdural puncture
dural puncture headache is classic and makes the diagnosis headache is one of exclusion.
straightforward if considering this diagnostic category of head-
ache. The diagnosis may be obscured if the clinician is unaware Testing
that dural puncture may have occurred or in the rare instance
when this type of headache occurs spontaneously after a bout of Magnetic resonance imaging (MRI) with and without gadolinium
sneezing or coughing. The symptoms and rare physical findings is highly accurate in helping confirm the diagnosis of postdural
associated with postdural puncture headache are due to low cere- puncture headache. Enhancement of the dura with low-lying
brospinal fluid pressure resulting from continued leakage of spinal cerebellar tonsils invariably is present. Poor visualization of the
fluid out of the subarachnoid space. cisterns and subdural and epidural fluid collections also may be
The symptoms of postdural puncture headache begin almost identified.
immediately after the patient moves from a horizontal to an No additional testing is indicated for a patient who has under-
upright position. The intensity peaks within 1 or 2 minutes and gone dural puncture and then develops a classic postural head-
abates within several minutes of the patient again assuming the ache, unless infection or subarachnoid hemorrhage is suspected.
horizontal position. The headache is pounding in character, and In this setting, lumbar puncture, complete blood cell count, and
its intensity is severe, with the intensity increasing the longer the erythrocyte sedimentation rate are indicated on an emergent basis.
patient remains upright. The headache is almost always bilateral
and located in the frontal, temporal, and occipital regions. Nausea Differential Diagnosis
and vomiting and dizziness frequently accompany the headache
pain, especially if the patient remains upright for long periods. If If the clinician is aware that the patient has undergone dural
cranial nerve palsy occurs, visual disturbance may occur. puncture, the diagnosis of postdural puncture headache is usu-
ally made. Delayed diagnosis most often occurs in settings in
which dural puncture is not suspected. Occasionally, postdural
Signs and Symptoms puncture headache is misdiagnosed as migraine headache because
The diagnosis of postdural puncture headache is most often of the associated nausea and vomiting coupled with visual dis-
made on the basis of clinical history rather than physical findings turbance. In any patient with dural puncture, infection remains
on examination. The neurological examination in most patients an ever-present possibility. If fever is present, immediate lumbar
suffering from postdural puncture headache is normal. If the puncture and blood cultures should be obtained and the patient
spinal fluid leak is allowed to persist, or if the patient remains in started on antibiotics that cover resistant strains of Staphylococ-
the upright position for long periods despite the headache, cranial cus. MRI to rule out epidural abscess also should be considered
nerve palsies may occur, with the sixth cranial nerve affected most if fever is present. Subarachnoid hemorrhage may mimic post
commonly. This complication may be transient, but may become dural puncture headache, but should be identified on MRI of
permanent, especially in patients with vulnerable nerves, such as the brain.
those with diabetes. If the neurological examination is abnormal,
other causes of headache should be considered, including sub- Treatment
arachnoid hemorrhage.
The onset of headache pain and other associated symptoms The mainstay of treatment of postdural puncture headache is
such as nausea and vomiting that occurs when the patient moves the administration of autologous blood into the epidural space.
30
12 PostDural Puncture Headache 31
Cauda equina
Dura mater
Figure 12-1 The onset of headache that occurs when the patient moves from the horizontal to the upright position is the sine qua non of postdural
puncture headache.
This technique is known as epidural blood patch and is highly associated with dural puncture. Failure to diagnose central ner-
successful in the treatment of postdural puncture headache. A vous system infection correctly can result in significant mortality
volume of 12 to 18 mL of autologous blood is injected slowly and morbidity.
into the epidural space at the level of dural puncture under
strict aseptic precautions. The patient should remain in the
horizontal position for the next 12 to 24 hours. Relief occurs Clinical Pearls
within 2 to 3 hours in more than 90% of patients. Approxi-
mately 10% of patients experience temporary relief and then a The diagnosis of postdural puncture headache is made by
recurrence of symptoms when assuming the upright position. obtaining a thorough, targeted headache history and per-
These patients should undergo a second epidural blood patch forming a careful physical examination. The postural nature
within 24 hours. is pathognomonic for postdural puncture headache, and
If the patient has experienced significant nausea and vomiting, its presence should lead the clinician to strongly consider
antiemetics combined with intravenous fluids help speed recov- the diagnosis of postdural puncture headache. The inci-
ery. Some clinicians have advocated the use of alcoholic beverages dence of postdural puncture headache after lumbar punc-
to suppress the secretion of antidiuretic hormone and increase ture, myelography, or spinal anesthesia can be decreased
cerebrospinal fluid production. Caffeine also has been reported to by using needles with a smaller diameter and placing the
be helpful in treating the headache pain. needle bevel parallel to the dural fibers. Special noncutting
needles may decrease further the incidence of postdural
puncture headache.
Complications and Pitfalls
Failure to recognize, diagnose, and treat postdural puncture
headache promptly may result in considerable pain and suffering SUGGESTED READINGS
for the patient. If the low cerebrospinal fluid pressure is allowed Ghaleb A, Pablo C, Mandoff VL, Albataniah J, Candido K: Postdural puncture
to persist, cranial nerve deficits may occur. In most instances, the cephalgia, Semin Pain Med 2:215219, 2004.
cranial nerve deficits are temporary, but in rare instances, these Harrington BE: Postdural puncture headache, Adv Anesth 28:121146, 2010.
Neal JM: Update on postdural puncture headache, Tech Reg Anesth Pain Manage
deficits may become permanent, especially in patients with vul- 2:202210, 1998.
nerable nerves, such as those with diabetes. MRI of the brain is Waldman SD, Feldstein GS, Allen ML: Cervical epidural blood patch for treatment
indicated in all patients thought to be suffering from headaches of cervical dural puncture headache, Anesth Rev 14:2325, 1987.
Chapter 13
32
13 Ramsay Hunt Syndrome 33
side effects of potent opioid analgesics (e.g., confusion or diz- cannot or will not undergo sympathetic neural blockade and do
ziness, which may cause a patient to fall) is warranted. Daily not tolerate pharmacological interventions.
dietary fiber supplementation and Milk of Magnesia should be Topical application of aluminium sulfate as a tepid soak pro-
started, along with opioid analgesics to prevent the side effect of vides excellent drying of the crusting and weeping lesions of acute
constipation. herpes zoster, and most patients find these soaks soothing. Zinc
oxide ointment also may be used as a protective agent, especially
Adjuvant Analgesics during the healing phase when temperature sensitivity is a prob-
The anticonvulsant gabapentin represents a first-line treatment in lem. Disposable diapers can be used as an absorbent padding to
the palliation of neuritic pain of acute herpes zoster involving the protect healing lesions from contact with clothing and sheets.
geniculate ganglion. Studies suggest that gabapentin also may help
prevent the development of postherpetic neuralgia. Treatment with
gabapentin should begin early in the course of the disease, and this
Complications and Pitfalls
drug may be used concurrently with neural blockade, opioid anal- In most patients, acute herpes zoster involving the geniculate gan-
gesics, and other adjuvant analgesics, including the antidepressant glion is a self-limited disease. In elderly and immunosuppressed
compounds if care is taken to avoid central nervous system side patients, complications may occur, however. Cutaneous and vis-
effects. Gabapentin is started at a bedtime dose of 300 mg and is ceral dissemination may range from a mild rash resembling chick-
titrated in 300-mg increments to a maximum dose of 3600 mg enpox to an overwhelming, life-threatening infection in patients
given in divided doses as side effects allow. Carbamazepine should already suffering from severe multisystem disease. Myelitis may
be considered in patients with severe neuritic pain who have failed cause bowel, bladder, and lower extremity paresis. Ocular compli-
to respond to nerve blocks and gabapentin. If this drug is used, rigid cations from trigeminal nerve involvement may range from severe
monitoring for hematological parameters is indicated, especially in photophobia to keratitis with loss of sight.
patients receiving chemotherapy or radiation therapy. Phenytoin
also may be beneficial to treat neuritic pain, but it should not be
used in patients with lymphoma because the drug may induce a Clinical Pearls
pseudolymphoma state that is difficult to distinguish from the Because the pain of herpes zoster usually precedes the erup-
actual lymphoma itself. tion of skin lesions by 5 to 7 days, erroneous diagnosis of
Antidepressants also may be useful adjuncts in the initial treat- other painful conditions (e.g., trigeminal neuralgia, glau-
ment of patients with acute herpes zoster. On an acute basis, these coma) may be made. In this setting, the astute clinician
drugs help alleviate the significant sleep disturbance that is com- advises the patient to call immediately if a rash appears
monly seen with acute herpes zoster. In addition, antidepressants because the diagnosis of acute herpes zoster is a possibility.
may be valuable in helping ameliorate the neuritic component of Some pain specialists believe that in a few immunocom-
the pain, which is treated less effectively with opioid analgesics. petent patients, when reactivation of virus occurs, a rapid
After several weeks of treatment, the antidepressants may exert immune response may attenuate the natural course of the
a mood-elevating effect that may be desirable in some patients. disease and the characteristic rash of acute herpes zoster may
Patients must be observed closely for central nervous system side not appear. This pain in the distribution of the geniculate
effects. These drugs may cause urinary retention and constipation ganglion without associated rash is termed zoster sine herpete
that may be mistakenly attributed to herpes zoster myelitis. and is, by necessity, a diagnosis of exclusion. Other causes
Antiviral Agents of head pain must be ruled out first before invoking this
diagnosis. Because of the potential for hearing loss in Ram-
A few antiviral agents, including famciclovir and acyclovir, have say Hunt syndrome, patients should be warned of this pos-
been shown to shorten the course of, and may help prevent the sibility to avoid erroneously blaming this complication on
development of, acute herpes zoster. They are probably useful a therapeutic intervention, such as stellate ganglion block.
in attenuating the disease in patients with immunosuppression.
These antiviral agents can be used in conjunction with the treat-
ment modalities mentioned earlier. Careful monitoring for side
effects is mandatory with these drugs. SUGGESTED READINGS
Bhagra A, Stead LG: Ramsay Hunt syndrome: a rare entity, Ann Emerg Med
Adjunctive Treatments 47:579, 2006.
Gantz BJ, Redleaf MI, Perry BP, Gubbels SP: Management of Bells palsy and
The application of ice packs to the lesions of acute herpes zoster Ramsay Hunt syndrome. In Brackmann DE, etal: Otologic surgery, ed 3, Phila-
may provide relief in some patients. Application of heat increases delphia, 2010, Saunders, pp 335346.
pain in most patients, presumably because of increased conduc- Persson A, Bergstrm T, Lindh M, Namvar L, Studahl M: Varicella-zoster virus
tion of small fibers, but it is beneficial occasionally and may be CNS disease: viral load, clinical manifestations and sequels, J Clin Virol 46:249
worth trying if application of cold is ineffective. Transcutaneous 253, 2009.
Taguchi T, Ueda S, Kudo T, etal: Ramsay-Hunt syndrome, J Infect 62:180181,
electrical nerve stimulation and vibration also may be effective in 2011.
a few patients. The favorable risk-to-benefit ratio of all of these Ulusoy , zkan G, Bekta D, etal: Ramsay Hunt syndrome in renal transplanta-
modalities makes them reasonable alternatives for patients who tion recipient: a case report, Transplant Proc 42:19861988, 2010.
Chapter 14
EAGLE SYNDROME
35
36 SECTION 1 Headache and Facial Pain Syndromes
Figure 14-2 Tumor (T) of the piriform sinus. The lesion protrudes Figure 14-3 An imaginary line from the mastoid process to the angle
through the thyroarytenoid gap between thyroid cartilage and aryte- of the mandible is an aid in needle placement for injection in a patient
noid (arrow). The tumor invades the paraglottic space (arrowhead) of with Eagle syndrome.
the supraglottic larynx. Compare with the fat in the paraglottic space on
the normal side. C, Carotid artery. (From Haaga JR, Lanzieri CF, Gilkeson
RC, editors: CT and MR imaging of the whole body, 4th ed, Philadelphia,
2003, Mosby, p 611.) blocked, dysphonia secondary to paralysis of the ipsilateral vocal
cord may occur. A reflex tachycardia secondary to vagal nerve
block also is observed in some patients. Inadvertent block of the
attached to a 14-mL syringe is advanced at this midpoint location hypoglossal and spinal accessory nerves during glossopharyngeal
in a plane perpendicular to the skin. The styloid process should be nerve block results in weakness of the tongue and trapezius muscle.
encountered within 3 cm. After contact is made, the needle is with-
drawn slightly out of the periosteum or substance of the calcified liga-
ment. After careful aspiration reveals no blood or cerebrospinal fluid,
Clinical Pearls
5 mL of 0.5% preservative-free lidocaine combined with 80 mg Eagle syndrome is an uncommon cause of facial pain.
of methylprednisolone is injected in incremental doses. Subsequent Because of the low incidence of Eagle syndrome relative
daily nerve blocks are performed in a similar manner, substituting to pain secondary to malignancy in this anatomical region,
40 mg of methylprednisolone for the initial 80-mg dose. Eagle syndrome must be considered a diagnosis of exclu-
The sharp, shooting pain associated with Eagle syndrome also sion. The clinician should always evaluate a patient with
may be treated with gabapentin. Gabapentin is started at a single pain in this anatomical region for occult malignancy.
nighttime dose of 300 mg and titrated by 300-mg increments Tumors of the larynx, hypopharynx, and anterior triangle
every 2 days in divided doses until pain relief is achieved or a total of the neck may manifest with clinical symptoms identical
daily dose of 3600 mg is reached. Alternatively, carbamazepine or to those of Eagle syndrome.
phenytoin may be tried.
ATYPICAL ODONTALGIA
Testing
Radiographs of the head are usually within normal limits in Figure 15-1 Patients with atypical odontalgia often rub the affected
patients suffering from atypical odontalgia, but they may be useful area; those with trigeminal neuralgia do not.
37
38 SECTION 1 Headache and Facial Pain Syndromes
A B
C D
Figure 15-2 Computed tomography (CT) scan and magnetic resonance imaging (MRI) of the lesion. CT shows a well-defined expansile lesion with
thin cortical margin and high-density area (A). MRI of the lesion revealed the well-circumscribed lesion (B) to be homogeneously and relatively
hypointense on T2-weighted imaging (C). The lesion was weakly enhanced by gadolinium (D). (From Nozaki S, Yamazaki M, Koyama T, etal: Primary
extracranial meningioma of the maxillary sinus presenting as buccal swelling, Asian J Oral Maxillofac Surg 23:134137, 2011.)
15 Atypical Odontalgia 39
40
16 Burning Mouth Syndrome 41
responsible for the patients pain. All underlying medical condi- a single bedtime dose of 300 mg, titrating the dosage upward in
tions (e.g., diabetes, deficiency syndromes) must be treated, along divided doses to a maximum dose of 3600 mg per day. Pregabalin
with the removal of any local irritants such as mouth washes, is a reasonable alternative to gabapentin and is better tolerated in
spicy foods, and cinnamon and mint products. Providing the some patients. Pregabalin is started at 50 mg three times per day
patient with a supportive and positive emotional environment and may be titrated upward to 100 mg three times per day as dis-
and reassurance that cancer is not the cause of the pain is para- ease effects allow. Pregabalin is excreted primarily by the kidneys,
mount if symptom relief is to be achieved. Coexistent behavioral and the dosage should be decreased in patients with compromised
and psychiatric abnormalities also must be addressed in a positive renal function.
therapeutic milieu. Empirical treatments, including anticandiadal Opioid analgesics and benzodiazepines should be avoided to
agents, vitamin B complex supplementation, and low-dose antide- prevent iatrogenic chemical dependence.
pressants, are also worthy of consideration.
Treatment often involves some combination of elimination of
any local irritants, treatment of underlying medical conditions, TABLE 16-2
pharmacological therapy, and behavioral therapy. Causes of Burning Mouth and Tongue Pain
First, any nidus of tissue trauma that is contributing to the
ongoing sympathetic dysfunction responsible for the symptoms Psychogenic,
Psychiatric,
must be identified and removed. Second, interruption of the sym- Systemic Local and Idiopathic
pathetic innervation of the face by stellate ganglion block with
local anesthetic must be implemented. This may require daily stel- Deficiencies Denture factors Psychiatric
late ganglion block for a considerable period. Occupational ther- Iron Dental work Depression
apy consisting of tactile desensitization of the affected mucosa also Vitamin B12 Mechanical Anxiety
may be of value. Underlying depression and sleep disturbance are Folate Oral habit or parafunc- Obsessive-
best treated with a tricyclic antidepressant such as nortriptyline, tional behavior compulsive
given as a single 25-mg dose at bedtime. Gabapentin may help pal- disorder
liate any neuritic pain component and is best started slowly with Zinc Clenching Somatoform
disorder
B complex vitamins Bruxism Cancerphobia
TABLE 161 Endocrine Tongue thrusting Psychosocial
stressors
Workup of Burning Mouth Syndrome
Diabetes mellitus Myofasical pain
Thorough history and review of symptoms
Hypothyroidism Allergic contact stomatitis
Medications causing xerostomia
Menopause or Dental restoration or
Dental or denture work hormonal denture materials
Oral care, oral products Foods
Oral habits or parafunctional behavior Xerostomia Preservative, additives,
History of depression, anxiety, cancerphobia flavorings
Family history of oral cancer, psychiatric diagnoses, and connective Connective tissue Neurologic
tissue disease disease
Oral examination Sjgrens syndrome Referred from tonsils or
teeth
Erythema, candidiasis, xerostomia, or other mucosal abnormalities
Sicca syndrome Lingual nerve neuropathy
Tongue disorders, such as a geographic, fissured, or atrophic
tongue Drug related Glossopharyngeal
neuropathy
Dental work or dentures
Anxiety or stress Acoustic neuroma
Laboratory tests
Medication Infection
Complete blood count
Angiotensin- Candidiasis
Iron, total iron binding capacity, iron saturation, ferreting
converting enzyme
Vitamin B12, folate, zinc inhibitor
Glucose, glycosylated hemoglobin Esophageal reflux Antibiotic related
Culture for Candida Anemia Denture related
Patch testing Local trauma
Include standard series, metal series, oral flavors, and preservatives Corticosteroid
Further consultation if indicated by history and review of systems Diabetes mellitus
Psychometric testing and psychiatric consultation Fusospirochetal
Dentistry Xerostomia
Neurology Irradiation
Otorhinolaryngology Local disease
From Drage LA, Rogers RSR III: Burning mouth syndrome, Dermatol Clin From Drage LA, Rogers RSR III: Burning mouth syndrome, Dermatol Clin
21:135145, 2003. 21:135145, 2003.
42 SECTION 1 Headache and Facial Pain Syndromes
SUGGESTED READINGS
Complications and Pitfalls
Drage LA, Rogers RSR III: Burning mouth syndrome, Dermatol Clin 21:135145,
The main complications surrounding the treatment of burn- 2003.
ing mouth syndrome are those associated with its misdiagnosis. Miziara ID, Arajo Filho BC, Oliveira R, Rodrigues dos Santos RM: Group psy-
chotherapy: an additional approach to burning mouth syndrome, Psychosom Res
Chemical dependence, depression, and multiple failed therapeutic 67:443448, 2009.
procedures are the rule rather than the exception. A diagnosis of a Mock D: Burning tongue/mouth syndrome, J Oral Maxillofac Surg 67(Suppl 1):5,
psychiatric basis for the patients pain should be made only after 2009.
all somatic causes of burning mouth syndrome have carefully been Moore PA, Guggenheimer J, Orchard T: Burning mouth syndrome and peripheral
ruled out. neuropathy in patients with type 1 diabetes mellitus, J Diabetes Complications
21:397402, 2007.
Clinical Pearls
The key to diagnosing burning mouth syndrome is a high
index of clinical suspicion. Once causes of burning mouth
and tongue that have clinically identifiable pathological
processes have been ruled out, a rational treatment plan
addressing the often multifactorial nature of the patients
pain can be initiated. A supportive therapeutic environment
is crucial if symptom reduction is to be achieved.
Chapter 17
Treatment
Drug Therapy
Carbamazepine
Carbamazepine is considered first-line treatment for nervus interme-
dius neuralgia. In fact, a rapid response to this drug helps confirms
the clinical diagnosis. Despite the safety and efficacy of carbamaze-
pine, some confusion and anxiety exist surrounding its use. This
medication, which may be the patients best chance for pain con-
trol, is sometimes discontinued because of laboratory abnormali-
ties erroneously attributed to it. Therefore baseline measurements
consisting of a complete blood count, urinalysis, and automated
blood chemistry profile should be obtained before starting the drug.
Axial Carbamazepine should be initiated slowly if the pain is not
out of control, with a starting dose of 100 to 200 mg at bedtime
for 2 nights. The patient should be cautioned about side effects,
including dizziness, sedation, confusion, and rash. The drug is
increased in 100- to 200-mg increments given in equally divided
doses over 2 days, as side effects allow, until pain relief is obtained
or a total dose of 1200 mg per day is reached. Careful monitoring
of laboratory parameters is mandatory to avoid the rare possibil-
ity of a life-threatening blood dyscrasia. At the first sign of blood
count abnormality or rash, this drug should be discontinued. Failure
to monitor patients on carbamazepine can be disastrous, because
aplastic anemia can occur. When pain relief is obtained, the
Coronal
patient should be kept at that dosage of carbamazepine for at least
Figure 17-2 Gadolinium-enhanced magnetic resonance imaging (MRI). 6 months before tapering of the medication is considered. The
Images show a centrally enhancing lesion in the geniculate ganglion
(arrow), measuring 5 mm 10 mm in diameter. (From Miyashita T,
patient should be informed that under no circumstances should
Hoshikawa H, Kagawa M, Mori N: A case report of facial nerve heman- the drug dosage be changed or the drug refilled or discontinued
gioma, Auris Nasus Larynx 34:519522, 2007.) without the physicians knowledge.
Gabapentin
intermedius or geniculate ganglion by aberrant blood vessels. In the uncommon event that carbamazepine does not adequately
Additional imaging of the sinuses should be considered in the control a patients pain, gabapentin may be considered. As with
case of any question of occult or coexisting sinus disease. If the carbamazepine, baseline blood tests should be obtained before
first division of the trigeminal nerve is affected, ophthalmologi- starting therapy and the patient should be cautioned about poten-
cal evaluation to measure intraocular pressure and rule out intra- tial side effects, including dizziness, sedation, confusion, and rash.
ocular pathological conditions is indicated. Screening laboratory The initial dose is 300 mg at bedtime for 2 nights. The drug is
tests consisting of a complete blood count, erythrocyte sedimen- then increased in 300-mg increments given in equally divided
tation rate, and automated blood chemistry should be performed doses over 2 days, as side effects allow, until pain relief is obtained
if the diagnosis of trigeminal neuralgia is in question. A complete or a total dose of 2400 mg per day is reached. At this point, if the
blood count is required for baseline comparisons before starting patient has experienced only partial pain relief, blood values are
treatment with carbamazepine (see discussion of treatment). measured and the drug is carefully titrated upward using 100-mg
tablets. Rarely is a dosage greater than 3600 mg per day required.
Differential Diagnosis Pregabalin
Nervus intermedius neuralgia is generally a diagnosis of exclu- Pregablin represents a reasonable alternative to gabapentin and
sion, although the clinical presentation makes it a straightforward is better tolerated in some patients. Pregablin is started at 50 mg
clinical diagnosis that can be made on the basis of a targeted his- three times per day and may be titrated upward to 100 mg three
tory and physical examination. Diseases of the eyes, ears, nose, times per day as side effects allow. Pregablin is excreted primarily
throat, and teeth may mimic nervus intermedius neuralgia or by the kidneys, and thus the dosage should be decreased in patients
may coexist and confuse the diagnosis. Atypical facial pain or with compromised renal function.
temporomandibular joint dysfunction is sometimes confused
with nervus intermedius neuralgia, but it can be distinguished by Baclofen
the character of the painatypical facial pain is dull and aching, Baclofen may be of value in some patients who fail to obtain relief
whereas the pain of nervus intermedius neuralgia is sharp and from carbamazepine, gabapentin, or pregabalin. As with those
neuritic. Additionally, the pain of nervus intermedius neuralgia drugs, baseline laboratory tests should be obtained before begin-
occurs in the distribution of the nervus intermedius, whereas the ning baclofen therapy and the patient should be warned about the
pain of atypical facial pain does not follow a specific nerve dis- same potential adverse effects. Start with a 10-mg dose at bedtime
tribution. Multiple sclerosis should be considered in all patients for 2 nights, then increase the drug in 10-mg increments given in
who present with nervus intermedius neuralgia before the fifth equally divided doses over 7 days, as side effects allow, until pain
decade of life. relief is obtained or a total dose of 100 mg per day is reached. This
17 Nervus Intermedius Neuralgia 45
drug has significant hepatic and central nervous system side effects, Clinical Pearls
including weakness and sedation. As with carbamazepine, careful
monitoring of laboratory values is indicated when using baclofen. Nervus intermedius neuralgia is an uncommon cause of otal-
When treating individuals with any of these drugs, the physi- gia. Because of the potential for disastrous clinical outcome
cian should make sure the patient knows that premature tapering should a more common cause of otic pain be overlooked
or discontinuation of the medication may lead to the recurrence (e.g., tumor or the temporal bone, brainstem, or nasophar-
of pain, which will be more difficult to control. ynx), the diagnosis of nervus intermedius neuralgia must by
necessity be one of exclusion. Because of the severity of the
pain associated with this syndrome, aggressive pharmaco-
Invasive Therapy
logical management in an inpatient setting may be required.
Section of the Nervus Intermedius Surgical treatment consisting of the sectioning of the nervus
This neurosurgical technique is the invasive treatment of choice intermedius is often the patients best option for complete
for those patients with nervus intermedius neuralgia who have and long-lasting pain relief.
failed to respond to conservative pharmacological management.
To perform this procedure, the nervus intermedius and geniculate
ganglion are identified and isolated and the nervus intermedius SUGGESTED READINGS
is sectioned in two places. Some surgeons also advocate extirpa-
tion of the geniculate ganglion. Section of the nervus intermedius Alcaraz N, King WA, Wackym PA: Endoscopy during neurotomy of the nervus
intermedius for geniculate neuralgia, Otolaryngol Head Neck Surg 121:334336,
alone provides excellent palliation of pain in 75% to 90% of cases. 1999.
Bhagra A, Stead LG: Nervus intermedius neuralgia: a rare entity, Ann Emerg Med
Complications and Pitfalls 47:579, 584, 2006.
Gantz BJ, Redleaf MI, Perry BP, Gubbels SP: Management of Bells palsy and
nervus intermedius neuralgia. In Brackmann DE, Shelton C, Arriaga MA,
The pain of nervus intermedius neuralgia is severe and can lead editors:Otologic surgery, ed 3, Philadelphia, 2010, Elsevier, pp 335346.
to suicide; therefore it must be considered a medical emergency, Persson A, Bergstrm T, Lindh M, Namvar L, Studahl M: Varicella-zoster
and strong consideration should be given to hospitalizing such virus CNS disease: viral load, clinical manifestations and sequels, J Clin Virol
patients. If a dull ache remains between the intense paroxysms of 46:249253, 2009.
pain, the clinician should have a high index of suspicion that the Taguchi T, Ueda S, Kudo T, etal: Ramsay-Hunt syndrome, J Infect 62:180181,
2011.
nidus of the patients pain is persistent compression of the nerve Ulusoy , zkan G, Bekta D, etal: Nervus intermedius neuralgia in renal trans-
by a structural lesion such as a brainstem tumor or schwannoma. plantation recipient: a case report, Transplant Proc 42:19861988, 2010.
Chapter 18
TABLE 18-1
The Trigeminal Autonomic Cephalgias
Cluster headache
Paroxysmal hemicranias
Figure 18-1 Red ear syndrome is characterized by the complaint of
Short-lasting unilateral neuralgiform headache with conjunctival severe paroxysms of sudden onset of unilateral ear redness associated
injection tearing (SUNCT) with ipsilateral ear pain.
46
18 Red Ear Syndrome 47
bony abnormality such as metastatic disease is considered in the Complications and Pitfalls
differential diagnosis.
Screening laboratory tests consisting of complete blood cell Failure to diagnose red ear syndrome correctly may put the
count, erythrocyte sedimentation rate, and automated blood chem- patient at risk if intracranial pathology or demyelinating disease,
istry should be performed if the diagnosis of red ear syndrome is in which may mimic the clinical presentation of red ear syndrome,
question. Additional testing to rule out collagen-vascular disease is is overlooked. MRI is indicated in all patients thought to have red
indicated if polychondritis is suspected. ear syndrome. A careful evaluation of the ear to rule out localized
pathological conditions is also indicated, as is laboratory testing
for collagen-vascular disease if polychondritis is suspected.
Differential Diagnosis
Red ear syndrome is a clinical diagnosis supported by a combi-
nation of clinical history, normal physical examination, radiogra- Clinical Pearls
phy, and MRI. Pain syndromes that may mimic red ear syndrome
include erythromelalgia of the ear, polychondritis, cluster head- Given the poor response to treatment with drugs tradi-
ache, temporal arteritis, trigeminal neuralgia, demyelinating tionally used to treat trigeminal neuralgia, facet block of
disease, primary stabbing headache, SUNCT, and chronic parox- the ipsilateral C2-C3 facet joints with local anesthetic and
ysmal hemicranias. However, because of the overlapping features steroids should be considered in patients thought to have
of all headache and facial pain syndromes, red ear syndrome easily red ear syndrome. Given the uncommon nature of this
can be mistaken for another type of headache or facial pain. Tri- headache syndrome and its overlap with the other trigemi-
geminal neuralgia is more common and is characterized by trigger nal autonomic cephalgias and other more serious forms of
areas and tic-like movements. Demyelinating disease is gener- intracranial pathological conditions such as tumors and
ally associated with other neurological findings, including optic vascular abnormalities, red ear syndrome must remain
neuritis and other motor and sensory abnormalities. The pain of a diagnosis of exclusion. All patients thought to have red
chronic paroxysmal hemicrania lasts much longer than the pain of ear syndrome require MRI of the brain with and without
red ear syndrome. gadolinium contrast material and thorough otic and neuro-
logical evaluation. Cervical facet block should be performed
only by clinicians familiar with the regional anatomy.
Treatment
The treatment of red ear syndrome is analogous to the treatment of
trigeminal neuralgia, although the pharmacological management
of this uncommon headache disorder is disappointing. The use of SUGGESTED READINGS
anticonvulsants such as lamotrigine and gabapentin represents a Kumar N, Swanson JW: The red ear syndrome revisited: two cases and a review
reasonable starting point. High-dose steroids tapered over 10 days of literature, Cephalalgia 24:305308, 2004.
also have been anecdotally reported to provide relief. For patients Lance JW: The red ear syndrome, Neurology 47:617620, 1996.
who do not respond to these treatments, a few case reports suggest Leone M, Bussone G: Pathophysiology of trigeminal autonomic cephalalgias, Lancet
Neurol 8:18551884, 2009.
that daily ipsilateral C2-C3 facet joint blocks with local anesthetic Purdy RA, Dodick DW: Red ear syndrome, Curr Pain Headache Rep 11:313316,
and steroid may provide relief of both the pain and the autonomic 2007.
dysfunction. Underlying sleep disturbance and depression associ- Waldman SD: Cervical facet block. In Waldman SD, editor: Atlas of interventional
ated with the pain of red ear syndrome are best treated with a pain management, ed 3, Philadelphia, 2009, Saunders, pp 165168.
tricyclic antidepressant compound, such as nortriptyline, which
can be started at a single bedtime dose of 25 mg.
Chapter 19
GLOSSOPHARYNGEAL NEURALGIA
Testing
Magnetic resonance imaging (MRI) of the brain and brainstem
should be performed in all patients thought to have glossopha-
ryngeal neuralgia. MRI of the brain provides the best informa-
tion regarding the cranial vault and its contents. MRI is highly Figure 19-1 The pain of glossopharyngeal neuralgia is in the distribution
accurate and helps identify abnormalities that may put the patient of cranial nerve IX.
48
19 Glossopharyngeal Neuralgia 49
fossa and piriform sinuses, may mimic the pain of glossopharyn- or a total dose of 1200 mg per day is reached. Careful monitoring
geal neuralgia, as may tumors at the cerebellopontine angle. Occa- of laboratory parameters is mandatory to avoid the rare possibility
sionally, demyelinating disease may produce a clinical syndrome of life-threatening blood dyscrasia. At the first sign of blood count
identical to glossopharyngeal neuralgia. The jaw claudication asso- abnormality or rash, this drug should be discontinued. Failure
ciated with temporal arteritis also sometimes confuses the clinical to monitor patients started on carbamazepine can be disastrous
picture, as does trigeminal neuralgia. because aplastic anemia can occur. When pain relief is obtained,
the patient should be kept at that dosage of carbamazepine for at
least 6 months before considering tapering of this medication. The
Treatment patient should be informed that under no circumstances should
the dosage of drug be changed or the drug refilled or discontinued
Pharmacological Treatment
without the physicians knowledge.
Carbamazepine
Carbamazepine is considered first-line treatment for glossopha- Gabapentin
ryngeal neuralgia. Rapid response to this drug essentially con- In the uncommon event that carbamazepine does not control a
firms a clinical diagnosis of glossopharyngeal neuralgia. Despite patients pain adequately, gabapentin may be considered. As with
the safety and efficacy of carbamazepine compared with other carbamazepine, baseline blood tests should be obtained before
treatments for glossopharyngeal neuralgia, much confusion and starting therapy. Gabapentin should be started with a 300-mg dose
unfounded anxiety surround its use. This medication, which may at bedtime for 2 nights; the patient should be cautioned about
be the patients best chance for pain control, is sometimes discon- potential side effects, including dizziness, sedation, confusion, and
tinued because of laboratory abnormalities erroneously attributed rash. The drug is increased in 300-mg increments, given in equally
to it. Baseline screening laboratory tests, consisting of a complete divided doses over 2 days, as side effects allow, until pain relief is
blood cell count, urinalysis, and automated chemistry profile, obtained or a total dose of 2400 mg per day is reached. At this
should be obtained before starting the drug. point, if the patient has experienced partial pain relief, blood val-
Carbamazepine should be started slowly, if the pain is not out ues are measured and the drug is carefully titrated using 100-mg
of control, at a starting dose of 100 to 200 mg at bedtime for tablets. More than 3600 mg per day is rarely required.
2 nights; the patient should be cautioned regarding side effects,
including dizziness, sedation, confusion, and rash. The drug is Baclofen
increased in 100- to 200-mg increments, given in equally divided Baclofen has been reported to be of value in some patients who
doses over 2 days, as side effects allow, until pain relief is obtained fail to obtain relief from carbamazepine and gabapentin. Baseline
B
Figure 19-2 Mixed cystic and solid acoustic nerve schwannoma in association with a solid schwannoma of the geniculate ganglion. A, Axial
enhanced image with fat saturation. A large mass with solid and cystic enhancing components is seen in the right cerebellopontine angle. A separate
solid erosive tumor is seen in the region of the right geniculate ganglion (arrowhead). B, Coronal enhanced image with fat saturation. The charac-
teristic mushroom appearance of an intracanalicular acoustic schwannoma with extension into the adjacent cerebellopontine angle is well seen. This
more anterior section through the internal auditory canal does not show the cystic portion of the tumor, but it does show the compression of the
adjacent brainstem. (From Stark DD, Bradley WG Jr, editors: Magnetic resonance imaging, 3rd ed, St Louis, 1999, Mosby, p 1219.)
50 SECTION 1 Headache and Facial Pain Syndromes
Complications and Pitfalls Figure 19-4 Vascular relationship between trigeminal nerve and the
superior cerebellar artery in the cerebellopontine cistern. The distortion
The pain of glossopharyngeal neuralgia is severe and can lead to of the trigeminal rootlets is evident from this intraoperative microscopic
suicide; therefore it must be considered a medical emergency, photograph. (From Franzini A, Ferroli P, Messina G, Broggi G: Surgical
and strong consideration should be given to hospitalizing such treatment of cranial neuralgias. In Bruyn G, Vinken P, editors: Handbook of
patients. If a dull ache remains after the intense, paroxysmal pain clinical neurology, vol 97, New York, 2010, Elsevier, pp 679692.)
of glossopharyngeal neuralgia subsides, this is highly suggestive of
persistent compression of the nerve by a structural lesion such as The major complications associated with glossopharyngeal
a brainstem tumor or schwannoma. Glossopharyngeal neuralgia nerve block are related to trauma to the internal jugular and
is almost never seen in persons younger than 30 years unless it carotid artery. Hematoma formation and intravascular injec-
is associated with multiple sclerosis, and all such patients should tion of local anesthetic with subsequent toxicity are significant
undergo MRI to identify demyelinating disease. problems for the patient. Blockade of the motor portion of the
19 Glossopharyngeal Neuralgia 51
Clinical Pearls
The pain of glossopharyngeal neuralgia is among the most
severe pain that humans can experience and must be con-
sidered a medical emergency. The uncontrolled pain of
glossopharyngeal neuralgia has led to suicide, and hospi-
talization of such patients should be strongly considered.
Between attacks of glossopharyngeal neuralgia, the patient
is relatively pain free. If a dull ache remains after the intense
pain subsides, this is highly suggestive of a persistent com-
pression of the nerve by a structural lesion, such as a brain-
stem tumor or schwannoma. Glossopharyngeal neuralgia
is almost never seen in individuals younger than 30 years
unless it is associated with multiple sclerosis, and all such
patients should undergo MRI with sequences designed to
identify demyelinating disease.
SECTION 2 Neck and Brachial Plexus Pain Syndromes
Chapter 20
52
20 Clival Chordoma Syndrome 53
neurological signs and symptoms and definitive diagnosis is an arteritis also sometimes confuses the clinical picture, as does
average of 2 years, a high index of clinical suspicion is necessary trigeminal neuralgia.
to avoid misdiagnosis. Obtaining a targeted history and per-
forming a careful physical examination are essential. Diseases of
the eye, ears, nose, throat, and teeth may mimic trigeminal neu-
Treatment
ralgia or may coexist and confuse the diagnosis. Tumors of the Treatment of clival chordoma requires surgery, radiation ther-
nasopharynyx and hypopharynx, including the tonsillar fossa apy, or both. Although clival chordomas are almost always
and piriform sinus, may mimic the pain of clival chordoma, as benign and rarely metastasize, the critical location of clival chor-
may tumors at the cerebellopontine angle. Occasionally, demy- domas relative to adjacent neural structures makes both forms
elinating disease may produce a clinical syndrome identical to of treatment challenging. Often, complete tumor resection is
clival chordoma. The jaw claudication associated with temporal impossible because of the location and postoperative radiation
Figure 20-1 Patients suffering from clival chordoma will often complain of headaches and associated facial pain, numbness, and diplopia.
A B
Figure 20-2 Sagittal (A) and axial (B) T2-weighted magnetic resonance imaging of the clival chordoma showing significant compression of the
spinal cord and brainstem plus destruction of cervical vertebra. (From Chau T, Lazzaro A, Mobbs RJ, Teo C: Surgical treatment of cranial neuralgias:
combined endoscopic endonasal and posterior cervical approach to a clival chordoma, J Clin Neurosci 17:14631465, 2010.)
54 SECTION 2 Neck and Brachial Plexus Pain Syndromes
Clinical Pearls
Clival chordoma is a rare neoplasm that is usually benign,
although aggressive clival chordomas have been reported.
Clival chordomas tend to be slow growing and produce
symptoms by compression of the adjacent brainstem and
cranial nerves. In spite of this fact, the long-term outcome
of patients diagnosed with clival chordoma remains poor
because of the location of these tumors and their tendency
to recur regardless of the treatment method chosen. Clival
chordomas can occur at any age.
Chapter 21
SPASMODIC TORTICOLLIS
Longus capitus
muscle
Scalene muscles:
Middle
Anterior
Posterior
Longus colli
muscle
Figure 21-1 The dystonia of spasmodic torticollis causes significant pain and functional disability.
may provide some symptomatic relief in mild cases. Trihexyphe- SUGGESTED READINGS
nidyl and diazepam also have been advocated. Maia FM, Kanashiro AK, Chien HF, Gonalves LR, Barbosa ER: Clinical changes
In patients for whom pharmacological treatment fails, injec- of cervical dystonia pattern in long-term botulinum toxin treated patients, Par-
tion of the affected muscles with botulinum toxin is a reasonable kinsonism Relat Disord 16:811, 2010.
Ochudo S, Drzyzga K, Drzyzga LR, Opala G: Various patterns of gestes antago-
next step. Frequent injections may result in the development of nistes in cervical dystonia, Parkinsonism Relat Disord 13:417420, 2007.
antibodies against the toxin, which makes the toxin less effec- Takeuchi N, Chuma T, Mano Y: Phenol block for cervical dystonia: effects and
tive. By changing to different subtypes of toxin, efficacy may be side effects, Arch Phys Med Rehabil 85:11171120, 2004.
restored. For intractable cases, bilateral thalamotomy has been Truong D, Brodsky M, Lew M, etal: Global Dysport Cervical Dystonia Study
advocated. The results of this radical treatment are variable at best. Group: Long-term efficacy and safety of botulinum toxin type A (Dysport) in
cervical dystonia, Parkinsonism Relat Disord 16:316323, 2010.
Clinical Pearls
Spasmodic torticollis is a devastating disease that responds
poorly to treatment. Injection of the affected muscles with
botulinum toxin to effect chemodenervation is probably the
best therapeutic option for most patients. The diagnosis of
the disease is straightforward. MRI of the brain is indicated
in all patients thought to have spasmodic torticollis.
Chapter 22
CERVICOTHORACIC INTERSPINOUS
BURSITIS
C7
T1
Figure 22-1 Patients with cervicothoracic interspinous bursitis attempt to relieve pain by assuming a position of dorsal kyphosis with a thrusting
forward of the neck.
well versed in the regional anatomy and experienced in perform- Because of the proximity of the epidural, subdural, and sub-
ing injection techniques. The proximity to the vertebral artery arachnoid space, placement of a needle too deeply could result
combined with the vascular nature of this anatomical region in inadvertent neuraxial block. Failure to recognize inadvertent
makes the potential for intravascular injection high. Even small epidural, subdural, or dural puncture can result in significant
amounts of a local anesthetic injected into the vertebral arteries motor and sensory block with the potential for associated loss of
result in seizures. Given the proximity of the brain and brainstem, consciousness, hypotension, and apnea. If subdural placement is
ataxia after trigger point injection as a result of vascular uptake unrecognized, and the previously mentioned doses of local anes-
of local anesthetic is common. Many patients also complain of a thetics are administered, the signs and symptoms are similar to
transient increase in pain after injection in this anatomical area. If those of subarachnoid injection, although the resulting motor and
long needles are used, pneumothorax also may occur. sensory block may be spotty.
22 Cervicothoracic Interspinous Bursitis 59
Kyphosis
Figure 22-3 Proper needle placement for injection for treatment of cer-
vicothoracic interspinous bursitis pain. (From Waldman SD: Atlas of pain
management injection techniques, Philadelphia, 2000, Saunders, p 33.)
Chapter 23
SCAPULOCOSTAL SYNDROME
Differential Diagnosis
The Clinical Syndrome Scapulocostal syndrome is most commonly misdiagnosed as cervi-
Scapulocostal syndrome is a clinical syndrome characterized by cal radiculopathy. In contrast to cervical radiculopathy, however,
pain and paresthesias over the medial border of the scapula that which is associated with numbness and weakness in the affected
radiate into the neck, upper triceps, chest wall, and distal upper dermatomes, the upper extremity neurological examination in
extremity. The pain is burning and aching. The intensity level of scapulocostal syndrome is normal. Osteoarthritis, rheumatoid
pain associated with scapulocostal syndrome is moderate. arthritis, posttraumatic arthritis, and rotator cuff tear arthropathy
Also known as traveling salesman shoulder, the scapulocostal also are common causes of shoulder pain secondary to arthritis
syndrome is thought to be an overuse syndrome resulting from that may be confused with scapulocostal syndrome. Less common
repetitive use of the shoulder stabilizing muscles, including the causes of arthritis-induced shoulder pain include the collagen-
serratus anterior, levator scapulae, pectoralis minor, and rhom- vascular diseases, infection, villonodular synovitis, and Lyme
boid, when carrying out activities such as reaching backward over disease. Acute infectious arthritis usually is accompanied by signif-
a car seat for samples and prolonged use of the telephone cradled icant systemic symptoms, including fever and malaise, and should
between the shoulder and neck (Figure 23-1). Racquet sports also be easily recognized by an astute clinician and treated appropri-
have been implicated in the evolution of scapulocostal syndrome. ately with culture and antibiotics, rather than injection therapy.
The collagen-vascular diseases generally manifest as a polyarthrop-
athy rather than a monarthropathy limited to the shoulder joint,
Signs and Symptoms and the pain does not radiate into the upper extremity. Pancoast
Physical examination reveals myofascial trigger points in the tumor and brachial plexopathy also may mimic the clinical pre-
rhomboid, infraspinatus, and subscapularis muscles. These trig- sentation of scapulocostal syndrome.
ger points are best shown by having the patient reach across the
chest and place his or her hand on the uninvolved shoulder. Pal- Treatment
pation of trigger points along the medial border of the scapula
produces a positive jump sign and causes pain to radiate into the Initial treatment of the pain and functional disability associated
ipsilateral upper extremity. The neurological examination of the with scapulocostal syndrome should include a combination of
upper extremity is normal in scapulocostal syndrome. Untreated, nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygen-
patients with scapulocostal syndrome develop decreased range of ase-2 (COX-2) inhibitors and physical therapy. The local applica-
motion of the shoulder and scapula, resulting in functional dis- tion of heat and cold also may be beneficial. Repetitive movements
ability and pain. that incite the syndrome should be avoided. For patients who do
not respond to these treatment modalities, injection of myofascial
trigger points with local anesthetic and steroid may be a reason-
Testing able next step.
Plain radiographs are indicated in all patients with scapulocos-
tal syndrome. Based on the clinical presentation, additional tests, Complications and Pitfalls
including complete blood cell count, erythrocyte sedimentation
rate, and antinuclear antibody level, may be indicated. Magnetic The major complication in the care of a patient thought to have
resonance imaging (MRI) of the shoulder is indicated if rotator scapulocostal syndrome is misdiagnosis. Tumors of the superior
cuff tear is suspected. Radionuclide bone scanning is indicated sulcus of the lung or primary or metastatic tumors of the shoulder
if metastatic disease or primary tumor involving the shoulder is and scapula must be included in the differential diagnosis.
60
23 Scapulocostal Syndrome 61
SUGGESTED READINGS
Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30,
2009.
Ge HU, Nie H, Madeleine P: Contribution of the local and referred pain from
active myofascial trigger points in fibromyalgia syndrome, Pain 147:233240,
2009.
Monach PA: Shoulder pain. In Mushlin SB, Greene HL II, editors: Decision making
in medicine, 3rd ed, New York, 2010, Elsevier, pp 522523.
Waldman SD: Scapulocostal syndrome. In Waldman SD, editor: Atlas of pain
Levator Supraspinatus management injection techniques, 2nd ed, Philadelphia, Saunders, pp 123126.
scapulae
Infraspinatus
Rhomboids Serratus
anterior
Clinical Pearls
Scapulocostal syndrome is a less common cause of shoulder
and upper extremity pain encountered in clinical practice,
with cervical radiculopathy occurring much more com-
monly. This painful condition must be separated from
other causes of shoulder pain, including rotator cuff tears.
Coexistent bursitis and tendinitis also may contribute to
shoulder pain and may require additional treatment with
more localized injection of local anesthetic and depot ste-
roid. Trigger point injections are a safe procedure if care-
ful attention is paid to the clinically relevant anatomy in
the areas to be injected. Care must be taken to use sterile
technique to avoid infection and universal precautions to
avoid risk to the operator. The incidence of ecchymosis and
hematoma formation can be decreased if pressure is placed
on the injection site immediately after injection. The use
of physical modalities, including local heat and gentle
range-of-motion exercises, should be introduced several
days after the patient undergoes trigger point injections for
scapulocostal syndrome. Avoidance of activities responsible
for the evolution of the disease must be considered or the
syndrome will recur. Vigorous exercises should be avoided
because they would exacerbate symptoms. Simple analgesics
and NSAIDs or a COX-2 inhibitor may be used concur-
rently with an injection technique.
Chapter 24
PARSONAGE-TURNER SYNDROME
Differential Diagnosis
Brachial plexopathy has many causes. In common to all of them is
the constellation of symptoms consisting of neurogenic pain and
associated weakness that radiates into the supraclavicular region
and upper extremity. More common causes of brachial plexopa-
thy include compression of the plexus by cervical ribs or abnor-
mal muscles (e.g., thoracic outlet syndrome), invasion of the Figure 24-1 The pain of Parsonage-Turner syndrome involves the
plexus by tumor (e.g., Pancoast syndrome), direct trauma to the shoulder and upper arm, preceding the onset of muscle weakness by
plexus (e.g., stretch injuries and avulsions), inflammatory causes hours to days.
62
24 Parsonage-Turner Syndrome 63
isolated nerve, the syndrome may be misdiagnosed as entrapment and rash. The drug is increased in 300-mg increments, given in
neuropathy. Electromyography is the cornerstone in sorting out equally divided doses over 2 days, as side effects allow, until pain
the differential diagnosis in patients with the acute onset of shoul- relief is obtained or a total dose of 2400 mg per day is reached. At
der and upper extremity pain. this point, if the patient has experienced partial pain relief, blood
Diseases of the cervical spinal cord, bony cervical spine, and values are measured, and the drug is carefully titrated upward
disc can mimic Parsonage-Turner syndrome. Appropriate testing, using 100-mg tablets. More than 3600 mg daily rarely is required.
including magnetic resonance imaging (MRI) and electromyog-
raphy, helps sort out the myriad possibilities, but the clinician Carbamazepine
also should be aware that more than one pathological process may Carbamazepine is useful in patients with Parsonage-Turner syn-
coexist and contribute to the patients symptoms. Syringomyelia, drome who do not experience pain relief with gabapentin. Despite
tumors of the cervical spinal cord, and tumors of the cervical nerve the safety and efficacy of carbamazepine compared with other
roots as they exit the spinal cord, such as schwannomas, can be of treatments for Parsonage-Turner syndrome, much confusion and
insidious onset and quite difficult to diagnose. Pancoast tumor unfounded anxiety surround its use. This medication, which may
should be high on the list of diagnostic possibilities in all patients be the best chance for pain control, is sometimes discontinued
with brachial plexopathy in the absence of clear antecedent because of laboratory abnormalities erroneously attributed to it.
trauma, especially in the presence of a history of tobacco abuse. Baseline screening laboratory tests, consisting of a complete blood
Lateral herniated cervical disc, metastatic tumor, or cervical spon- cell count, urinalysis, and automated chemistry profile, should be
dylosis that results in significant nerve root compression also may obtained before starting the drug.
manifest as a brachial plexopathy. Rarely, infection involving the Carbamazepine should be started slowly if the pain is not out
apex of the lung may compress and irritate the plexus. of control. The drug is started with a 100- to 200-mg dose at bed-
time for 2 nights; the patient should be cautioned regarding side
effects, including dizziness, sedation, confusion, and rash. The
Testing drug is increased in 100- to 200-mg increments, given in equally
All patients presenting with Parsonage-Turner syndrome must divided doses over 2 days, as side effects allow, until pain relief
undergo MRI of the cervical spine and the brachial plexus (Figure is obtained or a total dose of 1200 mg daily is reached. Careful
24-2). Computed tomography (CT) is a reasonable second choice monitoring of laboratory parameters is mandatory to avoid the
if MRI is contraindicated. Electromyography and nerve conduc- rare possibility of life-threatening blood dyscrasia. At the first sign
tion velocity testing are extremely sensitive, and a skilled electro- of blood count abnormality or rash, carbamazepine should be dis-
myographer can help delineate the specific portion of the plexus continued. Failure to monitor patients started on carbamazepine
that is abnormal. If an inflammatory basis for the plexopathy is can be disastrous because aplastic anemia can occur. When pain
suspected, serial electromyography is indicated. If Pancoast tumor relief is obtained, the patient should be kept at that dosage of
or other tumors of the brachial plexus are suspected, chest radio- carbamazepine for at least 6 months before considering tapering
graphs with apical lordotic views may be helpful. of this medication. The patient should be informed that under no
Screening laboratory tests consisting of complete blood cell circumstances should the dosage of drug be changed or the drug
count, erythrocyte sedimentation rate, antinuclear antibody test- refilled or discontinued without the physicians knowledge.
ing, and automated blood chemistry testing should be performed
if the diagnosis of brachial plexopathy is in question, to help rule Baclofen
out other causes of pain. Baclofen has been reported to be valuable in some patients who
fail to obtain relief from gabapentin and carbamazepine. Baseline
laboratory tests should be obtained before starting baclofen. The
Treatment drug is started with a 10-mg dose at bedtime for 2 nights; the
Pharmacological Therapy patient should be cautioned about potential adverse effects, which
are the same as those of carbamazepine and gabapentin.
Gabapentin Baclofen is increased in 10-mg increments, given in equally
Gabapentin is the first-line treatment for the neuritic pain of divided doses over 7 days, as side effects allow, until pain relief is
Parsonage-Turner syndrome. The drug is started with a 300-mg obtained or a total dose of 80 mg per day is reached. This drug
dose at bedtime for 2 nights; the patient should be cautioned about has significant hepatic and central nervous system side effects,
potential side effects, including dizziness, sedation, confusion, including weakness and sedation. As with carbamazepine, careful
TABLE 24-1
Comparison of Parsonage-Turner Syndrome and Cervical Radiculopathy
Disease History Examination Test Results
Parsonage-Turner Acute, intense burning pain that begins Neurological deficits that suggest Electromyogram positive for
syndrome spontaneously in shoulder and upper arm; more than one nerve is involved; brachial plexopathy; MRI of
pain unaffected by neck movement weakness that may progress to cervical spine noncontributory
flaccidity to diagnosis
Cervical Pain begins in neck and radiates down Weakness and numbness in the MRI of cervical spine reveals
radiculopathy arm; the pain is increased by neck move- distribution of a single nerve root herniated disc or osteophyte
ment; pain and muscle weakness occur formation or both
spontaneously
MRI, Magnetic resonance imaging.
64 SECTION 2 Neck and Brachial Plexus Pain Syndromes
A B
Figure 24-2 Pancoast tumor in a 46-year-old man. Sagittal T1-weighted (A) and sagittal T1-weighted gadolinium-enhanced with fat saturation (B)
sequences show left apical bronchogenic carcinoma (white arrow) invading the supraclavicular fossa, involving the brachial plexus, and encasing the
subclavian artery (black arrow). (From Knisely BL, Broderick LS, Kuhlman JE: MR imaging of the pleura and chest wall, MRI Clin North Am 8:125, 2000.)
monitoring of laboratory values is indicated during the initial use assist in activities of daily living also is important to avoid further
of this drug. deterioration of function.
When treating patients with any of the drugs mentioned, the
physician should inform the patient that premature tapering or
discontinuation of the medication may lead to the recurrence of
Complications and Pitfalls
pain. The pain becomes more difficult to control thereafter. The pain of Parsonage-Turner syndrome is difficult to treat. It
responds poorly to opioid analgesics and may respond poorly to
the previously mentioned medications. The uncontrolled pain
Interventional Treatment
of Parsonage-Turner syndrome has led to suicide, and hospital-
Brachial Plexus Block ization of such patients should be strongly considered. Correct
The use of brachial plexus block with a local anesthetic and steroid diagnosis is crucial to successfully treat the pain and dysfunction
is an excellent adjunct to drug treatment of Parsonage-Turner associated with brachial plexopathy because stretch injuries and
syndrome. This technique rapidly relieves pain while medications contusions of the plexus may respond with time, but plexopa-
are being titrated to effective levels. The initial block is performed thy secondary to tumor or avulsion of the cervical roots requires
with preservative-free bupivacaine combined with methylprednis- aggressive treatment.
olone. Subsequent daily nerve blocks are done in a similar manner,
substituting a lower dose of methylprednisolone. This approach
also may be used to obtain control of breakthrough pain. Clinical Pearls
Physical Modalities Brachial plexus block with a local anesthetic and steroid
represents an excellent stop-gap measure for patients with
The use of physical and occupational therapy to maintain func- the uncontrolled pain of Parsonage-Turner syndrome while
tion and help palliate pain is a crucial part of the treatment plan waiting for pharmacological treatments to take effect. As
for patients with Parsonage-Turner syndrome. Shoulder abnor- mentioned, correct diagnosis is paramount to allow the cli-
malities, including subluxation and adhesive capsulitis, must be nician to design a logical treatment plan.
aggressively searched for and treated. Occupational therapy to
24 Parsonage-Turner Syndrome 65
SUGGESTED READINGS Stutz CM: Neuralgic amyotrophy: Parsonage-Turner syndrome, J Hand Surg
35:21042106, 2010.
Marshall GB, McKenna E, Mahallati H: ParsonageTurner syndrome, Eur J Wendling D, Sevrin P, Bouchaud-Chabot A, etal: ParsonageTurner syndrome
Radiol Extra 6:5153, 2005. revealing Lyme borreliosis, Joint Bone Spine 76:202204, 2009.
Mileto A, Gaeta M: Calcific tendonitis of supraspinatus simulating acute brachial
neuritis (Parsonage-Turner syndrome), Clin Radiol 66:578581, 2011.
Chapter 25
HYOID SYNDROME
Styloid process
Figure 25-1 The pain of hyoid syndrome starts below the angle of the mandible and radiates into the anterolateral neck. It is triggered or worsened
with chewing, rotation of the cervical spine, or swallowing.
Hyoid Trachea
bone
Gentle pressure
on greater cornu
Figure 25-3 Injection technique for relieving the pain of hyoid syn-
drome. (From Waldman SD: Atlas of pain management injection tech-
niques, 2nd ed, Philadelphia, 2007, Saunders, p 17.)
Figure 25-2 Identification of the greater cornu of the hyoid bone. (From
Waldman SD: Atlas of pain management injection techniques, 2nd ed,
Philadelphia, 2007, Saunders, p 18.)
68 SECTION 2 Neck and Brachial Plexus Pain Syndromes
for tumors of the neck, apex of the lung, anterior triangle of the SUGGESTED READINGS
neck, and hypopharynx is indicated. If a significant history of vom- Auvenshine RC: Anatomy of the airway: an overview, Sleep Med Clin 5:4557,
iting is ascertained, esophageal tear should be considered. 2010.
Although the injection technique for hyoid syndrome is safe, Ernest EA III, Salter EG: Hyoid bone syndrome: a degenerative injury of the mid-
dle pharyngeal constrictor muscle with photomicroscopic evidence of insertion
complications can occur. In addition to the potential for com- tendinosis, J Prosthet Dentist 66:7883, 1991.
plications involving the vasculature, if the needle is placed too Nir D, Hefer T, Joachims HZ: Hyoid bone syndrome and its treatment with non-
laterally, the proximity of the brachial plexus, the central neuraxial steroidal anti-inflammatory drugs, Am J Otolaryngol 19:296300, 1998.
structures, and the phrenic nerve can result in side effects and com- Waldman SD: Hyoid syndrome. In Atlas of pain management injection techniques,
plications. Although these complications should be rare if proper 2nd ed, Philadelphia, 2007, Saunders. pp 1619.
technique is observed, the potential for inadvertent epidural, sub-
dural, or subarachnoid injection remains. Phrenic nerve block also
can occur when using this injection technique to treat hyoid syn-
drome if the needle placement is too posterolateral. In the absence
of significant pulmonary disease, unilateral phrenic nerve block
should rarely create respiratory embarrassment. Blockade of the
recurrent laryngeal nerve with its attendant vocal cord paralysis
combined with paralysis of the diaphragm may make the clearing
of pulmonary and upper airway secretions difficult. Because of the
proximity of the apex of the lung, pneumothorax is a distinct pos-
sibility, and the patient should be informed of this.
Clinical Pearls
The clinician should always evaluate a patient who has pain
in this anatomical region for occult malignancy. Tumors of
the larynx, hypopharynx, and anterior triangle of the neck
may manifest clinical symptoms identical to those of hyoid
syndrome. Given the low incidence of hyoid syndrome
relative to pain secondary to malignancy in this anatomical
region, hyoid syndrome must be considered a diagnosis of
exclusion.
The injection technique described for hyoid syndrome
is a simple technique that can produce dramatic relief for
patients with the previously mentioned pain problems.
As discussed earlier, the proximity of the greater cornu
of the hyoid bone to major vasculature makes postblock
hematoma and ecchymosis a distinct possibility. Although
these complications are usually transitory, their dramatic
appearance can be quite upsetting to the patient; therefore
the patient should be warned of this possibility before the
procedure. The vascularity of this region also increases the
incidence of inadvertent intravascular injection. Even small
amounts of local anesthetic injected into the carotid artery
at this level can result in local anesthetic toxicity and sei-
zures. Incremental dosing while carefully monitoring the
patient for signs of local anesthetic toxicity helps avoid this
complication.
Chapter 26
OMOHYOID SYNDROME
Testing
Magnetic resonance imaging (MRI) of the soft tissues of the neck
may reveal hematoma formation of the omohyoid muscle acutely
and calcification, fibrosis, or both as the syndrome becomes more
chronic. Injection of the belly of the omohyoid muscle with local Figure 26-1 The pain of omohyoid syndrome is localized in the supra-
anesthetic can serve as a diagnostic maneuver to help strengthen clavicular region at a point just lateral and superior to the attachment of
the diagnosis. the sternocleidomastoid muscle to the clavicle.
69
70 SECTION 2 Neck and Brachial Plexus Pain Syndromes
SUGGESTED READINGS Waldman SD: Omohyoid syndrome. In Waldman SD, editor: Atlas of pain man-
agement injection techniques, ed 2, Philadelphia, 2007, Saunders, pp 2931.
Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30, Wong DSY, Li HJC: The omohyoid sling syndrome, Am J Otolaryngol 21:318322,
2009. 2000.
Ge HU, Nie H, Madeleine P, et al: Contribution of the local and referred
pain from active myofascial trigger points in fibromyalgia syndrome, Pain
147:233240, 2009.
Chapter 27
NECK-TONGUE SYNDROME
C1 nerve root
C1 (Atlas)
Atlantoaxial joint
C2 nerve root
C2 (Axis)
Numbness
Hypoglossal nerve
Figure 27-1 The pain and numbness of the ipsilateral half of the tongue are aggravated by movement of the upper cervical spine.
Clinical Pearls
SUGGESTED READINGS
Neck-tongue syndrome is a unique and uncommon cause Bogduk N: An anatomical basis for the neck-tongue syndrome, J Neurol Neurosurg
of neck pain. The associated ipsilateral tongue numbness is Psychiatry 44:202208, 1981.
pathognomonic for the syndrome and is unusual in charac- Borody C: Neck-tongue syndrome, J Manipulative Physiol Ther 27:367, 2004.
ter. An analogous type of proprioceptive numbness is seen Chedrawi AK, Fishman MA, Miller G: Neck-tongue syndrome, Pediatr Neurol
22:397399, 2000.
in patients with Bells palsy. Given the rarity of this pain- Orrell RW, Marsden CD: The neck-tongue syndrome, J Neurol Neurosurg Psy-
ful condition, the clinician should search carefully for other chiatry 57:348352, 1994.
causes of the symptoms before attributing them to neck-
tongue syndrome.
SECTION 3 Shoulder Pain Syndromes
Chapter 28
SUPRASPINATUS TENDINITIS
Supraspinatus
tendon
Figure 28-1 Patients with supraspinatus tendinitis exhibit point tenderness of the greater tuberosity and a painful arc of abduction.
SUGGESTED READINGS
Chen SK, Chou PH, Lue YL, Lu YM: Treatment for frozen shoulder combined
Subdeltoid Supraspinatus with calcific tendinitis of the supraspinatus, Kaohsiung J Med Sci 2880;24:
synovial bursa tendon 78-84.
Gimblett PA, Saville J, Ebrall E: A conservative management protocol for calcific
tendinitis of the shoulder, J Manipulative Physiol Ther 22:622627, 1999.
Hsu HC, Wu JJ, Jim YF, Chang CY, etal: Calcific tendinitis and rotator cuff
tearing: a clinical and radiographic study, J Shoulder Elbow Surg 3:159164,
1994.
Deltoid muscle Waldman SD: Supraspinatus tendinitis. In Waldman SD, editor: Atlas of
pain management injection techniques, ed 3, Philadelphia, 2007, Saunders,
Head of humerus pp 6467.
Waldman SD: Functional anatomy of the shoulder joint. In Waldman SD, editor:
Periosteum
Pain review, Philadelphia, 2009, Saunders, pp 8081.
Posterior Anterior
Figure 28-3 Correct needle placement for injection into the supraspi-
natus tendon.
Clinical Pearls
The musculotendinous unit of the shoulder joint is suscep-
tible to the development of tendinitis for several reasons.
First, the joint is subjected to a wide range of repetitive
motions. Second, the space in which the musculotendi-
nous unit functions is restricted by the coracoacromial
arch, making impingement a likely possibility with extreme
movements of the joint. Third, the blood supply to the
musculotendinous unit is poor, making healing of micro-
trauma more difficult. All of these factors can contribute
to tendinitis of one or more of the tendons of the shoulder
joint. Calcium deposition around the tendon may occur if
the inflammation continues, making subsequent treatment
more difficult. Tendinitis of the musculotendinous unit of
the shoulder frequently coexists with bursitis of the associ-
ated bursae of the shoulder joint, creating additional pain
and functional disability.
The injection technique described is extremely effective
in the treatment of pain secondary to the causes of shoulder
pain mentioned earlier. Coexistent bursitis and arthritis also
may contribute to shoulder pain and may require additional
treatment with a more localized injection of local anesthetic
and depot steroid. This technique is a safe procedure if care-
ful attention is paid to the clinically relevant anatomy in
the areas to be injected. Care must be taken to use sterile
technique to avoid infection and universal precautions to
avoid risk to the operator. The incidence of ecchymosis and
hematoma formation can be decreased if pressure is placed
on the injection site immediately after injection.
Chapter 29
INFRASPINATUS TENDINITIS
Infraspinatus
tendon
Figure 29-1 Patients with infraspinatus tendinitis exhibit posterior point tenderness and a painful arc of abduction.
through the skin and subcutaneous tissues and the margin of Complications and Pitfalls
the deltoid muscle and underlying infraspinatus muscle until
it impinges on bone (Figure 29-3). The needle is withdrawn 1 The major complication of this injection technique is infection.
to 2 mm out of the periosteum of the humerus, and the con- This complication should be exceedingly rare if strict aseptic tech-
tents of the syringe are gently injected. There should be slight nique is followed. The possibility of trauma to the infraspinatus
resistance to injection. If no resistance is encountered, either tendon from the injection itself remains an ever-present possibil-
the needle tip is in the joint space itself or the infraspinatus ity. Tendons that are highly inflamed or previously damaged are
tendon is ruptured. If significant resistance to injection is felt, subject to rupture if they are directly injected. This complication
the needle tip is probably in the substance of a ligament or ten- can be greatly decreased if the clinician uses gentle technique and
don and should be advanced or withdrawn slightly until the stops injecting immediately if significant resistance to injection
injection proceeds without significant resistance. The needle is is encountered. Approximately 25% of patients complain of a
removed, and a sterile pressure dressing and ice pack are placed transient increase in pain after this injection technique; patients
at the injection site. should be warned of this possibility.
29 Infraspinatus Tendinitis 79
B C
B
Figure 29-2 Periarticular crystal deposition: shoulderinfraspinatus, teres minor, and subscapularis tendon calcification. A, In internal rotation,
calcific deposits in the infraspinatus and teres minor tendons appear lateral to the humeral head (arrow) and deposits in the subscapularis tendon are
located near the lesser tuberosity, overlying the joint space (arrowhead). B and C, Radiograph and photograph of a section of the humeral head out-
line these same calcifications (arrows, arrowhead). (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders.)
80 SECTION 3 Shoulder Pain Syndromes
SUGGESTED READINGS
Gimblett PA, Saville J, Ebrall P: A conservative management protocol for calcific
tendinitis of the shoulder, J Manipulative Physiol Ther 22:622627, 1999.
Hsu HC, Wu JJ, Jim YF, etal: Calcific tendinitis and rotator cuff tearing: a clinical
and radiographic study, J Shoulder Elbow Surg 3:159164, 1994.
Toriyama K, Fukuda H, Hamada K, Noguchi T: Calcifying tendinitis of the infra-
Infraspinatus spinatus tendon simulating a bone tumor, J Shoulder Elbow Surg 3:165168,
tendon 1994.
Synovial bursa Waldman SD: Functional anatomy of the shoulder joint. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 8081.
Waldman SD: Infraspinatus tendinitis. In Waldman SD, editor: Atlas of pain man-
Deltoid muscle
agement injection techniques, ed 3, Philadelphia, 2007, Saunders, pp 7175.
Head of humerus
Periosteum
Posterior Anterior
Figure 29-3 Correct needle placement for injection into the infraspina-
tus tendon.
Clinical Pearls
The musculotendinous unit of the shoulder joint is sus-
ceptible to the development of tendinitis for several rea-
sons. First, the joint is subjected to a wide range of often
repetitive motions. Second, the space in which the mus-
culotendinous unit functions is restricted by the coracoac-
romial arch, making impingement a likely possibility with
extreme movements of the joint. Third, the blood supply
to the musculotendinous unit is poor, making healing of
microtrauma more difficult. These factors can contribute
to tendinitis of one or more of the tendons of the shoulder
joint. Calcium deposition around the tendon may occur if
the inflammation continues, making subsequent treatment
more difficult. Tendinitis of the musculotendinous unit of
the shoulder frequently coexists with bursitis of the associ-
ated bursae of the shoulder joint, creating additional pain
and functional disability.
The injection technique described is extremely effective
in the treatment of pain secondary to the causes of shoul-
der pain mentioned. Coexistent bursitis and arthritis also
may contribute to shoulder pain and may require additional
treatment with a more localized injection of a local anes-
thetic and depot steroid. This technique is a safe procedure
if careful attention is paid to the clinically relevant anatomy
in the areas to be injected. Care must be taken to use sterile
technique to avoid infection and universal precautions to
avoid risk to the operator. The incidence of ecchymosis and
hematoma formation can be decreased if pressure is placed
on the injection site immediately after injection.
Chapter 30
SUBACROMIAL IMPINGEMENT
SYNDROME
Scapula Testing
MRI of the shoulder provides the best information regarding any
Humerus pathological process of the shoulder. MRI is highly accurate and
helps identify abnormalities that may put the patient at risk for
continuing damage to the rotator cuff and humeral head. MRI
of the shoulder also helps rule out unsuspected pathological con-
ditions that may harm the patient, such as primary and meta-
Figure 30-1 The subacromial space lies directly inferior to the acro-
static tumors of the shoulder joint and surrounding structures.
mion, the coracoid process, the acromioclavicular joint, and the cora- In patients who cannot undergo MRI, such as patients with
coacromial ligament. pacemakers, computed tomography (CT) is a reasonable second
81
82 SECTION 3 Shoulder Pain Syndromes
Subacromial
Coraco-clavicular ligament bursa
Acromioclavicular ligament
Coracoacromial ligament
Inflamed supraspinatus
tendon
Subacromial
Biceps Long head bursa
brachii m. Short head impinged
Subcapularis m.
Figure 30-2 The space between the acromion and the superior aspect of the humeral head is the impingement interval, and abduction of the arm
narrows the space further.
choice. Radionuclide bone scanning and plain radiography are combination of nonsteroidal antiinflammatory drugs (NSAIDs)
indicated if fracture or bony abnormality such as metastatic dis- or cyclooxygenase-2 (COX-2) inhibitors and gentle physical
ease is considered in the differential diagnosis. therapy. Local application of heat and cold also may be benefi-
Screening laboratory tests consisting of complete blood cell cial. For patients who do not respond to these treatment modali-
count, erythrocyte sedimentation rate, and automated blood ties, injection of the subacromial space with local anesthetic
chemistry testing should be performed if the diagnosis of subacro- and steroid is a reasonable next step while obtaining MRI and
mial impingement syndrome is in question. Arthrocentesis of the other appropriate testing to clarify further the working clinical
glenohumeral joint may be indicated if septic arthritis or crystal diagnosis. The use of physical therapy, including gentle range-
arthropathy is suspected. of-motion exercises, should be introduced several days after the
patient undergoes this injection technique for shoulder pain.
Vigorous exercises should be avoided because they would exac-
Differential Diagnosis erbate the patients symptoms. For patients who do not respond
Subacromial impingement syndrome is a clinical diagnosis sup- to these treatment modalities or radiographically have shown
ported by a combination of clinical history, physical examina- anatomical subacromial impingement that is producing ongoing
tion, radiography, and MRI. Pain syndromes that may mimic damage to the rotator cuff, open or arthroscopic acromioplasty
subacromial impingement syndrome include subacromial bursi- is required.
tis, tendinopathy and tendinitis of the rotator cuff, calcification
and thickening of coracoacromial ligament, and arthritis affecting Complications and Pitfalls
any of the shoulder joints. Adhesive capsulitis or frozen shoulder
may confuse the diagnosis, as may idiopathic brachial plexopathy Failure to diagnose subacromial impingement syndrome cor-
(Parsonage-Turner syndrome; see Chapter 24). Primary and met- rectly puts the patient at risk for the missed diagnosis of other
astatic tumors of the shoulder and surrounding structures remain syndromes that may result in ongoing damage to the shoulder
an ever-present possibility and should always be part of the differ- or lead to overlooked pathological processes in this anatomical
ential diagnosis of patients presenting with shoulder pain. region that may harm the patient, such as Pancoasts tumor or
primary or metastatic tumors of the shoulder. MRI is indicated in
all patients thought to have subacromial impingement syndrome,
Treatment and aggressive treatment of surgically correctable causes of such
Initial treatment of the pain and functional disability associ- impingement is generally indicated sooner rather than later to
ated with subacromial impingement syndrome should include a avoid ongoing irreversible shoulder damage.
30 Subacromial Impingement Syndrome 83
A B
C
Figure 30-3 Shoulder external subacromial impingement syndrome: Magnetic resonance imaging abnormalities. A, On sagittal oblique T1-weighted
(TR/TE, 800/20) spin echo MRI, a subacromial enthesophyte (solid arrow) containing marrow projects from the anterior surface of the acromion (a)
toward the coracoid process (c). Note its relationship to the coracoacromial ligament (open arrows) and supraspinatus tendon (arrowhead). B, In a
second patient, sagittal oblique T1-weighted (TR/TE, 800/12) spin echo MRI shows a large subacromial enthesophyte (arrows). The acromion (a) is
indicated. C, In a third patient, coronal oblique intermediate-weighted (TR/TE, 2000/30) spin echo MRI image reveals the flattened contour and low
signal intensity characteristic of a subacromial enthesophyte (arrows). Also observe osteoarthritis of the acromioclavicular joint manifested as osteo-
phytosis (arrowhead) and an elevated position of the humeral head, indicative of a rotator cuff tear. The tear was shown better on other MR images
(not shown). (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3084.)
84 SECTION 3 Shoulder Pain Syndromes
TABLE 30-1
Causes of Subacromial Impingement Syndrome
Subacromial osteophytes
Rotator cuff tears
Abnormal acromial anatomy (e.g., type 2 acromion, type 3 acromion)
Congenital acromial defect (e.g., os acromiale)
Acquired acromial defects (e.g., displaced fracture)
Inflammatory arthritis of the acromioclavicular joint
Abnormalities of the superior aspect of the humeral head
Glenohumeral joint instability LD
A
Crystal arthropathies of the acromioclavicular joint
Frozen shoulder (adhesive capsulitis)
Tendinopathy of the coracoacromial ligament
B
Figure 30-5 A, Lateral downsloping (LD) of the anterior acromion as
seen on coronal section (arrow). B, Coronal T2-weighted MR image with
fat suppression revealing LD (arrow). Note the corresponding alterations
on the bursal surface of the rotator cuff and the thickened subdeltoid
bursa filled with fluid (arrowheads). (From Zlatkin MB: MRI of the shoulder,
2nd ed, Philadelphia, 2003, Lippincott Williams & Wilkins, p 1639.)
Acromioclavicular joint
Clavicle
Acromion
Subacromial
bursa
Supraspinatus
tendon
Figure 30-7 Patients with subacromial impingement syndrome typically complain of increasing shoulder pain with activities that abduct or forward
flex the shoulder.
Clinical Pearls
The musculotendinous unit of the shoulder joint is sus-
ceptible to the development of tendinitis for several rea-
sons. First, the joint is subjected to a wide range of often
repetitive motions. Second, the space in which the mus-
culotendinous unit functions is restricted by the coracoac-
romial arch, making impingement a likely possibility with
extreme movements of the joint. Third, the blood supply
to the musculotendinous unit is poor, making healing of
microtrauma more difficult. These factors can contribute
to tendinitis of one or more of the tendons of the shoulder
joint. Calcium deposition around the tendon may occur if
the inflammation continues, making subsequent treatment
more difficult. Tendinitis of the musculotendinous unit of
the shoulder frequently coexists with bursitis of the associ-
ated bursae of the shoulder joint, creating additional pain
and functional disability. Patients with untreated subacro-
Figure 30-8 Neers test for subacromial impingement syndrome. (From mial impingement syndrome continue to experience pain
Waldman SD: Physical diagnosis of pain: An atlas of signs and symp- and functional disability and may continue to cause ongo-
toms, Philadelphia, 2006, Saunders, 2006.)
ing irreversible shoulder damage culminating in damage to
the humeral head and rotator cuff tear.
SUGGESTED READINGS
Dickens VA, Williams JL, Bhamra MS: Role of physiotherapy in the treatment
of subacromial impingement syndrome: a prospective study, Physiotherapy
91:159164, 2005.
Michener LA, McClure PW, Karduna AR: Anatomical and biomechanical mecha-
nisms of subacromial impingement syndrome, Clin Biomech 18:369379, 2003.
Neagle CE, Bennett JB: Subacromial anatomy and biomechanics related to the
impingement syndrome, Oper Tech Sports Med 2:8288, 1994.
Waldman SD: Functional anatomy of the shoulder joint. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 8081.
Chapter 31
Os acromiale
Figure 31-1 Os acromiale is a congenital defect caused by failure of the distal ossification center of the acromion to fuse.
A B
Figure 31-4 Os acromiale. A, T2-weighted gradient echo axial image. A high signal intensity line (arrows) runs through the acromion and demarcates
the division between the anterior os acromiale and the remainder of the acromion. B, T2-weighted sagittal oblique image also shows a dividing line
crossing the acromion (arrow). A large, full-thickness rotator cuff tear also is visible (asterisk). (From Haaga JR, Lanzieri CF, Gilkeson RC, editors: CT and
MR imaging of the whole body, 4th ed, Philadelphia, 2003, Mosby, p 1955.)
31 Os Acromiale Pain Syndrome 89
SUGGESTED READINGS Nissen CW: The acromion: fractures and os acromiale, Oper Tech Sports Med
12:3234, 2004.
Case DT, Burnett SE, Nielsen T: Os acromiale: population differences and their Pagnani MJ, Mathis CE, Solman CG: Painful os acromiale (or unfused acromial
etiological significance, HOMO 57:118, 2006. apophysis) in athletes, J Shoulder Elbow Surg 15:432435, 2006.
Nicholson GP, Goodman DA, Flatow EL, Bigliani LU: The acromion: morpho-
logic condition and age-related changesa study of 420 scapulas, J Shoulder
Elbow Surg 5:111, 1996.
Chapter 32
Testing
Figure 32-1 Frontal T1 MRI shows the calcification at the distal insertion
Magnetic resonance imaging (MRI) of the affected area often of the deltoid muscle in the area of the glomus tumor. (From Boretto J-G,
reveals the actual glomus tumor and may reveal erosion or a per- Lazerges C, Coulet B, Baldet P, Chammas M: Calcified glomus tumor of the
forating lesion of the phalanx beneath the tumor. The tumor shoulder: a case report, Chir Main 4:183186, 2008.)
90
32 Glomus Tumor Of The Shoulder 91
Figure 33-1 Microscopic tear of the pectoralis muscle with mild bleeding and slight edema.
Differential Diagnosis the sternum after acceleration/deceleration injuries also may con-
fuse the diagnosis. Fractures of all of the bony origins of the pecto-
Pectoralis major tear syndrome is a clinical diagnosis supported ralis major muscles (e.g., the sternum and ribs and fractures of the
by a combination of clinical history, physical examination, radi- anatomical or surgical neck of the humerus) may mimic the clini-
ography, and MRI. Pain syndromes that may mimic pectoralis cal presentation of pectoralis major tear syndrome. Primary and
major tear syndrome include injuries to the pectoralis minor, sub- metastatic tumors of the shoulder, humerus, and anterior chest
scapularis, or latissimus dorsi muscles and inferior glenohumeral wall and their surrounding structures remain an ever-present pos-
ligament injuries. Dislocation of the manubrium from the body of sibility and should be included as part of the differential diagnosis
94 SECTION 3 Shoulder Pain Syndromes
Complete rupture
of tendon
Pectoralis
major muscle
Figure 33-5 Patients with pectoralis major tear syndrome present with acute onset of anterior chest wall pain after trauma to the muscle sustained
while performing activities such as bench pressing.
of patients with symptoms thought to result from pectoralis major Complications and Pitfalls
tear syndrome.
Failure to diagnose pectoralis major tear syndrome correctly
puts the patient at risk for the missed diagnosis of other syn-
Treatment dromes that may result in ongoing damage to the shoulder or
Although the pain and functional disability associated with mild lead to overlooked pathological processes in this anatomical
microscopic tears of the pectoralis major muscle may be treated region that may harm the patient, such as Pancoasts tumor
conservatively with a combination of the nonsteroidal antiinflam- or primary or metastatic tumors of the shoulder, humerus, or
matory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors anterior chest wall. MRI is indicated in all patients thought to
and gentle physical therapy, more extensive tears and rupture of have pectoralis major tear syndrome, and aggressive treatment
the pectoralis major tendon require urgent surgical repair if per- of surgically correctable causes of the symptoms is indicated
manent cosmetic deformity and functional disability are to be on an urgent basis to avoid irreversible cosmetic deformity and
avoided. functional disability.
33 Pectoralis Major Tear Syndrome 95
Figure 33-8 Active internal rotation of the humerus may reveal weak-
ness. If significant disruption of the muscle or rupture of the tendon
occurs, the patient is unable to reach behind his or her back. (From
B Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms,
Philadelphia, 2006, Saunders, p 50.)
Figure 33-6 A, Resting axial gradient-recalled echo (GRE) MRI in
a patient with a known pectoralis tendon tear adjacent to the left
humerus at rest shows mild asymmetry of the pectoralis major muscles,
with apparent discontinuity of the left pectoralis major muscle at the
axillary line (arrow). B, Axial GRE MRI in the same patient with sustained Clinical Pearls
maximal contraction of the injured muscle shows a prominent bulge
in the medial aspect of the left pectoralis major muscle (arrow). (From Pectoralis major tear syndrome is an uncommon but easily
EdelmanRR, Hesselink JR, Zlatkin MB, etal, editors: Clinical magnetic reso- recognized cause of anterior chest wall and shoulder pain. A
nance imaging, 3rd ed, Philadelphia, 2006, Saunders, p 3468.) patient with complete pectoralis major muscle tear, tendon
rupture, or both may present with hematoma and ecchymo-
Biceps m. Ruptured proximal tendon sis formation that seems out of proportion to the patients
perception of the amount of trauma sustained; the patient
often requires reassurance that he or she will not bleed to
death. Such patients should undergo urgent surgical repair
and careful postoperative rehabilitation to avoid permanent
cosmetic deformity and functional disability.
SUGGESTED READINGS
Beloosesky Y, Grinblat J, Katz M, Hendel D, Sommer R: Pectoralis major rup-
ture in the elderly: clinical and sonographic findings, Clin Imaging 27:261264,
2003.
ElMaraghy AR, Devereaux MW: A systematic review and comprehensive clas-
sification of pectoralis major tears, J Shoulder Elbow Surg 21:412422, 2012.
Mellado JM, Calmet J, Gin J, Saur A: Pectoralis major muscle and tendon tears:
report of two cases with surgical correlation and postoperative follow-up, Eur
JRadiol Extra 50:101104, 2004.
Petilon J, Ellingson CI, Sekiya JK: Pectoralis major muscle ruptures, Oper Tech
Figure 33-7 Popeyes sign associated with rupture of the biceps ten- Sports Med 13:162168, 2005.
don. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and Weaver JS, Jacobson JA, Jamadar DA, etal: Sonography of the pectoralis major
symptoms, Philadelphia, 2006, Saunders, p 83.) tear, Ultrasound Med Biol 29:S15, 374383, 2003.
Chapter 34
SUPRASCAPULAR NERVE
ENTRAPMENT
Suprascapular nerve
Supraspinatus m.
Infraspinatus m. (cut)
Figure 34-1 Suprascapular nerve entrapment is caused by compression of the suprascapular nerve as it passes through the suprascapular notch.
m,Muscle.
96
34 Suprascapular Nerve Entrapment 97
Trapezius
Suprascapular
Supraspinatus nerve
Transverse Infraspinatus m.
suprascapular Suprascapular
ligament notch
Suprascapular
Infraspinatus m.
nerve
SUGGESTED READINGS Toussaint CP, Zager EL: Whats new in common upper extremity entrapment
neuropathies, Neurosurg Clin North Am 19:573581, 2008.
Fehrman DA, Orwin JF, Jennings RM: Suprascapular nerve entrapment by gan- Waldman SD: Suprascapular nerve block. In Waldman SD, editor: Pain review,
glion cysts: a report of six cases with arthroscopic findings and review of the Philadelphia, 2009, Saunders, pp 439440.
literature, Arthroscopy 11:727734, 1995.
Moore TP, Hunter RE: Suprascapular nerve entrapment, Oper Tech Sports Med
4:814, 1996.
Chapter 35
Figure 35-1 Anatomy of axillary nerve as it travels through the quadrilateral space.
A
B
Figure 35-2 Quadrilateral space: normal anatomy. Coronal oblique section (A) and T1-weighted (TR/TE, 600/20) spin echo magnetic resonance
imaging (B). The posterior humeral circumflex artery and the axillary nerve (51) are located in the quadrilateral space. Other identified structures are
the humeral diaphysis (7), infraspinatus muscle (13), teres minor muscle (15), deltoid muscle (16), teres major muscle (17), long head of the triceps
muscle (35), and lateral head of the triceps muscle (35). (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002,
Saunders, p 3145.)
35 Quadrilateral Space Syndrome 101
Axillary nerve
Teres minor muscle
Teres major muscle
Triceps muscle
Figure 35-3 If left untreated, quadrilateral space syndrome may result in permanent atrophy of the deltoid and teres minor muscles.
A B
Figure 35-4 Quadrilateral space syndrome: Magnetic resonance imaging (MRI). Coronal oblique (A) and transaxial (B) intermediate-weighted (TR/
TE, 2000/35) spin echo MRI show selective atrophy with fatty replacement of the teres minor muscle (arrows). The infraspinatus muscle (13), deltoid
muscle (16), teres major muscle (17), and long (35) and lateral (35) heads of the triceps muscle are identified and are not involved. The humeral
diaphysis (7) also is seen. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3145.)
Chapter 36
PRONATOR SYNDROME
103
104 SECTION 4 Elbow Pain Syndromes
Clinical Pearls
Avoidance techniques of the repetitive movements respon-
sible for pronator syndrome are often forgotten in the rush
to treatment. Median nerve block at the elbow is a simple
and safe technique in the evaluation and treatment of the
aforementioned painful conditions. Careful neurological
examination to identify preexisting neurological deficits
that may later be attributed to the nerve block should be
performed in all patients before beginning median nerve
block at the elbow.
Median nerve compression by the ligament of Struthers
manifests clinically as unexplained persistent forearm pain
caused by compression of the median nerve by an aberrant
ligament that runs from a supracondylar process to the
medial epicondyle. The diagnosis is made by electromy-
ography and nerve conduction velocity testing that show
Figure 36-2 A positive pronator syndrome test is highly indicative of compression of the median nerve at the elbow combined
pronator syndrome.
36 Pronator Syndrome 105
CUBITAL BURSITIS
Testing
The diagnosis of cubital bursitis usually can be made on clinical
grounds. Plain radiographs of the elbow may reveal calcification
of the bursa and associated structures consistent with chronic
inflammation. Magnetic resonance imaging (MRI) is indicated
the patient is thought to have a joint mouse or primary pathologi-
cal process of the elbow joint. Ultrasound imaging also may aid in
the diagnosis of cubital bursitis (Figure 37-2).
Laboratory testing to rule out hyperuricemia and collagen-
vascular disease also should be considered in appropriate patients. Figure 37-1 A patient with cubital bursitis reports pain and swelling on
Electromyography and nerve conduction velocity testing rule out any movement of the elbow.
106
37 Cubital Bursitis 107
Treatment
Cubital bursa
Initial treatment of the pain and functional disability associated
with cubital bursitis should include a combination of nonsteroidal Figure 37-3 Proper needle placement for injection for treatment of
cubital bursitis.
antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2)
inhibitors and physical therapy. Local application of heat and cold
also may be beneficial. The repetitive movements that incite the Clinical Pearls
syndrome should be avoided. For patients who do not respond to
these treatment modalities, injection of the cubital bursa with a local Bursae are formed from synovial sacs whose purpose is
anesthetic and steroid may be a reasonable next step (Figure 37-3). to allow easy sliding of muscles and tendons across one
To inject the cubital bursa, the patient is placed in the supine another at areas of repeated movement. These synovial sacs
position, with the arm fully adducted at the patients side and the are lined with a synovial membrane invested with a network
elbow extended and the dorsum of the hand resting on a folded of blood vessels that secrete synovial fluid. Inflammation of
towel. Using a 5-mL sterile syringe, 2 mL of local anesthetic and the bursa results in an increase in the production of syno-
40 mg of methylprednisolone is drawn. vial fluid with swelling of the bursal sac. With overuse or
After sterile preparation of skin overlying the anterior aspect misuse, these bursae may become inflamed, enlarged, and,
of the joint, the clinician identifies the pulsations of the brachial rarely, infected. Coexistent tendinitis and epicondylitis also
artery at the crease of the elbow. After preparation of the skin may contribute to elbow pain and may require additional
with antiseptic solution, a 25-gauge, 1-inch needle is inserted just treatment with more localized injection of local anesthetic
lateral to the brachial artery at the crease and slowly advanced in a and depot steroid. This technique is a safe procedure if care-
slightly medial and cephalad trajectory through the skin and sub- ful attention is paid to the clinically relevant anatomy in
cutaneous tissues. If bone is encountered, the needle is withdrawn the areas to be injected, in particular avoiding the median
back into the subcutaneous tissue. The contents of the syringe nerve by keeping the needle lateral to the brachial artery.
are gently injected. Little resistance to injection should be felt. If Care must be taken to use sterile technique to avoid infec-
resistance is encountered, the needle is probably in the tendon and tion and universal precautions to avoid risk to the opera-
should be withdrawn back until the injection proceeds without tor. The incidence of ecchymosis and hematoma formation
significant resistance. The needle is removed, and a sterile pressure can be decreased if pressure is placed on the injection site
dressing and ice pack are placed at the injection site. immediately after injection. The use of physical modalities,
including local heat and gentle range-of-motion exercises,
should be introduced several days after the patient under-
Complications and Pitfalls goes this injection technique for elbow pain. Vigorous
The major complication associated with cubital diagnosis is mis- exercises should be avoided because they exacerbate the
diagnosis. Failure of the clinician to recognize an acute inflamma- patients symptoms. Simple analgesics and NSAIDs may be
tory or infectious arthritis of the elbow may result in permanent used concurrently with this injection technique.
damage to the joint and chronic pain and functional disability.
Injection of the cubital bursa at the elbow is a safe block, with
SUGGESTED READINGS
the major complications being inadvertent intravascular injec-
tion and persistent paresthesia secondary to needle trauma to Chung CB, Kim HJ: Sports injuries of the elbow, Magn Res Imaging Clin N Am
11:239253, 2003.
the median nerve. This technique can be performed safely in the Hayter CL, Giuffre BM: Overuse and traumatic injuries of the elbow, Magn Res
presence of anticoagulation by using a 25- or 37-gauge needle, Imaging Clin N Am 17:617638, 2009.
although at increased risk for hematoma, if the clinical situation Howard TM, Shaw JL, Phillips J: Physical examination of the elbow. In Seiden-
dictates a favorable risk-to-benefit ratio. These complications berg PH, Beutler AI, editors: The sports medicine resource manual. Philadelphia,
can be decreased if manual pressure is applied to the area of the 2008, Saunders, pp 7178.
Sellards R, Kuebrich C: The elbow: diagnosis and treatment of common inju-
block immediately after injection. Application of cold packs for riesprimary care, Clin Office Pract 32:116, 2005.
20-minute periods after the block also decreases the amount of Waldman SD: Injection technique for cubital bursitis pain. In Waldman SD,
postprocedure pain and bleeding. editor: Pain review, Philadelphia, 2009, Saunders, pp 463464.
Chapter 38
ANCONEUS EPITROCHLEARIS
Anconeus
epitrochlearis
Anconeus m.
Inflamed and
compressed
ulnar nerve
Figure 38-1 Anconeus epitrochlearis is caused by entrapment and compression of the ulnar nerve at the elbow by an accessory anconeus muscle.
m, Muscle.
108
38 Anconeus Epitrochlearis 109
A B
Figure 38-2 Eliciting Froments sign. (From Waldman SD: Physical diag-
nosis of pain: an atlas of signs and symptoms, Philadelphia, 2006, Saun-
ders, p 126.)
SUGGESTED READINGS
of the radial nerve at the elbow with a local anesthetic and
steroid gives almost instantaneous relief. Careful examina- Dellon AL: Musculotendinous variations about the medial humeral epicondyle,
JHand Surg 11:175181, 1985.
tion to identify preexisting neurological deficits that may Kojima T: Ulnar compression neuropathy secondary to the anconeus epitrochle-
later be attributed to the nerve block should be performed aris muscle, J Hand Surg 14:918919, 1989.
on all patients before beginning ulnar nerve block at the Masear VR, Hill JJ Jr, Cohen SM: Ulnar compression neuropathy secondary to
elbow. the anconeus epitrochlearis muscle, J Hand Surg 13:720724, 1988.
Waldman SD: The ulnar nerve. In Waldman SD, editor: Pain review, Philadel-
phia, 2009, Saunders, pp 7677.
Chapter 39
OS SUPRATROCHLEARE-RELATED
ELBOW PAIN
Differential Diagnosis
Primary pathological processes of the elbow, including gout and
occult fractures, may mimic the pain and disability associated
with os supratrochleare. Entrapment neuropathies, such as ulnar
tunnel syndrome, also may confuse the diagnosis, as may bursitis,
tendinitis, and epicondylitis of the elbow, which may coexist with
os supratrochleare. Osteochondritis dissecans, Panners disease,
and synovial chondromatosis also may mimic the pain associated
with os supratrochleare. Primary and metastatic tumors of the
elbow may manifest in a manner similar to elbow pain secondary
to os supratrochleare.
Treatment
Initial treatment of the pain and functional disability associated
Figure 39-1 Elbow pain secondary to os supratrochleare is character- with os supratrochleare should include a combination of non-
ized by tenderness and pain over the posterior elbow. steroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2
111
112 SECTION 4 Elbow Pain Syndromes
A B C
Figure 39-2 Accessory ossicles. A, Os vesalianum. B, Os intermetatarseum. C, Os supratrochleare posterius (dorsale). (From Resnick D, editor: Diag-
nosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 4570.)
(COX-2) inhibitors and physical therapy. The local application Clinical Pearls
of heat and cold also may be beneficial. Avoidance of repetitive
activities that aggravate the patients symptoms also may provide Pain emanating from the elbow is a common problem
relief. For patients who do not respond to these treatment modali- encountered in clinical practice. Os supratrochleare must be
ties, injection of the os supratrochleare with a local anesthetic and distinguished from fractures of the elbow, fractures of the os
steroid may be a reasonable next step. For pain that persists, or if supratrochleare itself, entrapment neuropathies of the ulnar
the os supratrochleare is causing damage to the elbow joint, surgi- nerve, bursitis, tendinitis, and epicondylitis. Less common
cal removal is indicated. causes of posterior elbow pain are osteochondritis dissecans,
Panners disease, and synovial chondromatosis.
Complications and Pitfalls
The major complication of injection of os supratrochleare is infec- SUGGESTED READINGS
tion. This complication should be exceedingly rare if strict aseptic Gudmundsen E, stensen H: Accessory ossicles in the elbow, Acta Orthop Scand
technique is followed. Approximately 25% of patients report a 58:130132, 1987.
transient increase in pain after injection of the os supratrochleare McFarland EG, Gill HS, Laporte DM, Streiff M: Miscellaneous conditions about
and should be warned of this possibility. Another potential risk of the elbow in athletes [review], Clin Sports Med 23:743763, 2004.
Waldman SD: Functional anatomy of the elbow. In Waldman SD, editor: Pain
this injection technique is trauma to the extensor tendons from review, Philadelphia, 2009, Saunders, pp 7677.
the injection itself. Wood VE, Campbell GS: The supratrochleare dorsale accessory ossicle in the
elbow, J Shoulder Elbow Surg 3:395398, 1994.
Chapter 40
OSTEONECROSIS OF
THE ELBOW JOINT
TABLE 40-1
Predisposing Factors for Osteonecrosis of the Elbow Joint
Trauma to the elbow joint
Normal
Steroids
Cell death
Cushings disease
Ischemia
Alcohol abuse
Hyperemia
Connective tissue diseases, especially systemic lupus erythematosus
Osteomyelitis
Human immunodeficiency virus
Organ transplantation
Hemoglobinopathies, including sickle cell disease
Hyperlipidemia
Gout
Renal failure
Pregnancy
Figure 40-1 The blood supply to the elbow is easily disrupted, often Radiation therapy
leaving the proximal portion of the bone without nutrition and leading
to osteonecrosis. Sickle cell disease
113
114 SECTION 4 Elbow Pain Syndromes
the course of the disease, plain radiographs can be notoriously cysts, bone contusions, and fractures may mimic the pain of osteo-
unreliable; magnetic resonance imaging (MRI) reveals articular necrosis of the elbow joint, as can occult metastatic disease.
changes before significant changes are evident on plain radio-
graphs (Figure 40-2). Based on the patients clinical presenta-
tion, additional testing, including complete blood cell count,
Treatment
uric acid level, erythrocyte sedimentation rate, and antinuclear Initial treatment of the pain and functional disability associated
antibody testing, also may be indicated. MRI of the elbow joint with osteonecrosis of the elbow joint should include a combina-
is indicated in all patients thought to have osteonecrosis of the tion of the nonsteroidal antiinflammatory drugs (NSAIDs) or
elbow joint; if other causes of joint instability, infection, or cyclooxygenase-2 (COX-2) inhibitors and decreased weight bear-
tumor are suspected; or if plain radiographs are nondiagnostic. ing of the affected elbow joint or joints. Local application of heat
Computed tomography (CT) may be useful in early diagnosis, and cold may be beneficial. For patients who do not respond to
especially with three-dimensional reconstruction (Figure 40-3). these treatment modalities, an injection of a local anesthetic into
Administration of gadolinium followed by postcontrast imaging the elbow joint may be a reasonable next step to provide palliation
may help delineate the adequacy of blood supply, with contrast of acute pain. Vigorous exercises should be avoided because they
enhancement of the elbow joint being a good prognostic sign. will exacerbate the symptoms. Ultimately, surgical repair in the
Electromyography is indicated if coexistent cervical radiculopa- form of total joint arthroplasty is the treatment of choice.
thy or brachial plexopathy is suspected. A very gentle intraar-
ticular injection of the elbow joint with small volumes of local
anesthetic will provide immediate improvement of the pain and
Complications and Pitfalls
help demonstrate the nidus of the pain is in fact the elbow joint. Failure to surgically treat significant osteonecrosis of the elbow
Ultimately, total joint replacement will be required in most joint usually will result in continued pain and disability and in
patients with osteonecrosis of the elbow joint, although newer most patients will lead to ongoing damage to the elbow joint
joint preservation techniques are becoming more popular in (see Figure 40-2). Injection of the joint with local anesthetic is
younger, more active patients given the short life expectancy of a relatively safe technique if the clinician is attentive to detail,
total shoulder prosthesis. specifically using small amounts of local anesthetic and avoiding
high injection pressures, which may further damage the joint.
Another complication of this injection technique is infection.
Differential Diagnosis This complication should be exceedingly rare if strict aseptic
Coexistent arthritis and gout of the elbow joint, bursitis, and technique is followed. Approximately 25% of patients report
tendinitis may coexist with osteonecrosis of the elbow joints and a transient increase in pain after this injection technique and
exacerbate the pain and disability. Tears of the ligaments, bone should be warned of this possibility.
A B
Figure 40-2 A, Coronal T2-weighted with fat suppression (FST2W) MRI demonstrating an area of high-signal intensity marrow edema in the
capitellum (solid arrow) of an adolescent with elbow pain. An area of low SI is seen in the subchondral bone plate (dashed arrow), suggestive of an
osteochondral defect. B, The sagittal FST2W MRI more clearly shows the low-SI osteochondral defect (curved arrow), with a linear area of high SI
at its base, indicating that the lesion is likely to be unstable. These appearances are typical of Panners disease (osteochondritis dissecans). (From
Waldman SD: Osteonecrosis of the elbow. In Waldman SD, Campbell RSD, editors: Imaging of pain, New York, 2011, Elsevier, p 282.)
40 Osteonecrosis of the Elbow Joint 115
Po A
255/128 B 255/128 C
A
Figure 40-3 Multifocal aspect of elbow osteonecrosis. A, Anterior; P, posterior. (From Mukaza MM, Manicom O, Fillipini P, Hernigou P: Elbow osteone-
crosis in sickle cells anemia: a study of six cases, Orthop Traumatol 95:8284, 2009.)
TRICEPS TENDINITIS
ST
Figure 41-1 Tendon and soft tissue calcification. Calcified deposits are visualized in the triceps tendon (T) and soft tissues (ST) around the proximal
end of the radius. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 1581.)
116
41 Triceps Tendinitis 117
A B
Figure 41-2 Triceps tendon rupture imaged in flexion. This patient was unable to extend the elbow because of discomfort. The images were obtained
on a high-field scanner with the patient prone and the arm flexed overhead. Proton density (A) and fat-suppressed T2-weighted (B) coronal images
reveal a fluid-filled tear of the distal triceps tendon (arrows) from the olecranon (O). (From Edelman RR, Hesselink JR, Zlatkin MB, etal, editors: Clinical
magnetic resonance imaging, 3rd ed, Philadelphia, 2006, Saunders, p 3302.)
Differential Diagnosis
Triceps tendinitis generally is easily identified on clinical grounds,
but coexistent bursitis may confuse the diagnosis. Stress fractures
of the olecranon also may mimic triceps tendinitis and may be
identified on plain radiographs or radionuclide bone scanning.
Treatment
Initial treatment of the pain and functional disability associated with
triceps tendinitis should include a combination of nonsteroidal anti-
inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhib-
itors and physical therapy. The local application of heat and cold also
may be beneficial. Patients should be encouraged to avoid repetitive
activities responsible for the evolution of the tendinitis. For patients
who do not respond to these treatment modalities, injection with
local anesthetic and steroid may be a reasonable next step.
TABLE 42-1
Characteristics of Radial Tunnel Syndrome and Lateral Epicondylitis
Characteristic Radial Tunnel Syndrome Lateral Epicondylitis(Tennis Elbow)
Frequency Rare (2% of all peripheral nerve compressions of the upper Common cause of lateral elbow pain
limb)
Cause Compression of the radial nerve Caused by overuse of the extensor and supi-
nator muscles
Characteristic patient Anybody with repetitive, stressful pronation and supination Tennis players
(e.g., tennis players, Frisbee players, swimmers, powerlifters)
Pain location Pain over the neck of the radius and lateral aspect of the Pain and tenderness over the lateral epi-
proximal forearm over the extensor muscles themselves condyle and immediately distal to it (at the
(distal to where the pain is located in LE) origin of the extensor muscles)
Pain radiation Pain can radiate proximally and (more commonly) distally Usually localized without radiation
Provocative tests (much overlap Pain with resisted extension of the middle finger with the Pain with resisted wrist extension or elbow
between the two entities) forearm pronated and the elbow extended. Pain with resisted supination with the elbow extended. Pain with
forearm supination with the elbow fully extended forceful wrist flexion or forearm pronation
Modified from Mileti J, Largacha M, ODriscoll SW. Radial tunnel syndrome caused by ganglion cyst: treatment by arthroscopic cyst decompression, Arthroscopy
20:e39e44, 2004.
119
120 SECTION 4 Elbow Pain Syndromes
Differential Diagnosis
Cervical radiculopathy and tennis elbow can mimic radial tun-
nel syndrome. Radial tunnel syndrome can be distinguished from
tennis elbow because with radial tunnel syndrome, the maximal
tenderness to palpation is distal to the lateral epicondyle over the
posterior interosseous branch of the radial nerve, whereas with
tennis elbow, the maximal tenderness to palpation is over the
lateral epicondyle. Increased pain with active supination and a
positive middle finger test (see earlier discussion) helps strengthen
the diagnosis of radial tunnel syndrome. Acute gout affecting the
elbow manifests as a diffuse acute inflammatory condition that
Radial nerve may be difficult to distinguish from infection of the joint, rather
than a localized nerve entrapment.
Treatment
Extensor carpi
radialis brevis
Initial treatment of the pain and functional disability associated
muscle with radial tunnel syndrome should include a combination of
nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygen-
ase-2 (COX-2) inhibitors and physical therapy. The local applica-
tion of heat and cold also may be beneficial. Patients should avoid
the repetitive movements that incite the syndrome. For patients
who do not respond to these treatment modalities, injection of the
radial nerve at the elbow with a local anesthetic and steroid may be
a reasonable next step. If the symptoms of radial tunnel syndrome
persist, surgical exploration and decompression of the radial nerve
are indicated.
Figure 42-1 The pain of radial tunnel syndrome is localized to the deep
Complications and Pitfalls
extensor muscle mass and may radiate proximally and distally into the The major complications associated with radial tunnel syndrome
upper arm and forearm.
fall into two categories: (1) iatrogenically induced complications
resulting from persistent and overaggressive treatment of resistant
and (3) a positive result on the middle finger test. The middle tennis elbow and (2) the potential for permanent neurological
finger test is performed by having the patient extend the forearm, deficits as a result of prolonged untreated entrapment of the radial
wrist, and middle finger and sustain this action against resistance. nerve. Failure of the clinician to recognize an acute inflammatory
Patients with radial tunnel syndrome exhibit increased lateral or infectious arthritis of the elbow may result in permanent dam-
elbow pain secondary to fixation and compression of the radial age to the joint and chronic pain and functional disability.
nerve by the extensor carpi radialis brevis muscle.
Pre-op Post-op
Pre-op
A B C
Pre-op
Post-op
E
Post-op
D F
Figure 42-2 Preoperative and postoperative magnetic resonance imaging (MRI) (T2-weighted fast spin echo sequences with fat saturation). A,
Sagittal MRI shows cystic mass anterior to the capitellum. B, Postoperative sagittal MRI shows decompression of the cyst. C, Preoperative coronal
MRI shows cyst communication with the proximal radioulnar joint. D, Postoperative coronal MRI after decompression. E, Series of preoperative axial
MRIs showing the cyst from the anterior to the capitellum distally into the proximal radioulnar joint. F, Postoperative axial MRIs after decompression.
(From Mileti J, Largacha M, ODriscoll SW: Radial tunnel syndrome caused by ganglion cyst: treatment by arthroscopic cyst decompression, Arthroscopy
20:e39e44, 2004.)
SUGGESTED READINGS Tennent TD, Woodgate A: Posterior interosseous nerve dysfunction in the radial
tunnel, Curr Orthop 22:226232, 2008.
Clavert P, Lutz JC, Adam P: Frohses arcade is not the exclusive compression site Waldman SD: Radial tunnel syndrome. In Waldman SD, editor: Pain review,
of the radial nerve in its tunnel, Orthop Traumatol Surg Res 95:114118, 2009. Philadelphia, 2009, Saunders, pp 268269.
Lee JT, Azari K: Ford Jones N: Long term results of radial tunnel release: the effect Waldman SD: Radial tunnel syndrome. In Waldman SD, Campbell RSD, editors:
of co-existing tennis elbow, multiple compression syndromes and workers Imaging of pain, Philadelphia, 2011, Saunders, pp 287288.
compensation, J Plast Reconstr Aesthet Surg 61:10951099, 2008.
Huisstede B, Miedema HS, van Opstal T: Interventions for treating the radial tun-
nel syndrome: a systematic review of observational studies, J Hand Surg 33:72,
2008, e1-72.e10.
Chapter 43
Medial epicondyle
Ulnar
nerve
Medial
epicondyle
Figure 43-1 Patients with cubital tunnel syndrome exhibit weakness of the intrinsic muscles of the forearm, and the hand may take on a clawlike
appearance.
Figure 43-2 Adduction of the fifth digit is often present in cubital tun- Figure 43-3 A positive Wartenbergs sign is indicative of cubital tunnel
nel syndrome. (From Waldman SD: Physical diagnosis of pain: an atlas of syndrome. (From Waldman SD: Physical diagnosis of pain: an atlas of
signs and symptoms, Philadelphia, 2006, Saunders, p 127.) signs and symptoms, Philadelphia, 2006, Saunders, p 128.)
124 SECTION 4 Elbow Pain Syndromes
Patient
A Examiner B C
Figure 43-4 The scratch collapse test. The patient faces the examiner with arms adducted, elbows flexed, and hands outstretched with the wrists at
neutral. A, The patient resists bilateral shoulder adduction and internal rotation as the examiner applies these forces to the forearm. B, The examiner
scratches or swipes the fingertips over the course of the compressed ulnar nerve. C, The force is reapplied to the forearm. A positive result occurs
when the patient has a temporary loss of external rotation resistance tone (as seen in the diagram). (From Cheng CJ, Mackinnon-Patterson B, Beck JL,
Mackinnon SE: Scratch collapse test for evaluation of carpal and cubital tunnel syndromes, J Hand Surg 33A:15181524, 2008.)
A B
Figure 43-5 Thickening of the cubital tunnel retinaculum. A, T1-weighted axial MR image reveals the ulnar nerve (white arrow) deep to a thickened
cubital tunnel retinaculum (arrowheads) and superficial to the posterior bundle of the medial collateral ligament (curved arrow). B, Axial image further
distally in the same patient reveals the ulnar nerve (white arrow) deep to a normal, thin aponeurosis of the flexor carpi ulnaris (small black arrows) and
superficial to a mildly thickened medial joint capsule (open arrow). (From Edelman RR, Hesselink JR, Zlatkin MB, etal, editors: Clinical magnetic resonance
imaging, 3rd ed, Philadelphia, 2006, Saunders, p 3303.)
Ulna
Clinical Pearls
ME Cubital tunnel syndrome is a distinct clinical entity that is
often misdiagnosed as golfers elbow, which accounts for
the many patients with golfers elbow who fail to respond
to conservative measures. Cubital tunnel syndrome can be
distinguished from golfers elbow because in cubital tunnel
Tunnel syndrome, the maximal tenderness to palpation is over the
ulnar nerve and a positive Tinels sign is present, whereas
with golfers elbow, the maximal tenderness to palpation
is over the medial epicondyle. If cubital tunnel syndrome
is suspected, injection of the radial nerve at the elbow with
Figure 43-6 In this patient with UCT the ulnar nerve has a cross sec- a local anesthetic and steroid gives almost instantaneous
tional anatomy (CSA) of 0.29 cm2. The cross-section of the ulnar nerve is relief. Careful neurological examination to identify preex-
depicted by arrows outlining its periphery. The nerve also is hypoechoic,
a finding that can be seen with increased edema. ME, Medial epicon- isting neurological deficits that may later be attributed to
dyle; Tunnel, ulnar tunnel. (From Wiesler ER, Chloros GD, Cartwright MS, the nerve block should be performed on all patients before
Shin HW, Walker FO: Ultrasound in the diagnosis of ulnar neuropathy at the beginning ulnar nerve block at the elbow.
cubital tunnel, J Hand Surg 31:10881093, 2006.)
43 Cubital Tunnel Syndrome 125
SUGGESTED READINGS Palmer BA, Hughes TB: Cubital tunnel syndrome, J Hand Surg 35:153163,
2010.
Hariri S, McAdams TR: Nerve injuries about the elbow, Clin Sports Med 29:655 Rich BC, McKay MP: The cubital tunnel syndrome: a case report and discussion,
675, 2010. J Emerg Med 23:347350, 2002.
Heithoff SJ: Cubital tunnel syndrome: ulnar nerve subluxation, J Hand Surg
35:1556, 2010.
Chapter 44
DRIVERS ELBOW
and hand that are innervated by the ulnar nerve may be identi-
ICD-9 CODE 354.2 fied with careful manual muscle testing (Table 44-1). It should be
noted that the possibility always exists that a patient with drivers
elbow also may have an coexistent ulnar, median, or radial nerve
ICD-10 CODE G56.20 lesion distal to the elbow that may confuse the clinical picture.
Furthermore, it should be remembered that cervical radiculopathy
and ulnar nerve entrapment may coexist as the double crush
The Clinical Syndrome syndrome. The double crush syndrome is seen most commonly
with median nerve entrapment at the wrist or with carpal tunnel
The ulnar nerve is susceptible to compression when a driver or syndrome. The clinician should be aware that early in the course
passenger rests his or her elbow on the lower sill of the vehicle of the evolution of drivers elbow the only physical finding other
window while the shoulder is abducted and the elbow flexed. than tenderness over the nerve may be the loss of sensation on the
When the elbow is flexed, the proximal edge of the arcuate liga- ulnar side of the little finger.
ment becomes taut and the total volume of the cubital tunnel
is decreased, resulting in increased intratunnel pressure further
compromising the ulnar nerve. Vibration transmitted from the
Testing
car body to the elbow also may further contribute to compromise Drivers elbow should be differentiated from cervical radiculop-
of the ulnar nerve. This entrapment neuropathy presents as pain athy involving the C7 or C8 roots and golfers elbow. Electro-
and associated paresthesias in the lateral forearm that radiate to myography helps distinguish cervical radiculopathy and drivers
the wrist and ring and little finger. Untreated, progressive motor elbow from golfers elbow. Ultrasound imaging of the elbow
deficit and, ultimately, flexion contracture of the affected fingers may be useful in assessing the status of the ulnar nerve and can
can result. provide important anatomic information when combined with
the neurophysiological data obtained from electromyography.
Signs and Symptoms Plain radiographs and magnetic resonance imaging (MRI) are
indicated in all patients with drivers elbow to rule out intrinsic
Physical findings associated with drivers elbow include tenderness pathological conditions of the elbow joint (Figure 44-2). Based
over the ulnar nerve at the elbow. A positive Tinels sign over the on the patients clinical presentation, additional testing, includ-
ulnar nerve as it passes beneath the aponeuroses is usually present ing complete blood count, uric acid level, sedimentation rate,
(Figure 44-1). Weakness of the intrinsic muscles of the forearm and antinuclear antibody testing, may be indicated. The injection
technique described in this chapter serves as both a diagnostic and
therapeutic maneuver.
Differential Diagnosis
Drivers elbow is an entrapment neuropathy resulting from exter-
nal compression of the ulnar nerve that clinically mimics cubital
tunnel syndrome. It is often is misdiagnosed as golfers elbow,
which accounts for the many patients with golfers elbow who
fail to respond to conservative measures. Drivers elbow can be dis-
tinguished from golfers elbow in that in drivers elbow, the maxi-
mal tenderness to palpation is over the ulnar nerve 1 inch below
the medial epicondyle, whereas with golfers elbow, the maximal
tenderness to palpation is directly over the medial epicondyle.
Treatment
Figure 44-1 Tinels sign at elbow. (From Waldman SD: Atlas of pain man- Initial treatment of the pain and functional disability associated
agement injection techniques, 3rd ed, Philadelphia, 2013, Saunders, p 129.) with drivers elbow should include a combination of nonsteroidal
126
44 Drivers Elbow 127
TABLE 44-1
Summary of Ulnar Nerve Motor Signs and Tests Grouped by Affected Musculature
Test Name Description Positive Result
Motor signs involving the adductor pollicis muscle
Froments sign The patient holds a piece of paper using a lateral pinch. Thumb IP flexion compensates for a weak adductor
The examiner then pulls the paper distally along the pollicis muscle.
thumbs longitudinal axis and assesses the patients
method of stabilization.
Jeannes sign The patient holds a piece of paper using a lateral pinch. Thumb MP hyperextension compensates for a weak
The examiner then pulls the paper distally along the adductor pollicis muscle.
thumbs longitudinal axis and assesses the patients
method of stabilization.
Motor signs and tests involving the interosseous muscles
Finger flexion sign Performed bilaterally at the same time. Both forearms and The involved side will use MP flexion to compensate
wrists are in neutral. Examiner first places a piece of paper for interossei weakness.
between the middle and ring fingers in both hands and
then pulls the paper distally.
Crossed finger test Examiner asks the patient to cross the middle finger over Inability to cross the fingers. Compare with unin-
the index finger. volved side.
Egawas sign Examiner then asks the patient to flex the middle finger Inability to perform this action in contrast to unin-
MP joint and then to abduct it to both sides. This can volved side.
be difficult to perform; therefore bilateral assessment is
recommended.
Motor signs involving the ulnar nerveinnervated lumbrical muscles
Duchennes sign Sign is identified by observing the posture of the small Clawing posture (MP hyperextension and IP flexion)
and ring fingers on the involved side. present in the ring and small fingers.
Andr-Thomas sign Sign is identified by observing the compensatory pattern Wrist tends to flex with ring and small finger EDC
used in the ring and small fingers during actions involv- activation.
ing EDC use.
Motor signs involving the hypothenar musculature
Wartenbergs sign Patient actively abducts the fingers with the forearm in Inability of the small finger to fully adduct and
pronation and the wrist in neutral. Observe the small touch the ring finger. Compare with the uninvolved
fingers ability to fully adduct. side.
Masses sign Observe the metacarpal arch as compared with the unin- Flattened metacarpal arch.
volved side. The convex nature of the ulnar aspect of the
hand is altered by hypothenar atrophy.
Pitres-Testut sign Noted after the examiner asks the patient to shape the Inability to shape the hand in the form of a cone.
hand in the form of a cone. Although present in the lit-
erature, this sign is not commonly used in clinical practice
settings.
Palmaris brevis sign A rarely observed sign in lower ulnar nerve palsy in which The sparing of the palmaris brevis muscle in con-
the lesion selectively affects the deep branch. Determine trast to the uninvolved side.
the presence of this sign by observing and evaluating the
palmaris brevis muscle in contrast to the uninvolved side.
Motor signs involving the extrinsic ulnar nerveinnervated muscles
Nail file sign Patient attempts to make a hook fist. Examiner places an Decreased small and ring finger FDP strength in
index finger along the volar surface of the patients small contrast to the uninvolved side.
and ring fingers, leaving the DIPs free to contract.
Modified from Goldman SB, Brininger TL, Schrader JW, Koceja DM: A review of clinical tests and signs for the assessment of ulnar neuropathy, J Hand Ther 22:209220,
2009.
DIP, Distal interphalangeal; EDC, extensor digitorum communis; FDP, flexor digitorum profundus; IP, interphalangeal; MP, metacarpophalangeal.
LE
ME
O
A B
C D
Figure 44-2 A, Axial T1-weighted magnetic resonance imaging (MRI) of a patient with symptoms of ulnar nerve compression. Soft tissue is seen
within the region of the cubital tunnel (white arrow); it is isointense, with normal muscle and represents an accessory anconeus muscle. The ulnar
nerve is not clearly visible. B, Compare this axial T1-weighted image of a normal elbow with high signal intensity fat suppression (FS) within the
cubital tunnel around the ulnar nerve (broken black arrow) and no accessory muscle tissue. The axial (C) and sagittal FS T2-weighted MRI demonstrate
high signal intensity within the nerve (white arrows) resulting from compression neuritis. LE, Lateral epicondyle; ME, medial epicondyle; O, olecranon.
(From Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, p 290.)
44 Drivers Elbow 129
ANTERIOR INTEROSSEOUS
SYNDROME
Muscle paralysis:
Nerve compression:
Normal
Pronator digitorum
superficialis muscle
Flexor pollicis
Anterior interosseous longus muscle
branch of median nerve
Flexor digitorum
profundus muscle
Figure 45-1 Patients with anterior interosseous syndrome exhibit acute forearm pain and progressive weakness of pinch.
132 SECTION 4 Elbow Pain Syndromes
A B
C
Figure 45-2 A, Axial T1-weighted magnetic resonance imaging (MRI) of the mid-forearm in a patient with weakness in muscles in the distribution of
the anterior interosseous nerve. The forearm appears normal on the T1-weighted image, but the axial FST2-weighted image (B) shows high signal
intensity within the muscles of the flexor pollicis longus (FPL), index finger tendon (FDP2) and middle finger tendon (FDP3) (arrows), which are sig-
nificantly reduced in bulk. This pattern is typical of denervation edema and atrophy. C, The axial FST2-weighted image of the distal forearm shows
similar high signal intensity denervation edema in the pronator quadratus muscle (arrows). (Waldman SD:. In Waldman SD, Campbell RSD, editors:
Imaging of pain, Philadelphia, 2011, Saunders, p 291)
SUGGESTED READINGS
Clinical Pearls
Chi Y, Harness NG: Anterior interosseous nerve syndrome, J Hand Surg 35:2078
Avoidance techniques for the repetitive movements respon- 2080, 2010.
sible for pronator syndrome are often forgotten in the rush Douglas H, Chin CL, Meals RA: Anterior interosseous nerve syndrome, J Am Soc
Surg Hand 1:249257, 2001.
to treatment. Median nerve block at the elbow is a simple Feldman MI, Muhammad K, Beltran J: Preoperative diagnosis of anterior inter-
and safe technique in the evaluation and treatment of the osseous nerve syndrome resulting in complete recovery, Eur J Radiol Extra
aforementioned painful conditions. Careful neurological 69:e73e76, 2009.
examination to identify preexisting neurological deficits Waldman SD: Anterior interosseous syndrome. In Waldman SD, editor: Pain
that may later be attributed to the nerve block should be review, Philadelphia, 2009, Saunders, pp 271272.
Waldman SD: Anterior interosseous syndrome. In Waldman SD, Campbell RSD,
performed in all patients before beginning median nerve editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 291293.
block at the elbow.
SECTION 5 Wrist and Hand Pain Syndromes
Chapter 46
133
134 SECTION 5 Wrist and Hand Pain Syndromes
B C
Figure 46-2 Entrapment of the ulnar nerve: Guyons canal syndrome (ulnar tunnel syndrome). A, Ganglion cyst. Transverse T2-weighted (TR/TE,
2000/80) spin echo magnetic resonance imaging shows a ganglion cyst (arrow) adjacent to the ulnar nerve and vessels (arrowhead). B and C, Anoma-
lous muscle. This accessory muscle (i.e., accessory abductor digiti minimi muscle) (arrows) is well shown in transverse T1-weighted (TR/TE, 550/12)
spin echo (B) and fat-suppressed fast spin echo (TR/TE, 3000/11) (C) images. Note the abnormal high signal intensity in the muscle and subjacent
Guyons canal in C. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3527.)
T L
A B
C
Figure 46-3 A, Axial T2-weighted magnetic resonance imaging through the level of the proximal carpal row in a patient with symptoms of ulnar
nerve compression. A high signal intensity lesion (white arrow) adjacent to the ulnar artery and vein (broken white arrows) displaces the ulnar nerve
(curved white arrow). B, The postcontrast (obtained after administration of a contrast agent) T1-weighted image shows low SI within the lesion (white
arrow) without enhancement, and the displaced ulnar nerve is again demonstrated. The appearances are consistent with a ganglion within Guyons
canal. C, The cystic nature of the lesion is further confirmed on the transverse Doppler ultrasound image, on which the ganglion can be seen as an
anechoic mass (white arrow) with flow evident in the ulnar artery and vein (black arrows). L, Lunate; P, pisiform; S, scaphoid; T, triquetrum. (Repro-
duced with permission from Spratt JD, etal: The role of diagnostic radiology in compressive and entrapment neuropathies, Eur Radiol 12:23522364, 2002.)
CHEIRALGIA PARESTHETICA
Testing
Electromyography can help identify the exact source of neurologi- Figure 47-1 Cheiralgia paresthetica manifests as pain, paresthesias, and
cal dysfunction and clarify the differential diagnosis; this should numbness of the radial aspect of the dorsum of the hand to the base
be the starting point of the evaluation of all patients thought to of the thumb.
136
47 Cheiralgia Paresthetica 137
TABLE 47-1
Causes of Compressive Radial Neuropathies
Site Cause
High radial nerve Trauma
Fractures: Diaphyseal, distal third of the humerus
Aneurysms
Tumors
Infection
Inflammation: Local
Anomalous muscles and arteries
Idiopathic: Nerve torsion or localized constrictions
Muscular effort: Lateral triceps
Muscular hypertrophy
Hereditary neuropathies
External compression: Casts, crutches, braces, sleeping positions, tourniquets, walkers
Radial nerve Radial tunnel: Pain without muscular weakness
Anatomy: (1) Fibrous band, (2) vasculature leash (of Henry), (3) extensor carpi radialis brevis,
(4) arcade of Frohse, (5) distal edge of supinator
Musculature compression: Rowers, tennis players, weightlifters
Metabolic: Pseudogout (joint swelling), rheumatoid arthritis
Tumor: Synovial chondromatosis, ganglion, bicipital bursitis
Infection: Septic arthritis
External compression: Casts
Posterior interosseous nerve (PIN) Same sites as the radial tunnel
Surgical: Arthroscopy portals
Tumor: Scapholunate ganglion, lipoma, intramuscular myxoma, ganglion
Metabolic: Pseudogout
Arteriovenous malformation, vasculitis
Trauma: Dislocated radial head
External compression: Casts, weight
Idiopathic nerve constriction
Superficial branch Wrist ganglion
Anatomical: Fascia at brachoradialis/extensor carpi radialis brevis
External compression: Casts, watch bands
Crush injury
Modified from Markiewitz AD, Merryman J: Radial nerve compression in the upper extremity, J Am Soc Surg Hand 5:8799, 2005.
Radial nerve block at the wrist is an effective treatment for Markiewitz AD, Merryman J: Radial nerve compression in the upper extremity,
JAm Soc Surg Hand 5:8799, 2005.
the symptoms of cheiralgia paresthetica. Careful neurologi- Massey EW, Pleet AB: Handcuffs and cheiralgia paresthetica, Neurology 28:1312
cal examination to identify preexisting neurological defi- 1313, 1978.
cits that may later be attributed to the nerve block should Smith MS: Handcuff neuropathy, Ann Emerg Med 10:668, 1981.
be performed in all patients before beginning radial nerve Waldman SD: Cheiralgia paresthetica. In Waldman SD, editor: Pain review, Phil-
adelphia, 2009, Saunders, pp 275276.
block at the wrist when treating cheiralgia paresthetica. If
cheiralgia paresthetica is identified early, removal of the
offending pressure and radial nerve block with a local anes-
thetic and steroid should lead to marked improvement in
most patients.
Chapter 48
SECRETANS SYNDROME
Differential Diagnosis
Coexistent arthritis, gout of the metacarpal and interphalangeal
joints, and tendinitis also may coexist with Secretans syndrome and
exacerbate the pain and disability of Secretans syndrome. Reflex
sympathetic dystrophy may manifest in a similar clinical manner,
but can be distinguished from Secretans syndrome because the pain
of reflex sympathetic dystrophy responds to sympathetic neural
blockade and the pain of Secretans syndrome does not.
Treatment
Initial treatment of the pain and functional disability associated
with Secretans syndrome should include a combination of non-
steroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
(COX-2) inhibitors and physical therapy. Local application of
heat and cold also may be beneficial. For patients who do not
respond to these treatment modalities, an injection of a local anes-
thetic and steroid into the areas of the peritendinous fibrosis may
be a reasonable next step. The use of physical therapy, including
gentle range-of-motion exercises, should be introduced several
days after the patient undergoes this injection technique. Vigor-
Figure 48-1 Secretans syndrome is caused by a peritendinous fibrosis ous exercises should be avoided because they would exacerbate the
that occurs after trauma to the dorsum of the hand. patients symptoms.
139
140 SECTION 5 Wrist and Hand Pain Syndromes
Clinical Pearls
This injection technique is extremely effective in the treat-
ment of pain and dysfunction secondary to Secretans syn-
drome. Coexistent arthritis, tendinitis, and gout also may
contribute to the pain and may require additional treatment
with more localized injection of a local anesthetic and depot
steroid. This technique is a safe procedure if careful atten-
tion is paid to the clinically relevant anatomy in the areas
to be injected. Care must be taken to use sterile technique
to avoid infection and universal precautions to avoid risk
to the operator. The incidence of ecchymosis and hema-
toma formation can be decreased if pressure is placed on
the injection site immediately after injection. The use of
physical modalities, including local heat, massage, and gen-
tle range-of-motion exercises, should be introduced several
days after the patient undergoes this injection technique.
Vigorous exercises should be avoided because they would
exacerbate the patients symptoms. Simple analgesics and
NSAIDs may be used concurrently with this injection tech-
nique.
Chapter 49
Middle phalanx
Joint cavity
Thorn
Inflamed synovial
membrane
Proximal phalanx
Figure 49-1 Foreign body synovitis manifests as a monarthritis without apparent cause.
Testing
Figure 50-1 The classic bluish discoloration of the nail plate is seen on
Magnetic resonance imaging (MRI) of the affected digit often the right proximal corner of the nail. (From McDermott EM, Weiss A-P C:
reveals the actual glomus tumor and may reveal erosion or a Glomus tumors, J Hand Surg Am 31:13971400, 2006.)
144
50 Glomus Tumor of the Hand 145
Treatment
The mainstay of treatment of glomus tumor is surgical removal.
Medication management is uniformly disappointing. Injection of
the affected digit in the point of maximal tenderness may provide
temporary relief of the pain of glomus tumor and blocks the posi-
tive ice water test response, further strengthening the diagnosis.
Clinical Pearls
The diagnosis of glomus tumor of the hand is usually
straightforward if the clinician identifies the unique nature
of its clinical presentation. Because of the rare potential for
aggressive, invasive behavior, complete excision and careful
follow-up are important.
SUGGESTED READINGS
B
Abou Jaoude JF, Roula Farah A, Sargi Z, Khairallah S, Fakih C: Glomus tumors:
Figure 50-2 Glomus tumor: MRI abnormalities. A, On a sagittal report on eleven cases and a review of the literature, Chirurg Main 19:243252,
T1-weighted (TR/TE, 350/25) spin echo magnetic resonance image, a 2000.
glomus tumor (arrows) led to subtle erosion of the dorsal surface of Constantinesco A, Arbogast S, Foucher G, etal: Detection of glomus tumor of the
the distal phalanx. Its signal intensity is identical to that of the nail bed finger by dedicated MRI at 0.1 T, Magn Reson Imaging 12:11311134, 1994.
(arrowhead). B, After intravenous gadolinium administration, a sagit- Gandon F, Legaillard Ph, Brueton R, Le Viet D, Foucher G: Forty-eight glomus
tal fat-suppressed T1-weighted (TR/TE, 500/25) spin echo image shows tumours of the hand: retrospective study and four-year follow-up, Ann Chir
the glomus tumor (arrows) and nail bed (arrowhead) as regions of high Main Memb Super 11:401405, 1992.
signal intensity. (From Resnick D, editor: Diagnosis of bone and joint dis- Gombos Z, Fogt F, Zhang PJ: Intraosseous glomus tumor of the great toe: a case
orders, 4th ed, Philadelphia, 2002, Saunders, p 3999.) report with review of the literature, J Foot Ankle Surg 47:299301, 2008.
McDermott EM, Weiss A-P C: Glomus tumors, J Hand Surg Am 31:13971400,
2006.
Chapter 51
BOXERS KNUCKLE
Differential Diagnosis
The tentative diagnosis of boxers knuckle is made on clinical
grounds and confirmed by radiographic testing. Arthritis, teno-
synovitis, or gout of the affected digits may accompany boxers
knuckle and exacerbate the patients pain. Occult fractures
occasionally confuse the clinical presentation.
Treatment
Initial treatment of the pain and functional disability associated
with carpal boss consists of nonsteroidal anti-inflammatory drugs
(NSAIDs), simple analgesics, or cyclooxygenase-2 (COX-2)
inhibitors. Physical modalities, including local heat and gentle
range-of-motion exercises, should be introduced to avoid loss of
function. Vigorous exercises should be avoided, because they will
exacerbate the patients symptoms. A nighttime splint to protect
the fingers may be helpful. If sleep disturbance is present, low-
Figure 51-1 Subluxation of the central tendon and rupture of the
dose tricyclic antidepressants are indicated. Ultimately, surgical
extensor hood mechanism create the classic deformity associated with repair is required to alleviate the patients pain and functional
boxers knuckle. disability.
146
51 Boxers Knuckle 147
Normal anatomy
Interosseous muscles
Joint capsule
Sagittal band
Central
extensor tendon
Metacarpal
Torn capsule
Boxers knuckle
Injured joint
cartilage
Figure 51-2 Normal anatomy of
the metacarpophalangeal (MP)
Torn sagittal joint extensor hood mechanism
band and the pathoanatomy of boxers
knuckle. Despite variations in extent
and exact location, the characteris-
tic lesion consistently comprised
rupture of the sagittal band with
subluxation or overt dislocation of
the central extensor tendon. (From
Melone CP JR, Polatsch DB, Beldner
S: Disabling hand injuries in boxing:
boxers knuckle and traumatic carpal
boss, Clin Sports Med 28:609621,
2009.)
Clinical Pearls
Pain emanating from the hand is a common problem.
Boxers knuckle must be distinguished from stress frac-
ture, arthritis, and other occult pathological conditions of
the wrist and hand. Although NSAIDs may palliate the
pain of carpal boss, patients often require surgical repair to
obtain long-lasting relief and restore functionality. Coexis-
Figure 51-3 Radiograph demonstrating a subchondral cyst at the head tent arthritis bursitis and tendinitis may contribute to the
of the index metacarpal highly suggestive of boxers knuckle associated
with osteochondral fracture (arrow). (From Polatsch DB, Beldner S: Dis- patients pain, necessitating additional treatment with more
abling hand injuries in boxing: boxers knuckle and traumatic carpal boss, localized injection of local anesthetic and steroid.
Clin Sports Med 28:609621, 2009.)
148 SECTION 5 Wrist and Hand Pain Syndromes
SUGGESTED READINGS
Aronowitz AR, Leddy JP: Closed tendon injuries of the hand and wrist in athletes, Posner MA, Ambrose L: Boxers knuckle: dorsal capsular rupture of the metacar-
Clin Sports Med 17:449467, 1998. pophalangeal joint of a finger, J Hand Surg Am 14:229236, 1989.
Melone CP Jr, Polatsch DB, Beldner S: Disabling hand injuries in boxing: boxers Waldman SD: Painful conditions of the wrist and hand. Physical diagnosis of pain:
knuckle and traumatic carpal boss, Clin Sports Med 28:609621, 2009. an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, pp 153154.
Chapter 52
149
150 SECTION 5 Wrist and Hand Pain Syndromes
Distraction of
radius and ulna
from metacarpals
FIGURE 52-2 Common injuries that lead to triangular fibrocartilage tear syndrome include waterskiing and horseback riding injuries, in which the
patient is dragged by the wrist by a tangled ski rope or reins, causing critical distraction forces to be applied to the volar forearm and wrist.
Protruding ulna
A
B
C
Figure 52-4 Ulnar-sided triangular fibrocartilage complex (TFCC) tears. A, Coronal two-dimensional T2 gradient echo magnetic resonance imaging.
A large amount of fluid signal is seen replacing the ulnar attachment of the TFCC, extending beyond the ulnar capsule, along the extensor carpi ulna-
ris tendon sheath more proximally (long arrows). A tear of the scapholunate ligament also is present (short arrow). B, Coronal T2 fast spin echo image
with fat saturation reveals fluid signal and altered morphology indicating disruption of the ulnar attachment (arrow) of the TFCC. C, Coronal short tau
inversion recovery MR image. The ulnar aspect of the TFCC is torn and detached (white arrows). A fracture of the ulnar styloid tip can be seen (black
arrow). (From Edelman RR, Hesselink JR, Zlatkin MB, etal, editors: Clinical magnetic resonance imaging, 3rd ed, Philadelphia, 2006, Saunders, p 3325.)
52 Triangular Fibrocartilage Tear Syndrome 153
C
Figure 52-5 Radial-sided triangular fibrocartilage complex (TFCC) tears. Coronal two-dimensional T2* gradient echo magnetic resonance imaging
(A) and T2 fast spin echo image with fat saturation (B) show fluid signal intensity in the radial aspect of the TFCC (arrow), which extends to the
radiocarpal and the distal radioulnar joint articular surfaces. Fluid is seen in the distal radioulnar joint. C, Coronal high-resolution T1 fast spin echo
image after intra-articular contrast injection into the radiocarpal joint in another patient illustrates high signal intensity contrast extending through
a TFCC defect into the distal radioulnar joint (arrow). (From Edelman RR, Hesselink JR, Zlatkin MB, etal, editors: Clinical magnetic resonance imaging,
3rd ed, Philadelphia, 2006, Saunders, p 3324.)
154 SECTION 5 Wrist and Hand Pain Syndromes
A B C
Figure 52-6 A, Digital subtraction magnetic resonance arthrogram image demonstrating a leak of contrast agent from the radiocarpal joint into the
distal radioulnar joint (DRUJ) (broken black arrow) resulting from a TFC tear. B, The postinjection radiograph also shows contrast agent within the
DRUJ. In addition, contrast agent is seen in the midcarpal joint because of a leak through an asymptomatic central perforation of the scapholunate
ligament. C, The coronal gradient echo magnetic resonance arthrogram image shows the tear of the TFC (white arrow). The articular cartilage of the
wrist is well demonstrated and normal. (From In Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, p 310.)
Triangular fibrocartilage tear syndrome is a straightforward Buterbaugh GA, Brown TR, Horn PC: Ulnar-sided wrist pain in athletes, Clin
diagnosis in the presence of obvious antecedent trauma. The Sports Med 17:567583, 1998.
diagnosis is less obvious in the absence of trauma, however, Coggins CA: Imaging of ulnar-sided wrist pain, Clin Sports Med 25:505526,
unless the clinician includes it in the differential diagno- 2006.
sis with all patients with ulnar-sided wrist pain. Coexistent Kovachevich R, Elhassan BT: Arthroscopic and open repair of the TFCC,
Hand Clin 26:485494, 2010.
arthritis, tendinitis, and gout also may contribute to the Sachar K: Ulnar-sided wrist pain: evaluation and treatment of triangular fibro-
pain and may require additional treatment with more local- cartilage complex tears, ulnocarpal impaction syndrome, and lunotriquetral
ized injection of a local anesthetic and depot steroid. The ligament tears, J Hand Surg Br 33:16691679, 2008.
use of physical modalities, including local heat and cold
and immobilization of the wrist, may provide symptomatic
relief. Vigorous exercises should be avoided because they
would exacerbate the patients symptoms and may cause
further damage to the wrist. Simple analgesics and NSAIDs
may be used concurrently with this injection technique.
Chapter 53
Scapholunate
ligament
complex
Figure 53-2 Common injuries that lead to scapholunate ligament tear include falls onto a hyperextended wrist.
53 Scapholunate Ligament Tear Syndrome 157
Figure 53-3 Watsons test (scaphoid displacement test) for the diag- Figure 53-4 Posteroanterior radiograph of the wrist depicting severe
nosis of scapholunate dissociation is performed by pushing upward on scapholunate dissociation with increased scapholunate gap, also
the scaphoid tuberosity while the hand is in ulnar deviation. This action referred to as a positive Terry Thomas sign. The scaphoid is foreshort-
tends to cause the scaphoid to ride out of the radial fossa over the dor- ened with respect to the longitudinal axis of the forearm. The scaphoid
sal rim, at times producing a painful snap. The test might be positive tuberosity is seen in profile providing the ring sign. The lunate appears
in loose-jointed individuals and should always be compared with the to be trapezoidal in shape because the palmar pole is rotated under
contralateral side. (From Manuel J, Moran SL: The diagnosis and treatment the capitate. (From Manuel J, Moran SL: The diagnosis and treatment of
of scapholunate instability, Hand Clin 26:129144, 2010.) scapholunate instability, Hand Clin 26:129144, 2010.)
A B
Figure 53-5 Intercarpal ligaments: three-dimensional Fourier transform gradient recalled magnetic resonance imaging. Normal and abnormal scaph-
olunate interosseous ligament. A, Normal scapholunate interosseous ligament. Coronal three-dimensional Fourier transform (TR/TE, 60/11; flip
angle, 10 degrees) MRI shows the low signal intensity and linear morphology that characterize normal scapholunate (arrow) and lunotriquetral
(arrowhead) interosseous ligaments. The triangular fibrocartilage also is normal. B, Communicating defect of the scapholunate interosseous ligament.
Coronal oblique three-dimensional Fourier transform (TR/TE, 60/10; flip angle, 30 degrees) MRI shows altered morphology (arrow) of the scapholu-
nate interosseous ligament. (From Resnick D, editor: Diagnosis of bone and Joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3039.)
158 SECTION 5 Wrist and Hand Pain Syndromes
LUNOTRIQUETRAL INSTABILITY
PAIN SYNDROME
Testing
Lunotriquetral
Plain radiographs are indicated in all patients who present with ligament complex
lunotriquetral instability pain syndrome to rule out underlying
occult bony pathological processes and identify widening of the
lunotriquetral gap. Based on the patients clinical presentation,
additional tests, including complete blood cell count, uric acid
level, erythrocyte sedimentation rate, and antinuclear antibody
testing, may be indicated. Magnetic resonance imaging (MRI) of
the wrist is indicated in all patients suspected to have lunotriquetral Figure 54-1 Anatomy of the lunotriquetral ligament complex.
159
160 SECTION 5 Wrist and Hand Pain Syndromes
Treatment
Initial treatment of the pain and functional disability associated
with lunotriquetral instability pain syndrome should include a
combination of nonsteroidal anti-inflammatory drugs (NSAIDs)
or cyclooxygenase-2 (COX-2) inhibitors and short-term immobi-
lization of the wrist. Local application of heat and cold also may
be beneficial. For patients who do not respond to these treatment
modalities, an injection of a local anesthetic and steroid into the
lunotriquetral joint may be a reasonable next step. Vigorous exer-
cises should be avoided because they would exacerbate the patients
symptoms. Ultimately, surgical repair is the treatment of choice.
Right
A B C
D E
Figure 54-3 A, Lateral radiograph demonstrating the lunate (white arrows) with its axis (white line) tilted in a volar direction compared with the axis
of capitate and radius (broken white line); this tilting is consistent with a volar intercalated segment instability (VISI) deformity. B, A digital subtraction
arthrogram of the same patient after injection of contrast agent into the radiocarpal joint demonstrates contrast agent passing through the lunotriquetral
(LT) joint (black arrow) and into the metacarpal joint (broken black arrow), indicating a tear of the LT ligament. The coronal T1-weighted (C) and
T2-weighted with fat suppression (D) magnetic resonance arthrogram images show sclerosis, subchondral cyst formation, and marrow edema within
the lunate resulting from secondary osteoarthritis change in the LT joint. E, The gradient echo magnetic resonance image best demonstrates absence
of the LT ligament (white arrow) and loss of articular cartilage. Compare with the normal appearance of the scapholunate ligament (broken white arrow).
(From: Lunotriquetral instability pain syndrome. In Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 307308.)
KIENBCKS DISEASE
Testing
Plain radiographs are indicated in all patients who present with
Kienbcks disease to rule out underlying occult bony pathological
conditions and identify sclerosis and fragmentation of the lunate.
Based on the patients clinical presentation, additional tests,
including complete blood cell count, uric acid level, erythrocyte
sedimentation rate, and antinuclear antibody testing, may also
be indicated. Magnetic resonance imaging (MRI) of the wrist is
indicated in all patients suspected to have Kienbcks disease or if
Figure 55-1 Repetitive microtrauma to the wrist from repetitive compres-
other causes of joint instability, infection, or tumor are suspected sive loading and unloading and recurrent compression of the lunate by the
(Figure 55-2). Electromyography is indicated if coexistent ulnar capitate and distal radius owing to extreme wrist positions have been impli-
or carpal tunnel syndrome is suspected. A very gentle injection of cated in the evolution of this painful condition of the wrist and forearm.
162
55 Kienbcks Disease 163
B C
Figure 55-2 Kienbcks disease and nonunion of a scaphoid fracture: Magnetic resonance imaging (MRI). A, Conventional tomography shows cystic
changes and sclerosis in the lunate bone and an ununited fracture of the midportion of the scaphoid bone. The fracture lines are smooth with sclerotic
margins. Mild negative ulnar variance is seen. B, Coronal T1-weighted (TR/TE, 800/20) spin echo MRI reveals low signal intensity throughout the
lunate bone and in the fracture gap of the scaphoid bone. C, Coronal T2-weighted (TR/TE, 2500/60) spin echo MRI shows foci of high signal intensity
(arrowhead) in the lunate bone. Fluid of high signal intensity (arrow) is evident in a portion of the fracture gap in the scaphoid bone. (From Resnick D,
editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3044.)
A B
C
Figure 55-3 Kienbcks disease mimics. Posteroanterior x-ray (A) and B T1-weighted coronal MRI of a patient with stage 1 Kienbcks disease (B).
(From Beredjiklian PK: Kienbcks disease, J Hand Surg Am 34:167175, 2009.)
165
166 SECTION 5 Wrist and Hand Pain Syndromes
Treatment
Initial treatment of the pain and functional disability associated
with avascular necrosis of the scaphoid should include a com-
bination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and short-term immobili-
zation of the wrist. Local application of heat and cold also may
be beneficial. For patients who do not respond to these treatment
modalities, an injection of a local anesthetic and steroid into the
radial aspect of the distal radioulnar joint may be a reasonable next
step to provide palliation of acute pain. Vigorous exercises should
be avoided because they would exacerbate the patients symptoms.
Ultimately, surgical repair is the treatment of choice.
A B
Figure 56-3 A, Radiograph obtained 12 weeks after a scaphoid fracture. There is an apparent cyst in the scaphoid but no fracture line. B, The com-
puted tomography scan, however, confirms fracture nonunion. (From In Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011,
Saunders, pp 313-315.
56 Avascular Necrosis of the Scaphoid 167
A B
Figure 56-4 Osteonecrosis of the scaphoid bone after a fracture. A, Four months after a scaphoid fracture, coronal T1-weighted (TR/TE, 500/14) spin
echo magnetic resonance imaging (MRI) reveals nonunion of the bone and low signal intensity at the fracture line and in the proximal pole of the
scaphoid. B, After intravenous gadolinium administration, fat-suppressed coronal T1-weighted (TR/TE, 550/14) spin echo MRI image shows enhance-
ment in both portions of the scaphoid, a good prognostic sign. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia,
2002, Saunders, p 3045.)
Figure 56-5 A split-screen side-by-side comparison of the fractured scaphoid (right) and normal scaphoid (left). The arrows identify two cortical frac-
tures in the palmar cortex. (From Senall JA, Failla JM, Bouffard A, Holsbeeck M: Ultrasound for the early diagnosis of clinically suspected scaphoid fracture,
J Hand Surg Am 29:400405, 2004.)
168 SECTION 5 Wrist and Hand Pain Syndromes
Testing
Plain radiographs and magnetic resonance imaging (MRI) are indi- Figure 57-1 Improper grip of golf clubs and tennis racquets is often
cated for all patients who present with ulnar-sided wrist pain. Based implicated as the inciting cause of acute extensor carpi ulnaris tendinitis.
169
170 SECTION 5 Wrist and Hand Pain Syndromes
Figure 57-2 Tenosynovitis of the extensor carpi ulnaris tendon sheath: magnetic resonance imaging. Transaxial T1-weighted (TR/TE, 600/20) spin
echo MRI of the wrist at the level of the radiocarpal joint shows fluid of intermediate signal intensity (arrows) around the extensor carpi ulnaris ten-
don in the sixth extensor compartment. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3048.)
* * *
* *
Ulna
Triquetrum
Figure 57-3 Longitudinal ultrasound image of a patient with simple tenosynovitis of the extensor carpi ulnaris (ECU) tendon. There is anechoic fluid
(white arrows) within the ECU tendon sheath. The ECU tendon (asterisks) is not thickened. (From Waldman SD: Extensor carpi ulnaris tendinitis. In Wald-
man SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 329330.)
SUGGESTED READINGS
Allende C, Le Viet D: Extensor carpi ulnaris problems at the wrist: classification, Waldman SD: Extensor carpi ulnaris tendinitis. In Waldman SD, Campbell RSD,
surgical treatment and results, J Hand Surg Br 30:265272, 2005. editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 329330.
Jeantroux J, Becce F, Guerini H, et al: Athletic injuries of the extensor carpi Watanabe A, Souza F, Vezeridis PS, Blazar P, Yoshioka H: Ulnar-sided wrist pain.
ulnaris subsheath: MRI findings and utility of gadolinium-enhanced fat- II. Clinical imaging and treatment, Skeletal Radiol 39:837857, 2010.
saturated T1-weighted sequences with wrist pronation and supination, Eur
Radiol 21:160166, 2011.
Chapter 58
Testing
Figure 58-1 Exercise and repetitive trauma, such as prolonged use of
Plain radiographs and magnetic resonance imaging (MRI) are a heavy hammer, are often implicated as inciting factors of acute flexor
indicated for all patients who present with ulnar-sided wrist carpi radialis tendinitis.
172
58 Flexor Carpi Radialis Tendinitis 173
Figure 58-2 Tenosynovitis of the flexor carpi radialis tendon sheath: magnetic resonance imaging (MRI). Coronal T1-weighted (TR/TE, 600/14) spin
echo MRI of the volar aspect of the wrist shows the enlarged tendon sheath (arrow) containing fluid or inflammatory tissue. (From Resnick D, editor:
Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3049.)
MN
Scaphoid
FCR
tra
Scaphoid
A C
Figure 58-3 Flexor carpi radialis (FCR) tendinopathy in a 65-year-old woman with a painful palpable lump over the ventral radial aspect of the right wrist.
The patient was referred for ultrasound examination for a suspected ventral ganglion cyst. A, Anteroposterior radiograph reveals scapholunate diasta-
sis and advanced triscaphe arthritis (arrows). B, Transverse ultrasound image over the lump demonstrates a swollen and heterogeneous FCR tendon
(arrows) stabilized over the scaphoid tubercle by a thickened retinaculum (white arrowhead). C, Longitudinal ultrasound image shows bony spurs (hollow
arrowhead) from the ventral aspect of the scaphoid and the trapezium (tra) impinging on the undersurface of the abnormal tendon. The retinaculum
is thickened (solid arrowheads). (From Allen PL, Baxter GM, Weston MJ: Clinical ultrasound, 3rd ed, vol 2, New York, 2011, Churchill Livingstone p 1060.)
174 SECTION 5 Wrist and Hand Pain Syndromes
SUGGESTED READINGS
Treatment
Bishop AT, Gabel G, Carmichael SW: Flexor carpi radialis tendinitis. I. Operative
Initial treatment of the pain and functional disability associated anatomy, J Bone Joint Surg Am 76:10091014, 1994.
with flexor carpi radialis tendinitis should include a combination Cowey AJ, Carmont MR, Tins B, Ford DJ: Flexor carpi radialis rupture reined in!,
Injury Extra 38:9093, 2007.
of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxy- Fitton JM, Shea FW, Goldie W: Lesions of flexor carpi radialis tendon and sheath
genase-2 (COX-2) inhibitors and physical therapy. Local applica- causing pain at the wrist, J Bone Joint Surg Br 50:359363, 1968.
tion of heat and cold also may be beneficial. Repetitive activities Gabel G, Bishop AT, Wood MB: Flexor carpi radialis tendinitis. II. Results of
responsible for the evolution of the tendinitis should be avoided. operative treatment, J Bone Joint Surg Am 76:10151018, 1994.
For patients who do not respond to these treatment modalities, Kosiyatrakul A, Luenam S, Prachaporn S: Symptomatic flexor carpi radialis brevis:
case report, J Hand Surg 35:633635, 2010.
injection with local anesthetic and steroid may be a reasonable
next step.
Clinical Pearls
The flexor carpi radialis is a very strong tendon, yet it is also
very susceptible to rupture. Coexistent bursitis and arthritis
may contribute to wrist pain and may require additional
treatment with a more localized injection of local anesthetic
and methylprednisolone acetate.
Injection of the flexor carpi radialis tendon is a safe pro-
cedure if careful attention is paid to the clinically relevant
anatomy in the areas to be injected. The use of physical
modalities, including local heat and gentle range-of-motion
exercises, should be introduced several days after the patient
undergoes this injection technique for elbow pain. Vigorous
exercises should be avoided because they would exacerbate
the patients symptoms. Simple analgesics and NSAIDs
may be used concurrently with this injection technique.
Chapter 59
TRIGGER WRIST
175
176 SECTION 5 Wrist and Hand Pain Syndromes
Clinical Pearls
The injection technique described is extremely effective in
Figure 59-3 Giant cell tumour of the flexor sheath compressing the the treatment of pain secondary to trigger wrist. Coexistent
median nerve. (From Chalmers RL, Mandalia M, Contreras R, Schreuder F: arthritis or gout may contribute to the patients pain, neces-
Acute trigger wrist and carpal tunnel syndrome due to giant-cell tumour of
the flexor sheath, J Plast Reconstr Aesthet Surg 61:1557, 2008.)
sitating additional treatment with more localized injection
of local anesthetic and methylprednisolone. A hand splint
to protect the wrists also may help relieve the symptoms of
trigger wrist. Simple analgesics and NSAIDs can be used
concurrently with the injection technique, although surgi-
cal treatment may ultimately be required to provide perma-
nent relief.
59 Trigger Wrist 177
SUGGESTED READINGS
Chalmers RL, Mandalia M, Contreras R, Schreuder F: Acute trigger wrist and Sonoda H, Takasita M, Taira H, Higashi T, Tsumura H: Carpal tunnel syndrome
carpal tunnel syndrome due to giant-cell tumour of the flexor sheath, J Plast and trigger wrist caused by a lipoma arising from flexor tenosynovium: a case
Reconstr Aesthet Surg 61:1557, 2008. report, J Hand Surg Am 27:10561058, 2002.
Giannikas D, Karabasi A, Dimakopoulos P: Trigger wrist, J Hand Surg Br 32: Waldman SD: Trigger finger. Atlas of pain management injection techniques, 2nd
214216, 2007. ed, Philadelphia, 2007, Saunders, pp 244247.
Pople IK: Trigger wrist due to idiopathic synovial hypertrophy, J Hand Surg Br Waldman SD: Painful conditions of the wrist and hand. Physical diagnosis of pain:
11:453454, 1986. an atlas of signs and symptoms, 2nd ed, Philadelphia, 2010, Saunders, pp 153159.
Ragheb D, Stanley A, Gentili A, Hughes T, Chung CB: MR imaging of the wrist
tendons: normal anatomy and commonly encountered pathology, Eur J Radiol
56:296306, 2005.
SECTION 6 Thoracic Pain Syndromes
Chapter 60
DEVILS GRIP
Testing
Plain radiographs are indicated in all patients with pain thought
to be the result of infection with coxsackievirus to rule out
occult chest wall pathology, pulmonary tumors, pneumonia, or
empyema (Figure 60-2). Ventilation/perfusion studies of the
lungs are indicated if pulmonary embolism is being considered Figure 60-1 Deep inspiration markedly increases the pain of devils grip.
178
60 Devils Grip 179
*
*
*
B
C E
Figure 60-2 A, This patient presented with a right upper lobe pneumonia (*) and a pleural effusion (arrow) seen in. B, Chest computed tomography
shows the effusion (*) that appears to be free-flowing as it is dependent. C, An ultrasound shows multiple septations in the pleural fluid (arrows). D,
Radiograph after image-guided insertion of a small-bore chest tube and fibrinolytic therapy. The empyema is nearly resolved, with persistent pneu-
monia (*) causing persistent fevers. E, Minimal residual pleural thickening (arrow) seen after removal of the chest tube and completion of antibiotics.
(From Hogan MJ, Coley BD: Interventional radiology treatment of empyema and lung abscesses, Paediatr Respir Rev 9:7784, 2008.)
Rib
Figure 60-3 Injection technique to relieve the pain of devils grip. a, Artery; n, nerve; v, vertebra.
inflame the pleura, such as pulmonary embolus, infection, and to be blocked is identified by palpating its path at the posterior
tumor, also need to be considered. axillary line. The index and middle fingers are placed on the rib,
bracketing the site of needle insertion. The skin is prepared with
antiseptic solution. A 22-gauge, 112-inch needle is attached to a
Treatment 12-mL syringe and is advanced perpendicular to the skin, aim-
Initial treatment of devils grip should include a combination ing for the middle of the rib between the index and middle fin-
of simple analgesics and nonsteroidal anti-inflammatory drugs gers. The needle should impinge on bone after being advanced
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. If these med- approximately 34 inch. After bony contact is made, the needle is
ications do not control the patients symptoms adequately, opioid withdrawn into the subcutaneous tissues and the skin and subcu-
analgesics may be added during the period of acute pain. Local taneous tissues are retracted with the palpating fingers inferiorly;
application of heat and cold also may be beneficial to provide this allows the needle to be walked off the inferior margin of the
symptomatic relief of the pain of devils grip. The use of an elastic rib. As soon as bony contact is lost, the needle is slowly advanced
rib belt may help provide symptomatic relief in some patients. approximately 2 mm deeper; this places the needle in proximity
For patients who do not respond to the aforementioned treat- to the costal groove, which contains the intercostal nerve and the
ment modalities, the following injection technique using a local intercostal artery and vein (Figure 60-3). After careful aspiration
anesthetic and steroid may be a reasonable next step. The patient reveals no blood or air, 3 to 5 mL of 1% preservative-free lidocaine
is placed in the prone position with the patients arms hanging is injected. If the pain has an inflammatory component, the local
loosely off the side of the cart. Alternatively, this block can be anesthetic is combined with 80 mg of methylprednisolone and
done with the patient in the sitting or lateral position. The rib is injected in incremental doses. Subsequent daily nerve blocks
60 Devils Grip 181
STERNOCLAVICULAR SYNDROME
ICD-9 CODE 786.59 Pain emanating from the sternoclavicular joint often mimics the
pain of cardiac origin.
Sternoclavicular
joint
Figure 61-1 Acute protraction or retraction of the shoulder reproduces the pain of sternoclavicular syndrome.
182
61 Sternoclavicular Syndrome 183
A
A
B
B
Figure 61-3 Three-dimensional computed tomography images show
Figure 61-2 A, Anterior view shows anterior dislocation of the right bipolar dislocation of the clavicle. (From Schemitsch LA, Schemitsch EH,
sternoclavicular joint. B, Superior view shows posterior dislocation of McKee MD: Bipolar clavicle injury: posterior dislocation of the acromiocla-
the acromioclavicular joint. (From Schemitsch LA, Schemitsch EH, McKee vicular joint with anterior dislocation of the sternoclavicular jointa report
MD: Bipolar clavicle injury: posterior dislocation of the acromioclavicular of two cases, J Shoulder Elbow Surg 20:e18e22, 2011.)
joint with anterior dislocation of the sternoclavicular jointa report of two
cases, J Shoulder Elbow Surg 20:e18e22, 2011.)
associated with viral infections, can be confused with sternocla-
vicular syndrome.
Neuropathic pain involving the chest wall also may be confused
the patients clinical presentation, additional tests, including com- or coexist with sternoclavicular syndrome. Examples of such neu-
plete blood cell count, prostate-specific antigen level, erythrocyte ropathic pain include diabetic polyneuropathies and acute herpes
sedimentation rate, and antinuclear antibody testing, may be zoster involving the thoracic nerves. The possibility of diseases of
indicated. Computed tomography (CT) or magnetic resonance the structures of the mediastinum is ever present and these diseases
imaging (MRI) of the joint is indicated if joint instability, tumor, sometimes can be difficult to diagnose. Pathological processes that
or infection is suspected (Figure 61-3). Injection of the sterno- inflame the pleura, such as pulmonary embolus, infection, and
clavicular joint with a local anesthetic, steroid, or both serves as a Bornholms disease, also should be considered.
diagnostic and therapeutic maneuver.
Treatment
Differential Diagnosis Initial treatment of the pain and functional disability associated with
As mentioned earlier, the pain of sternoclavicular syndrome is sternoclavicular syndrome should include a combination of non-
often mistaken for pain of cardiac origin and can lead to visits steroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
to the emergency department and unnecessary cardiac workups. (COX-2) inhibitors. Local application of heat and cold also may
If trauma has occurred, sternoclavicular syndrome may coexist be beneficial. The use of an elastic clavicle splint may help pro-
with fractured ribs or fractures of the sternum itself, which can vide symptomatic relief and help protect the sternoclavicular joints
be missed on plain radiographs and may require radionucleo- from additional trauma. For patients who do not respond to these
tide bone scanning for proper identification. Tietzes syndrome, treatment modalities, injection of the sternoclavicular joint using a
which is painful enlargement of the upper costochondral cartilage local anesthetic and steroid may be a reasonable next step.
184 SECTION 6 Thoracic Pain Syndromes
Clinical Pearls
Patients with pain emanating from the sternoclavicular
joint often attribute their pain symptoms to a heart attack.
Reassurance is required, although it should be remem-
bered that this musculoskeletal pain syndrome and coro-
nary artery disease can coexist. Tietzes syndrome, which
is painful enlargement of the upper costochondral cartilage
associated with viral infections, can be confused with ster-
noclavicular syndrome, although both respond to the injec-
tion technique described. The use of physical modalities,
including local heat and gentle range-of-motion exercises,
should be introduced several days after the patient under-
goes this injection technique for sternoclavicular joint pain.
Vigorous exercises should be avoided because they would
exacerbate the patients symptoms. Simple analgesics and
NSAIDs may be used concurrently with this injection tech-
nique. Laboratory evaluation for collagen-vascular disease
is indicated in patients with sternoclavicular joint pain in
whom other joints are involved.
Chapter 62
POSTMASTECTOMY PAIN
ICD-9 CODE 611.71 The clinician should always be alert to the possibility of
metastatic disease or direct extension of tumor into the chest
wall, which may mimic the pain of postmastectomy syndrome.
ICD-10 CODE N64.4 The findings of the targeted history and physical examination
assist the clinician in making an assessment of the sympathetic,
neuropathic, and musculoskeletal components of the pain and
designing a rational treatment plan.
The Clinical Syndrome
Postmastectomy pain syndrome is a constellation of symptoms that Testing
include pain in the anterior chest, breast, axilla, and medial upper
extremity after surgical procedures on the breast. Postmastectomy Plain radiographs are indicated in all patients who present with
pain is a misnomer because the clinical syndrome includes the pain pain thought to be due to postmastectomy syndrome to rule out
mentioned here even if the patient has only a lumpectomy or if occult bony pathology, including tumor. Electromyography helps
another, less extensive surgical procedure is performed on the breast. rule out damage to the intercostobrachial nerve or plexopathy
The pain is often described as constricting, with a continuing dull that may be contributing to the patients pain. Radionucleotide
ache. In addition to these symptoms, many patients with postmas-
tectomy pain syndrome also report sudden paresthesia radiating into
the breast, axilla, or both. In some patients, a burning, allodynic pain
reminiscent of reflex sympathetic dystrophy may be the principal
manifestation. The intensity of postmastectomy pain is moderate
to severe. The onset of postmastectomy pain may be immediately
after surgery and initially be confused with expected postsurgical
pain, or the onset may be more insidious, occurring gradually 2 to 6
weeks after the inciting surgical procedure. If complete mastectomy
is performed, phantom breast pain may confound the diagnosis fur-
ther, as may associated lymphedema. Sleep disturbance is a common
finding in patients with postmastectomy pain.
185
186 SECTION 6 Thoracic Pain Syndromes
STERNALIS SYNDROME
ICD-9 CODE 786.52 and antinuclear antibody testing, may be indicated. Computed
tomography (CT) and magnetic resonance imaging (MRI) of
the chest are indicated if a retrosternal mass, such as thymoma,
ICD-10 CODE R07.1 is suspected, as well as to help confirm the presence of a sternalis
muscle or other anterior chest wall mass (Figures 63-2 and 63-3).
Electromyography is indicated in patients with sternalis syndrome
to help rule out cervical radiculopathy or plexopathy that may
The Clinical Syndrome be considered because of the referred arm pain. Injection of the
Chest wall pain syndromes are commonly encountered in clini- sternalis muscle with a local anesthetic and steroid serves as a
cal practice. Some occur with relatively greater frequency and are diagnostic and therapeutic maneuver.
more readily identified by the clinician, such as costochondritis
and Tietzes syndrome. Others occur so infrequently that they are
often misdiagnosed, resulting in suboptimal outcome. Sternalis
Differential Diagnosis
syndrome is one such infrequent cause of anterior chest wall pain. As mentioned earlier, the pain of sternalis syndrome is often
Sternalis is a constellation of symptoms affecting the midline mistaken for pain of cardiac origin and can lead to visits to the
anterior chest wall that can radiate to the retrosternal area and the emergency department and unnecessary cardiac workups. If
medial aspect of the arm. Sternalis syndrome can mimic the pain
of myocardial infarction and is frequently misdiagnosed as such.
Sternalis syndrome is a myofascial pain syndrome and is char-
acterized by trigger points in the midsternal area. In contrast to
costosternal syndrome, which also manifests as midsternal pain,
the pain of sternalis syndrome is not exacerbated by movement Myofascial
of the chest wall and shoulder. The intensity of the pain associ- trigger points
ated with sternalis syndrome is mild to moderate and described as
having a deep, aching character. The pain of sternalis syndrome
is intermittent.
Testing
Plain radiographs are indicated in all patients thought to have
sternalis syndrome to rule out occult bony pathological processes,
including metastatic lesions. Based on the patients clinical pre-
sentation, additional tests, including complete blood cell count, Figure 63-1 Patients with sternalis syndrome exhibit myofascial trigger
prostate-specific antigen level, erythrocyte sedimentation rate, points at the midline over the sternum.
188
63 Sternalis Syndrome 189
ICD-9 CODE 786.52 from primary malignancies, including thymoma, metastatic dis-
ease, and infection.
ICD-10 CODE R07.1
Signs and Symptoms
On physical examination, the physical deformity of joint sub-
luxation after traumatic injury may be obvious on inspection
The Clinical Syndrome (Figure 64-3). The patient vigorously attempts to splint the
The manubriosternal joint can serve as a source of pain that joint by keeping the shoulders stiffly in neutral position. Pain is
often may mimic pain of cardiac origin. The manubriosternal reproduced by active protraction or retraction of the shoulder,
joint is susceptible to the development of arthritis, including deep inspiration, and full elevation of the arm. Shrugging of the
osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, Reit- shoulder also may reproduce the pain. The manubriosternal joint
ers syndrome, and psoriatic arthritis (Figure 64-1). The joint is may be tender to palpation and feel hot and swollen if acutely
often traumatized during acceleration/deceleration injuries and inflamed. The patient may report a clicking sensation with
blunt trauma to the chest. With severe trauma, the joint may movement of the joint.
sublux or dislocate (Figure 64-2). Overuse or misuse can result
in acute inflammation of the manubriosternal joint, which can Testing
be quite debilitating. The joint is subject to invasion by tumor
Plain radiographs are indicated for all patients who present with
pain thought to be emanating from the manubriosternal joint
to rule out occult bony pathological processes, including tumor.
Based on the patients clinical presentation, additional testing may
be indicated, including complete blood count, prostate-specific
antigen level, erythrocyte sedimentation rate, and antinuclear
antibody testing. Computed tomography (CT) or magnetic reso-
nance imaging (MRI) of the joint is indicated if infection, tumor,
or joint instability is suspected (Figure 64-4). Injection of the
manubriosternal joint with local anesthetic and steroid serves as a
diagnostic maneuver and a therapeutic maneuver.
Differential Diagnosis
As mentioned earlier, manubriosternal joint pain is often mis-
taken for cardiac pain. A careful search for metastatic disease or
tumor invasion of the chest wall is mandatory in all patients with
manubriosternal joint pain because this pain may coexist with
pathological rib fractures or pathological fractures of the sternum
itself, which can be missed on plain radiographs and may require
radionucleotide bone scanning for proper identification.
Neuropathic pain involving the chest wall and sternum also
may be confused or coexist with manubriosternal joint pain.
Examples of such neuropathic pain include diabetic polyneuropa-
thies and acute herpes zoster involving the thoracic nerves. The
Figure 64-1 Abnormalities of the manubriosternal joint. Radiographic possibility of diseases of the structures of the mediastinum is ever
abnormalities of the manubriosternal joint are illustrated in this coro- present, and these diseases sometimes can be difficult to diagnose.
nal section of the sternum. They include osseous erosions and sclerosis.
Note the irregularity of the costosternal joints (arrow). (From Resnick D,
Pathological processes that inflame the pleura, such as pulmonary
editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, embolus, infection, and Bornholms disease, also may mimic the
Saunders, p 924.) pain emanating from the manubriosternal joint.
190
64 Manubriosternal Joint Pain 191
Dislocated
manubriosternal
joint
Figure 64-2 With severe trauma, the manubriosternal joint may sublux or dislocate.
Treatment
Initial treatment of manubriosternal joint pain should include a conditions. Controlled studies have shown the efficacy of ami-
combination of simple analgesics and nonsteroidal anti-inflam- triptyline for this indication. Other tricyclic antidepressants,
matory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibi- including nortriptyline and desipramine, also have been shown
tors. If these medications do not control the patients symptoms to be clinically useful. This class of drugs is associated with
adequately, or if considerable sleep disturbance exists, a tricyclic considerable anticholinergic side effects, including dry mouth,
antidepressant should be added. constipation, sedation, and urinary retention. These drugs
Traditionally, tricyclic antidepressants have been a mainstay should be used with caution in patients with glaucoma, car-
in the palliation of sleep disturbance associated with painful diac arrhythmia, and prostatism. To minimize side effects and
192 SECTION 6 Thoracic Pain Syndromes
encourage compliance, the primary care physician should start Clinical Pearls
amitriptyline or nortriptyline at a 10-mg dose at bedtime. The
dose can be titrated upward to 25 mg at bedtime as side effects Patients with pain emanating from the manubriosternal
allow. Upward titration of dosage in 25-mg increments can joint often attribute their pain symptoms to a heart attack.
be done each week as side effects allow. Even at lower doses, Reassurance is required, although it should be remembered
patients generally report a rapid improvement in sleep dis- that this musculoskeletal pain syndrome and coronary
turbance and begin to experience pain relief in 10 to 14 days. artery disease can coexist. Care must be taken to use sterile
Selective serotonin reuptake inhibitors, such as fluoxetine, also technique to avoid infection and universal precautions to
have been used to treat the pain of diabetic neuropathy, and avoid risk to the operator. The incidence of ecchymosis and
although better tolerated than tricyclic antidepressants, they hematoma formation can be decreased if pressure is placed
seem to be less efficacious than the tricyclic antidepressants. on the injection site immediately after injection. The use of
Local application of heat and cold may be beneficial to pro- physical modalities, including local heat and gentle range-
vide symptomatic relief of the pain of manubriosternal joint pain. of-motion exercises, should be introduced several days after
The use of an elastic rib belt may help provide symptomatic relief. the patient undergoes this injection technique for manu-
For patients who do not respond to these treatment modalities, briosternal joint pain. Vigorous exercise should be avoided
injection of the manubriosternal joint using local anesthetic and because it exacerbates the symptoms. Simple analgesics and
steroid may be a reasonable next step. NSAIDs may be used concurrently with this injection tech-
nique. Laboratory evaluation for collagen-vascular disease is
indicated for patients who have manubriosternal joint pain
Complications and Pitfalls with other joints involved.
The major problem in the care of patients thought to have manu-
briosternal pain is the failure to identify potentially serious pathol-
ogy of the thorax or upper abdomen secondary to metastatic SUGGESTED READINGS
disease or invasion of the chest wall and thorax by tumor. Given Al-Dahiri A, Pallister I: Arthrodesis for osteoarthritis of the manubriosternal joint,
the proximity of the pleural space, pneumothorax after injection Eur J Cardiothorac Surg 29:119121, 2006.
of the manubriosternal joint is a possibility. The incidence of the Ellis H: The superior mediastinum, Anaesth Intens Care Med 10:360361, 2009.
complication is less than 1%, but it occurs with greater frequency Lyons I, Saha S, Arulampalam T: Manubriosternal joint dislocation: an unusual
in patients with chronic obstructive pulmonary disease. Although risk of trampolining, J Emerg Med 39:596598, 2010.
Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders,
uncommon, infection is an ever-present possibility, especially in Med Clin North Am 94:259273, 2010.
an immunocompromised patient with cancer. Early detection of Waldman SD: Manubriosternal joint syndrome. In Waldman SD, editor: Pain
infection is crucial to avoid potentially life-threatening sequelae. review, Philadelphia, 2009, Saunders, pp 247248.
Chapter 65
XIPHODYNIA
ICD-9 CODE 733.90 (MRI) of the joint is indicated if joint instability or an occult mass
is suspected (Figure 65-3). The following injection technique
serves as a diagnostic and therapeutic maneuver.
ICD-10 CODE M94.9
Differential Diagnosis
As with costochondritis, costosternal joint pain, devils grip, Tie-
The Clinical Syndrome tzes syndrome, and rib fractures, many patients with xiphodynia
An uncommon cause of anterior chest wall pain, xiphodynia is first seek medical attention because they believe they are having a
often misdiagnosed as pain of cardiac or upper abdominal origin. heart attack. Patients also may believe they have ulcer or gallblad-
Xiphodynia syndrome is a constellation of symptoms consisting der disease. In contrast to most other causes of pain involving
of severe intermittent anterior chest wall pain in the region of the chest wall that are musculoskeletal or neuropathic in origin,
the xiphoid process that worsens with overeating, stooping, and the pain of devils grip results from infection. The constitutional
bending. The patient may report a nauseated feeling associated symptoms associated with devils grip may lead the clinician to
with the pain of xiphodynia syndrome. This xiphisternal joint
seems to serve as the nidus of pain for xiphodynia syndrome.
The xiphisternal joint is often traumatized during acceleration/ Xiphisternal joint
deceleration injuries and blunt trauma to the chest. With severe
trauma, the joint may sublux or dislocate. The xiphisternal joint
also is susceptible to the development of arthritis, including osteo-
arthritis, rheumatoid arthritis, ankylosing spondylitis, Reiters
syndrome, and psoriatic arthritis. The joint is subject to invasion
by tumor from either primary malignancies, including thymoma,
or metastatic disease.
Testing
Plain radiographs are indicated in all patients with pain thought to
be emanating from the xiphisternal joint to rule out occult bony
pathological conditions, including tumor. Based on the patients
clinical presentation, additional tests, including complete blood
cell count, prostate-specific antigen level, erythrocyte sedimen-
tation rate, and antinuclear antibody testing, may be indicated.
Computed tomography (CT) or magnetic resonance imaging Figure 65-1 The xiphisternal joint is swollen in patients with xiphodynia.
193
194 SECTION 6 Thoracic Pain Syndromes
Clinical Pearls
Patients with pain emanating from the xiphisternal joint
often attribute their pain symptoms to a heart attack or
ulcer disease. Reassurance is required, although it should
be remembered that this musculoskeletal pain syndrome,
ulcer disease, and coronary artery disease can coexist. The
xiphoid process articulates with the sternum via the xiphi-
sternal joint. The xiphoid process is a plate of cartilaginous
bone that becomes calcified in early adulthood. The xiphi-
sternal joint is strengthened by ligaments, but it can be sub-
luxed or dislocated by blunt trauma to the anterior chest.
The xiphisternal joint is innervated by the T4-7 intercostal
nerves and the phrenic nerve. It is thought that this innerva-
tion by the phrenic nerve is responsible for the referred pain
associated with xiphodynia syndrome. Tietzes syndrome,
which is painful enlargement of the upper costochondral
cartilage associated with viral infections, can be confused
with xiphisternal syndrome, although both respond to the
injection technique described.
The use of physical modalities, including local heat and
gentle range-of-motion exercises, should be introduced sev-
eral days after the patient undergoes this injection technique
for xiphisternal joint pain. Vigorous exercises should be
avoided because they would exacerbate the patients symp-
toms. Simple analgesics and NSAIDs may be used concur-
Figure 65-3 The xiphosternal angle was 105 degrees. The curved shape rently with this injection technique. Laboratory evaluation
of the xyphoid process hindered the measurement of the angle. (From for collagen-vascular disease is indicated in patients with
Maigne J-Y, Vareli M, Rousset P, Cornelis P: Xiphodynia and prominence of xiphisternal joint pain in whom other joints are involved.
the xyphoid process: value of xiphosternal angle measurementthree case
reports, Joint Bone Spine 77:474476, 2010.)
SUGGESTED READINGS
consider pneumonia, empyema, and occasionally pulmonary
Howell J: Xiphodynia: an uncommon cause of exertional chest pain, Am J Emerg
embolus as the most likely diagnosis. Med 8:176, 1990.
Howell JM: Xiphodynia: a report of three cases, J Emerg Med 10:435438, 1992.
Treatment Jelenko C III, Cowan GSM Jr: Perichondritis (Tietzes syndrome) at the xiphisternal
joint: a mimic of severe disease, J Am Coll Emerg Physicians 6:536542, 1977.
Koren W, Shahar A: Xiphodynia masking acute myocardial infarction: a diagnostic
Initial treatment of xiphodynia should include a combination cul-de-sac, Am J Emerg Med 16:177178, 1998.
of simple analgesics and nonsteroidal anti-inflammatory drugs Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders,
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. If these Med Clin North Am 94:259273, 2010.
Chapter 66
ICD-9 CODE 729.1 indicated, including complete blood cell count, prostate-specific
antigen level, sedimentation rate, and antinuclear antibody test-
ing. Magnetic resonance imaging (MRI) of the chest is indicated
ICD-10 CODE M79.7 if a retrosternal mass such as thymoma is suspected or if trauma
to the serratus anterior muscle itself has occurred (Figure 66-2).
Electromyography is indicated in patients with serratus ante-
The Clinical Syndrome rior muscle syndrome to help rule out cervical radiculopathy
or plexopathy that may be considered because of the referred
Chest wall pain syndromes are commonly encountered in clini- arm pain. Injection of the serratus anterior muscle with a local
cal practice. Some occur with relatively greater frequency and are anesthetic and steroid serves as both a diagnostic and therapeutic
more readily identified by the clinician, such as costochondritis maneuver.
and Tietzes syndrome. Others occur so infrequently that they are
often misdiagnosed, resulting in less-than-optimal outcome. Ser-
ratus anterior muscle syndrome is one such infrequent cause of
Differential Diagnosis
anterior chest wall pain. The syndrome is a constellation of symp- As mentioned, the pain of serratus anterior muscle syndrome is
toms consisting of pain overlying the fifth to the seventh ribs in often mistaken for pain of cardiac origin and can lead to visits
the midaxillary line, with referred pain that may radiate down the to the emergency department and unnecessary cardiac workups.
ispilateral upper extremity into the palmar aspect of the ring and If trauma has occurred, serratus anterior muscle syndrome may
little finger. Serratus anterior muscle syndrome can mimic the pain coexist with fractured ribs or fractures of the sternum itself, which
of myocardial infarction and is frequently misdiagnosed as such. It can be missed on plain radiographs and may require radionucleo-
is a myofascial pain syndrome. The intensity of the pain associated tide bone scanning for proper identification. Tietzes syndrome,
with serratus anterior muscle syndrome is mild to moderate and is which is painful enlargement of the upper costochondral cartilage
described as having a deep, aching character. The pain of serratus associated with viral infections, can be confused with sternalis
anterior muscle syndrome is intermittent. syndrome, as can costosternal syndrome.
Neuropathic pain involving the chest wall may be confused or
Signs and Symptoms coexist with costosternal syndrome. Examples of such neuropathic
pain include diabetic polyneuropathies and acute herpes zoster
On physical examination, the patient with serratus anterior muscle involving the thoracic nerves. The possibility of diseases of the
syndrome will exhibit myofascial trigger points overlying the 5th structures of the mediastinum remains ever present and at times
to 7th ribs in the midaxillary line, with referred pain that may radi- can be difficult to diagnose. Pathological processes that inflame
ate down the ispilateral upper extremity into the palmar aspect of the pleura, such as pulmonary embolus, infection, and tumor, also
the ring and little fingers (Figure 66-1). Pain is reproduced with should be considered.
palpation of these trigger points rather than with movement of
the chest wall and shoulders. A positive jump sign will be pres-
ent when these trigger points are stimulated. Trigger points at the
Treatment
lateral border of the scapula may be present and amenable to injec- Initial treatment of serratus anterior muscle syndrome should
tion therapy. As mentioned, movement of the shoulders and chest include a combination of simple analgesics and the nonsteroidal
wall will not exacerbate the pain. anti-inflammatory agents or the cyclooxygenase-2 (COX-2)
inhibitors. The local application of heat and cold may be benefi-
Testing cial to provide symptomatic relief of the pain of serratus anterior
muscle syndrome. The use of an elastic rib belt may help provide
Plain radiographs are indicated in all patients with suspected symptomatic relief in some patients. For patients who do not
serratus anterior muscle syndrome to rule out occult bony respond to these treatment modalities, injection of the trigger
pathological processes, including metastatic lesions. Based on areas located in the sternalis muscle using a local anesthetic and
the patients clinical presentation, additional testing may be steroid may be a reasonable next step.
195
196 SECTION 6 Thoracic Pain Syndromes
Side view
Serratus
anterior m.
Trigger point
Referred pain
Figure 66-1 Serratus anterior muscle syndrome is a constellation of symptoms consisting of anterior chest wall pain that can radiate to the retrosternal
area and the medial aspect of the arm.
ICD-9 CODE 786.59 imaging (MRI) of the affected ribs and cartilage is indicated if
joint instability or occult mass is suspected. The injection tech-
nique discussed in this chapter serves as a diagnostic and thera-
ICD-10 CODE R07.82 peutic maneuver.
Differential Diagnosis
The Clinical Syndrome As mentioned earlier, the pain of slipping rib syndrome is often
Encountered more frequently in clinical practice since the mistaken for pain of cardiac or gallbladder origin and can lead
increased use of across-the-chest seat belts and airbags, slipping to visits to the emergency department and unnecessary cardiac
rib syndrome is often misdiagnosed, leading to prolonged suffer- and gastrointestinal workups. If trauma has occurred, slipping rib
ing and excessive testing for intra-abdominal and intrathoracic syndrome may coexist with rib fractures or fractures of the ster-
pathological conditions. Slipping rib syndrome is a constellation num, which can be missed on plain radiographs and may require
of symptoms consisting of severe knifelike pain emanating from radionucleotide bone scanning for proper identification. Tietzes
the lower costal cartilages associated with hypermobility of the syndrome, which is painful enlargement of the upper costochon-
anterior end of the lower costal cartilages. The tenth rib is most dral cartilage associated with viral infections, can be confused with
commonly involved, but the eighth and ninth ribs also can be
affected. This syndrome is also known as the rib-tip syndrome.
Slipping rib syndrome is almost always associated with trauma
to the costal cartilage of the lower ribs. These cartilages are often
8th rib
traumatized during acceleration/deceleration injuries and blunt
trauma to the chest. With severe trauma, the cartilage may sublux
9th rib
or dislocate from the ribs. Patients with slipping rib syndrome
may report a clicking sensation with movement of the affected 10th rib
ribs and associated cartilage.
Testing
Plain radiographs are indicated in all patients who present with
pain thought to be emanating from the lower costal cartilage and
ribs to rule out occult bony pathological processes, including rib
fracture and tumor. Based on the patients clinical presentation,
additional tests, including complete blood cell count, prostate-
specific antigen level, erythrocyte sedimentation rate, and anti- Figure 67-1 Patients with slipping rib syndrome exhibit pain on hook-
nuclear antibody testing, may be indicated. Magnetic resonance ing of the affected costochondral cartilage.
198
67 Slipping Rib Syndrome 199
slipping rib syndrome, as can devils grip, which is a pleura-based pathological conditions of the thorax or upper abdomen. Given
pain syndrome of infectious origin. the proximity of the pleural space, pneumothorax after the injec-
Neuropathic pain involving the chest wall also may be con- tion technique described is a possibility. The incidence of the
fused or coexist with slipping rib syndrome. Examples of such complication is less than 1%, but it occurs with greater frequency
neuropathic pain include diabetic polyneuropathies and acute in patients with chronic obstructive pulmonary disease. Because
herpes zoster involving the thoracic nerves. The possibility of dis- of the proximity to the intercostal nerve and artery, the clinician
eases of the structures of the mediastinum is ever present, and should calculate carefully the total milligram dosage of local anes-
these diseases sometimes can be difficult to diagnose. Pathologi- thetic administered, in consideration of the high vascular uptake
cal processes that inflame the pleura, such as pulmonary embolus, via these vessels. Although uncommon, infection is an ever-pres-
infection, and tumor, also should be considered. ent possibility, especially in an immunocompromised patient with
cancer. Early detection of infection is crucial to avoid potentially
Treatment life-threatening sequelae.
Scapula
Long thoracic
nerve (C5-C7)
Serratus anterior
muscle
Figure 68-1 Scapular winging is best viewed by having the patient push his or her hands against the wall.
result not of an isolated lesion of the long thoracic nerve of Bell but SUGGESTED READINGS
rather a part of a larger neurological problem. Akgun K, Aktas I, Terzi Y: Winged scapula caused by a dorsal scapular nerve
lesion: a case report, Arch Phys Med Rehabil 89:20172020, 2008.
Belville RG, Seupaul RA: Winged scapula in the emergency department: a case
Clinical Pearls report and review, J Emerg Med 29:279282, 2005.
Nakatsuchi Y, Saitoh S, Hosaka M, Uchiyama S: Long thoracic nerve paralysis
Winged scapula syndrome is a distinct clinical entity that associated with thoracic outlet syndrome, J Shoulder Elbow Surg 3:2833, 1994.
is difficult to treat. Early removal of the offending cause Sherman SC, OConnor M: An unusual cause of shoulder pain: winged scapula,
of nerve entrapment should allow rapid recovery of nerve J Emerg Med 28:329331, 2005.
function with resultant improvement in pain and shoulder
dysfunction. A careful search for other causes of winging of
the scapula should occur before attributing this neurologi-
cal finding to winged scapula syndrome.
SECTION 7 Abdominal and Groin Pain Syndromes
Chapter 69
ICD-9 CODE 355.9 the affected nerve by keeping the thoracolumbar spine slightly
flexed to avoid increasing tension on the abdominal musculature
(Figure 69-2). Having the patient do a sit-up often reproduces
ICD-10 CODE G58.9 the pain, as does a Valsalva maneuver. Patients with anterior cuta-
neous nerve entrapment will also exhibit a positive Carnetts test
when the patient is asked to tense his or her abdominal muscula-
ture, which is indicative of abdominal wall pain rather than pain
The Clinical Syndrome with an intra-abdominal nidus (Figure 69-3).
Anterior cutaneous nerve entrapment is an uncommon cause of
anterior abdominal wall pain that is a frequently overlooked clinical Testing
diagnosis. Anterior cutaneous nerve entrapment syndrome is a con-
stellation of symptoms consisting of severe knifelike pain emanating Plain radiographs are indicated in all patients with pain thought
from the anterior abdominal wall associated with the physical find- to be emanating from the lower costal cartilage and ribs to rule
ing of point tenderness over the affected anterior cutaneous nerve. out occult bony pathological conditions, including rib fracture
The pain radiates medially to the linea alba but in almost all cases and tumor. Radiographic evaluation of the gallbladder is indi-
does not cross the midline. Anterior cutaneous nerve entrapment cated if cholelithiasis is suspected. Based on the patients clini-
syndrome occurs most commonly in young women. The patient cal presentation, additional tests, including complete blood cell
can often localize the source of pain accurately by pointing to the count, rectal examination with stool guaiac, erythrocyte sedi-
spot at which the anterior cutaneous branch of the affected inter- mentation rate, and antinuclear antibody testing, may be indi-
costal nerve pierces the fascia of the abdominal wall at the lateral cated. Ultrasonography and computed tomography (CT) scan
border of the abdominus rectus muscle (Figure 69-1). At this point, of the abdomen are indicated if intra-abdominal pathological
the anterior cutaneous branch of the intercostal nerve turns sharply process or occult mass is suspected. Injection of the anterior
in an anterior direction to provide innervation to the anterior wall. cutaneous nerve with or without ultrasound guidance at the
The nerve passes through a firm fibrous ring as it pierces the fascia, point at which it pierces the fascia serves as a diagnostic and
and at this point the nerve becomes subject to entrapment. The therapeutic maneuver (Figure 69-4).
nerve is accompanied through the fascia by an epigastric artery and
vein. The potential exists for small amounts of abdominal fat to Differential Diagnosis
herniate through this fascial ring and become incarcerated, which
results in further entrapment of the nerve. The pain of anterior The differential diagnosis of anterior cutaneous nerve entrapment
cutaneous nerve entrapment is moderate to severe in intensity. syndrome should consider ventral hernia, peptic ulcer disease,
cholecystitis, intermittent bowel obstruction, renal calculi,
angina, mesenteric vascular insufficiency, diabetic polyneuropa-
Signs and Symptoms thy, and pneumonia (Table 69-1). Rarely, the collagen-vascular
As mentioned earlier, the patient often can point to the exact diseases, including systemic lupus erythematosus and polyarteri-
spot that the anterior cutaneous nerve is entrapped. Palpation tis nodosa, may cause intermittent abdominal pain; porphyria
of this point often elicits sudden sharp, lancinating pain in the also may cause intermittent abdominal pain. Because the pain of
distribution of the affected anterior cutaneous nerve. Voluntary acute herpes zoster may precede the rash by 24 to 72 hours, the
contraction of the abdominal muscles puts additional pressure on pain may be attributed erroneously to anterior cutaneous nerve
the nerve and may elicit the pain. The patient attempts to splint entrapment.
202
69 Anterior Cutaneous Nerve Entrapment 203
Linea alba
Rectus
abdominis Entrapped anterior
cutaneous nerve
Transverse
abdominis
Figure 69-1 The course of the anterior cutaneous nerve within the abdominal wall.
Rectus
sheath
Anterior
cutaneous
nerve
Figure 69-2 Patients with anterior cutaneous nerve entrapment often
attempt to splint the affected nerve by keeping the thoracolumbar
spine slightly flexed to avoid increasing tension on the abdominal
musculature.
Treatment
Initial treatment of the pain and functional disability associated B
with anterior cutaneous entrapment syndrome should include a Figure 69-3 A, The patient is asked to completely relax the abdominal
combination of nonsteroidal anti-inflammatory drugs (NSAIDs) muscles and point with one finger to the most painful area. B, The
or the cyclooxygenase-2 (COX-2) inhibitors and physical patient is then asked to maximally tense the abdominal muscles. The
therapy. Local application of heat and cold may be beneficial. Carnetts test is positive if the localized pain increases at the previously
identified painful area.
The repetitive movements that incite the syndrome should be
avoided. For patients who do not respond to these treatment
modalities, injection of the anterior cutaneous nerve at the point Complications and Pitfalls
at which the nerve pierces the fascia with a local anesthetic and
steroid may be a reasonable next step. If the symptoms of anterior The major complications associated with anterior cutaneous
cutaneous entrapment syndrome persist, surgical exploration and entrapment syndrome fall into two categories: (1) iatrogenically
decompression of the anterior cutaneous nerve are indicated. induced complications secondary to incorrect diagnosis and (2)
204 SECTION 7 Abdominal and Groin Pain Syndromes
Figure 69-4 Transverse ultrasound image demonstrating the linea alba, rectus muscles, and the skin and subcutaneous tissues.
TABLE 69-1
The Differential Diagnosis of Anterior Cutaneous Nerve Entrapment Syndrome
Differential Diagnosis Investigations and Characteristics
Anterior cutaneous nerve entrapment syndrome Carnetts test, injection of local anesthetics
Thoracic lateral cutaneous nerve entrapment History of previous surgery, clinical examination
Ilioinguinal or iliohypogastric nerve entrapment History of previous groin surgery, clinical examination, injection of local anesthetics
Endometriosis History of cyclic abdominal pain, laparoscopy
Myofascial pain syndrome Clinical examination, myofascial strain
Slipping rib syndrome Hypermobile, luxating eighth to tenth ribs, clinical examination
Diabetic radiculopathy Paraspinal EMG, patient with diabetes mellitus
Abdominal wall tear History of acute pain related to lifting or stretching, athletes
Abdominal wall or rectus sheath hematoma Abdominal ultrasound or CT scan, after laparoscopy, after coughing in anticoagulated
patient
Herpes zoster History and clinical examination, dermatomal
Abdominal wall tumor (lipoma, desmoid, metastasis) History and clinical examination, abdominal CT scan
Spinal nerve irritation Referred pain by thoracic spine pathological condition
Hernia Abdominal ultrasound, clinical examination
Traction symphysitis or pubalgia Athletes, positive findings on MRI or scintigraphy
CT, Computed tomographic; EMG, electromyography; MRI, magnetic resonance imaging.
failure of the clinician to recognize that a hernia coexists with the SUGGESTED READINGS
nerve entrapment until bowel ischemia occurs. Hall MW, Sowden DS, Gravestock H, et al: Abdominal wall tenderness test,
Lancet 7:16061607, 1991.
Kanakarajan S, High K, Nagaraja R: Chronic abdominal wall pain and ultrasound-
Clinical Pearls guided abdominal cutaneous nerve infiltration: a case series, Pain Med 12:
382386, 2011.
Patients with pain from anterior cutaneous nerve entrap- Kuan L-C, Li Y-T, Chen F-M, etal: Efficacy of treating abdominal wall pain by
ment syndrome often attribute their pain symptoms to a local injection, Taiwan J Obstet Gynecol 45:239243, 2006.
gallbladder attack or ulcer disease. Reassurance is required, Srinivasan R, Greenbaum DS: Chronic abdominal wall pain: a frequently overlooked
although it should be remembered that this musculoskeletal problem: practical approach to diagnosis and management, Am J Gastroenterol
97:824830, 2002.
pain syndrome and intra-abdominal pathological conditions
can coexist. The use of physical modalities, including local
heat and gentle range-of-motion exercises, should be intro-
duced several days after the patient undergoes this injec-
tion technique for anterior cutaneous nerve entrapment
syndrome. Vigorous exercises should be avoided because
they would exacerbate the symptoms. Simple analgesics and
NSAIDs may be used concurrently with the aforementioned
injection technique. Radiographic evaluation for intra-
abdominal pathological conditions is indicated in patients
with anterior abdominal pain of unclear origin.
Chapter 70
ICD-9 CODE 277.1 as may dehydration, calorie restriction, hormonal alterations, and
infection.
ICD-10 CODE E802.9
Testing
Given the usual delay in the diagnosis of acute intermittent por-
The Clinical Syndrome phyria, a considerable amount of testing is done. Most standard
laboratory testing does not point the clinician toward a diagnosis
Acute intermittent porphyria is an uncommon cause of abdominal of acute intermittent porphyria, however. Specifically, liver func-
pain that frequently confounds the diagnostic efforts of even the tion tests are normal. A mild normocytic, normochromic anemia
most astute clinician. The porphyrias are disorders of heme syn- is sometimes present. Freshly passed urine is colorless, but it turns
thesis that can produce a wide range of clinical symptoms. Many a port wine color if exposed to light. Given the low incidence of
different types of porphyrias occur, each of which manifests in a porphyria, qualitative urine screening tests, such as the Watson-
distinct clinical manner that reflects the specific enzyme deficiency Schwartz test, is a reasonable first step in diagnosing porphyria. If
of the heme biosynthetic pathway. The porphyrias can be inher- the qualitative tests are positive, quantitative testing, such as gas
ited or acquired. The main clinical manifestations of the porphyr- chromatographic measurements for aminolevulinic acid, should
ias are neurological dysfunction and the unique clinical finding of be performed.
cutaneous sensitivity to sunlight.
Acute intermittent porphyria is an autosomal dominant trait
with variable clinical expression. The incidence of the gene
responsible for acute intermittent porphyria is thought to be 1 in
100,000 individuals. The disease rarely manifests before puberty.
Acute abdominal pain is usually the first clinical expression of
the disease. As the name implies, the pain of acute intermittent
porphyria is intermittent and colicky. The pain may be localized
to the abdomen or may radiate to the flanks. The patient also
may exhibit neurological symptoms, suggesting dysfunction of the
central and peripheral nervous systems. Port wine urine, which is
characteristic of hepatic porphyrias, including acute intermittent
porphyria, is often seen during acute attacks.
205
206 SECTION 7 Abdominal and Groin Pain Syndromes
RADIATION ENTERITIS
207
208 SECTION 7 Abdominal and Groin Pain Syndromes
Clinical Pearls
Treatment of the symptoms associated with radiation enter-
itis should be part of the overall management of a patient
with cancer. The recognition and treatment of symptoms
other than pain are often delayed while the clinician focuses
on pain control, further compounding the patients suffer-
ing. Vigilance for life-threatening complications of radia-
tion enteritis, including bowel perforation, is mandatory to
avoid disaster.
SUGGESTED READINGS
Andreyev HJ: Gastrointestinal problems after pelvic radiotherapy: the past, the
present and the future, Clin Oncol 1979019799, 2007.
Chon BH, Loeffler JS: The effect of nonmalignant systemic disease on tolerance to
radiation therapy, Oncologist 7:136143, 2002.
Theis VS, Sripadam R, Ramani V, Lal S: Chronic radiation enteritis, Clin Oncol
22:7083, 2010.
Waddell BE, Rodriguez-Bigas MA, Lee RJ, Weber TK, Petrelli NJ: Prevention of
chronic radiation enteritis, J Am Coll Surg 189:611624, 1999.
LIVER PAIN
209
210 SECTION 7 Abdominal and Groin Pain Syndromes
rule out occult bony pathological conditions, including tumor. Based hypertension, or hepatic metastatic disease. Pain emanating from
on the patients clinical presentation, additional tests, including the liver is often mistaken for pain of cardiac or gallbladder origin
complete blood cell count, automated chemistries, liver function test, and can lead to visits to the emergency department and unneces-
erythrocyte sedimentation rate, and antinuclear antibody testing, may sary cardiac and gastrointestinal workups. If trauma has occurred,
be indicated. Computed tomography (CT) and magnetic resonance liver pain may coexist with rib fractures or fractures of the sternum
imaging (MRI) of the lower thoracic contents and abdomen are itself that can be missed on plain radiographs and may require
indicated in most patients with liver pain to rule out occult pulmo- radionucleotide bone scanning for proper identification.
nary and intra-abdominal pathological processes, including cancer of Neuropathic pain involving the chest wall may be confused or
the gallbladder and pancreas (Figures 72-2 and 72-3). Differential coexist with liver pain. Examples of neuropathic pain include dia-
neural blockade on an anatomical basis can serve as a diagnostic and betic polyneuropathies and acute herpes zoster involving the lower
therapeutic maneuver (see discussion of treatment). thoracic and upper lumbar nerves. The possibility of diseases of the
structures of the inferior mediastinum and retroperitoneum is ever
present, and these diseases sometimes can be difficult to diagnose.
Differential Diagnosis Pathological processes that inflame the pleura, such as pulmonary
Pain of hepatic origin must be taken seriously. It is often the result embolus, infection, and Bornholms disease, may mimic or coexist
of an underlying serious disease, such as biliary malignancy, portal with pain of hepatic origin.
Treatment
Initial treatment of liver pain should include a combination of sim-
ple analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs)
or cyclooxygenase-2 (COX-2) inhibitors. If these medications do
not control the patients symptoms adequately, an opioid analgesic
may be added. Local application of heat and cold may be beneficial
to provide symptomatic relief of liver pain. The use of an elastic rib
belt over the liver may help provide symptomatic relief.
For patients who do not respond to these treatment modalities,
an intercostal nerve block using a local anesthetic and steroid may
be a reasonable next step. If the pain is thought to be sympatheti-
cally mediated, a celiac plexus block is a reasonable next step. This
technique provides diagnostic and therapeutic benefit. If the pain
is thought to be somatic, intercostal nerve blocks should be the
next step. Pain of hepatic origin may be somatic and sympathetic
and require celiac plexus and intercostal nerve block for complete
control.
Figure 72-2 Gallbladder carcinoma (small arrows) manifesting as thicken-
ing of the gallbladder wall with a gallstone (large arrow) and metastasis to
lymph nodes (n). (From Haaga JR, Lanzieri CF, Sartoris UJ, etal: Computed Complications and Pitfalls
tomography and magnetic resonance imaging of the whole body, 3rd ed,
St Louis, 1994, Mosby, p 1359.)
The major problem in the care of patients thought to have liver
pain is the failure to identify potentially serious pathological pro-
cesses of the thorax or upper abdomen. Given the proximity of
the pleural space, pneumothorax after intercostal nerve block is a
possibility. The incidence of the complication is less than 1%, but
it occurs with greater frequency in patients with chronic obstruc-
tive pulmonary disease. Although uncommon, infection, includ-
ing liver abscess, remains an ever-present possibility, especially in
an immunocompromised patient with cancer. Early detection of
infection is crucial to avoid potentially life-threatening sequelae.
Clinical Pearls
Liver pain is often poorly diagnosed and treated. Correct
diagnosis of the cause of liver pain and the nerves subserving
the pain is necessary to treat this painful condition prop-
erly and to avoid overlooking serious intrathoracic or intra-
abdominal pathological processes. Intercostal nerve block
is a simple technique that can produce dramatic relief for
patients with liver pain thought to be somatically mediated.
Figure 72-3 Axial precontrast T1-weighted magnetic resonance imaging Celiac plexus block is technically more demanding and
shows numerous bright metastases within the liver and vertebral body. should be performed only by clinicians well versed in the
(From Edelman RR, Hesselink JR, Zlatkin MB, etal, editors: Clinical magnetic technique and potential complications.
resonance imaging, 3rd ed, Philadelphia, 2006, Saunders, p 2572.)
72 Liver Pain 211
SUGGESTED READINGS
Goodman CC: Screening for medical problems in patients with upper extremity Tsunekawa K, Matsuda R, Ohgushi N, Ogasawara A: Ohnishi: Basic problems of
signs and symptoms, J Hand Ther 23:105126, 2010. the pain from the gallbladder and liver, Pain 30(Suppl 1):S24, 1987.
Hansen L, Sasaki A, Zucker B: End-stage liver disease: challenges and practice Waldman SW, Feldstein GS, Donohoe CD, Waldman KA: The relief of body
implications, Nurs Clin North Am 45:411426, 2010. wall pain secondary to malignant hepatic metastases by intercostal nerve block
Khoury GF, Stein C, Ramming KP: Neck and shoulder pain associated with with bupivacaine and methylprednisolone, J Pain Symptom Manage 3:3943,
hepatic arterial chemotherapy using an implantable infusion pump, Pain 1988.
32:275277, 1988.
Chapter 73
ABDOMINAL ANGINA
Testing
The diagnosis of abdominal angina is based on clinical history.
Angiography of the celiac artery provides proof of vascular insuf-
ficiency and often identifies the cause of the problem. Barium
enema shows the classic finding of thumbprinting that is strongly
suggestive of mucosal ischemia (Figure 73-2). Colonoscopy reveals
localized hemorrhage and ulceration of the affected mucosa. Based
on the patients clinical presentation, additional tests, including
complete blood cell count, erythrocyte sedimentation rate, and Figure 73-1 Abdominal angina is an uncommon cause of intermittent
stool and blood cultures for infectious enteritis, may be indicated. abdominal pain. Patients with abdominal angina report severe cramping
Given the possibility that the patients abdominal angina is due to abdominal pain that begins 15 to 30 minutes after eating.
212
73 Abdominal Angina 213
B
Figure 73-4 Ischaemic colitis. A, Longitudinal view shows thickened
descending colon with absence of blood flow. The mural stratification is
maintained. B, Transverse view shows diffuse, poorly reflective thicken-
ing (arrow), loss of the mural stratification and absence of blood flow.
Focal area of pneumatosis is seen (arrow) with edema of the paracolic
fat and ascites (arrowhead). (From Allen PL, Baxter GM, Weston MJ: Clini-
cal ultrasound, vol 1, ed 3, New York, 2011, Churchill Livingstone, p 402.)
Chapter 74
EPIDURAL ABSCESS
ICD-9 CODE 324.1 onset may be delayed. As the abscess increases in size, the patient
appears acutely ill, with fever, rigors, and chills. The clinician
may be able to identify neurological findings suggestive of spinal
ICD-10 CODE G06.1 nerve root compression, spinal cord compression, or both. Subtle
findings that point toward the development of myelopathy (e.g.,
Babinskis sign, clonus, and decreased perineal sensation) may be
The Clinical Syndrome overlooked if not carefully sought. As compression of the involved
neural structures continues, the patients neurological status may
Epidural abscess is an uncommon cause of spine pain that, if undi- deteriorate rapidly. If the diagnosis is not made, irreversible motor
agnosed, can result in paralysis and life-threatening complications. and sensory deficit occurs.
Epidural abscess can occur anywhere in the spine and intracranially.
It can occur spontaneously via hematogeneous seeding, most fre-
quently as a result of urinary tract infections that spread to the spinal
Testing
epidural space via Batsons plexus. More commonly, epidural abscess Myelography is still considered the best test to ascertain compro-
occurs after instrumentation of the spine, including surgery and epi- mise of the spinal cord and exiting nerve roots by an extrinsic
dural nerve blocks. The literature suggests that the administration of mass such as an epidural abscess. In this era of readily available
steroids into the epidural space results in immunosuppression, with magnetic resonance imaging (MRI) and high-speed computed
a resultant increase in the incidence of epidural abscess. Although tomography (CT), it may be more prudent to perform this non-
theoretically plausible, the statistical evidencegiven the thousands invasive testing first, rather than wait for a radiologist or spine
of epidural steroid injections performed around the United States on surgeon to perform a myelogram (Figure 74-2). MRI and CT are
a daily basiscalls this belief into question. highly accurate in the diagnosis of epidural abscess and are prob-
A patient with epidural abscess initially presents with ill-defined ably more accurate than myelography in the diagnosis of intrinsic
pain in the segment of the spine affected (e.g., cervical, thoracic, disease of the spinal cord and spinal tumor. All patients suspected
or lumbar) (Figure 74-1). This pain becomes more intense and to have epidural abscess should undergo laboratory testing con-
localized as the abscess increases in size and compresses neural sisting of complete blood cell count, erythrocyte sedimentation
structures. Low-grade fever and vague constitutional symptoms, rate, and automated blood chemistries. Blood and urine cultures
including malaise and anorexia, progress to frank sepsis with should be performed immediately in all patients thought to have
a high-grade fever, rigors, and chills. At this point, the patient epidural abscess to allow immediate implementation of antibiotic
begins to experience sensory and motor deficits and bowel and therapy while the workup is in progress. Gram stains and cultures
bladder symptoms as the result of neural compromise. As the of the abscess material also should be performed, but antibiotic
abscess continues to expand, compromise of the vascular supply to treatment should not be delayed waiting for this information.
the affected spinal cord and nerve occurs with resultant ischemia
and, if untreated, infarction and permanent neurological deficits.
Differential Diagnosis
Signs and Symptoms The diagnosis of epidural abscess should be strongly considered
in any patient with spine pain and fever, especially if the patient
A patient with epidural abscess initially has ill-defined pain in the has undergone spinal instrumentation or epidural nerve blocks for
general area of the infection. At this point, mild pain may occur on either surgical anesthesia or pain control. Other pathological pro-
range of motion of the affected segments. The neurological exami- cesses that must be considered in the differential diagnosis include
nation is within normal limits. A low-grade fever, night sweats, intrinsic disease of the spinal cord, such as demyelinating disease
or both may be present. Theoretically, if the patient has received and syringomyelia, and other processes that can result in compres-
steroids, these constitutional symptoms may be attenuated or their sion of the spinal cord and exiting nerve roots, such as metastatic
215
216 SECTION 8 Lumbar Spine and Sacroiliac Joint Pain Syndromes
Lumbar
vertebrae
Spinal cord
Cauda equina
Dura mater
Epidural
space
Abscess
Figure 74-1 Patients with epidural abscess initially present with ill-defined pain in the affected segment of the spine.
tumor, Pagets disease, and neurofibromatosis. As a general rule, use of CT or MRI guidance. Serial CT or MRI scans are useful
unless the patient has concomitant infection, these diseases are in following the resolution of epidural abscess; scans should be
routinely associated with only back pain and not with fever. repeated immediately at the first sign of negative change in the
patients neurological status.
Treatment
The rapid initiation of treatment of epidural abscess is manda-
Complications and Pitfalls
tory if the patient is to avoid the sequelae of permanent neuro- Failure to diagnose and treat epidural abscess rapidly and accu-
logical deficit or death. The treatment of epidural abscess has rately can result in disaster for the clinician and patient alike. The
two goals: (1) treatment of the infection with antibiotics and (2) insidious onset of neurological deficit associated with epidural
drainage of the abscess to relieve compression on neural struc- abscess can lull the clinician into a sense of false security that can
tures. Because most epidural abscesses are caused by Staphylococcus result in permanent neurological damage to the patient. If epidu-
aureus, antibiotics such as vancomycin that treat staphylococcal ral abscess or other causes of spinal cord compression is suspected,
infection should be started immediately after blood and urine cul- the algorithm shown in Table 74-1 should be followed.
ture samples are taken. Antibiotic therapy can be tailored to the
culture and sensitivity reports as they become available. As men-
tioned, antibiotic therapy should not be delayed while waiting for Clinical Pearls
definitive diagnosis if epidural abscess is being considered as part Delay in diagnosis puts the patient and clinician at tremen-
of the differential diagnosis. dous risk for a poor outcome. The clinician should assume
Antibiotics alone rarely treat an epidural abscess successfully that all patients who present with fever and back pain have
unless the diagnosis is made very early in the course of the disease; an epidural abscess until proved otherwise and should treat
drainage of the abscess is required to effect full recovery. Drainage accordingly. Overreliance on a single negative or equivo-
of the epidural abscess is usually accomplished via decompression cal imaging test is a mistake. Serial CT or MRI scans are
laminectomy and evacuation of the abscess. More recently, inter- indicated should there be any deterioration in the patients
ventional radiologists have been successful in draining epidural neurological status.
abscesses percutaneously using drainage catheters placed with the
74 Epidural Abscess 217
A B C
D E F
Figure 74-2 Sagittal (A and B) and axial (C and D) T2-weighted magnetic resonance imaging (MRI) of discitis at the LF-S1 disk level showing high-
signal-intensity fluid within the disk. High-signal-intensity fluid collections (white arrows) are seen in the epidural space, consistent with abscesses. The
sagittal postcontrast T1-weighted MRI with fat saturation (E and F) show the abscesses as low-signal-intensity areas with only peripheral enhancement
(broken white arrows). (In Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, p 152.)
TABLE 74-1
Algorithm for Evaluation of Spinal Cord Compression Caused by Epidural Abscess
Immediately obtain blood and urine samples for cultures.
Immediately start high-dose antibiotics that cover Staphylococcus aureus.
Immediately order the most readily available spinal imaging technique (computed tomography, magnetic resonance imaging, myelography)
that can confirm the presence of spinal cord compression (e.g., abscess, tumor).
Simultaneously obtain emergency consultation from a spine surgeon.
Continuously and carefully monitor patients neurological status.
If any of the measures listed here are unavailable, arrange emergency transfer of patient to tertiary care center by the most rapidly available
transportation.
Repeat imaging, and obtain repeat surgical consultation if any deterioration occurs in the patients neurological status.
218 SECTION 8 Lumbar Spine and Sacroiliac Joint Pain Syndromes
SUGGESTED READINGS
Bandikatla VB, Rizwan B, Skalimis A, Patel H: Spinal epidural abscess and menin- Recinos PF, Pradilla G, Crompton P, Thai Q-A, Rigamonti D: Spinal epidural
gitis following an epidural catheterisation, Acute Pain 9:3538, 2007. abscess: diagnosis and treatment, Oper Techn Neurosurg 7:188192, 2004.
Esteves Pereira C, Lynch JC: Spinal epidural abscess: an analysis of 24 cases, Surg Rigamonti D, Liem L, Sampath P, et al: Spinal epidural abscess: contemporary
Neurol 63(Suppl 1):S26S29, 2005. trends in etiology, evaluation, and management, Surg Neurol 52:189197, 1999.
Chapter 75
MULTIPLE MYELOMA
ICD-9 CODE 203.0 secondary to hypercalcemia also may be elicited. Anasarca result-
ing from renal failure, if present, is an ominous prognostic sign.
ICD-10 CODE C90.00
Testing
The presence of Bence Jones protein in the urine, anemia, and
The Clinical Syndrome increased M protein on serum protein electrophoresis point
219
220 SECTION 8 Lumbar Spine and Sacroiliac Joint Pain Syndromes
A B C
D E F
Figure 75-2 Elderly patient with low back pain. Anteroposterior (A) and lateral (B) radiographs show a presumed insufficiency fracture of
L2 with minor end-plate collapse of L3. The sagittal T1-weighted (C), T2-weighted (D), and short tau inversion recovery (STIR) (E) magnetic
resonance images acquired a few months later show multilevel vertebral fractures. Diffuse abnormalities of the bone marrow are seen, with
a generally patchy appearance and some rounded areas of high signal intensity on the T2-weighted and STIR images. The appearances are
strongly suspicious for disorders such as plasma cell dyscrasias and other reticuloendothelial disorders. Immunoglobin testing yielded results
positive for myeloma, and a subsequent skeletal survey showed lytic lesions in the skull (F) typical of multiple myeloma. (In Waldman SD,
Campbell RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, p 192.)
strongly to the diagnosis of multiple myeloma. Classic punched-out bony destruction. Magnetic resonance imaging (MRI) is indicated
bone lesions in the skull and spine on plain radiographs are pathog- in any patient thought to have multiple myeloma who exhibits
nomonic for the disease (Figures 75-2 and 75-3). Because little signs of spinal cord compression. Serum creatine testing and auto-
osteoclastic activity is present in patients with multiple myeloma, mated blood chemistries that include serum calcium determina-
radionucleotide bone scanning can be negative in the face of diffuse tions are indicated in all patients with multiple myeloma.
75 Multiple Myeloma 221
PAGETS DISEASE
renal calculi and gout may occur, especially in men with Pagets
ICD-9 CODE 731.1 disease. In less than 1% of patients, a pagetic bone lesion may
transform into a malignant osteosarcoma.
ICD-10 CODE M90.60
Signs and Symptoms
Although the disease is often asymptomatic, pain is the most com-
mon clinical symptom that ultimately leads the clinician to the
The Clinical Syndrome diagnosis of Pagets disease (Figure 76-1). Seemingly minor trauma
Pagets disease is an uncommon cause of back pain that is frequently may cause pathological vertebral compression fractures. Pain on
diagnosed on plain radiographs obtained for other purposes or movement of the affected bones is a common finding on physical
when the patient notices swelling of a long bone. Pagets disease is examination, as is excess bone growth on palpation of the skull and
also known as osteitis deformans, and its cause is unknown. The other affected bones. Neurological findings based on neural com-
incidence of Pagets disease is approximately 2%, with the disease pression secondary to either excessive bone growth or pathological
occurring much less commonly in India, Japan, the Middle East, fracture may be present. Pain on range of motion of the peripheral
and Scandinavia. joints, especially the hip, owing to calcific periarthritis is a common
In the early phase of the disease, resorption of bone occurs, and physical finding in patients with Pagets disease. Hearing loss may
the affected areas become vascular. The resorption phase is followed be noted on physical examination. In rare patients with Pagets
by the formation of new pagetic bone that is laid down in a dense, disease, high-output cardiac failure resulting from increased blood
haphazard fashion. This process of bone resorption and formation flow to new bone may be present.
can be quite active, with the bone turnover rate increased 20 times
above normal. This process results in a characteristic pattern on Testing
plain radiographs that includes areas of bone resorption termed
osteoporosis circumscripta. Areas of new bone formation show an As mentioned previously, Pagets disease is often fortuitously
irregularly widened cortex, with a dense, striated pattern and focal diagnosed when the patient is undergoing radiographic testing
variations in density that reflect the chaotic nature in which the for an unrelated problem, such as intravenous pyelography for
pagetic bone is laid down. renal calculi. The classic radiographic appearance of areas of bone
Although many patients with Pagets disease are asymptom- resorption with surrounding areas of dense, chaotic bone points
atic, and their disease is a fortuitous finding when radiographs are strongly to the diagnosis of Pagets disease. In patients with Pagets
obtained for other reasons, back pain also may occur. It is thought disease, radionucleotide bone scanning can be used to assess the
that the cause of the back pain associated with Pagets disease is extent of the disease because many bone lesions are clinically silent
multifactorial. The pain may be caused by the bone resorption (Figure 76-2). Magnetic resonance imaging (MRI) is indicated in
process itself or distortion of the facet joints as new pagetic bone is any patient thought to have Pagets disease who exhibits signs of
formed. Both of these processes may alter the functional stability spinal cord compression. Serum creatine testing and automated
of the spine and exacerbate preexisting facet arthropathy. blood chemistries, including serum calcium determinations, are
Patients with Pagets disease may experience thickening and indicated in all patients with Pagets disease. Alkaline phosphatase
widening of the long bones or enlargement of the skull resulting levels are elevated, especially during the resorption phase of the
from new bone formation. Rarely, exuberant bone growth at the disease. Given the increased incidence of hearing loss in patients
base of the skull may cause compression of the brainstem, with with Pagets disease, audiometric testing is indicated.
disastrous results. Hearing loss secondary to compression of the
eighth cranial nerve by new bone formation or by direct involve- Differential Diagnosis
ment of the ossicles themselves may occur. Occasionally, exces-
sive bone formation in the dorsal spine may result in spinal cord Numerous other diseases of the bone, including osteoporosis, mul-
compression, which, if untreated, may result in paraplegia. Patho- tiple myeloma, osteopetrosis, and primary and metastatic bone
logical fractures resulting from excessive resorption of the vertebra tumors, can mimic the clinical presentation of Pagets disease.
may occur, with resultant acute back pain. Hip pain secondary to Acromegaly also shares many common clinical signs and symptoms.
calcific periarthritis also may be present. An increased incidence of Metastatic disease from prostate and breast cancer can produce
222
76 Pagets Disease 223
Spine pain
Thickening of
long bones
ICD-9 CODE 733.99 numbness, weakness, and lack of coordination in the extremi-
ties subserved by the spinal segments affected by DISH. Muscle
spasms, back pain, and pain referred to the buttocks are common
ICD-10 CODE M89.30 (Figure 77-1). Occasionally, a patient with DISH experiences
compression of the spinal cord, nerve roots, and cauda equina,
resulting in myelopathy or cauda equina syndrome. DISH is the
The Clinical Syndrome second most common cause of cervical myelopathy after cervical
spondylosis. Patients with lumbar myelopathy or cauda equina
Diffuse idiopathic skeletal hyperostosis (DISH) is a disease of syndrome experience varying degrees of lower extremity weakness
the ligamentous structures of the spine. The cause of DISH is and bowel and bladder symptoms; this represents a neurosurgical
unknown. The hallmark of this disease is confluent ossification of emergency and should be treated as such.
the spinal ligamentous structures that spans at least three spinal
interspaces (Table 77-1). DISH occurs most commonly in the
thoracolumbar spine, but it also can affect the cervical spine, ribs,
Testing
and bones of the pelvis. DISH is diagnosed by plain radiographs. Confluent ossification of
DISH causes stiffness and pain of the cervical and thoracolum- the spinal ligamentous structures spanning at least three interspaces
bar spine. The symptoms are worse on wakening and at night. is pathognomonic for the disease. Disk space height is preserved
When the disease affects the cervical spine, cervical myelopathy in patients with DISH. If myelopathy is suspected, magnetic reso-
may result. If anterior spurring of the cervical spine occurs, dys- nance imaging (MRI) of the spine provides the best information
phagia may result. DISH is a disease of the late fifth and early regarding the status of the spinal cord and nerve roots. MRI is
sixth decades. It also can cause a relative spinal stenosis with highly accurate and helps identify other abnormalities that may
intermittent claudication. It affects men twice as commonly as put the patient at risk for the development of permanent spinal
women. DISH is a disease that affects primarily whites. Patients cord injury (Figure 77-2). In patients who cannot undergo MRI,
with DISH have a higher incidence of diabetes mellitus, hyperten- such as a patient with a pacemaker, computed tomography (CT)
sion, and obesity than the general population. DISH usually is or myelography is a reasonable second choice. Radionucleotide
diagnosed by plain radiographs of the spine. bone scanning and plain radiographs are indicated if fracture or
bony abnormality, such as metastatic disease, is being considered.
Signs and Symptoms Although this testing provides useful neuroanatomical infor-
mation, electromyography and nerve conduction velocity test-
A patient with DISH reports stiffness and pain in the area of ing provide neurophysiological information that can delineate
the affected spinal segments or bone. Patients also may note the actual status of each individual nerve root and the lumbar
plexus. Screening laboratory tests, consisting of complete blood
cell count, erythrocyte sedimentation rate, and automated blood
TABLE 77-1 chemistry testing, should be performed if the diagnosis of DISH
is in question.
Causes of Abnormal Bone Growth in and About the
Axial Skeleton
Seronegative spondyloathropathies
Differential Diagnosis
Acromegaly DISH is a radiographic diagnosis that is supported by a combina-
Charcot neuroarthropathy
tion of clinical history, physical examination, and MRI. Pain syn-
dromes that may mimic DISH include neck and low back strain;
Trauma
bursitis; fibromyositis; inflammatory arthritis; ankylosing spondy-
Degenerative changes litis; and disorders of the spinal cord, roots, plexus, and nerves.
Diffuse idiopathic skeletal hyperostosis Thirty percent of patients with multiple myeloma or Pagets
Abnormal urate deposition disease also have DISH. Screening laboratory tests consisting of
Excessive fluoride intake
complete blood cell count, erythrocyte sedimentation rate, anti-
nuclear antibody testing, human leukocyte antigen (HLA) B-27
Onchronosis antigen screening, and automated blood chemistry testing should
225
226 SECTION 8 Lumbar Spine and Sacroiliac Joint Pain Syndromes
Figure 77-1 Patients with DISH report stiffness and pain in the area of
the affected spinal segments or bone. They also may note numbness,
weakness, and lack of coordination in the extremities subserved by the to paraparesis or paraplegia. Electromyography helps distinguish
spinal segments affected by DISH. Muscle spasms, back pain, and pain
referred to the buttocks are common.
between plexopathy from radiculopathy and helps identify coex-
istent entrapment neuropathy, which may confuse the diagnosis.
SPONDYLOLISTHESIS
ICD-9 CODE 756.12 imaging (MRI) of the lumbar spine provides the best information
regarding the contents of the lumbar spine (Figure 78-3). MRI is
highly accurate and helps identify abnormalities that may put the
ICD-10 CODE Q76.2 patient at risk for the development of lumbar myelopathy, such as
the trefoil spinal canal of congenital spinal stenosis (Figure 78-4).
In patients who cannot undergo MRI, such as patients with pace-
The Clinical Syndrome makers, computed tomography (CT) and myelography are rea-
sonable second choices. Radionucleotide bone scanning and plain
Spondylolisthesis is a degenerative disease of the lumbar spine that radiographs are indicated if fracture or bony abnormality, such as
results in pain and functional disability. It occurs more commonly metastatic disease, is being considered.
in women and is most often seen after age 40. This disease is caused Although this testing provides useful neuroanatomical infor-
by the slippage of one vertebral body onto another as a result of mation, electromyography and nerve conduction velocity testing
degeneration of the facet joints and intervertebral disk. Usually, provide neurophysiological information that can delineate the
the upper vertebral body moves anteriorly relative to the vertebral actual status of each individual nerve root and the lumbar plexus.
body below it, which causes narrowing of the spinal canal. This Screening laboratory tests, consisting of complete blood cell count,
narrowing results in a relative spinal stenosis and back pain. Occa- erythrocyte sedimentation rate, and automated blood chemistry
sionally, the upper vertebral body slides posteriorly relative to the
vertebral body below it, which compromises the neural foramina.
Clinically, a patient with spondylolisthesis reports back pain
with lifting, twisting, or bending of the lumbar spine. Patients
may state that they feels like they have a catch in their back.
Patients with spondylolisthesis often report radicular pain of the
lower extremity and often experience pseudoclaudication with
walking. Rarely, the slippage of the vertebra is so extreme that
myelopathy or cauda equina syndrome develops.
Testing
Plain radiographs of the lumbar spine usually are sufficient to Figure 78-1 Patients with spondylolisthesis often report back pain with
diagnose spondylolisthesis (Figure 78-2). The lateral view shows motion of the lumbar spine. Rising from a sitting to a standing position
the slippage of one vertebra onto another. Magnetic resonance often reproduces the pain.
227
228 SECTION 8 Lumbar Spine and Sacroiliac Joint Pain Syndromes
L4
testing, should be performed if the diagnosis of spondylolisthesis Figure 78-3 Spondylolisthesis. Grade II spondylolisthesis of L4 on L5.
is in question. This leads to the false impression of L4-5 disk herniation. The posterior
disk margin has not extended beyond the L5 vertebral margin (arrows),
however. (From Haaga JR, Lanzieri CF, Gilkeson RC, editors: Computed
Differential Diagnosis tomography and magnetic resonance imaging of the whole body, ed 4,
St Louis, 2003, Mosby, p 732.)
Spondylolisthesis is a radiographic diagnosis that is supported by a
combination of clinical history, physical examination, radiography,
and MRI. Pain syndromes that may mimic spondylolisthesis include treated with a tricyclic antidepressant compound, such as nortrip-
lumbar radiculopathy; low back strain; lumbar bursitis; lumbar fibro- tyline, which can be started at a single bedtime dose of 25 mg.
myositis; inflammatory arthritis; and disorders of the lumbar spinal
cord, roots, plexus, and nerves. MRI of the lumbar spine should be
performed in all patients thought to have spondylolisthesis. Screening
Complications and Pitfalls
laboratory tests consisting of complete blood cell count, erythrocyte Failure to diagnose spondylolisthesis accurately may put the
sedimentation rate, antinuclear antibody testing, human leukocyte patient at risk for the development of lumbar myelopathy, which,
antigen (HLA) B-27 antigen screening, and automated blood chem- if untreated, may progress to paraparesis or paraplegia. Electro-
istry testing should be performed if the diagnosis of spondylolisthesis myography helps distinguish plexopathy from radiculopathy and
is in question to help rule out other causes of pain. helps identify coexistent entrapment neuropathy, such as tarsal
tunnel syndrome, which can confuse the diagnosis.
Treatment
Spondylolisthesis is best treated with a multimodality approach. Clinical Pearls
Physical therapy, including flexion exercises, heat modalities, The diagnosis of spondylolisthesis should be considered in
and deep sedative massage, combined with nonsteroidal anti- any patient reporting back pain, radicular pain, or both or
inflammatory drugs (NSAIDs) and skeletal muscle relaxants repre- symptoms of pseudoclaudication. Patients with symptoms
sents a reasonable starting point. The addition of steroid epidural of myelopathy should undergo MRI on an urgent basis.
nerve blocks is a reasonable next step. Caudal or lumbar epidural Physical therapy may help prevent recurrent episodes of
blocks with a local anesthetic and steroid have been shown to be pain, but, ultimately, surgical stabilization of the affected
extremely effective in the treatment of pain secondary to spondy- segments may be required.
lolisthesis. Underlying sleep disturbance and depression are best
78 Spondylolisthesis 229
SUGGESTED READINGS
Agabegi SA, Fischgrund JS: Contemporary management of isthmic spondylolis-
thesis: pediatric and adult, Spine J 10:530543, 2010.
Butt S, Saifuddin A: The imaging of lumbar spondylolisthesis, Clin Radiol
60:533546, 2005.
Denard PJ, Holton KF, Miller J, etal: Lumbar spondylolisthesis among elderly
men: prevalence, correlates and progression, Spine 35:10721078, 2010.
Denard PJ, Holton KF, Miller J, etal: Osteoporotic Fractures in Men (MrOS)
Study Group: Back pain, neurogenic symptoms, and physical function in rela-
tion to spondylolisthesis among elderly men, Spine J 10:865873, 2010.
L4
B
Figure 78-4 Congenital spinal stenosis. A 12-year-old boy developed
leg numbness and pain after a soccer game. A, Sagittal T2-weighted
magnetic resonance imaging shows progressive narrowing of the sagit-
tal dimension of the lumbar spinal canal from the upper to lower lev-
els. B, On an axial proton densityweighted image at L4, short stubby
pedicles are the primary cause of small lateral recesses and congenital
spinal stenosis. (From Edelman RR, Hesselink JR, Zlatkin MB, etal, editors:
Clinical magnetic resonance imaging, ed 3, Philadelphia, 2006, Saunders,
p 2227.)
Chapter 79
ANKYLOSING SPONDYLITIS
ICD-9 CODE 720.0 the knee. Spinal fracture with resultant spinal cord injury may
occur as a result of the rigid and inflexible nature of the spine.
Anterior uveitis manifests with photophobia, decreased visual acu-
ICD-10 CODE M45.9 ity, and excessive lacrimation and represents an ophthalmological
emergency.
Spine
Ilium
Sacroiliac
joint
Sacrum
Greater
trochanter
Figure 79-1 Patients with ankylosing spondylitis often report back and sacroiliac pain and stiffness that are worse in the morning and after periods
of prolonged activity.
Treatment
Ankylosing spondylitis is best treated with a multimodality
approach. Physical therapy, including exercises to maintain func-
tion, heat modalities, and deep sedative massage, combined with
nonsteroidal anti-inflammatory drugs (NSAIDs) and skeletal mus-
cle relaxants represents a reasonable starting point. Sulfasalazine Figure 79-3 Lateral radiograph of the lumbar spine with squaring of the
may be useful in managing the arthritis associated with the disease. vertebral bodies, which is typical of early ankylosing spondylitis. Gener-
The addition of steroid epidural nerve blocks is a reasonable next alized osteopenia and early inflammatory arthropathy of the lower facet
step. Caudal or lumbar epidural blocks with a local anesthetic and joints are seen. (From Waldman SD: Seronegative spondyloarthropathy. In
steroid have been shown to be extremely effective in the treatment Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011,
Saunders, pp 141144.)
of pain secondary to ankylosing spondylitis. Underlying sleep dis-
turbance and depression are best treated with a tricyclic antide-
pressant compound, such as nortriptyline, which can be started at
232 SECTION 8 Lumbar Spine and Sacroiliac Joint Pain Syndromes
Figure 79-4 Ankylosing spondylitis. Parasagittal and sagittal T1-weighted images show extensive L2-L3 discovertebral erosion and associated marrow
edema and a posterior neural arch pseudofracture that is depicted as a horizontal dark signal abnormality (arrows). Note the presence of a prevertebral
inflammatory mass. Magnetic resonance imaging findings are indistinguishable from the findings of infectious spondylodiscitis. Plain film radiographs
showing characteristic findings of ankylosing spondylitis and clinical history are useful for differentiating the two entities. (From Edelman RR, Hesselink
JR, Zlatkin MB, etal, editors: Clinical magnetic resonance imaging, 3rd ed, Philadelphia, 2006, Saunders, p 2346.)
TABLE 79-1
disability. Myelopathy, which may progress to paraplegia or quad-
riplegia, is a serious problem if diagnosis is delayed. Electromyog-
Common Causes of Sacroilitis-Related Pain raphy helps distinguish plexopathy from radiculopathy and helps
Psoriatic arthritis identify coexistent entrapment neuropathy, such as tarsal tunnel
Reiters syndrome syndrome, which confuse the diagnosis.
Septic arthritis
Ulcerative colitis
Crohns disease
Clinical Pearls
Synovitis-acne-pustulosis hyperostosis-osteomyelitis (SAPHO) The diagnosis of ankylosing spondylitis should be consid-
syndrome ered in any patient reporting back or sacroiliac pain and
Seronegative arthropathies, including ankylosing spondylitis stiffness that are worse in the morning or after prolonged
Tuberculosis periods of inactivity. Patients with symptoms of myelopathy
should undergo MRI on an urgent basis. Physical therapy
Intestinal bypassinduced arthritis
combined with NSAIDs may help prevent recurrent epi-
Sarcoidosis sodes of pain and help preserve function.
Whipples disease
Brucellosis
Hyperparathyroidism
SUGGESTED READINGS
Joseph A, Brasington R, Kahl L, etal: Immunologic rheumatic disorders, J Allergy
a single bedtime dose of 25 mg. Acute uveitis should be managed Clin Immunol 125(Suppl 2):S204S215, 2010.
with corticosteroids and mydriatic agents. Mansour M, Cheema GS, Naguwa SM, et al: Ankylosing spondylitis: a con-
temporary perspective on diagnosis and treatment, Semin Arthritis Rheum
36:210223, 2007.
Complications and Pitfalls Reveille JD, Arnett FC: Spondyloarthritis: update on pathogenesis and management,
Am J Med 118:592603, 2005.
Failure to diagnose ankylosing spondylitis accurately may put Waldman SD: Seronegative spondyloarthropathy. In Waldman SD, Campbell
the patient at risk for the development of significant functional RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 141144.
Chapter 80
ICD-9 CODE 355.9 bony pathological processes. Based on the patients clinical presen-
tation, additional testing may be warranted, including a complete
blood count, uric acid level, erythrocyte sedimentation rate, and
ICD-10 CODE G58.9 antinuclear antibody testing. Magnetic resonance imaging (MRI)
of the back is indicated if herniated disk, spinal stenosis, or space-
occupying lesion is suspected. The injection technique described
The Clinical Syndrome later serves as both a diagnostic and therapeutic maneuver.
Entrapped, inflamed,
and flattened
cluneal nerves
Gluteus medius
Gluteus maximus
Figure 80-1 Distribution of the superior cluneal nerves as they pass over the posterior iliac crest and provide cutaneous innervation of the buttocks.
The medial superior cluneal nerve is shown crossing the iliac crest 7 cm from midline. The wearing of low-cut jeans with tight waistbands or wide
belts can compress the nerve and exacerbate the symptoms of superior cluneal nerve entrapment.
ICD-9 CODE 724.2 and bending may result in the development of myofascial pain in
the muscles of the back. Myofascial pain syndrome is a chronic
pain syndrome that affects a focal or regional portion of the body.
ICD-10 CODE M54.5 The sine qua non of myofascial pain syndrome is the finding
of myofascial trigger points on physical examination. Although
these trigger points are generally localized to the regional part of
The Clinical Syndrome the body affected, the pain of myofascial pain syndrome often is
referred to other areas. This referred pain often is misdiagnosed or
The muscles of the back work together as a functional unit to attributed to other organ systems, leading to extensive evaluations
stabilize and allow coordinated movement of the low back and and ineffective treatment. Patients with myofascial pain syndrome
allow maintaining an upright position. Trauma to an individual involving the muscles of the low back often have referred pain into
muscle can result in dysfunction of the entire functional unit. the hips, sacroiliac joint, and buttocks.
The rhomboids, latissimus dorsi, iliocostalis quadratus lumbo-
rum, multifidus, and psoas muscles are frequent sites of myo-
fascial pain syndrome. The points of origin and attachments of
Signs and Symptoms
these muscles are particularly susceptible to trauma and the sub- The trigger point is the pathognomonic lesion of myofascial pain
sequent development of myofascial trigger points (Figure 81-1). and is thought to be the result of microtrauma to the affected
Injection of these trigger points serves as a diagnostic and thera- muscles. This pathological lesion is characterized by a local point
peutic maneuver. of exquisite tenderness in affected muscle. Mechanical stimulation
The muscles of the back are particularly susceptible to the devel- of the trigger point by palpation or stretching produces not only
opment of myofascial pain syndrome. Flexion/extension injuries intense local pain, but also referred pain. In addition to this local
to the back or repeated microtrauma secondary to improper lifting and referred pain, an involuntary withdrawal of the stimulated
Multifidus m.
Figure 81-1 Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body.
235
236 SECTION 8 Lumbar Spine and Sacroiliac Joint Pain Syndromes
muscle often occurs that is called a jump sign. This jump sign also spondylolisthesis also may mimic the clinical presentation of lum-
is characteristic of myofascial pain syndrome. bar myofascial pain syndrome.
Taut bands of muscle fibers often are identified when myo-
fascial trigger points are palpated. Despite this consistent physi-
cal finding in patients with myofascial pain syndrome, the
Treatment
pathophysiology of the myofascial trigger point remains elusive, Lumbar myofascial pain syndrome is best treated with a multi-
although many theories have been advanced. Common to all modality approach. Physical therapy, including correction of
of these theories is the belief that trigger points are the result of functional abnormalities (e.g., poor posture, improper chair or
microtrauma to the affected muscle. This microtrauma may occur computer height) and the use of heat modalities and deep sedative
as a single injury to the affected muscle or as the result of repeti- massage, combined with nonsteroidal anti-inflammatory drugs
tive microtrauma or chronic deconditioning of the agonist and (NSAIDs) and skeletal muscle relaxants represents a reasonable
antagonist muscle unit. starting point. If these treatments fail to provide rapid symptomatic
In addition to muscle trauma, a variety of other factors seem relief, local trigger point injection of anesthetic and steroid into the
to predispose to development of myofascial pain syndrome. The myofascial trigger point area is a reasonable next step. Underlying
weekend athlete who subjects his or her body to unaccustomed diffuse muscle pain and sleep disturbance and depression are best
physical activity often develops myofascial pain syndrome. Poor treated with a tricyclic antidepressant compound, such as nortrip-
posture while sitting at a computer keyboard or watching television tyline, which can be started at a single bedtime dose of 25 mg.
has been implicated as a predisposing factor to the development of When performing trigger point injections, careful prepara-
myofascial pain syndrome. Previous injuries may result in abnormal tion of the patient before injection helps optimize results. Trigger
muscle function and predispose to the subsequent development of point injections are directed at the primary trigger point, rather
myofascial pain syndrome. All of these predisposing factors may be than the area of referred pain. It should be explained to the patient
intensified if the patient also has poor nutritional status or coex- that the goal of trigger point injection is to block the trigger of the
isting psychological or behavioral abnormalities, including chronic persistent pain and, it is hoped, provide long-lasting relief. It is
stress and depression. The muscles of the low back seem to be par- important that the patient understand that for most patients with
ticularly susceptible to stress-induced myofascial pain syndrome. myofascial pain syndrome, more than one treatment modality is
Stiffness and fatigue often coexist with the pain of myofascial required to provide optimal pain relief. The use of the prone or
pain syndrome, increasing the functional disability associated with lateral position when identifying and marking trigger points and
this disease and complicating its treatment. Myofascial pain syn- when performing the actual trigger point injection helps decrease
drome may occur as a primary disease state or may occur in con- the incidence of vasovagal reactions. The skin overlying the trig-
junction with other painful conditions, including radiculopathy ger point to be injected should always be prepared with antiseptic
and chronic regional pain syndromes. Psychological or behavioral solution before injection to avoid infection.
abnormalities, including depression, frequently coexist with the After the goals of trigger point injection are explained to the
muscle abnormalities associated with myofascial pain syndrome. patient and proper preparation of the patient has been carried out,
Treatment of these psychological and behavioral abnormalities the trigger point to be injected is reidentified by palpation with a
must be an integral part of any successful treatment plan for myo- sterile gloved finger (Figure 81-2). A syringe containing 10 mL of
fascial pain syndrome.
Testing
No specific test exists for lumbar myofascial pain syndrome. Test-
ing is aimed primarily at identifying occult pathology or other
Trapezius m. Erector spinae m.
diseases that may mimic myofascial pain syndrome (see discussion
of differential diagnosis). Plain radiographs help delineate bony
abnormality of the lumbar spine, including arthritis, fracture,
congenital abnormalities (e.g., trefoil spinal canal), and tumor. All
patients with recent onset of myofascial pain syndrome should
undergo magnetic resonance imaging (MRI) of the lumbar spine
to rule out occult pathological processes. Screening laboratory
tests, consisting of complete blood count, erythrocyte sedimen-
tation rate, antinuclear antibody testing, and automated blood
Latissimus dorsi m. Serratus posterior m.
chemistry testing, should be performed to rule out occult inflam-
matory arthritis, infection, and tumor. Trigger points
Differential Diagnosis
Lumbar myofascial pain syndrome is a clinical diagnosis of exclu-
sion that is supported by a combination of clinical history, physi-
cal examination, radiography, and MRI. Pain syndromes that
may mimic lumbar myofascial pain syndrome include lumbar Carrico & Shavell
strain, inflammatory arthritis, and disorders of the lumbar spi- Figure 81-2 Injection technique to relieve lumbar myofascial pain.
nal cord, roots, plexus, and nerves. Congenital abnormalities, (From Waldman SD: Atlas of pain management injection techniques, ed
such as arteriovenous malformations and trefoil spinal canal, and 2, Philadelphia, 2007, Saunders, p 330.)
81 Lumbar Myofascial Pain Syndrome 237
Clinical Pearls
Trigger point injections are an extremely safe procedure if
careful attention is paid to the clinically relevant anatomy in
the areas to be injected. Care must be taken to use sterile tech-
nique to avoid infection and universal precautions to avoid
risk to the operator. Most side effects of trigger point injec-
tion are related to needle-induced trauma to the injection
site and underlying tissues. The incidence of ecchymosis and
hematoma formation can be decreased if pressure is placed
on the injection site immediately after trigger point injec-
tion. The avoidance of overly long needles helps decrease the
incidence of trauma to underlying structures. Special care
must be taken to avoid pneumothorax when injecting trig-
ger points in proximity to the underlying pleural space.
Antidepressant compounds are the primary pharmaco-
logical treatment for myofascial pain syndrome. Tricyclic
antidepressants are thought to be more effective than selec-
tive serotonin reuptake inhibitors in the treatment of this
painful condition. The precise mechanism of action of anti-
depressant compounds in the treatment of myofascial pain
syndrome is unknown. Some investigators believe that the
primary effect of this class of drugs is to treat the underlying
depression that is present in many patients with myofascial
pain syndrome. Drugs such as amitriptyline and nortrip-
tyline represent good first choices and should be given as a
single bedtime dose, starting with 10 to 25 mg and titrating
upward as side effects allow.
SECTION 9 Pelvic Pain Syndromes
Chapter 82
PROCTALGIA FUGAX
Rectum
Anal canal
Figure 82-1 The pain of proctalgia fugax is sharp or gripping and severe. Increased stress and sitting for prolonged periods can increase the
frequency and intensity of attacks.
PROSTATODYNIA
ICD-9 CODE 608.9 neuropathy can occur after radiation therapy for the treatment of
malignancy of the prostate and rectum and can mimic the pain of
prostatodynia.
ICD-10 CODE R10.2
Testing
The Clinical Syndrome Digital examination of the prostate is the cornerstone of the
diagnosis of patients with prostatodynia. Careful examination
Prostatodynia is an uncommon cause of perineal pain in men. for tenderness, nodules, or tumor is crucial to avoid overlooking
Also known as chronic nonbacterial prostatitis and chronic pel- prostatic malignancy. Ultrasound examination of the prostate is
vic pain syndrome, prostatodynia probably is not a single clini- indicated in all patients with prostatodynia. If any question of
cal entity, but rather the conglomeration of a variety of disorders occult malignancy of the prostate or pelvic contents exists, mag-
that can cause pain in this anatomical region. Included in these netic resonance imaging (MRI) or computed tomography (CT) of
disorders are chronic infections of the prostate, chronic inflam- the pelvis is mandatory, as is laboratory determination of prostate-
mation of the prostate without demonstrable infection, bladder specific antigen level (Figure 83-2). Acute infection of the pros-
outflow abnormalities, pelvic floor muscle disorders, reflex sym- tate can elevate the prostate-specific antigen level. Urinalysis to
pathetic dystrophy, and psychogenic causes. All have in common rule out urinary tract infection is indicated in all patients with
the ability to cause chronic, ill-defined perineal pain, which is the prostatodynia. The role of laboratory examination of postpros-
hallmark of prostatodynia. tatic massage prostatic fluid in the evaluation of prostatodynia is
The pain of prostatodynia is characterized by dull, aching, unclear, although anecdotal reports exist of the consistent finding
or burning pain of the perineum and underlying structures of an elevated uric acid level in the prostatic fluid of patients with
(Figure 83-1). The intensity of pain is mild to moderate and prostatodynia.
may worsen with urination or sexual activity. The pain may be Electromyography helps distinguish radiation neuropathy
referred to the penis, testicles, scrotum, or inner thigh. Irritative from lumbar plexopathy or lumbar radiculopathy. Based on the
urinary outflow symptoms and sexual dysfunction often coex- patients clinical presentation, additional tests, including com-
ist with the pain of prostatodynia. The history of all patients plete blood cell count, uric acid, erythrocyte sedimentation rate,
with chronic prostatodynia should include specific questioning and antinuclear antibody testing, may be indicated. MRI of the
regarding a history of sexual abuse. lumbar plexus is indicated if tumor or hematoma is suspected.
Sitz bath
Prostate
Urethra
Penis
Testicle
Scrotum
Figure 83-1 The pain of prostatodynia is characterized by dull, aching, or burning pain of the perineum and underlying structures.
Figure 83-3 Prostate cancer (arrows) infiltrating and displacing the nor-
mal high signal intensity peripheral zone. The fibrous prostate capsule
is intact, separating the cancer from the high signal intensity lateral
periprostatic venous plexus. (From Stark DD, Bradley WG Jr: Magnetic
Figure 83-2 Coronal T2-weighted magnetic resonance imaging of resonance imaging, 3rd ed, St Louis, 1999, Mosby, p 626.)
the prostate in a patient with a prostate-specific antigen level of 9.2,
Gleason cancer score of 7 on biopsy, and organ-confined disease on
digital rectal examination. The patient was being assessed for radical An arbitrary treatment course of antibiotics, such as doxycycline
prostatectomy. Low T2 signal intensity is seen extending into the left 100 mg twice daily for 2 weeks, may be worth trying, even though
seminal vesicle (arrow), consistent with T3B disease. In view of this urine cultures are negative. Anecdotal reports of decreased pain
unequivocal finding, the patient opted to undergo radiation treat-
ment instead of surgery. (From Edelman RR, Hesselink JR, Zlatkin MB,
after treatment with allopurinol make this drug a consideration
etal, editors: Clinical magnetic resonance imaging, 3rd ed, Philadel- for patients who continue to have pain. For patients who do not
phia, 2006, Saunders, p 2925.) respond to these treatment modalities, caudal epidural nerve
83 Prostatodynia 243
TABLE 83-1
Distinguishing Features of Prostate Syndromes
Prostatic Fluid
Prostate Response to Impaired
Syndrome Confirmed UTI Examination WBC Culture Antibiotics Urinary Flow
Acute bacterial Yes Tender, warm Yes Yes Yes Yes
prostatitis
Chronic bacterial Usually Varied Yes Yes Slow
prostatitis
Nonbacterial No Varied Yes No Poor
prostatitis
Prostatodynia No Usually normal No No No Yes
From Lummus WE, Thompson I: Prostatitis, Emerg Med Clin North Am 19:691707, 2001.
UTI, Urinary tract infection.
blocks with a local anesthetic and steroid may be a reasonable next SUGGESTED READINGS
step. Psychological evaluation and interventions should occur Lummus WE, Thompson I: Prostatitis, Emerg Med Clin North Am 19:691707,
concurrently with the aforementioned treatment modalities, given 2001.
the high incidence of coexistent psychological issues associated Rarbalias GA: Prostatodynia or painful male urethral syndrome? Urology
36:146153, 1990.
with all pelvic pain syndromes. Turner JA, Hauge S, Von Korff M, et al: Primary care and urology patients
with the male pelvic pain syndrome: symptoms and quality of life, J Urol
Complications and Pitfalls 167:17681773, 2002.
Wesselmann U, Burnett AL, Heinberg LJ: The urogenital and rectal pain
The major pitfalls in the care of a patient with prostatodynia are syndromes, Pain 73:269294, 1997.
threefold: (1) the misdiagnosis of extraprostate pathological pro-
cesses responsible for the patients pain, (2) the failure to identify
prostate malignancy, and (3) the failure to address the psychologi-
cal issues surrounding the patients pain.
Clinical Pearls
The clinician should be aware that the relationship of the
genitalia to the male psyche presents some unique chal-
lenges for the clinician treating patients with prostatodynia.
The behavioral and psychological issues must be addressed
concurrently with the medical issues if treatment is to be
successful. The possibility for prostate malignancy is ever
present and should be carefully sought in all patients with
prostatodynia.
Chapter 84
syndrome may occur as a primary disease state or may occur in testing, and automated blood chemistry testing, should be per-
conjunction with other painful conditions, including radiculopa- formed to rule out occult inflammatory arthritis, infection, and
thy and chronic regional pain syndromes. Psychological or behav- tumor.
ioral abnormalities, including depression, frequently coexist with
the muscle abnormalities associated with myofascial pain syn-
drome. Treatment of these psychological and behavioral abnor-
Differential Diagnosis
malities must be an integral part of any successful treatment plan Gluteus maximus pain syndrome is a clinical diagnosis of exclu-
for myofascial pain syndrome. sion supported by a combination of clinical history, physical
examination, radiography, and MRI. Pain syndromes that may
mimic gluteus maximus pain syndrome include lumbosacral
Signs and Symptoms radiculopathy and plexopathy, stress fractures of the pelvis and
The trigger point is the pathognomonic lesion of myofascial pain hip, muscle strain, inflammatory arthritis, and disorders of the
and is thought to be the result of microtrauma to the affected lumbar spinal cord, roots, plexus, and nerves. Intrapelvic tumors
muscles. This pathological lesion is characterized by a local point also may mimic the clinical presentation of gluteus maximus pain
of exquisite tenderness in affected muscle. Mechanical stimulation syndrome.
of the trigger point by palpation or stretching produces not only
intense local pain but also referred pain. In addition to this local
and referred pain, an involuntary withdrawal of the stimulated
Treatment
muscle, termed the jump sign, often occurs. The jump sign also is Gluteus maximus pain syndrome is best treated with a multi-
characteristic of myofascial pain syndrome. Patients with gluteus modality approach. Physical therapy, including correction of
maximus pain syndrome exhibit trigger points in the medial and functional abnormalities (e.g., poor posture, improper chair or
lower aspects of the muscle that are referred across the buttocks computer height) and the use of heat modalities and deep sedative
and into the coccygeal area. massage, combined with nonsteroidal anti-inflammatory drugs
(NSAIDs) and skeletal muscle relaxants, represents a reasonable
starting point. If these treatments fail to provide rapid symptom-
Testing atic relief, local trigger point injection of local anesthetic and ste-
No specific test exists for gluteus maximus pain syndrome. Testing roid into the myofascial trigger point area is a reasonable next step.
is aimed primarily at identifying occult pathological conditions or Underlying diffuse muscle pain and sleep disturbance and depres-
other diseases that may mimic myofascial pain syndrome (see dis- sion are best treated with a tricyclic antidepressant compound,
cussion of differential diagnosis). Plain radiographs help delineate such as nortriptyline, which can be started at a single bedtime
bony abnormality of the pelvis and hip, including arthritis, avas- dose of 25 mg.
cular necrosis of the hip, fracture, congenital abnormalities, and When performing trigger point injections, careful prepara-
tumor. All patients with the recent onset of myofascial pain syn- tion of the patient before trigger point injection helps optimize
drome should undergo magnetic resonance imaging (MRI) of the results. Trigger point injections are directed at the primary trig-
lumbar spine and pelvis to rule out occult pathological processes ger point, rather than in the area of referred pain. It should be
(Figure 84-3). Screening laboratory tests, consisting of complete explained to the patient that the goal of trigger point injection is
blood count, erythrocyte sedimentation rate, antinuclear antibody to block the trigger of the persistent pain and, it is hoped, provide
Trigger point
Referred pain
Gluteus maximus m.
Figure 84-2 Injection technique to relieve gluteus maximus pain. (From Waldman SD: Atlas of pain management injection techniques, 2nd ed, Phila-
delphia, 2007, Saunders, p 379.)
246 SECTION 9 Pelvic Pain Syndromes
A B
Figure 84-3 Gluteal intramuscular hematoma. A, Axial T1-weighted magnetic resonance imaging. Subacute left gluteal region hematoma manifests
as a hyperintense rim, consistent with the presence of methemoglobin. B, Axial T2-weighted image. The left gluteal hematoma exhibits a hyper-
intense signal pattern. (From Edelman RR, Hesselink JR, Zlatkin MB, et al, editors: Clinical magnetic resonance imaging, 3rd ed, Philadelphia, 2006,
Saunders, p 3387.)
SUGGESTED READINGS Marsh M: Milnacipran. The comprehensive pharmacology reference, Philadelphia, 2008,
Elsevier, pp 14.
Arnold LM: The pathophysiology, diagnosis and treatment of fibromyalgia, Waldman SD: Atlas of pain management injection techniques, Philadelphia, 2007,
Psychiatr Clin North Am 33:375408, 2010. Saunders, pp 378380.
Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30,
2009.
Imamura M, Cassius DA, Fregni F: Fibromyalgia: from treatment to rehabilita-
tion, Eur J Pain Suppl 3:117122, 2009.
Chapter 85
ICD-9 CODE 729.1 are localized to the regional part of the body affected, the pain
of myofascial pain syndrome often is referred to other anatomi-
cal areas. This referred pain often is misdiagnosed or attributed
ICD-10 CODE M79.7 to other organ systems, thereby leading to extensive evaluations
and ineffective treatment. Patients with myofascial pain syndrome
involving the gluteus medius often have primary pain along the
The Clinical Syndrome posterior iliac crest that is referred down the buttocks across the
sacroiliac joint and into the posterior lower extremity.
The gluteus medius muscles primary function is as a hip abduc- The trigger point is the pathognomonic lesion of myofascial
tor, and the muscle also assists in medial and lateral rotation of the pain and is thought to be the result of microtrauma to the affected
hip. The gluteus medius muscle finds its origin at the dorsal ilium muscles. This pathological lesion is characterized by a local point
just below the iliac crest. The gluteus medius muscle is susceptible of exquisite tenderness in affected muscle. Mechanical stimulation
to the development of myofascial pain syndrome. Such pain most of the trigger point by palpation or stretching produces not only
often occurs as a result of repetitive microtrauma to the muscle intense local pain but also referred pain. In addition to this local
from activities such as running on soft surfaces and overuse of and referred pain, often an involuntary withdrawal of the stimu-
exercise equipment or other repetitive activities that require hip lated muscle, termed a jump sign, occurs. The jump sign also is
abduction (Figure 85-1). Blunt trauma to the muscle may also characteristic of myofascial pain syndrome. Patients with gluteus
incite gluteus medius myofascial pain syndrome. medius syndrome will exhibit a trigger point along the posterior
Myofascial pain syndrome is a chronic pain syndrome that iliac crest.
affects a focal or regional portion of the body. The sine qua non of Taut bands of muscle fibers often are identified when myo-
myofascial pain syndrome is the finding of myofascial trigger points fascial trigger points are palpated. In spite of this consistent
on physical examination. Although these trigger points generally physical finding in patients with myofascial pain syndrome, the
pathophysiology of the myofascial trigger point remains elusive,
although many theories have been advanced. Common to all
of these theories is the belief that trigger points are the result of
microtrauma to the affected muscle. This microtrauma may occur
as a single injury to the affected muscle or as the result of repeti-
tive microtrauma or chronic deconditioning of the agonist and
antagonist muscle unit.
In addition to muscle trauma, a variety of other factors seem to
predispose the patient to develop myofascial pain syndrome. The
weekend athlete who subjects his or her body to unaccustomed
physical activity often may develop myofascial pain syndrome.
Poor posture while sitting at a computer keyboard or while watch-
ing television also has been implicated as a predisposing factor
to the development of myofascial pain syndrome. Previous inju-
ries may result in abnormal muscle function and predispose to
the subsequent development of myofascial pain syndrome. All of
these predisposing factors may be intensified if the patient also has
poor nutritional status or coexisting psychological or behavioral
abnormalities, including chronic stress and depression. The glu-
teus medius muscle seems to be particularly susceptible to stress-
induced myofascial pain syndrome.
Stiffness and fatigue often coexist with the pain of myofas-
cial pain syndrome, increasing the functional disability associ-
Figure 85-1 Gluteus medius syndrome usually results from repetitive
microtrauma to the muscle during such activities as running on soft
ated with this disease and complicating its treatment. Myofascial
surfaces, overuse of exercise equipment, or other repetitive activities pain syndrome may occur as a primary disease state or in con-
that require hip extension. junction with other painful conditions, including radiculopathy
248
85 Gluteus Medius Syndrome 249
and chronic regional pain syndromes. Psychological or behavioral patient thought to have gluteus medius syndrome. It is incumbent
abnormalities, including depression, frequently coexist with the on the clinician to rule out other coexisting disease processes that
muscle abnormalities associated with myofascial pain syndrome. may mimic gluteus medius syndrome, including primary inflam-
Treatment of these psychological and behavioral abnormalities matory muscle disease, primary hip pathological processes, glu-
must be an integral part of any successful treatment plan for myo- teal bursitis, and superior cluneal and gluteal nerve entrapment
fascial pain syndrome. (Figure 85-2). The use of electrodiagnostic and radiographic test-
ing can identify coexisting pathological conditions such as rectal
Signs and Symptoms or pelvic tumors or lumbosacral nerve lesions. The clinician must
also identify coexisting psychological and behavioral abnormali-
The trigger point is the pathological lesion of gluteus medius syn- ties that may mask or exacerbate the symptoms associated with
drome, and it is characterized by a local point of exquisite ten- gluteus medius syndrome.
derness in gluteus medius muscle. Mechanical stimulation of the
trigger point by palpation or stretching produces both intense
local pain in the medial and lower aspects of the muscle and
Treatment
referred primary pain along the posterior iliac crest that is referred Treatment is focused on eliminating the myofascial trigger and
down the buttocks across the sacroiliac joint and into the posterior achieving relaxation of the affected muscle. It is hoped that inter-
lower extremity. In addition, the jump sign is often present. rupting the pain cycle in this way will allow the patient to obtain
prolonged pain relief. The mechanism of action of the treatment
modalities used is poorly understood, so an element of trial and
Testing error is involved in developing a treatment plan.
Biopsies of clinically identified trigger points have not revealed Conservative therapy consisting of trigger point injection with
consistently abnormal histological findings. The muscle hosting local anesthetic or saline is the initial treatment of gluteus medius
the trigger points has been described as moth eaten and as con- syndrome. Because underlying depression and anxiety are present
taining waxy degeneration. Increased plasma myoglobin has in many patients, antidepressants are an integral part of most treat-
been reported in some patients with gluteus medius syndrome, but ment plans. Other methods, including physical therapy, therapeu-
this finding has not been corroborated by other investigators. Elec- tic heat and cold, transcutaneous nerve stimulation, and electrical
trodiagnostic testing has revealed an increase in muscle tension in stimulation, may be helpful on a case-by-case basis. For patients
some patients, but again, this finding has not been reproducible. who do not respond to these traditional measures, consideration
Because of the lack of objective diagnostic testing, the clinician should be given to the use of botulinum toxin type A. Although
must rule out other coexisting disease processes that may mimic not currently approved by the Food and Drug Administration for
gluteus medius syndrome (see discussion of differential diagnosis). this indication, the injection of minute quantities of botulinum
toxin type A directly into trigger points has been successful in the
treatment of persistent gluteus medius syndrome.
Differential Diagnosis
The diagnosis of gluteus medius syndrome is based on clinical
findings rather than specific laboratory, electrodiagnostic, or
Complications and Pitfalls
radiographic testing. For this reason, a targeted history and physi- Trigger point injections are extremely safe if careful attention is
cal examination, with a systematic search for trigger points and paid to the clinically relevant anatomy. Sterile technique must
identification of a positive jump sign, must be carried out in every be used to avoid infection, along with universal precautions to
A B
Figure 85-2 Possible entrapment of the superior gluteal nerve. A, Transverse, T1-weighted, spin echo magnetic resonance imaging (MRI) shows
denervation hypertrophy of the tensor fasciae latae muscle (arrow). B, Similar hypertrophy and high signal intensity are seen in the muscle (arrow)
on transverse, fat-suppressed, T1-weighted, spin echo MRI obtained after intravenous gadolinium administration. (From Resnick D: Diagnosis of bone
and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3551.)
250 SECTION 9 Pelvic Pain Syndromes
minimize any risk to the operator. Most complications of trigger SUGGESTED READINGS
point injection are related to needle-induced trauma at the injec- Arnold LM: The pathophysiology, diagnosis and treatment of fibromyalgia, Psychiatr
tion site and in underlying tissues. The incidence of ecchymosis Clin North Am 33:375408, 2010.
and hematoma formation can be decreased if pressure is applied Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30,
2009.
to the injection site immediately after injection. The avoidance Imamura M, Cassius DA, Fregni F: Fibromyalgia: from treatment to rehabilitation,
of overly long needles can decrease the incidence of trauma to Eur J Pain Suppl 3:117122, 2009.
underlying structures. Special care must be taken to avoid trauma Marsh M: Milnacipran, The comprehensive pharmacology reference, Philadelphia, 2008,
to the sciatic nerve. Elsevier, pp 14.
Waldman SD: Atlas of pain management injection techniques, Philadelphia, 2007,
Saunders, pp 378380.
Clinical Pearls
Although gluteus medius syndrome is a common disorder,
it is often misdiagnosed. Therefore, in patients thought
to have gluteus medius syndrome, a careful evaluation to
identify underlying disease processes is mandatory. Gluteus
medius syndrome often coexists with a variety of somatic
and psychological disorders.
Chapter 86
ORCHIALGIA
ICD-9 CODE 608.9 tapping over the ilioinguinal nerve at the point it pierces the trans-
verse abdominis muscle. A patient with ilioinguinal or genitofem-
oral neuralgia may assume a bent-forward novice skiers position
ICD-10 CODE R10.2 to eliminate pressure on the affected nerve.
Testing
The Clinical Syndrome Ultrasound examination of the scrotal contents is indicated in all
Orchialgia, or testicular pain, can be a difficult clinical situation patients with orchialgia. Radionucleotide and Doppler studies are
for the patient and clinician because of the unique significance the indicated if vascular compromise is suspected. Transillumination
testicle has as part of the male psyche. This fact is crucial if the cli- of the scrotal contents also can help identify varicocele. Electro-
nician is to evaluate and treat successfully patients with orchialgia. myography helps distinguish ilioinguinal nerve entrapment from
Acute orchialgia represents a medical emergency and may be the lumbar plexopathy, lumbar radiculopathy, and diabetic polyneu-
result of trauma, infection, or inflammation of the testes or tor- ropathy. Based on the patients clinical presentation, additional
sion of the testes and spermatic cord. Chronic orchialgia is defined tests, including complete blood cell count, uric acid level, eryth-
as testicular pain that is of more than 3 months duration and rocyte sedimentation rate, and antinuclear antibody testing, may
significantly interferes with the patients activities of daily living. be indicated. Magnetic resonance imaging (MRI) of the lumbar
Chronic orchialgia can be the result of pathological processes that plexus and pelvis is indicated if tumor or hematoma is suspected
are extrascrotal in origin (e.g., ureteral calculi, inguinal hernia, (Figure 86-2).
ilioinguinal or genitofemoral nerve entrapment), diseases of the
lumbar spine and roots, or pathological processes that are intra-
scrotal in origin (e.g., chronic epididymitis, hydrocele, varicocele).
Differential Diagnosis
The history of all patients with chronic orchialgia should include Extrascrotal pathology, including inguinal hernia, ilioinguinal neu-
specific questioning regarding a history of sexual abuse. ralgia, and lesions of the lumbar plexus, nerve roots, and spinal cord,
can mimic the pain of orchialgia and must be included in the dif-
Signs and Symptoms ferential diagnosis, as can a variety of systemic diseases (Table 86-1).
Considerable intrapatient variability exists in the anatomy of the
Physical examination of patients with acute orchialgia is directed ilioinguinal and genitofemoral nerves, which can result in variation
at identifying acute torsion of the testes and spermatic cord, which in patients clinical presentation. The ilioinguinal nerve is a branch
is a surgical emergency. Patients with acute orchitis secondary to of the L1 nerve root with contribution from T12 in some patients.
infections, including sexually transmitted diseases, present with The nerve follows a curvilinear course that takes it from its origin of
testes that are exquisitely tender to palpation. For patients with the L1 and occasionally T12 somatic nerves to inside the concavity
chronic orchialgia, the physical findings are often nonspecific, with of the ilium. The ilioinguinal nerve continues anteriorly to perforate
the testicle mildly tender to palpation, unless specific pathological the transverse abdominis muscle at the level of the anterior supe-
processes are present (Figure 86-1). Patients with chronic testicu- rior iliac spine. The nerve may interconnect with the iliohypogastric
lar pain secondary to varicocele present with a scrotum that feels nerve as it continues along its course medially and inferiorly, where
like a bag of worms. Patients with chronic epididymitis pres- it accompanies the spermatic cord through the inguinal ring and
ent with tenderness that is localized to the epididymis. Testicular into the inguinal canal. The distribution of the sensory innervation
malignancy always should be considered in any patient presenting of the ilioinguinal nerves varies among patients because considerable
with orchialgia. Physical findings in this setting vary, but testicular overlap may occur with the iliohypogastric nerve. In general, the
enlargement is often an early finding. ilioinguinal nerve provides sensory innervation to the upper portion
As mentioned earlier, extrascrotal pathological processes also of the skin of the inner thigh and the root of the penis and upper
can manifest with the primary symptom of orchialgia. One of the scrotum in men.
most common causes of orchialgia of extrascrotal origin is ilioin-
guinal or genitofemoral neuralgia. Ilioinguinal neuralgia manifests
as a sensory deficit in the inner thigh and scrotum in the distribu-
Treatment
tion of the ilioinguinal nerve. Weakness of the anterior abdominal Many treatments have been advocated for orchialgia, with vary-
wall musculature may be present. Tinels sign may be elicited by ing degrees of success (Table 86-2). Initial treatment of the pain
251
252 SECTION 9 Pelvic Pain Syndromes
Testicle
Figure 86-1 For patients with chronic orchialgia, the physical findings are often nonspecific, with the testicle mildly tender to palpation unless specific
pathological processes are present.
TABLE 86-1
Causes of Chronic Orchialgia
Diabetic neuropathy
Epididymal cyst/spermatocele
Epididymitis
Infectious (e.g., Chlamydia trachomatis, Neisseria gonorrhea, Urea-
plasma urealyticum, coliform bacteria)
Noninfectious (e.g., reflux of urine)
Fourniers gangrene
Henoch-Schnlein purpura
Hydrocele
Idiopathic swelling
Inguinal hernia
Interstitial cystitis
Nephrolithaisis in the mid-ureter
Orchitis (e.g., mumps)
Polyarteritis nodosa
Previous surgical interventions (e.g., vasectomy, herniorrhaphy,
scrotal procedures)
Prostatitis
Psychogenic (e.g., history of sexual abuse, relationship stress)
Referred pain from abdomen or pelvis resulting from entrapment of
Figure 86-2 Tumor in an undescended testis. Computed tomography genitofemoral or ilioinguinal nerve roots (T10-L1), with or without
scan through the pelvis shows a large cystic-necrotic mass (M) invading a history of surgery
the left iliopsoas muscles. Excision revealed testicular teratoma within a Testicular torsion or torsion of the appendix testis (intermittent)
nodal mass. (From Haaga JR, Lanzieri CF, Gilkeson RC, editors: CT and MR Testicular vasocongestion from sexual arousal without ejaculation
imaging of the whole body, 4th ed, Philadelphia, 2003, Mosby, p 1727.) Trauma
Tumor (e.g., testicle, epididymis, spermatic cord)
Statin use
Varicocele
Vasectomy (postvasectomy pain syndrome)
From Heidelbaugh JJ: Academic mens health: case studies in clinical practice:
chronic orchialgia, J Mens Health 6:220225, 2009.
86 Orchialgia 253
SUGGESTED READINGS
associated with orchialgia should include a combination of non-
Christiansen CG, Sandlow JI: Testicular pain following vasectomy: a review of
steroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 postvasectomy pain syndrome, J Androl 24:293298, 2003.
(COX-2) inhibitors and physical therapy. Local application of Heidelbaugh JJ: Academic mens health: case studies in clinical practice: chronic
heat and cold may be beneficial. The use of supportive undergar- orchialgia, J Mens Health 6:220225, 2009.
ments or an athletic supporter may provide symptomatic relief. Linnebur S, Hiatt WH: Probable statin-induced testicular pain, Ann Pharmacother
For patients who do not respond to these treatment modalities, 41:138142, 2007.
Masarani M, Cox R: The aetiology, pathophysiology and management of chronic
injection of the spermatic cord or ilioinguinal and genitofemoral orchialgia, BJU Int 91:435437, 2003.
nerves with a local anesthetic and steroid may be a reasonable next Waldman SD: Orchialgia. In Waldman SD, editor: Pain review, Philadelphia,
step. If the symptoms of orchialgia persist, surgical exploration of 2009, Saunders, pp 304305.
the scrotal contents should be considered. Psychological evalua- Wampler SM, Llanes M: Common scrotal and testicular problems primary care,
Clin Office Pract 37:613626, 2010.
tion and interventions should take place concurrently with the Wesselman U, Burnett AL, Heinburg LJ: The urogenital and rectal pain syndromes,
previously mentioned treatment modalities. Pain 73:269294, 1997.
Chapter 87
VULVODYNIA
ICD-9 CODE 625.9 Extravulvar pathological processes can manifest with the pri-
mary symptom of vulvodynia. One of the most common causes
of vulvodynia of extravulvar origin is malignancy involving the
ICD-10 CODE R10.2 pelvic contents other than the vulva. Tumor involving the lum-
bar plexus, cauda equina, or hypogastric plexus rarely can mani-
fest as pain localized to the vulva and perineum. Postradiation
neuropathy can occur after radiation therapy for the treatment of
The Clinical Syndrome malignancy of the vulva and rectum and can mimic the pain of
Vulvodynia is an uncommon cause of pelvic pain encountered vulvodynia. Ilioinguinal or genitofemoral entrapment neuropathy
in clinical practice. Vulvodynia probably is not a single clini- also can manifest clinically as vulvodynia.
cal entity, but rather the conglomeration of a variety of disor-
ders that can cause pain in this anatomical region. Included in Testing
these disorders are chronic infections of the female urogenital
tract; chronic inflammation of the skin and mucosa of the vulva Pelvic examination is the cornerstone of the diagnosis of patients
without demonstrable bacterial, viral, or fungal infection; and with vulvodynia. Careful examination for infection, cutaneous or
bladder abnormalities, including interstitial cystitis, pelvic floor mucosal abnormalities, tenderness, muscle spasm, or tumor is cru-
muscle disorders, reflex sympathetic dystrophy, and psychogenic cial to avoid overlooking vulvar malignancy. Ultrasound examina-
causes. All of these disorders have in common the ability to tion of the pelvis is indicated in all patients with vulvodynia. If any
cause chronic, ill-defined pain of the vulva that is the hallmark question of occult malignancy of the vulva or pelvic contents exists,
of vulvodynia. magnetic resonance imaging (MRI) or computed tomography
The pain of vulvodynia is characterized by dull, stinging, aching, (CT) of the pelvis is mandatory to rule out malignancy or disease of
or burning pain of the vulva. The intensity of pain is mild to mod- the pelvic organs, such as endometriosis, which may be responsible
erate and may worsen with bathing, urination, or sexual activity. for the pain symptoms (Figure 87-2). Urinalysis to rule out urinary
The pain may be referred to the perineum, rectum, or inner thigh. tract infection also is indicated in all patients with vulvodynia. Cul-
Irritative urinary outflow symptoms and sexual dysfunction often ture for sexually transmitted diseases, including herpes, is indicated
coexist with the pain of vulvodynia, with vulvodynia being one in the evaluation of all patients thought to have vulvodynia.
of the leading causes of dyspareunia (Figure 87-1). All patients Electromyography helps distinguish entrapment neuropathy of
with chronic vulvodynia should be questioned regarding a history the genitofemoral or ilioinguinal nerves from lumbar plexopathy or
of sexual abuse, sexually transmitted diseases, and psychological lumbar radiculopathy. Based on the patients clinical presentation,
abnormalities related to sexuality. additional tests, including complete blood cell count, erythrocyte
sedimentation rate, and antinuclear antibody testing, may be indi-
cated. MRI of the lumbar plexus is indicated if tumor or hematoma
Signs and Symptoms is suspected.
Physical examination of patients with acute vulvodynia is directed
at identifying acute infections of the vulva, urinary tract, or both Differential Diagnosis
that may be readily treatable. Patients with acute infections, includ-
ing yeast infections and sexually transmitted diseases, have a vulva Extravulvar pathological findings, including reflex sympathetic dys-
that is irritated, inflamed, raw to the touch, and tender to palpa- trophy and lesions of the lumbar plexus, nerve roots, and spinal
tion. For patients with chronic vulvodynia, the physical findings cord, can mimic the pain of vulvodynia and must be included in
are often nonspecific, with the vulva mildly tender to palpation the differential diagnosis. As mentioned earlier, because of the disas-
and an otherwise normal pelvic examination. Changes of the skin trous results of missing a diagnosis of pelvic or vulvar malignancy
and mucous membranes of the vulva resulting from herpes infec- when evaluating and treating patients thought to have vulvodynia,
tion, chronic itching, irritation, or douching also may be present. it is mandatory that malignancy be high on the list of differential
In a few patients with vulvodynia, spasm of the muscles of the diagnostic possibilities.
pelvic floor may be shown on pelvic examination. Allodynia of the
vulva and perineum may be present, especially if the patient has a Treatment
history of trauma, such as surgery, radiation therapy, or straddle
injuries. Vulva malignancy always should be considered in any A variety of treatments have been advocated in the treatment of
patient with vulvodynia. vulvodynia with varying degrees of success (Tables 87-1 and 87-2).
254
87 Vulvodynia 255
Rectum
Bladder
Perineum
Vulva
Inner thigh
Figure 87-1 The pain of vulvodynia is characterized by dull, stinging, aching, or burning pain of the vulva. The pain may be referred to the perineum,
rectum, or inner thigh.
Initial treatment of the pain associated with vulvodynia should Complications and Pitfalls
include implementation of the approaches listed in Table 87-1
along with a combination of nonsteroidal anti-inflammatory drugs The major pitfalls in the care of a patient with vulvodynia are
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. Local applica- threefold: (1) the misdiagnosis of extravulvar pathological pro-
tion of heat and cold with sitz baths may be beneficial. An arbitrary cesses responsible for the patients pain, (2) the failure to identify
treatment course of antibiotics, such as doxycycline 100 mg twice vulvar or pelvic malignancy or both, and (3) the failure to address
daily for 2 weeks, may be worth trying, even though urine cultures the psychological issues surrounding the patients pain.
are negative. A course of treatment for vaginal yeast infection con-
currently with the antibiotics also should be considered. Anecdotal
reports of decreased pain after treatment with adjuvant analgesics Clinical Pearls
such as a tricyclic antidepressant (e.g., nortriptyline 25 mg at bed- The clinician should be aware that the relationship of
time and titrating upward as side effects allow) or gabapentin make the genitalia to the female psyche presents some unique
these drugs a consideration for patients who continue to have pain challenges when treating patients with vulvodynia. The
in the absence of demonstrable treatable disease. behavioral and psychological issues must be addressed
For patients who do not respond to these treatment modalities, concurrently with the medical issues if treatment is to be
caudal epidural nerve blocks with a local anesthetic and steroid may successful. The possibility for vulvar or pelvic malignancy
be a reasonable next step. If the symptoms of vulvodynia persist, is ever present and should be carefully sought out in all
laparoscopy should be considered. Psychological evaluation and patients with vulvodynia.
interventions should take place concurrently with the previously
mentioned treatment modalities given the high incidence of coexis-
tent psychological issues associated with all pelvic pain syndromes.
256 SECTION 9 Pelvic Pain Syndromes
A B
C D
Figure 87-2 A 41-year-old woman with chronic pelvic pain and a suspicious multicystic pelvic mass at sonography. A, Axial T2-weighted magnetic
resonance imaging shows a complex cystic mass associated with normal hyperintense follicles at the right posterior (large arrow) and anterior left side
suggesting a bilateral adnexal origin. Shadowing of the left part of the cyst suggests blood products. The anterior rectal wall is abnormally thickened
and contains hyperintense spots (small arrow). B, Axial T1-weighted image at the same level as in A shows hyperintense portions (asterisks). C, Fat-
suppressed T1-weighted image shows that the hyperintense areas seen in B persist, confirming the suspicion of bilateral endometrioma. Multiple
smaller, high-intensity foci are better seen with fat suppression (arrows). D, Sagittal T2-weighted image confirms abnormal thickening of the anterior
rectal wall posterior to the ovary (arrow) and a hypointense nodule in the pouch of Douglas posterior to the cervix (asterisk). Subsequent laparotomy
with bilateral oophorectomy and anterior rectal resection confirmed bilateral endometriomas (8 cm rectal and 2 cm peritoneal endometriosis of the
pouch of Douglas), associated with functional ovarian cysts. (From Edelman RR, Hesselink JR, Zlatkin MB, etal, editors: Clinical magnetic resonance
imaging, 3rd ed, Philadelphia, 2006, Saunders, p 2980.)
TABLE 87-1
First-Line Treatment Options for Vulvodynia
Cease use of potentially irritating perfumed soaps, lotions, sprays,
or douches
After urination, rinse vulvar skin with distilled water
Rinse all underwear in a separate cycle with only water after
laundering with detergent
Do not use fabric softener on underwear
Use only 100% cotton menstrual pads and tampons
Wear only 100% cotton underwear and stockings, not nylon
pantyhose
Bathe in water with oatmeal, baking soda, Aveeno, or sitz baths
with tea; no bubble baths; cold compresses
Lubricate with vitamin E oil or vegetable oil, Desitin, or A&D
ointment
From Glazer HI, Ledger WJ: Clinical management of vulvodynia, Rev Gynaecol
Pract 2:8390, 2002.
87 Vulvodynia 257
CLITORAL PRIAPISM
ICD-9 CODE 625.8 (Figure 88-1). The erection may last from minutes to hours and
is often described as painful, with the pain being characterized
as burning and often involving not only the clitoris but also the
ICD-10 CODE N94.89 vulva. The patient may be hesitant to describe the exact nature
or location of the painful erection because of embarrassment or
a lack of understanding as to what is actually causing the pain.
The Clinical Syndrome Often, the patient may report a painful swelling of her vagina
and attribute her symptoms to an insect bite, urinary tract or
In health, an integral part of the human sexual response is tumes- vaginal infection, or allergic reaction. On physical examination,
cence of the penis in males and the clitoris and vulva in females, the examiner will note that the clitoris is erect and firm, with the
known as erection. The physiological process that results in tumes- glans of the clitoris retracted beneath the engorged clitoral hood.
cence is the result of a complex interplay of the parasympathetic Rubor is often present, as well as significant allodynia. Vaginal
and sympathetic nervous system and vasoactive neurotransmitters, transudation, which is seen as part of female sexual arousal, is
including prostaglandin E1 and the vasoactive intestinal polypep- usually absent. It should be noted that enlargement of the clitoris
tide, as well as nitric oxide. Rarely, tumescence of the penis and has other causes, some of which are painful and some not, such
clitoris can occur in the absence of sexual arousal and can be the as infiltrative tumors (Table 88-2).
result of systemic disease, for example, sickle cell disease or drugs
such as sildenafil and trazodone (Table 88-1). Occasionally, no
causative factor can be identified. If the duration of tumescence
Testing
is prolonged, it is termed priapism. Although most attention has Pelvic examination is the cornerstone of the diagnosis of patients
been paid to cases of priapism occurring in males, more recently with vulvodynia. Careful examination for infection, cutaneous
cases of clitoral priapism have been identified as an uncommon or mucosal abnormalities, tenderness, muscle spasm, or tumor
cause of female pelvic pain. is crucial to avoid overlooking clitoral, vulvar, or pelvic malig-
nancy. Ultrasound examination of the pelvis is indicated in all
Signs and Symptoms patients with clitoral priapism. If any question exists regard-
ing occult malignancy of the vulva or pelvic contents, magnetic
Priapism of the clitoris is defined as a painful and often pro-
longed erection of the clitoris in the absence of sexual arousal
TABLE 88-1
Drugs Implicated in Priapism in Men and Women
Trazodone
Bupropion
Risperidone
Olanzapine
Fluoxetine
Bromocriptine
Nefazodone
Citalopram
Papaverine
Cocaine
Sildenafil
Vardenafil Figure 88-1 Clitoral tumescence. (From Bruni V, Pontello V, Dei M, etal:
Hemangioma of the clitoris presenting as clitoromegaly: a case report,
Tadalafil J Pediatr Adolesc Gynecol 22:el37e138, 2009.)
258
88 Clitoral Priapism 259
SUGGESTED READINGS
Compton MT, Miller AH: Priapism associated with conventional and atypical
antipsychotic medications: a review, J Clin Psychiatry 62:362366, 2001.
Fedele L, Fontana E, Bianchi S, Frontino G, Berlanda N: An unusual case of clito-
romegaly, Eur J Obstet Gynecol Reprod Biol 140:287288, 2008.
Gharahbaghian L: Clitoral priapism with no known risk factors, West J Emerg Med
9:235237, 2008.
Levin R, Riley A: The physiology of human sexual function, Psychiatry 6:9094,
Figure 88-2 Clitoral carcinoma. (From Matsuo K, Hew KE, Im DD, Rosen- 2007.
shein NB: Clitoral metastasis of anal adenocarcinoma associated with rec- Rosenberg I, Aniskin D, Bernay L: Psychiatric treatment of patients predisposed to
tovaginal fistula in long standing Crohns disease, Eur J Obstet Gynecol priapism induced by quetiapine, trazodone and risperidone: a case report, Gen
Reprod Biol 144:182183, 2009.) Hosp Psychiatry 31:98, 2009.
Chapter 89
GLUTEAL BURSITIS
260
89 Gluteal Bursitis 261
be distinguished by the presence of motor and sensory changes extremity, indicating that the needle has impinged on the sciatic
involving the sciatic nerve. These motor and sensory changes are nerve. Should a paresthesia occur, the needle should be withdrawn
limited to the distribution of the sciatic nerve below the sciatic immediately and repositioned more medially. The needle is care-
notch. Lumbar radiculopathy and sciatic nerve entrapment may fully advanced perpendicular to the skin at the previously identi-
coexist as the double crush syndrome. The pain of gluteal bur- fied point until it impinges on the wing of the ilium (Figure 89-2).
sitis may cause alteration of gait, which may result in secondary Care must be taken to keep the needle medial and not to advance
back and radicular symptoms that may coexist with this entrap- it laterally, or it could impinge on the sciatic nerve. After careful
ment neuropathy. aspiration and if no paresthesia is present, the contents of the
syringe are gently injected into the bursa. Minimal resistance to
Treatment injection should be felt.
ICD-9 CODE 729.1 attributed to other organ systems, leading to extensive evalua-
tions and ineffective treatment. Patients with levator ani syndrome
exhibit a trigger point along the rectum or perineum (Figure 90-2).
ICD-10 CODE M79.7 Taut bands of muscle fibers often are identified when myofascial
trigger points are palpated. Despite this consistent physical finding
in patients who have myofascial pain syndrome, the pathophysiol-
The Clinical Syndrome ogy of the myofascial trigger point remains elusive, although many
theories have been advanced. Common to all of these theories is
The primary function of the levator ani muscle is active support the thought that trigger points are the result of microtrauma to the
of the pelvic contents, compressing the urethra and vagina by ele- affected muscle. This microtrauma may occur as a single injury to
vating the pelvic floor, and maintaining a physiological anorectal the affected muscle or may occur as the result of repetitive micro-
angle by pulling the anorectal junction forward. The levator ani trauma or chronic deconditioning of the agonist and antagonist
muscle originates at the posterior surface of the body of the pubis, muscle unit.
the fascia of the obturator internus muscle, and the ischial spine In addition to muscle trauma, a variety of other factors seem to
(Figure 90-1). The muscle inserts on the anococcygeal raphe and predispose the patient to develop myofascial pain syndrome. The
coccyx. The muscle is innervated by the branches of the ventral weekend athlete who subjects his or her body to unaccustomed
primary rami of spinal nerves S3-4. The levator ani muscle is sus- physical activity often develops myofascial pain syndrome. Poor
ceptible to trauma and to wear and tear from overuse and misuse. posture while sitting at a computer keyboard or while watching
It may develop myofascial pain syndrome that may also be associ- television also has been implicated as a predisposing factor to the
ated with gluteal bursitis and coccygodynia, which may confuse
the clinical picture further.
Myofascial pain syndrome is a chronic pain syndrome that
affects a focal or regional portion of the body. The sine qua non
of myofascial pain syndrome is the finding of myofascial trigger
points on physical examination. Although these trigger points
generally are localized to the regional part of the body affected,
the pain of myofascial pain syndrome often is referred to other
anatomical areas. This referred pain often is misdiagnosed or
Trigger point
Referred pain
Levator ani m.
Figure 90-1 The levator ani muscle originates at the posterior surface of Figure 90-2 Patients with levator ani syndrome exhibit a trigger point
the body of the pubis, the fascia of the obturator internus muscle, and along the rectum or perineum. (From Waldman SD: Atlas of pain manage-
the ischial spine. ment injection techniques, 2nd ed, Philadelphia, 2007, Saunders, p 385.)
262
90 Levator Ani Pain Syndrome 263
development of myofascial pain syndrome. Previous injuries may muscles. This pathological lesion is characterized by a local point
result in abnormal muscle function and predispose to the sub- of exquisite tenderness in affected muscle. Mechanical stimula-
sequent development of myofascial pain syndrome. All of these tion of the trigger point by palpation or stretching produces not
predisposing factors may be intensified if the patient also has poor only intense local pain but also referred pain. In addition to this
nutritional status or coexisting psychological or behavioral abnor- local and referred pain, an involuntary withdrawal of the stimu-
malities, including chronic stress and depression. The levator lated muscle, termed a jump sign, may occur. The jump sign also
ani muscle seems to be particularly susceptible to stress-induced is characteristic of myofascial pain syndrome. Patients with glu-
myofascial pain syndrome. teus medius syndrome exhibit a trigger point along the rectum or
Stiffness and fatigue often coexist with the pain of myofascial perineum (see Figure 90-2).
pain syndrome, increasing the functional disability associated with
this disease and complicating its treatment. Myofascial pain syn-
drome may occur as a primary disease state or may occur in con-
Testing
junction with other painful conditions, including radiculopathy No specific test exists for levator ani pain syndrome. Testing
and chronic regional pain syndromes. Psychological or behavioral is aimed primarily at identifying occult pathological conditions
abnormalities, including depression, frequently coexist with the or other diseases that may mimic myofascial pain syndrome
muscle abnormalities associated with myofascial pain syndrome. (see discussion of differential diagnosis). Plain radiographs
Treatment of these psychological and behavioral abnormalities help delineate bony abnormality of the pelvis and hip, includ-
must be an integral part of any successful treatment plan for myo- ing arthritis, avascular necrosis of the hip, fracture, congenital
fascial pain syndrome. abnormalities, and tumor. All patients with recent onset of
myofascial pain syndrome should undergo magnetic resonance
imaging (MRI) of the lumbar spine and pelvis to rule out occult
Signs and Symptoms pathological processes. Screening laboratory tests, consisting of
The trigger point is the pathognomonic lesion of myofascial pain complete blood count, erythrocyte sedimentation rate, antinu-
and is thought to be the result of microtrauma to the affected clear antibody testing, and automated blood chemistry testing,
A B
C
Figure 90-3 Crohns disease with enterorectal fistula. A, Small-bowel follow-through examination shows an enterorectal fistula (arrow). B, Com-
puted tomography (CT) scan shows diffuse pericolonic, perirectal, and perienteric inflammatory infiltrates with bowel wall thickening of pelvic ileal
loops. C, Gadolinium-enhanced MR image shows marked contrast enhancement in the thickened rectal wall (arrows) and inflammatory tissues
(arrowheads) surrounding the fistula. (From Haaga JR, Lanzieri CF, Gilkeson RC, editors: CT and MR imaging of the whole body, 4th ed, Philadelphia,
2003, Mosby, p 1244.)
264 SECTION 9 Pelvic Pain Syndromes
should be performed to rule out occult inflammatory arthritis, well versed in the regional anatomy and experienced in perform-
infection, and tumor. ing interventional pain management techniques. Many patients
also report a transient increase in pain after injection of trigger
Differential Diagnosis points. If long needles are used, damage to the retroperitoneal
organs also may occur.
Levator ani pain syndrome is a clinical diagnosis of exclusion
supported by a combination of clinical history, physical exami-
nation, radiography, and MRI. Pain syndromes that may mimic Clinical Pearls
levator ani pain syndrome include lumbosacral radiculopathy and
plexopathy; stress fractures of the pelvis and hip; myofascial pain Trigger point injections are an extremely safe procedure if
syndromes such as gluteus medius pain syndrome; pelvic floor careful attention is paid to the clinically relevant anatomy
muscle strain; inflammatory arthritis; and disorders of the lumbar in the areas to be injected. Care must be taken to use ster-
spinal cord, roots, plexus, and nerves. Intrapelvic tumors also may ile technique to avoid infection and universal precautions
mimic the clinical presentation of gluteus medius pain syndrome to avoid risk to the operator. Most side effects of trigger
(Figure 90-3). point injection are related to needle-induced trauma to
the injection site and underlying tissues. The incidence of
ecchymosis and hematoma formation can be decreased if
Treatment pressure is placed on the injection site immediately after
Levator ani pain syndrome is best treated with a multimodality trigger point injection. The avoidance of overly long nee-
approach. Physical therapy, including correction of functional dles helps decrease the incidence of trauma to underlying
abnormalities (e.g., poor posture, improper chair or computer structures. Special care must be taken to avoid pneumo-
height) and use of heat modalities and deep sedative massage, thorax when injecting trigger points in proximity to the
combined with nonsteroidal anti-inflammatory drugs (NSAIDs) underlying pleural space. The antidepressant compounds
and skeletal muscle relaxants is a reasonable starting point. If these represent the primary pharmacological treatment for
treatments fail to provide rapid symptomatic relief, local trigger myofascial pain syndrome. Tricyclic antidepressants are
point injection of local anesthetic and steroid into the myofas- thought to be more effective than selective serotonin reup-
cial trigger point area is a reasonable next step. Underlying diffuse take inhibitors in the treatment of this painful condition.
muscle pain, sleep disturbance, and depression are best treated The precise mechanism of action of the antidepressant
with a tricyclic antidepressant compound, such as nortriptyline, compounds in the treatment of myofascial pain syndrome
which can be started at a single bedtime dose of 25 mg. is unknown. Some investigators believe that the primary
When performing trigger point injections, careful preparation effect of this class of drugs is to treat the underlying depres-
of the patient before trigger point injection helps optimize results. sion that is present in many patients who have myofas-
Trigger point injections are directed at the primary trigger point, cial pain syndrome. Drugs such as amitriptyline and
rather than in the area of referred pain. It should be explained nortriptyline represent good first choices and should be
to the patient that the goal of trigger point injection is to block given as a single bedtime dose, starting with 10 to 25 mg
the trigger of the persistent pain and, it is hoped, provide long- and titrating upward as side effects allow.
lasting relief. It is important that the patient understand that with
most patients who have myofascial pain syndrome, more than one
treatment modality is required to provide optimal pain relief. The
SUGGESTED READINGS
use of the prone or lateral position when identifying and marking
trigger points and when performing the actual trigger point injec- Arnold LM: The pathophysiology, diagnosis and treatment of fibromyalgia,
Psychiatr Clin North Am 33:375408, 2010.
tion helps decrease the incidence of vasovagal reactions. The skin Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30,
overlying the trigger point to be injected always should be pre- 2009.
pared with antiseptic solution before injection to avoid infection. Imamura M, Cassius DA, Fregni F: Fibromyalgia: from treatment to rehabilitation,
Eur J Pain Suppl 3:117122, 2009.
Shobeiri SA, Chesson RR, Gasser RF: The internal innervation and morphology of
Complications and Pitfalls the human female levator ani muscle, Am J Obstet Gynecol 199:686.e1686.e6,
2008.
The proximity to the rectum, vagina, and pelvic viscera makes it Singh K, Reid WMN, Berger LA: Magnetic resonance imaging of normal levator
imperative that this procedure be performed only by clinicians ani anatomy and function, Obstet Gynecol 99:433438, 2002.
SECTION 10 Hip and Lower Extremity Pain Syndromes
Chapter 91
ICD-9 CODE 733.40 collagen-vascular disease. The disease is bilateral in 50% to 55%
of cases.
Predisposing factors to avascular necrosis of the hip are listed
ICD-10 CODE M87.00 in Table 91-1 and include trauma to the proximal femur and
acetabulum; corticosteroid use; Cushings disease; alcohol abuse;
connective tissue diseases, especially systemic lupus erythema-
The Clinical Syndrome tous; osteomyelitis; human immunodeficiency virus (HIV); organ
transplantation; Legg-Calv-Perthes disease; hemoglobinopathies,
Avascular necrosis of the hip is an often missed diagnosis. It is including sickle cell disease; hyperlipidemia; gout; renal failure;
also known as osteonecrosis. Similar to the scaphoid, the hip is pregnancy; and radiation therapy involving the femoral head. A
extremely susceptible to this disease because of its tenuous blood patient with avascular necrosis of the hip reports pain over the
supply. The blood supply of the hip is easily disrupted, often leav- affected hip or hips, which may radiate into the groin, buttocks,
ing the proximal portion of the bone without nutrition, thereby and proximal lower extremity. The pain is deep and aching,
leading to osteonecrosis. Avascular necrosis of the hip is a disease and the patient often reports a catching sensation with range of
of the fourth and fifth decades of life and is more common in motion of the affected hip or hips. Range of motion decreases as
men, with an 8:1 male-to-female preponderance (Figure 91-1), the disease progresses.
except for patients with avascular necrosis of the hip secondary to
Signs and Symptoms
Physical examination of patients with avascular necrosis of the hip
reveals pain to deep palpation of the hip joint. The pain becomes
TABLE 91-1
Predisposing Factors for Avascular Necrosis of the Hip
Trauma to proximal femur and acetabulum
Corticosteroid use
Cushings disease
Alcohol abuse
Connective tissue diseases, especially systemic lupus erythematosus
Osteomyelitis
Human immunodeficiency virus
Organ transplantation
Legg-Calv-Perthes disease
Hemoglobinopathies, including sickle cell disease
Hyperlipidemia
Gout
Renal failure
Figure 91-1 Avascular necrosis of the hip is a disease of the fourth and Pregnancy
fifth decades of life and is more common in men, with an 8:1 male-to-
female ratio. Radiation therapy
265
266 SECTION 10 Hip and Lower Extremity Pain Syndromes
B C
Figure 91-2 Osteonecrosis of the right hip in a 35-year-old man. A left hip replacement was performed because of advanced osteonecrosis and
secondary osteoarthritis. A, Coronal T1-weighted magnetic resonance imaging. A well-defined reactive rim surrounds a zone of osteonecrosis that
appears isointense with normal fatty marrow. B, Axial T2-weighted image. The region of femoral head osteonecrosis remains relatively isointense with
normal marrow. C, Coronal fat-saturated T2-weighted image. The double line sign represents an inner hyperintense component, corresponding with
hypervascular granulation tissue and fibrovascular proliferation, and an outer, hypointense, fibrotic band. (From Edelman RR, Hesselink JR, Zlatkin MB,
etal, editors: Clinical magnetic resonance imaging, 3rd ed, Philadelphia, 2006, Saunders, p 3369.)
worse with passive range of motion and weight bearing on a single erythrocyte sedimentation rate, and antinuclear antibody testing,
extremity. A click or crepitus may be appreciated by the examiner may be indicated. Magnetic resonance imaging (MRI) of the hip is
when putting the hip joint through range of motion. A Tren- indicated in all patients suspected to have avascular necrosis of the
delenburg gait may be noted, and decreased range of motion is hip or if other causes of joint instability, infection, or tumor are
invariably present. suspected (Figures 91-2 and 91-3). Administration of gadolinium
followed by postcontrast imaging may help delineate the adequacy
of blood supply, with contrast enhancement of the proximal hip
Testing being a good prognostic sign. Electromyography is indicated if
Plain radiographs are indicated in all patients with avascular coexistent lumbar radiculopathy, plexopathy, or both are sus-
necrosis of the hip to rule out underlying occult bony pathological pected. A gentle injection of the hip joint with small volumes of
processes and identify sclerosis and fragmentation of the femoral local anesthetic provides immediate improvement of the pain and
head, although early in the course of the disease, plain radio- helps show the nidus of the patients pain is, in fact, the hip. Ulti-
graphs are unreliable. Based on the patients clinical presentation, mately, total joint replacement is required in most patients with
additional tests, including complete blood cell count, uric acid, avascular necrosis of the hip.
91 Avascular Necrosis of the Hip 267
Treatment
Initial treatment of the pain and functional disability associated
with avascular necrosis of the hip should include a combination
of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxy-
genase-2 (COX-2) inhibitors and decreased weight bearing of the
affected hip or hips. Local application of heat and cold may be
beneficial. For patients who do not respond to these treatment
modalities, an injection of a local anesthetic into the hip joint
may be a reasonable next step to provide palliation of acute pain.
Vigorous exercises should be avoided because they would exac-
erbate the patients symptoms. Ultimately, surgical repair in the
A form of total joint arthroplasty is the treatment of choice.
Clinical Pearls
Avascular necrosis of the hip is a diagnosis that is often
missed, leading to much unnecessary pain and disability.
The clinician should include avascular necrosis of the hip
in the differential diagnosis with all patients with hip pain,
B especially if any of the predisposing factors listed in Table
91-1 are present. Coexistent arthritis, tendinitis, and gout
Figure 91-3 Osteonecrosis of the left hip with subchondral osseous col- may contribute to the pain and may require additional treat-
lapse and osteoarthritis. A, Coronal T1-weighted magnetic resonance
imaging. Decreased marrow signal intensity is identified within the
ment. The use of physical modalities, including local heat
superior lateral aspect of the left femoral head and the adjacent lateral and cold and decreased weight bearing, may provide symp-
aspect of the acetabulum. Lateral subluxation of the femoral head also is tomatic relief. Vigorous exercises should be avoided because
present. B, Coronal fat-saturated T2-weighted image. Flattening of the they would exacerbate the symptoms and may cause further
articular surface of the superior lateral portion of the left femoral head damage to the hip. Simple analgesics and NSAIDs may be
is evident, indicating subchondral osseous collapse. Increased marrow
signal intensity involving the lateral acetabulum and the proximal femur used concurrently with this injection technique.
is observed, which is compatible with reactive edema and fibrovascular
proliferation. A large left hip joint effusion also is present. (From Edelman
RR, Hesselink JR, Zlatkin MB, et al, editors: Clinical magnetic resonance
imaging, 3rd ed, Philadelphia, 2006, Saunders, p 3371.) SUGGESTED READINGS
Israelite CL, Garino JP: Osteonecrosis of the hip, Semin Arthroplasty 16:2732,
Differential Diagnosis 2005.
Malizos KN, Karantanas AH, Varitimidis SE, etal: Osteonecrosis of the femoral
Coexistent arthritis and gout of the hip joints, bursitis, and ten- head: etiology, imaging and treatment, Eur J Radiol 63:1628, 2007.
Waldman SD: Osteonecrosis of the hip. In Waldman SD, Campbell RSD, editors:
dinitis may coexist with avascular necrosis of the hips and exac- Imaging of pain, Philadelphia, 2011, Saunders, pp 339341.
erbate the pain and disability of the patient. Tears of the labrum, Zibis AH, Karantanas AH, Roidis NT, etal: The role of MR imaging in staging
ligament tears, bone cysts, bone contusions, bone fractures, and femoral head osteonecrosis, Eur J Radiol 63:39, 2007.
Chapter 92
PSOAS BURSITIS
Psoas muscle
Psoas bursa
Figure 92-1 The psoas muscle flexes the thigh on the trunk or, if the thigh is fixed, flexes the trunk on the thigh as when moving from a supine to
a sitting position. This action can irritate the psoas bursa, as can repeated trauma from repetitive activity, including running up stairs or overuse of
exercise equipment for lower extremity strengthening.
268
92 Psoas Bursitis 269
markedly increases the pain. Examination of the hip is normal, nerve. These motor and sensory changes are limited to the distri-
unless there is coexistent internal derangement of the hip. bution of the femoral nerve below the inguinal ligament. Ilioin-
guinal and genitofemoral neuropathy also can be confused with
psoas bursitis. Lumbar radiculopathy and these nerve entrapments
Testing may coexist as the double crush syndrome. The pain of psoas
Plain radiographs of the hip may reveal calcification of the bursa bursitis also may cause alteration of gait, which may result in sec-
and associated structures consistent with chronic inflammation ondary back and radicular symptoms that may coexist with this
(Figure 92-2). Magnetic resonance imaging (MRI) is indicated entrapment neuropathy.
if occult mass, abscess, or tumor of the hip or groin is suspected.
Complete blood cell count and automated chemistry profile,
including uric acid level, erythrocyte sedimentation rate, and anti-
Treatment
nuclear antibody testing, are indicated if collagen-vascular disease Initial treatment of the pain and functional disability associated
is suspected. Injection of the psoas bursa with a local anesthetic with psoas bursitis should include a combination of nonste-
and steroid serves as a diagnostic maneuver and a therapeutic roidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
maneuver. (COX-2) inhibitors and physical therapy. Local application of
heat and cold also may be beneficial. The repetitive movements
that incite the syndrome should be avoided. For patients who do
Differential Diagnosis not respond to these treatment modalities, injection of the psoas
Psoas bursitis is often misdiagnosed as an inguinal hernia or bursa with a local anesthetic and steroid may be a reasonable
attributed to a primary hip pathological process. Radiographs of next step.
the hip and electromyography help distinguish psoas bursitis from
radiculopathy of pain emanating from the hip. Most patients
with lumbar radiculopathy have back pain associated with reflex,
Complications and Pitfalls
motor, and sensory changes, whereas patients with psoas bursi- The proximity to the femoral nerve of the psoas bursa makes it
tis have only secondary back pain as a result of altered gait and imperative that the injection procedure be done only by clinicians
no neurological changes. Femoral diabetic neuropathy sometimes well versed in the regional anatomy and experienced in perform-
may be confused with psoas bursitis, but can be distinguished by ing injection techniques. Many patients report a transient increase
the presence of motor and sensory changes involving the femoral in pain after injection of the bursa.
C B
Figure 92-2 Tuberculous spondylitis: Psoas abscess. A, The typical appearance of bilateral and fusiform psoas abscesses is illustrated in a cross-
sectional drawing through a lumbar vertebral body. B, A large left noncalcified psoas abscess (arrows) can be seen. C, Diffusely calcified psoas
abscesses are noted in association with spinal abnormalities. (From Resnick D, editor: Diagnosis of bone and Joint disorders, 4th ed, Philadelphia, 2002,
Saunders, p 2530.)
270 SECTION 10 Hip and Lower Extremity Pain Syndromes
FEMORAL NEUROPATHY
Testing
Electromyography can help identify the exact source of neurologi-
cal dysfunction and clarify the differential diagnosis and should be
the starting point of the evaluation of all patients thought to have
femoral neuropathy. Plain radiographs of the spine, hip, and pelvis
are indicated in all patients with femoral neuropathy to rule out
occult bony pathological conditions. Based on the patients clinical
presentation, additional tests, including complete blood cell count,
uric acid level, erythrocyte sedimentation rate, and antinuclear Figure 93-1 Patients with femoral neuropathy present with pain that
antibody testing, may be indicated. Magnetic resonance imaging radiates into the anterior thigh and medial calf.
271
272 SECTION 10 Hip and Lower Extremity Pain Syndromes
Clinical Pearls
Figure 93-2 Amyotrophy of the left quadriceps femoris. (From Jellad A, Femoral neuropathy always should be differentiated from
Boudokhane S, Ezzine S, etal: Femoral neuropathy caused by compressive
iliopsoas hydatid cyst: a case report and review of the literature, Joint Bone lumbar plexopathy and radiculopathy of the nerve roots,
Spine 77:371372, 2010.) which sometimes may mimic femoral nerve compression.
Lumbar radiculopathy and femoral nerve entrapment
may coexist in the double crush syndrome. The double
crush syndrome is seen most commonly with median nerve
entrapment at the wrist.
Injection of the femoral nerve is a simple and safe tech-
nique in the evaluation and treatment of the previously
mentioned painful conditions. Careful neurological exami-
nation to identify preexisting neurological deficits that may
later be attributed to the nerve block should be performed
on all patients before beginning femoral nerve block, espe-
cially in patients with clinical symptoms of diabetes or clini-
cally significant femoral neuropathy.
SUGGESTED READINGS
Busis NA: Femoral and obturator neuropathies, Neurol Clin 17:633653, 1999.
Hsin HT, Hwang JJ: Isolated femoral nerve neuropathy after intra-aortic balloon
pump treatment, J Formos Med Assoc 106:S29S32, 2007.
Parmer SS, Carpenter JP, Fairman RM, etal: Femoral neuropathy following ret-
Figure 93-3 T2-Weighted coronal magnetic resonance imaging show-
roperitoneal hemorrhage: case series and review of the literature, Ann Vasc Surg
ing the hematoma as an area of increased signal intensity in the mus-
20:536540, 2006.
cle belly (arrowhead). Fascial edema/hemorrhage is depicted as linear
Seijo-Martnez M, Castro del Ro M, Fontoira E, Fontoira M: Acute femoral neu-
hyperintensity. An ill-defined area of high signal intensity can be seen
ropathy secondary to an iliacus muscle hematoma, J Neurol Sci 209:119122,
at the distal myotendinous junction of the left psoasiliacus complex,
2003.
indicating a partial injury (arrow). (From Seijo-Martnez M, Castro del Ro
M, Fontoira E, Fontoira M: Acute femoral neuropathy secondary to an iliacus
muscle hematoma, J Neurol Sci 209:119122, 2003.)
Chapter 94
SAPHENOUS NEURALGIA
tests, including complete blood cell count, uric acid level, erythro-
ICD-9 CODE 355.8 cyte sedimentation rate, and antinuclear antibody testing, may be
indicated. Magnetic resonance imaging (MRI) of the spine, pelvis,
and proximal lower extremity is indicated if tumor or hematoma
ICD-10 CODE G57.90 is suspected. Injection of the saphenous nerve with a local anes-
thetic and steroid as it exits Hunters canal serves as a diagnostic
and therapeutic maneuver.
The Clinical Syndrome
Saphenous neuralgia is an uncommon cause of medial calf pain
Differential Diagnosis
that may occur after vascular surgery on the lower extremity It is difficult to separate saphenous neuralgia from a lumbar radic-
(Figure 94-1). With the increased number of total knee arthro- ulopathy on purely clinical grounds, and electromyography is
plasties being performed, trauma to the infrapatellar branch of strongly recommended. Electromyography and nerve conduction
the saphenous nerve may cause damage, producing pain and testing also help rule out the presence of peripheral neuropathy.
numbness over the patellar tendon. Patients with saphenous Intrapelvic or retroperitoneal tumor or hematoma may compress
neuralgia often experience the medial pseudoclaudication type the lumbar plexus and mimic the clinical presentation of saphe-
of pain that may confuse the clinical evaluation and lead the nous neuralgia.
clinician to suspect lumbar spinal stenosis. Saphenous neuralgia
also may be due to compression of the nerve by tumor, hemor-
rhage, or abscess. This compression usually occurs at the level
Treatment
at which the nerve exits from Hunters canal. Stretch injuries to Mild cases of saphenous neuralgia usually respond to conservative
the saphenous nerve also can occur at this point. The nerve is therapy, and surgery should be reserved for more severe cases. Ini-
subject to compression as it crosses to the medial knee. Compres- tial treatment of saphenous neuralgia should consist of treatment
sion of the saphenous nerve at the knee is known as surfers knee with simple analgesics, nonsteroidal anti-inflammatory drugs
because of compression of the saphenous nerve by the edge of (NSAIDs), or cyclooxygenase-2 (COX-2) inhibitors and avoid-
the surfboard. Diabetes can affect the saphenous nerve, but this ance of repetitive activities that exacerbate the symptoms. If diabe-
is usually in conjunction with neuropathy of the other nerves of tes is thought to be the cause of the patients saphenous neuralgia,
the lower extremity. tight control of blood glucose levels is mandatory. Avoidance of
repetitive activities thought to be responsible for the exacerbation
Signs and Symptoms of saphenous neuralgia helps ameliorate the symptoms. The use
of gabapentin or a tricyclic antidepressant such as nortriptyline
A patient with saphenous neuralgia presents with pain that radi- as an adjuvant analgesic also may help ameliorate the symptoms
ates into the medial calf to the medial malleolus (Figure 94-2). of saphenous neuralgia. If the patient fails to respond to these
This pain may be paresthetic or burning; the intensity is moderate conservative measures, a next reasonable step is injection of the
to severe. There is no motor deficit associated with saphenous neu- saphenous nerve with a local anesthetic and steroid. Ultrasound
ropathy, unless the spinal nerve roots or plexus or other peripheral guidance may be useful in patients in whom anatomical land-
nerves are involved. Patients with saphenous neuralgia may report marks are difficult to identify (Figure 94-3).
a sunburned feeling over the distribution of the saphenous nerve.
Complications and Pitfalls
Testing It is imperative that the clinician rule out causes of saphenous
Electromyography can help identify the exact source of neurologi- neuralgia that, if undiagnosed, could harm the patient, such as
cal dysfunction and clarify the differential diagnosis and should uncontrolled diabetes and retroperitoneal or pelvic tumor. The
be the starting point of the evaluation of all patients suspected main side effect of saphenous nerve block is postblock ecchymosis
to have saphenous neuralgia. Plain radiographs of the spine, hip, and hematoma. Potential exists for needle-induced trauma to the
pelvis, and femur are indicated in all patients who present with saphenous nerve. By advancing the needle slowly and then with-
saphenous neuralgia to rule out occult bony pathological pro- drawing the needle slightly away from the nerve, needle-induced
cesses. Based on the patients clinical presentation, additional trauma to the saphenous nerve can be avoided.
273
274 SECTION 10 Hip and Lower Extremity Pain Syndromes
Sartorius
A B
Medial condyle
of femur
Femur
Tibia
Tibia
D
Figure 94-1 Axial T1-weighted (A) and PD-weighted fat-suppressed (B) images, sagittal PD-weighted fat-suppressed (C) and ultrasound (arrows
delineate postsurgical neuroma) (D) images of a right knee. Postsurgery neuroma of the sartorial branch of the saphenous nerve at the point where
it becomes superficial between the sartorius (S) and gracilis (G) tendons. GSV, Great saphenous vein; SSV, small saphenous vein. (From Damarey B,
Demondion X, Wavreille G, etal: Imaging of the nerves of the knee region, Eur J Radiol 82:27-37, 2013.)
94 Saphenous Neuralgia 275
Saphenous
nerve
Patellar
tendon
Medial
malleolus
Figure 94-2 Patients with saphenous neuralgia present with pain that radiates into the medial calf to the medial malleolus.
Posterior
Anterior
A
Vastus medialis Needle Subsartorial Femoral
muscle tip plexus artery
Sartorius muscle Subsartorial plexus
Posterior
Anterior
B
Vastus medialis Local Femoral
muscle anesthetic artery
Figure 94-3 Image sequence showing subsartorial block of the saphenous nerve in the midthigh with the sartorius muscle and subsartorial plexus
imaged in short-axis view. An in-plane approach is demonstrated in which the needle tip is placed through the sartorius muscle, targeting the fascial
plane on the anterior side of the femoral artery (A). In this example, after injection, the local anesthetic is distributed around a single nerve complex
underneath the sartorius muscle (B). (From Gray AT: Atlas of ultrasound-guided regional anesthesia, Philadelphia, 2010, Saunders, p 158.)
276 SECTION 10 Hip and Lower Extremity Pain Syndromes
OBTURATOR NEURALGIA
Testing
Electromyography can help identify the exact source of neurologi-
cal dysfunction and clarify the differential diagnosis and should
be the starting point of the evaluation of all patients thought to
have obturator neuralgia. Plain radiographs of the spine, hip, pel-
vis, and proximal femur are indicated in all patients with obtu-
rator neuralgia to rule out occult bony pathology. Based on the
patients clinical presentation, additional tests, including com-
plete blood cell count, uric acid level, erythrocyte sedimentation
rate, and antinuclear antibody testing, may be indicated. Mag-
netic resonance imaging (MRI) of the spine, pelvis, and proximal
lower extremity is indicated if tumor or hematoma is suspected
(Figure 95-2). Injection of the obturator nerve with a local anes- Figure 95-1 Patients with obturator neuralgia have pain that radiates
thetic and steroid serves as a diagnostic and therapeutic maneuver. into the medial thigh and does not extend below the knee.
277
Sigmoid colon
Endometriosis tumor in
right obturator fossae Left obturator nerve
Figure 95-2 Transversal magnetic resonance image of the pelvis, with entrapment of the obturator nerve on the right side. (From Langebrekke A,
Qvigstad E: Endometriosis entrapment of the obturator nerve after previous cervical cancer surgery, Fertil Steril 91:622623, 2009.)
B C
Figure 95-3 Skeletal metastasis: Medulloblastoma. A, Radiograph of the pelvis was obtained in a 23-year-old woman 2 years after a craniotomy with
excision of a medulloblastoma. Patchy osteosclerosis is evident in the left iliac crest, right acetabulum, symphyseal regions, ischial tuberosities, and
left femoral neck. B, After the removal of a medulloblastoma in a 20-year-old man, extensive osteoblastic metastases developed in the spine and,
as shown here, throughout the pelvic bones and proximal portions of the femora. C, In a 12-year-old boy who had undergone excision of a medul-
loblastoma, widespread osteoblastic skeletal metastases developed, shown here in the tubular bones of the lower extremity. (From Resnick D, editor:
Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 4313.)
95 Obturator Neuralgia 279
Clinical Pearls
Obturator neuralgia always should be differentiated from
lumbar plexopathy and radiculopathy of the nerve roots
that may sometimes mimic obturator nerve compression.
Lumbar radiculopathy and obturator nerve entrapment
may coexist in the double crush syndrome. The double
crush syndrome is seen most commonly with median nerve
entrapment at the wrist.
Injection of the obturator nerve is a simple and safe
technique in the evaluation and treatment of the previously
mentioned painful conditions. Careful neurological exami-
nation to identify preexisting neurological deficits that may
later be attributed to the nerve block should be performed
on all patients before beginning obturator nerve block,
especially in patients with clinical symptoms of diabetes or
clinically significant obturator neuralgia.
Chapter 96
ADDUCTOR TENDINITIS
Sartorius
Signs and Symptoms
Vastus medialis
On physical examination, a patient with adductor tendinitis
reports pain on palpation of the origins of the adductor tendons.
Active resisted adduction and passive abduction reproduce the Adductor magnus
pain (Figure 96-1). Patients with adductor tendinitis also exhibit
a positive Waldman knee squeeze test for adductor tendinitis.
For this test, the patient places a tennis ball between the knees
and gently holds it there (Figure 96-2, A). The patient is asked to
squeeze the ball as hard as possible. Patients with adductor tendi-
nitis reflexively abduct their knees, causing the tennis ball to fall Figure 96-1 The patient with adductor tendinitis reports pain on palpa-
(Figure 96-2, B). Tendinitis of the musculotendinous unit of the tion of the origins of the adductor tendons. Active resisted adduction
hip frequently coexists with bursitis of the associated bursa of the and passive abduction reproduce the pain.
280
96 Adductor Tendinitis 281
Tennis
ball
A B
Figure 96-2 Patients with adductor tendinitis also exhibit a positive Waldman knee squeeze test for adductor tendinitis. A, The patient places a ten-
nis ball between the knees and gently holds it there. B, Patients with adductor tendinitis reflexively abduct their knees, causing the tennis ball to fall.
(From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, Philadelphia, 2006, Saunders, pp 306307.)
ILIOPECTINATE BURSITIS
the point at which the ilium and the pubis bone merge. The psoas
ICD-9 CODE 726.5 and iliacus muscles join at the lateral side of the psoas, and the
combined fibers are referred to as the iliopsoas muscle. Similar to
the psoas, the iliacus flexes the thigh on the trunk or, if the thigh
ICD-10 CODE M77.9 is fixed, flexes the trunk on the thigh, as when moving from a
supine to sitting position. This action can irritate the iliopectinate
bursa, as can repeated trauma from repetitive activity, includ-
The Clinical Syndrome ing sit-ups or overuse of exercise equipment for lower extremity
strengthening (Figure 97-1). The iliacus muscle is innervated by
A patient with iliopectinate bursitis frequently reports pain in the the femoral nerve.
anterior hip and groin. The pain is localized to the area just below
the crease of the groin anteriorly, with referred pain noted into
the hip joint and anterior pelvis. Often, the patient is unable to
Signs and Symptoms
sleep on the affected hip and may report a sharp, catching sen- Physical examination may reveal point tenderness in the upper
sation with range of motion of the hip. Iliopectinate bursitis often thigh just below the crease of the groin. Passive flexion, adduc-
coexists with arthritis of the hip joint. tion, and abduction and active resisted flexion and adduction of
The iliopectinate bursa lies between the psoas and iliacus mus- the affected lower extremity reproduce the pain. Sudden release
cles and the iliopectinate eminence. The iliopectinate eminence is of resistance during this maneuver markedly increases the pain.
Iliopsoas m.
Gluteus medius m.
Inflamed
iliopectineal
bursa
Figure 97-1 The iliacus muscle flexes the thigh on the trunk or, if the thigh is fixed, flexes the trunk on the thigh, as when moving from a supine to
sitting position. This action can irritate the iliopectinate bursa, as can repeated trauma from repetitive activity, including sit-ups or overuse of exercise
equipment for lower extremity strengthening.
283
284 SECTION 10 Hip and Lower Extremity Pain Syndromes
Examination of the hip and of the sacroiliac joint is normal. heat and cold may be beneficial. The repetitive movements that
Careful neurological examination of the affected lower extrem- incite the syndrome should be avoided. For patients who do not
ity should reveal no neurological deficits. If neurological deficits respond to these treatment modalities, injection of the iliopecti-
are present, evaluation for plexopathy, radiculopathy, or entrap- nate bursa with a local anesthetic and steroid may be a reasonable
ment neuropathy should be undertaken. These neurological next step.
symptoms can coexist with iliopectinate bursitis, confusing the The goals of this injection technique are first explained to
clinical diagnosis. the patient. The patient is placed in the supine position, and the
pulsation of the femoral artery at the midpoint of the inguinal
Testing ligament is identified. At a point 212 inches down and 312 inches
lateral to these femoral arterial pulsations lies the entry point of
Plain radiographs of the hip may reveal calcification of the bursa the needle. This point should be at the lateral edge of the sartorius
and associated structures consistent with chronic inflamma- muscle. Proper preparation with antiseptic solution of the skin
tion. Magnetic resonance imaging (MRI) is indicated if occult overlying this point is done. A syringe containing 9 mL of 0.25%
mass or tumor of the hip or groin is suspected and help confirm preservative-free bupivacaine and 40 mg of methylprednisolone is
the diagnosis (Figure 97-2). The injection technique described attached to a 25-gauge, 312-inch needle.
subsequently serves as a diagnostic maneuver and a therapeutic Before needle placement, the patient should be advised to say
maneuver. There! as soon as a paresthesia into the lower extremity is felt,
indicating that the needle has impinged on the femoral nerve. If a
paresthesia occurs, the needle should be withdrawn immediately
Differential Diagnosis and repositioned more laterally. The needle is advanced carefully
Iliopectinate bursitis is often attributed to primary hip or groin through the previously identified point at a 45-degree angle ceph-
pathological conditions. Radiographs of the hip and pelvis com- alad to allow the needle to pass safely beneath the femoral artery,
bined with electromyography help distinguish iliopectinate bursi- vein, and nerve. The needle is advanced slowly to avoid trauma
tis from radiculopathy or plexopathy from pain emanating from to the femoral nerve until it hits the bone at the point where the
the hip. Most patients with a lumbar radiculopathy have back ilium and pubis bones merge (Figure 97-3). The needle is with-
pain associated with reflex, motor, and sensory changes, whereas drawn out of the periosteum, and after careful aspiration for blood
patients with iliopectinate bursitis have only secondary back pain and if no paresthesia is present, the contents of the syringe are
and no neurological changes. Ilioinguinal or genitofemoral neu- gently injected into the bursa. There should be minimal resistance
ralgia sometimes may be confused with iliopectinate bursitis, to injection.
but can be distinguished by the presence of motor and sensory
changes involving these nerves. Lumbar radiculopathy and ilioin-
guinal nerve entrapment may coexist as the double crush syn-
Complications and Pitfalls
drome. The pain of iliopectinate bursitis may cause alteration of The proximity to the femoral artery, vein, and nerve makes it
gait, which may result in secondary back and radicular symptoms imperative that this procedure be done only by clinicians well
that may coexist with less common forms of bursitis. versed in the regional anatomy and experienced in perform-
ing injection techniques. Many patients also report a transient
increase in pain after injection of the iliopectinate bursa.
Treatment
Initial treatment of the pain and functional disability associated
with iliopectinate bursitis should include a combination of non- Psoas major m.
steroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
Femoral n.
(COX-2) inhibitors and physical therapy. Local application of
Femoral a.
inflamed iliopectineal bursa
Psoas major m.
Femoral v.
Iliopsoas m.
Superficial
Iliopsoas bursa trochanteric
bursa
Iliotibial tract
Inflamed superficial
trochanteric bursa
Gluteus medius m.
Tensor fasciae
latae m.
Superficial
trochanteric
Iliotibial tract bursa
Figure 98-1 The snapping sensation and pain are the result of the iliopsoas tendon subluxing over the greater trochanter or iliopectinate eminence.
syringe are gently injected. There should be minimal resistance which makes it imperative that this procedure be done only by
to injection. clinicians well versed in the regional anatomy and experienced
in performing injection techniques. Many patients report a
transient increase in pain after this injection technique. Infec-
Complications and Pitfalls tion, although rare, can occur, and careful attention to sterile
Care must be taken to rule out other conditions that may technique is mandatory.
mimic the pain of snapping hip syndrome. The main pitfall
of the described nerve block is proximity to the sciatic nerve,
Gluteus medius
muscle
Gluteus maximus
muscle
Trochanteric bursa
Greater trochanter
Figure 98-2 The symptoms of snapping
hip syndrome occur most commonly when
the patient rises from a sitting to a standing
position or when walking briskly. Often, tro-
chanteric bursitis coexists with snapping hip
syndrome, increasing the patients pain and
disability further. The type of pain often mim-
ics sciatica. (From Waldman SD: Atlas of com-
mon pain syndromes, 3rd ed, Philadelphia,
2012, Saunders, p 297.)
Gluteus
medius m
Piriformis m & t
Iliotibial tract Coccygeus m
Sciatic n
Ischium, spine
Sup gemellus m
Obturator internus
Greater trochanter m&t
Inf gemellus m
Ischium
Semimembranosus t
Vastus lateralis m
Gluteus minimus m
Gluteus medius m
Piriformis m
Sciatic n
Iliotibial tract Ischium, spine
Sup gemellus m
Inf gemellus m
Greater trochanter Obturator internus
m and t
Gluteus
maximus m
Ischium
Vastus lateralis m Semimembranosus t
Figure 98-3 The trochanteric bursa lies between the greater trochanter and the tendon of the gluteus medius and the iliotibial tract. Inf, Inferior; m,
muscle; n, nerve; t, tendon. (From Kang HS, Ahn JM, Resnick D, editors: MRI of the extremities, 2nd ed, Philadelphia, 2002, Saunders, p 221.)
98 Snapping Hip Syndrome 289
Figure 98-4 Physical examination reveals that the patient can recreate
the snapping and pain by moving from a sitting to a standing position
and adducting the hip. (From Waldman SD: Physical diagnosis of pain:
an atlas of signs and symptoms, Philadelphia, 2006, Saunders, p 320.)
A B
Figure 98-5 Resisted abduction release test is performed by having the patient assume the lateral position with the unaffected leg down. A, The
examiner firmly grasps the patients lateral thigh and has the patient abduct the hip against the examiners resistance. B, The examiner suddenly
releases the resistance against the patients active abduction. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, Philadel-
phia, 2006, Saunders, p 316.)
290 SECTION 10 Hip and Lower Extremity Pain Syndromes
Lat. femoral
cutaneous n.
Greater trochanter
Iliotibial band
Inguinal ligament
Clinical Pearls
Snapping hip syndrome frequently coexists with trochan-
teric bursitis and arthritis of the hip, which may require Figure 98-7 Injection technique to relieve the pain of snapping hip syn-
drome. (From Waldman SD: Atlas of pain management injection tech-
specific treatment to provide palliation of pain and return niques, 2nd ed, Philadelphia, 2007, Saunders, p 368.)
of function. This injection technique is extremely effective
in the treatment of snapping hip syndrome. It is a safe pro-
cedure if careful attention is paid to the clinically relevant
anatomy in the areas to be injected. Most side effects of this SUGGESTED READINGS
injection technique are related to needle-induced trauma to
Allen WC, Cope R: Coxa saltans: the snapping hip revisited, J Am Acad Orthop
the injection site and underlying tissues. Special care must Surg 3:303308, 1995.
be taken to avoid trauma to the sciatic nerve. Byrd WT: Snapping hip, Oper Techn Sports Med 13:4654, 2005.
The use of physical modalities, including local heat and Fery A, Sommelet J: The snapping hip: late results of 24 surgical cases, Int Orthop
gentle stretching exercises, should be introduced several 12:277282, 1988.
Ilizaliturri VM Jr, Camacho-Galindo J, Ramirez ANE, Lizette Y, etal: Soft tissue
days after the patient undergoes this injection technique. pathology around the hip, Clin Sports Med 30:391415, 2011.
Vigorous exercises should be avoided because they would Waldman SD: Snapping hip. In Waldman SD, Campbell RSD, editors: Imaging
exacerbate the symptoms. Simple analgesics, NSAIDs, and of pain, Philadelphia, 2011, Saunders, pp 365366.
antimyotonic agents may be used concurrently with this
injection technique.
SECTION 11 Knee Pain Syndromes
Chapter 99
Testing
The Clinical Syndrome Plain radiographs of the knee are indicated in all patients with
Tibiofibular joint pain is most often the result of arthritis of tibiofibular joint pain. Based on the patients clinical presentation,
the joint. Osteoarthritis of the joint is the most common form additional tests, including complete blood cell count, erythrocyte
of arthritis that results in tibiofibular joint pain. Rheumatoid
arthritis and posttraumatic arthritis also are common causes of
tibiofibular pain secondary to arthritis. The tibiofibular joint
is frequently damaged from falls with the foot fully medially
rotated and the knee flexed, and such trauma frequently results
in posttraumatic arthritis. Less common causes of arthritis- Posterior knee
induced tibiofibular pain include collagen-vascular diseases,
infection, villonodular synovitis, and Lyme disease. In addition
to arthritis, the tibiofibular joint is susceptible to the develop-
ment of tendinitis, bursitis, and disruption of the ligaments, car-
tilage, and tendons, all of which may cause pain and functional
disability.
Most patients with tibiofibular pain secondary to osteoarthritis
and posttraumatic arthritis report pain localized around the tibio-
fibular joint and the lateral aspect of the knee. Activity, especially
involving flexion and medial rotation of the knee, makes the pain
worse; rest and heat provide some relief. The pain is constant and
characterized as aching. The pain may interfere with sleep.
Osteoarthritis of
Signs and Symptoms tibiofibular joint
291
292 SECTION 11 Knee Pain Syndromes
sedimentation rate, and antinuclear antibody testing, may be indi- Complications and Pitfalls
cated. Magnetic resonance imaging (MRI) of the tibiofibular joint
is indicated if aseptic necrosis or occult mass or tumor is suspected Failure to identify primary or metastatic tumor of the knee or
and to help confirm the diagnosis. Bone scan may be useful to spine that is responsible for the patients pain may yield disastrous
identify occult stress fractures involving the joint, especially if results. The major complication of intra-articular injection of the
trauma has occurred. knee is infection. This complication should be exceedingly rare if
strict aseptic technique is followed. Approximately 25% of patients
report a transient increase in pain after intra-articular injection of
Differential Diagnosis the knee joint; patients should be warned of this possibility.
The tibiofibular joint is susceptible to the development of arthri-
tis from a variety of conditions that have in common the ability Clinical Pearls
to damage the joint cartilage. Acute infectious arthritis usually is
accompanied by significant systemic symptoms, including fever Coexistent bursitis and tendinitis may contribute to tib-
and malaise, and should be easily recognized by an astute clini- iofibular pain and may require additional treatment with
cian and treated appropriately with culture and antibiotics, rather more localized injection of a local anesthetic and depot ste-
than with injection therapy. The collagen-vascular diseases gener- roid. Injection of the tibiofibular joint is extremely effective
ally manifest as a polyarthropathy rather than a monarthropathy in the treatment of pain secondary to the previously men-
limited to the tibiofibular joint, although tibiofibular pain second- tioned causes of arthritis of the knee joint. This technique is
ary to collagen-vascular disease responds well to the intra-articular a safe procedure if careful attention is paid to the clinically
injection technique described subsequently. Lumbar radiculopa- relevant anatomy in the areas to be injected. Care must be
thy may mimic the pain and disability associated with arthritis of taken to use sterile technique to avoid infection and uni-
the tibiofibular joint. In patients with lumbar radiculopathy, the versal precautions to avoid risk to the operator. The use of
knee examination should be negative. Entrapment neuropathies, physical modalities, including local heat and gentle range-
such as meralgia paresthetica, and bursitis of the knee also may of-motion exercises, should be introduced several days after
confuse the diagnosis; both may coexist with arthritis of the tib- the patient undergoes this injection technique for knee
iofibular joint. Primary and metastatic tumors of the femur and pain. Vigorous exercises should be avoided because they
spine also may manifest clinically in a manner analogous to arthri- would exacerbate the symptoms.
tis of the knee.
SUGGESTED READINGS
Treatment Bozkurt M, Ylmaz E, Akseki D, Havtcolu H: Gnal : The evaluation of
Initial treatment of the pain and functional disability associ- the proximal tibiofibular joint for patients with lateral knee pain, Knee 11:
ated with arthritis of the knee should include a combina- 307312, 2004.
ztuna V, Yldz A, zer C, etal: Involvement of the proximal tibiofibular joint
tion of nonsteroidal anti-inflammatory drugs (NSAIDs) or in osteoarthritis of the knee, Knee 10:347349, 2003.
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Rethnam U, Sinha A: Instability of the proximal tibiofibular joint, an unusual
Local application of heat and cold may be beneficial. For cause for knee pain, Injury Extra 37:190192, 2006.
patients who do not respond to these treatment modalities, an Waldman SD: Arthritis pain of the knee. In Waldman SD, editor: Pain review,
Philadelphia, 2009, Saunders, p 316.
intra-articular injection of a local anesthetic and steroid may be Waldman SD: Functional anatomy of the knee. In Waldman SD, editor: Pain
a reasonable next step. review, Philadelphia, 2009, Saunders, pp 144149.
Chapter 100
JUMPERS KNEE
Figure 100-1 Patients with jumpers knee present with pain over the superior or inferior pole (or both) of the sesamoid. Jumpers knee affects the
medial and the lateral sides of the quadriceps and the patellar tendons.
Clinical Pearls
Injection of the knee is extremely effective in the treatment
of pain secondary to the previously mentioned causes of
jumpers knee. Coexistent bursitis, tendinitis, arthritis, and
internal derangement of the knee may contribute to the
patients pain and may require additional treatment with
more localized injection of local anesthetic and depot ste-
roid preparation. Injection of jumpers knee is safe if careful
attention is paid to the clinically relevant anatomy in the
areas to be injected. Care must be taken to use sterile tech-
nique to avoid infection; universal precautions should be
used to avoid risk to the operator. The incidence of ecchy-
mosis and hematoma formation can be decreased if pressure
is placed on the injection site immediately after injection.
The use of physical modalities, including local heat and
gentle range-of-motion exercises, should be introduced
several days after the patient undergoes this injection tech-
nique for tibiofibular pain. Vigorous exercises should be
avoided because they would exacerbate the symptoms. Sim-
ple analgesics and NSAIDs may be used concurrently with
this injection technique.
SUGGESTED READINGS
A B Benjamin M, Kumai T, Milz S, etal: The skeletal attachment of tendons: tendon
entheses, Comp Biochem Physiol A Mol Integr Physiol 133:931945, 2002.
Figure 100-3 Chronic patellar tendinosis. Sagittal intermediate- Draghi F, Danesino GM, Coscia D, Precerutti M, Pagani C: Overload syndromes
weighted (TR/TE, 2200/30) (A) and T2-weighted (TR/TE, 2200/80) (B) of the knee in adolescents: sonographic findings, J Ultrasound 11:151157, 2008.
spin echo magnetic resonance imaging show marked thickening of the Eifert-Mangine M, Brewster C, Wong M, etal: Patellar tendinitis in the recre-
entire patellar tendon, more pronounced in the middle and distal seg- ational athlete, Sports Med Rehabil Series 15:13591367, 1992.
ments, and indistinctness of the anterior margin of the tendon. (From Fritschy D: Jumpers knee, Oper Techn Sports Med 5:150152, 1997.
Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, Terslev L, Qvistgaard E, Torp-Pedersen S, et al: Ultrasound and power Dop-
2002, Saunders, p 3236.) pler findings in jumpers knee: preliminary observations, Eur J Ultra-
sound1318313189, 2001.
Chapter 101
SEMIMEMBRANOSUS INSERTION
SYNDROME
Semimembranosus
m&t
Vastus medialis
m
Med sup
genicular a
Adductor magnus t
Med femoral
condyle
Semitendinosus t
Med patellar
Gracilis t
retinaculum
Sartorius t
296
101 Semimembranosus Insertion Syndrome 297
Semimembranosus
Femur
Tibia
Fibula
Figure 101-2 Direct trauma to the posterior knee by kicks or tackles may cause semimembranosus insertion syndrome to develop. Semimembrano-
sus insertion syndrome is a constellation of symptoms including localized tenderness over the posterior aspect of the medial knee joint, with severe
pain elicited on palpation of the attachment of the semimembranosus muscle at the posterior medial condyle of the tibia. (Modified from Waldman
SD: Atlas of pain management injection techniques, 3rd ed, Philadelphia, 2013, Saunders, p 353.)
A C
B D
E
Figure 101-4 Injury to the semimembranosus insertion. A, Sagittal fat-suppressed proton density weighted fast spin echo (PDW FSE) image showing
bone bruising in the posteromedial tibial plateau and a hypointense fracture line (arrowheads). B, Axial fat-suppressed PDW FSE image showing com-
plete absence of the main semimembranosus tendon (arrow). C, Sagittal fat-suppressed PDW FSE image showing edema around the tibial insertions
of the semimembranosus tendon (arrows). D, Sagittal fat-suppressed PDW FSE image showing thickening and edema of the posteromedial capsule
(arrows). E, Sagittal T1-weighted spin echo image showing marked thickening and intermediate signal intensity within the tibial insertions of semi-
membranosus (arrows). (From House CV, Connell DA, Saifuddin A: Posteromedial corner injuries of the knee, Clin Radiol 62:539546, 2007.)
300 SECTION 11 Knee Pain Syndromes
of the knee, makes the pain worse (Figure 102-1); rest and heat
ICD-9 CODE 844.8 provide some relief. The pain is constant and characterized as ach-
ing; it may interfere with sleep. Coexistent bursitis, tendinitis,
arthritis, or internal derangement of the knee, in particular of the
ICD-10 CODE S83.8X9A medial meniscus, may confuse the clinical picture after trauma to
the knee joint.
Articular portion of
femur
Medial portion
of coronary ligament
Tibia
Figure 102-1 Patients with coronary ligament syndrome have pain over the medial joint and increased pain on passive external rotation of the knee.
Activity, especially involving flexion and external rotation of the knee, often makes the pain worse.
301
302 SECTION 11 Knee Pain Syndromes
Treatment
Initial treatment of the pain and functional disability associ- SUGGESTED READINGS
ated with coronary ligament strain should include a combina- Colletti JE, Kilgore KP, Derrick J: Traumatic knee pain, Ann Emerg Med
tion of nonsteroidal anti-inflammatory drugs (NSAIDs) or 53(403):409, 2009.
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local El-Khoury GY, Usta HY, Berger RA: Meniscotibial (coronary) ligament tears, Ske-
let Radiol 11:191196, 1984.
application of heat and cold may be beneficial. For patients who Lougher L, Southgate CRW, Holt MD: Coronary ligament rupture as a cause of
do not respond to these treatment modalities, injection of the medial knee pain, Arthroscopy 19:e157e158, 2003.
coronary ligament with a local anesthetic and steroid may be a Parvizi J, Kim GK: Knee ligament injuries, In Parvizi J (ed) High yield orthopaedics,
reasonable next step. Philadelphia, 2010, Saunders, pp 261264.
Chapter 103
BREASTSTROKERS KNEE
Figure 1031 The whip kick subjects the knee to extreme valgus torque and rotational forces and compression of the lateral compartment, resulting
in repetitive microtrauma to the knee.
303
304 SECTION 11 Knee Pain Syndromes
Lat patellar
retinaculum
Med patellar
retinaculum
Vastus lateralis t
Lat femoral
condyle
Figure 1032 Transverse section of the knee demonstrating the anatomy of the medial (tibial) collateral ligament. a, Artery; lat, lateral; lig, ligament;
m, muscle; med, medial; mm, muscles; n, nerve; post, posterior; t, tendon; v, vein. (From Kang A, Resnick D: MRI of the extremities: an anatomic atlas,
2nd ed, Philadelphia, 2002, Saunders, p 319.)
Differential Diagnosis
Any condition affecting the medial compartment of the knee joint
may mimic the pain of breaststrokers knee. Bursitis, meniscal
injuries, arthritis, and entrapment neuropathies may also confuse
Figure 1033 The valgus stress test for medial collateral ligament integ- the diagnosis, as may primary tumors of the knee and spine.
rity. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and
symptoms, 2nd ed, Philadelphia, 2006, Saunders, p 291.)
Treatment
Testing Initial treatment of the pain and functional disability associated
with injury to the medial collateral ligament includes a combi-
MRI is indicated in all patients with medial collateral ligament nation of nonsteroidal anti-inflammatory drugs (NSAIDs) or
pain, particularly if internal derangement or occult mass or tumor cyclooxygenase-2 (COX-2) inhibitors and physical therapy.
is suspected. In addition, MRI should be performed in all patients The local application of heat and cold may also be beneficial.
103 Breaststrokers Knee 305
Lt. fem
m
tib
Complications and Pitfalls
The major complication of injection is infection, although this
should be exceedingly rare if strict aseptic technique is followed.
Approximately 25% of patients report a transient increase in pain
A after injection of the medial collateral ligament; patients should be
warned of this possibility.
Clinical Pearls
fem m
tib
Patients with injury to the medial collateral ligament are
best examined with the knee in the slightly flexed posi-
tion. The clinician may want to examine the nonpainful
knee first to reduce the patients anxiety and ascertain the
B findings of a normal examination. The injection technique
described is extremely effective in the treatment of pain sec-
Figure 1034 A, Grade 2 tear of the medial collateral ligament with ondary to breaststrokers knee. Coexistent bursitis, tendi-
an interrupted superficial part of tibial collateral ligament (arrow). B,
A normal contralateral MCL. Fem, Femoral; Lt, left; m, meniscus; tib, tibial.
nitis, arthritis, and internal derangement of the knee may
(From Wakefield SD, DAgostino MA: Essential application of musculoskel- contribute to the patients pain, necessitating additional
etal ultrasound in rheumatology, Philadelphia, 2010, Saunders, p 271.) treatment with more localized injection of local anesthetic
and methylprednisolone.
QUADRICEPS EXPANSION
SYNDROME
Vastus lateralis
Rectus femoris
Vastus medialis
Patella
Figure 104-1 Patients with quadriceps expansion syndrome present with pain over the superior pole of the patella, more commonly on the medial
side. Pain is often increased with walking down slopes or stairs.
306
104 Quadriceps Expansion Syndrome 307
Testing
Plain radiographs of the knee are indicated in all patients with
Carrico & Shavell
quadriceps expansion syndrome pain. Based on the patients
clinical presentation, additional tests, including complete blood Figure 104-2 Injection technique to relieve pain secondary to quadri-
ceps expansion syndrome. (From Waldman SD: Atlas of pain management
cell count, erythrocyte sedimentation rate, and antinuclear anti- injection techniques, Philadelphia, 2000, Saunders, p 266.)
body testing, may be indicated. Magnetic resonance imaging
(MRI) of the knee is indicated if internal derangement, occult
mass, or tumor is suspected. Bone scan may be useful to identify
occult stress fractures involving the joint, especially if trauma has
occurred.
Complications and Pitfalls
The major complication of this injection technique is infection.
Differential Diagnosis This complication should be exceedingly rare if strict aseptic tech-
nique is followed. Approximately 25% of patients report a tran-
Anterior knee pain most commonly is due to arthritis of the knee; sient increase in pain after injection of the quadriceps tendon of
this should be readily identifiable on plain radiographs of the knee the knee, and patients should be warned of this possibility. The
and may coexist with quadriceps expansion syndrome. Another clinician also should identify coexistent internal derangement of
common cause of anterior knee pain that may mimic or coexist the knee, primary and metastatic tumors, and infection, which, if
with quadriceps expansion syndrome is suprapatellar or prepa- undiagnosed, may yield disastrous results.
tellar bursitis. Internal derangement of the knee or torn medial
meniscus may confuse the clinical diagnosis, but should be readily
identifiable on MRI of the knee.
Clinical Pearls
Treatment This injection technique is extremely effective in the treat-
ment of pain secondary to the causes of quadriceps extension
Initial treatment of the pain and functional disability associated syndrome mentioned earlier. Coexistent bursitis, tendinitis,
with quadriceps expansion syndrome should include a combi- arthritis, and internal derangement of the knee may con-
nation of nonsteroidal anti-inflammatory drugs (NSAIDs) or tribute to the patients pain and may require additional
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local treatment with more localized injection of a local anesthetic
application of heat and cold may be beneficial. For patients who and depot steroid. This technique is a safe procedure if care-
do not respond to these treatment modalities, injection of the ful attention is paid to the clinically relevant anatomy in
quadriceps expansion with a local anesthetic and steroid may be a the areas to be injected. Care must be taken to use sterile
reasonable next step. technique to avoid infection and universal precautions to
To inject the quadriceps expansion, the patient is placed in the avoid risk to the operator. The use of physical modalities,
supine position with a rolled blanket underneath the knee to flex including local heat and gentle range-of-motion exercises,
the joint gently. The skin overlying the medial aspect of the knee should be introduced several days after the patient under-
joint is prepared with antiseptic solution. A sterile syringe con- goes this injection technique for tibiofibular pain. Vigorous
taining 2 mL of 0.25% preservative-free bupivacaine and 40 mg exercises should be avoided because they would exacerbate
of methylprednisolone is attached to a 25-gauge, 112-inch needle the patients symptoms. Simple analgesics and NSAIDs
using strict aseptic technique. With strict aseptic technique, the may be used concurrently with this injection technique.
medial edge of the superior patella is identified (Figure 104-2). At
this point, the needle is inserted horizontally toward the medial
edge of the patella. The needle is advanced carefully through the
skin and subcutaneous tissues until it impinges on the medial edge SUGGESTED READINGS
of the patella. The needle is withdrawn slightly out of the peri-
Greenhill BJ: The importance of the medial quadriceps expansion in medial liga-
osteum of the patella, and the contents of the syringe are gently ment injury, Can J Surg 10:312317, 1967.
injected. There should be little resistance to injection. If resistance Heng RC, Haw CS: Patello-femoral pain syndrome: diagnosis and management
is encountered, the needle is probably in a ligament or tendon from an anatomical and biomechanical perspective, Curr Orthop 10:256266,
and should be advanced or withdrawn slightly until the injection 1996.
Waldman SD: Quadriceps expansion syndrome. In Waldman SD, editor: Atlas
proceeds without significant resistance. The needle is removed, of pain management injection techniques, Philadelphia, 2013, Saunders, p 364.
and a sterile pressure dressing and ice pack are placed at the injec- Waldman SD: Functional anatomy of the knee. In Waldman SD, editor: Pain
tion site. review, Philadelphia, 2009, Saunders, pp 144149.
Chapter 105
RUNNERS KNEE
Testing
Plain radiographs of the knee may reveal calcification of the
bursa and associated structures, including the iliotibial band
tendon, consistent with chronic inflammation. Magnetic reso-
nance imaging (MRI) and ultrasound are indicated if runners
knee, iliotibial band bursitis, internal derangement, occult mass,
or tumor of the knee is suspected. Electromyography helps
distinguish iliotibial band bursitis from neuropathy, lumbar
Figure 105-1 Also known as iliotibial band friction syndrome, runners
radiculopathy, and plexopathy. Injection of the iliotibial band knee is an overuse syndrome caused by friction injury to the iliotibial
at the friction point may serve as a diagnostic and therapeutic band as it rubs back and forth across the lateral epicondyle of the femur
maneuver. during running.
308
105 Runners Knee 309
Iliotibial band
Femur
Lateral
epicondyle
SUGGESTED READINGS
Costa ML, Marshall T, Donell ST, Phillips H: Knee synovial cyst presenting as Hamill J, Miller R, Noehren B, Davis I: A prospective study of iliotibial band
iliotibial band friction syndrome, Knee 11:247248, 2004. strain in runners, Clin Biomech 23:10181025, 2008.
Draghi F, Danesino GM, Coscia D, Precerutti M, Pagani C: Overload syndromes Waldman SD: Iliotibial band syndrome. In Waldman SD, Campbell RSD, editors:
of the knee in adolescents: sonographic findings, J Ultrasound 11:151157, 2008. Imaging of pain, Philadelphia, 2011, Saunders, pp 387388.
Ellis R, Hing W, Reid D: Iliotibial band friction syndrome: a systematic review,
Man Ther 12:200208, 2007.
Chapter 106
of the rarity of glomus tumor in areas other than the digits, diag-
ICD-9 CODE 228.00 nosis is often delayed.
A B
Figure 106-1 Axial magnetic resonance imaging of the right knee after a 40-mL saline injection into the joint showed the mass of which intensity
was low on (A) T1-weighted sequences and high on (B) T2-weighted sequences. (From Kato S, Fujii H, Yoshida A, Hinoki S: Glomus tumor beneath the
plica synovialis in the knee: a case report, Knee 14:164166, 2007.)
311
312 SECTION 11 Knee Pain Syndromes
Figure 106-3 Arthroscopy showed the soft tissue mass beneath the plica
Figure 106-2 Axial T2 fast-spin echo magnetic resonance imaging of synovialis. (From Kato S, Fujii H, Yoshida A, Hinoki S: Glomus tumor beneath
the right knee showing the lesion marked by an arrow. (From Waseem M, the plica synovialis in the knee: a case report, Knee 14:164166, 2007.)
Jari S, Paton RW: Glomus tumour, a rare cause of knee pain: a case report,
Knee 9:161163, 2002.)
Differential Diagnosis
Clinical Pearls
The triad of localized, intermittent, lancinating excruciating pain;
tenderness to palpation; and cold intolerance makes the diagnosis The diagnosis of glomus tumor of the knee is usually
apparent to an astute clinician. Glomus tumor of the knee must straightforward if the clinician identifies its unique clinical
be distinguished from other causes of localized knee pain. If a his- presentation. Because of the rare potential for aggressive,
tory of trauma is present, fracture, osteomyelitis, tenosynovitis, invasive behavior, complete excision and careful follow-up
and foreign body synovitis should be considered. If the patient are important.
has no history of trauma, tumors and diseases of the glenohumoral
joint and associated soft tissues should be considered. Reflex sym-
pathetic dystrophy should be distinguishable from glomus tumor
of the knee because the pain of reflex sympathetic dystrophy is SUGGESTED READINGS
less localized and is associated with distal trophic skin and nail Clark ML, OHara C, Dobson PJ, Smith AL: Glomus tumor and knee pain: a
changes and vasomotor and sudomotor abnormalities. report of four cases, Knee 16:231234, 2009.
Kato S, Fujii H, Yoshida A, Hinoki S: Glomus tumor beneath the plica synovialis
in the knee: a case report, Knee 14:164166, 2007.
Treatment ztekin HH: Popliteal glomangioma mimicking Bakers cyst in a 9-year-old child:
an unusual location of a glomus tumor, Arthroscopy 19:e67e71, 2003.
The mainstay of treatment of glomus tumor is surgical removal. Waseem M, Jari S, Paton RW: Glomus tumour, a rare cause of knee pain: a case
Medication management is uniformly disappointing. Injection of report, Knee 9:161163, 2002.
Chapter 107
Iliotibial band
Iliotibial bursa
Figure 107-1 The onset of iliotibial bursitis frequently occurs after long-distance cycling or jogging with worn-out shoes without proper cushioning.
Flexion of the affected knee may reproduce the pain. Often, the patient is unable to kneel or walk down stairs.
Clinical Pearls
Coexistent bursitis and tendinitis may contribute to knee
Inflamed iliotibial bursa pain and may require additional treatment with more local-
ized injection of a local anesthetic and depot steroid. Injec-
tion of the iliotibial band bursa is extremely effective in the
Inflamed iliotibial band treatment of pain secondary to iliotibial band bursitis. This
technique is a safe procedure if careful attention is paid to
the clinically relevant anatomy in the areas to be injected.
The use of physical modalities, including local heat and
gentle range-of-motion exercises, should be introduced
several days after the patient undergoes this injection tech-
nique for knee pain. Vigorous exercises should be avoided
because they would exacerbate the symptoms.
Figure 107-2 Injection technique to relieve pain secondary to iliotibial
band bursitis. (From Waldman SD: Atlas of pain management injection SUGGESTED READINGS
techniques, Philadelphia, 2000, Saunders, p 283.)
Beaman FD, Peterson JJ: MR imaging of cysts, ganglia, and bursae about the knee,
Radiol Clin North Am 45:969982, 2007.
OKeeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee,
resistance is encountered, the needle is probably in a ligament or Magn Res Imaging Clin North Am 17:725739, 2009.
tendon and should be advanced or withdrawn slightly until the Waldman SD: Injection technique to relieve pain secondary to iliotibial band bur-
sitis. In Waldman SD, editor: Atlas of pain management injection techniques,
injection proceeds without significant resistance. The needle is Philadelphia, 2000, Saunders, p 283.
removed, and a sterile pressure dressing and ice pack are placed Waldman SD: The iliotibial band bursa. In Waldman SD, editor: Pain review,
at the injection site. Philadelphia, 2009, Saunders, pp 154155.
Chapter 108
FABELLA SYNDROME
Testing
Plain radiographs are indicated in all patients with fabella to
rule out fractures and identify other accessory ossicles that may
have become inflamed. Plain radiographs also will often identify
loose bodies or joint mice. Based on the patients clinical presen- Figure 108-1 The fabella is located in the lateral head of the gastrocne-
tation, additional testing, including complete blood cell count, mius muscle in approximately 25% of patients.
315
316 SECTION 11 Knee Pain Syndromes
Clinical Pearls
Pain emanating from the knee is a common problem
Popliteal fossa encountered in clinical practice. Fabella must be distin-
Fabella guished from other more common causes of knee pain,
including Bakers cyst, bursitis, tendonitis, and synovitis.
Medial head of Careful differential diagnosis will help the clinician distin-
gastrocnemius Lateral head of guish symptomatic fabella from other causes of knee pain.
gastrocnemius
SUGGESTED READINGS
Clark AM, Matthews JG: Osteoarthritis of the fabella: a fourth knee compartment?
JR Coll Surg Edinb 36:58, 1991.
Franceschi F, Giuseppe Longo U, Ruzzini L, et al: Dislocation of an enlarged
fabella as uncommon cause of knee pain: a case report, Knee 14:330332, 2007.
Kuur E: Painful fabella: a case report with review of the literature, Acta Orthop
Scand 57:453454, 1986.
Robertson A, Jones SCE, Paes R, Chakrabarty G: The fabella: a forgotten source
of knee pain? Knee 11:243245, 2004.
Weiner DS, McNab I: The fabella syndrome: an update, J Paediatr Orthop
2:405408, 1982.
HAMSTRING TENDINITIS
Semitendinosus muscle
Signs and Symptoms
Semimembranosus muscle
Patients with hamstring tendinitis experience severe pain on
palpation over the tendinous insertion, with the medial portion Gracilis muscle
of the tendon more commonly affected than the lateral portion
(Figure 109-1). Crepitus or a creaking sensation may be felt when
palpating the tendon while the patient flexes the affected knee.
No mass in the popliteal fossa is present as is seen with Bakers
cyst. The neurological examination of a patient with hamstring
tendinitis is normal.
Testing
Plain radiographs are indicated in all patients with posterior knee
pain. Based on the patients clinical presentation, additional tests,
including complete blood cell count, erythrocyte sedimentation
rate, and antinuclear antibody testing, may be indicated. Mag-
netic resonance imaging (MRI) of the knee is indicated if internal
derangement, occult mass, Bakers cyst, or partial tendon disrup- Figure 109-1 Patients with hamstring tendinitis experience severe pain
tion is suspected. Injection of the hamstring tendons serves as a on palpation over the tendinous insertion, with the medial portion of
diagnostic and therapeutic maneuver. the tendon more commonly affected than the lateral portion.
318
109 Hamstring Tendinitis 319
should avoid the repetitive activities responsible for the develop- SUGGESTED READINGS
ment of this painful condition. For patients who do not respond Bencardino JT, Mellado JM: Hamstring injuries of the hip, Magn Res Imaging Clin
to these treatment modalities, injection of the hamstring tendons North Am 13:677690, 2005.
with a local anesthetic and steroid may be a reasonable next step. OKeeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee,
Magn Res Imaging Clin North Am 17:725739, 2009.
Orava S: Hamstring syndrome, Oper Techn Sports Med 5:143149, 1997.
Complications and Pitfalls Ptasznik R: Ultrasound in acute and chronic knee injury, Radiol Clin North Am
37:797830, 1999.
Failure to diagnose primary knee pathological processes (e.g., tears
of the medial meniscus) may lead to further pain and disability.
MRI should help identify internal derangement of the knee. The
possibility of trauma to the hamstring tendon from the injection
itself is ever present. Tendons that are highly inflamed or previ-
ously damaged are subject to rupture if they are directly injected.
This complication can be greatly decreased if the clinician uses
gentle technique and stops injecting immediately if significant
resistance to injection is encountered. The proximity to the com-
mon peroneal and tibial nerve and the popliteal artery and vein
makes it imperative that this procedure be done only by clinicians
well versed in the regional anatomy and experienced in perform-
ing injection techniques. Many patients report a transient increase
in pain after the injection technique. Although rare, infection may
occur if careful attention to sterile technique is not followed.
Clinical Pearls
The musculotendinous insertion of the hamstring group
of muscles is susceptible to the development of tendinitis
for two reasons. First, the knee joint is subjected to signifi-
cant repetitive motion under weight-bearing conditions.
Second, the blood supply to the musculotendinous unit is
poor, making healing of microtrauma difficult. Calcium
deposition around the tendon may occur if the inflamma-
tion continues, complicating subsequent treatment. Tendi-
nitis of the musculotendinous insertion of the hamstring
frequently coexists with bursitis of the associated bursa of
the knee joint, creating additional pain and functional dis-
ability. This injection technique is extremely effective in the
treatment of pain secondary to hamstring tendinitis. Coex-
istent bursitis and arthritis may contribute to knee pain
and may require additional treatment with a more localized
injection of a local anesthetic and depot steroid. This tech-
nique is a safe procedure if careful attention is paid to the
clinically relevant anatomy in the areas to be injected. The
use of physical modalities, including local heat and gentle
range-of-motion exercises, should be introduced several
days after the patient undergoes this injection technique.
Vigorous exercises should be avoided because they would
exacerbate the symptoms.
Chapter 110
320
110 Pes Anserine Bursitis 321
Sartorius muscle
Gracilis muscle
Semitendinosus
muscle
Pes anserine
bursa
Figure 110-1 Patients with pes anserine bursitis present with pain over the medial knee joint and increased pain on passive valgus and external rotation
of the knee. The patient often is unable to kneel or walk down stairs.
A B
Figure 110-3 Pes anserinus spurs. A, In this 65-year-old woman with a history of pes anserine bursitis, a conventional radiograph reveals a small
excrescence in the medial portion of the tibia. B, On coronal fat-suppressed fast spin echo (TR/TE, 3600/34) magnetic resonance imaging, fluid of
high signal intensity (arrow) is seen around the bone outgrowth. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia,
2002, Saunders, p 3898.)
Tibia
Tendons
A B
Figure 110-4 A, Drawing illustrating an anserine bursitis. This axial view shows the anserine bursa (blue) located between the medial aspect of the
tibia and the tendons forming the pes anserinus (from anterior to posterior: sartorius, gracilis, and semitendinosus). B, Axial proton density (PD)-
weighted image with fat suppression shows a fluid collection (*) located between the pes anserinus (arrowheads) and the surface of the medial
tibial condyle (T), consistent with anserine bursitis. (From Marra MD, Crema MD, Chung M, etal: MRI features of cystic lesions around the knee, Knee
15:423438, 2008.)
110 Pes Anserine Bursitis 323
Chapter 111
Extensor Peroneus
digitorum brevis m tertius m Tibia
Extensor Peroneus
digitorum longus t brevis m
Lat cuneiform Lat malleolus
Interosseous Talus
cuneocuboid lig Post inf
tibiofibular lig
3th metatarsal Post
talofibular lig
4th metatarsal Interosseous
Interosseous talocalcaneal lig
mm
Calcaneus
Plantar apon,
lat cord
Cuboid Peroneus Long Abductor digiti
longus t plantar lig minimi m
Figure 111-1 The subtalar joint is a synovial planetype articulation between the talus and the calcaneus. apon, Aponeurosis; inf, inferior; lat, lateral;
lig, ligament; m, muscle; mm, muscles; post, post; t, tendon. (From Kang A, Resnick D: MRI of the extremities: an anatomic atlas, 2nd ed, Philadelphia,
2002, Saunders, p 447.)
Clinical Pearls
Calcaneus Coexistent bursitis and tendinitis may contribute to ankle
pain and may require additional treatment with more
localized injection of a local anesthetic and depot steroid.
Injection of the subtalar joint is extremely effective in the
Figure 111-2 Most patients with subtalar joint pain secondary to osteo- treatment of pain secondary to the causes of arthritis of
arthritis and posttraumatic arthritis complain of pain that is localized the joint mentioned. This technique is a safe procedure if
deep within the heel, with a secondary dull aching pain in the ankle. careful attention is paid to the clinically relevant anatomy
in the areas to be injected. The use of physical modalities,
including local heat and gentle range-of-motion exercises,
activities that aggravate the symptoms and short-term immobili- should be introduced several days after the patient under-
zation of the ankle joint also may provide relief. For patients who goes this injection technique for ankle pain. Vigorous exer-
do not respond to these treatment modalities, an intra-articular cises should be avoided because they would exacerbate the
injection of the subtalar joint with a local anesthetic and steroid symptoms.
may be a reasonable next step. Computed tomography (CT),
326 SECTION 12 Ankle and Foot Pain Syndromes
A B C
Figure 111-3 Arthrography of the posterior subtalar joint: Abnormalities after trauma. A, In the initial coronal computed tomography (CT) scan,
aneedle has been introduced into an osteoarthritic posterior subtalar joint from a lateral approach. Also note degenerative disease with subchondral
cysts involving the ankle. B, In a similar scan after injection of anesthetic and contrast material, opacification of the posterior subtalar joint (solid arrow),
talocalcaneonavicular joint (open arrow), and ankle (arrowhead) is evident. Pain relief occurred, but could have been caused by anesthesia reaching any
of these articulations. C, In a second case, opacification of the posterior subtalar joint has resulted in similar opacification of the talocalcaneonavicular,
calcaneocuboid, and ankle joints. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 303.)
CALC
TAL
PSTJ
SUGGESTED READINGS
Henning T, Finnoff JT, Smith J: Sonographically guided posterior subtalar joint Waldman SD: Functional anatomy of the ankle and foot. In Waldman SD, editor:
injections: anatomic study and validation of 3 approaches, PM R 1:925931, Pain review, Philadelphia, 2009, Saunders, pp 155156.
2009. Ward ST, Williams PL, Purkayastha S: Intra-articular corticosteroid injections in
Anatomy: special imaging considerations of the ankle and foot. In the foot and ankle: a prospective 1-year follow-up investigation, J Foot Ankle
Surg 47:138144, 2008.
Chapter 112
Navicular bone
Cuneiform bones
Calcaneus
Talus
Cuboid bone
Figure 112-1 Midtarsal joint pain is seen in patients who repeatedly point their toes, such as ballet dancers and football punters.
112 Midtarsal Joint Pain 329
A B C
D E
Figure 112-2 Midfoot sprain suspected on radiographs and confirmed on magnetic resonance imaging (MRI). A 25-year-old woman injured her foot
while running and twisting. Radiographs initially were interpreted as normal, and the patient was told to bear weight as tolerated. Radiographs at the
authors institution were considered suspicious but not diagnostic for midfoot sprain, and MRI was performed. Fluoroscopy under anesthesia confirmed
the MRI diagnosis of Lisfranc ligament complex rupture and instability of the first through third tarsometatarsal joints. A, Anteroposterior weight-bear-
ing radiograph shows a tiny chip fracture (arrow) arising either from the medial cuneiform or the first metatarsal. B, Axial T2-weighted fat-saturated MRI
obtained through the dorsum of foot shows a ruptured dorsal Lisfranc ligament (arrow) and bone marrow edema in the medial cuneiform (arrowhead).
C, Axial T2-weighted fat-saturated MRI through midportion of Lisfranc joint shows midsubstance rupture of interosseous Lisfranc ligament (long arrow).
The first interosseous intercuneiform ligament (short arrow) is ruptured also. D, Axial T2-weighted fat-saturated MRI through the plantar aspect of the
Lisfranc joint shows small avulsion fragment from second metatarsal base (long arrow) that is not visible on radiographs. The first plantar intercuneiform
ligament (short arrow) also is ruptured. E, Coronal T2-weighted fat-saturated MRI through the Lisfranc joint demonstrates disruption of the dorsal
Lisfranc ligament (black arrow), the interosseous Lisfranc ligament (white arrow), and the plantar Lisfranc ligament (black arrowhead). (From Crim J: MR
imaging evaluation of subtle Lisfranc injuries: the midfoot sprain, Magn Res Imaging Clin North Am 16:1927, 2008.)
330 SECTION 12 Ankle and Foot Pain Syndromes
331
332 SECTION 12 Ankle and Foot Pain Syndromes
Normal
Flattened
Tibialis posterior
tendon ruptured
and frayed
Figure 113-2 Tendinitis of the posterior tibial tendon. Calcium deposition around the tendon may occur if the inflammation continues, making
subsequent treatment more difficult. Continued trauma to the inflamed tendon ultimately may result in tendon rupture.
Testing
Plain radiographs, ultrasound imaging, and magnetic resonance
imaging (MRI) are indicated for all patients with posterior ankle
pain; weight-bearing radiographs often reveal the deformity asso-
ciated with rupture of the posterior tibial tendon (Figures 113-3,
113-4, and 113-5). Based on the patients clinical presentation, B
additional tests, including complete blood count, erythrocyte
sedimentation rate, and antinuclear antibody testing, may be Figure 113-3 Injuries of the tibialis posterior tendon: Complete tears.
indicated. MRI of the ankle is indicated if joint instability is sus- Although a lateral radiograph obtained without weight bearing (A)
pected. Radionuclide bone scanning identifies stress fractures of appears normal, a lateral radiograph obtained with weight bearing (B)
shows plantar flexion of the distal portion of the talus with malalign-
the tibia not seen on plain radiographs. Injection of the posterior ment at the talonavicular joint. (From Myerson M, Solomon G, Shereff M:
tibial tendon with local anaesthetic and steroid serves as a diagnostic Posterior tibial tendon dysfunction: its association with seronegative inflam-
and therapeutic maneuver. matory disease, Foot Ankle 9:219225, 1989.)
Differential Diagnosis coexistent bursitis may confuse the diagnosis. Stress fractures
Posterior tibial tendinitis generally is identified easily on clini- of the ankle and hindfoot may mimic posterior tibial tendinitis
cal grounds. Because a bursa is located between the Achilles ten- and may be identified on plain radiographs or radionuclide bone
don and the base of the tibia and the upper posterior calcaneus, scanning.
113 Posterior Tibial Tendinitis 333
A B
Figure 113-4 Injuries of the tibialis posterior tendon: acute complete tear. A, Sagittal T1-weighted (TR/TE, 800/12) spin echo magnetic resonance
imaging (MRI) shows disorganization of the tibialis posterior tendon (white arrows) near its navicular site of insertion. Note a mass of intermediate
signal intensity around the tendon. B, Coronal T1-weighted (TR/TE, 650/20) spin echo MRI obtained with fat suppression after the intravenous
administration of a gadolinium compound reveals the torn tibialis posterior tendon (black arrow). Note the enhancement of signal intensity around
the torn tendon. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3313.)
SUGGESTED READINGS
Bowring B, Chockalingam N: Conservative treatment of tibialis posterior tendon Waldman SD: Posterior tibial tendinitis. In Waldman SD, editor: Atlas of
dysfunction: a review, Foot 20:1826, 2010. pain management injection techniques, 2nd ed, Philadelphia, 2004, Saunders,
Imhauser CW, Siegler S, Abidi NA, Frankel DZ: The effect of posterior tibialis pp 560562.
tendon dysfunction on the plantar pressure characteristics and the kinematics of Waldman SD: Posterior tibial tendon rupture. In Waldman SD, Campbell RSD,
the arch and the hindfoot, Clin Biomech 19:161169, 2004. editors: Imaging of pain, Philadelphia, 2010, Saunders, pp 435436.
Noon M, Hoch AZ, McNamara L, Schimke J: Injury patterns in female Irish
dancers, PM R 2:10301034, 2010.
Chapter 114
ACHILLES BURSITIS
Differential Diagnosis
The Clinical Syndrome Achilles bursitis generally is identified easily on clinical grounds.
Achilles bursitis is being seen with increasing frequency in clinical Because tendinitis frequently accompanies Achilles bursitis, the
practice as jogging has increased in popularity. The Achilles tendon specific diagnosis may be unclear. Stress fractures of the ankle also
is susceptible to the development of bursitis at its insertion on the may mimic Achilles bursitis and tendinitis and may be identified
calcaneus and at its narrowest part at a point approximately 5 cm on plain radiographs, MRI, or radionucleotide bone scanning.
above its insertion. The Achilles tendon also is subject to repetitive
motion injury that may result in microtrauma, which heals poorly
because of the tendons avascularity. Running is often implicated as
Treatment
the inciting factor of acute Achilles bursitis. Bursitis of the Achilles Initial treatment of the pain and functional disability associated
tendon frequently coexists with Achilles tendinitis, creating addi- with Achilles bursitis should include a combination of nonste-
tional pain and functional disability. Calcium deposition around roidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
the Achilles bursa may occur if the inflammation continues, making (COX-2) inhibitors and physical therapy. Local application of
subsequent treatment more difficult. heat and cold may be beneficial. The patient should be encour-
aged to avoid repetitive activities responsible for the evolution of
Signs and Symptoms the bursitis, such as jogging. For patients who do not respond to
these treatment modalities, the following injection technique with
The onset of Achilles bursitis is usually acute, occurring after a local anesthetic and steroid may be a reasonable next step.
overuse or misuse of the ankle joint. Inciting factors include For injection, the patient is placed in the prone position with
activities such as running and sudden stopping and starting as the affected foot hanging off the end of the table. The foot is
when playing tennis (Figure 114-1). Improper stretching of the gently dorsiflexed to facilitate identification of the margin of the
gastrocnemius and Achilles tendons before exercise has been tendon to aid in avoiding injection directly into the tendon. The
implicated in the development of Achilles bursitis, acute tendinitis, tender points at the tendinous insertion or at its narrowest part
and tendon rupture. The pain of Achilles bursitis is constant and approximately 5 cm above the insertion are identified and marked
severe and is localized in the posterior ankle. Significant sleep with a sterile marker.
disturbance is often reported. The patient may attempt to splint Proper preparation with antiseptic solution of the skin
the inflamed Achilles bursa by adopting a flat-footed gait to avoid overlying these points is carried out. A sterile syringe contain-
plantar flexion of the affected foot. Patients with Achilles bursitis ing 2 mL of 0.25% preservative-free bupivacaine and 40 mg of
experience pain with resisted plantar flexion of the foot. A creak- methylprednisolone is attached to a 25-gauge, 1-inch needle
ing or grating sensation may be palpated when passively plantar using strict aseptic technique. With strict aseptic technique, the
flexing the foot because of coexistent tendinitis. As mentioned previously marked points are palpated. The needle is carefully
previously, a chronically inflamed Achilles tendon may suddenly advanced at this point alongside the tendon through the skin and
rupture with stress or during vigorous injection procedures to subcutaneous tissues, with care taken not to enter the substance
treat Achilles bursitis. of the tendon (Figure 114-2). The contents of the syringe are
gently injected while slowly withdrawing the needle. Minimal
Testing resistance to injection should be felt. If significant resistance to
injection is noted, the needle tip is probably in the substance of
Plain radiographs are indicated in all patients with posterior the Achilles tendon and should be withdrawn slightly until the
ankle pain. Based on the patients clinical presentation, addi- injection proceeds without significant resistance. The needle is
tional tests, including complete blood cell count, erythrocyte removed, and a sterile pressure dressing and ice pack are placed
sedimentation rate, and antinuclear antibody testing, may be at the injection site.
335
336 SECTION 12 Ankle and Foot Pain Syndromes
Posterior view
Lateral view
Achilles
tendon
(narrowest
part)
5 cm
Soleus
muscle
Lateral
malleolus Calcaneus
Subtendinous
calcaneal bursa
Achilles tendon
(insertion)
Calcaneus
Figure 114-1 The onset of Achilles bursitis is usually acute, occurring after overuse or misuse of the ankle joint. Inciting factors include activities such
as running and sudden stopping and starting.
Clinical Pearls
The Achilles tendon is the thickest and strongest tendon
in the body, but it also is very susceptible to rupture. The
Achilles tendon common tendon of the gastrocnemius muscle, the Achilles
tendon begins at midcalf and continues downward to attach
Inflamed Achilles bursa to the posterior calcaneus, where it may become inflamed.
The Achilles tendon narrows during this downward course,
becoming most narrow approximately 5 cm above its calca-
neal insertion. Tendinitis and bursitis may occur at this nar-
rowest point. The previously mentioned injection technique
is extremely effective in the treatment of pain secondary to
Figure 114-2 Injection technique to relieve pain of Achilles bursitis.
(From Waldman SD: Atlas of pain management injection techniques, ed 3,
the causes of posterior ankle pain. Coexistent tendinitis and
Philadelphia, 2013, Saunders, p 443.) arthritis may contribute to posterior ankle pain and may
require additional treatment with a more localized injection
of a local anesthetic and depot steroid.
Complications and Pitfalls The injection technique is a safe procedure if careful
attention is paid to the clinically relevant anatomy in the
The possibility of trauma to the Achilles tendon from the injec- areas to be injected. The use of physical modalities, includ-
tion itself is ever present. Tendons that are highly inflamed or ing local heat and gentle range-of-motion exercises, should
previously damaged are subject to rupture if they are directly be introduced several days after the patient undergoes this
injected. This complication can be greatly decreased if the cli- injection technique for ankle pain. Vigorous exercises should
nician uses gentle technique and stops injecting immediately if be avoided because they would exacerbate the symptoms.
significant resistance to injection is encountered. Approximately Simple analgesics and NSAIDs may be used concurrently
25% of patients report a transient increase in pain after this injec- with this injection technique.
tion technique, and patients should be warned of this possibility.
114 Achilles Bursitis 337
SUGGESTED READINGS
Aronow MS: Posterior heel pain (retrocalcaneal bursitis, insertional and noninser- Van der Wall H, Lee A, Magee M, etal: Radionuclide bone scintigraphy in sports
tional Achilles tendinopathy), Clin Podiatr Med Surg 22192243, 2005. injuries, Semin Nucl Med 40:1630, 2010.
Hochman MG, Ramappa AJ, Newman JS, Farraher SW: Imaging of tendons Vyce SD, Addis-Thomas E, Mathews EE, Perez SL: Painful prominences of the
and bursae imaging of arthritis and metabolic bone disease, Philadelphia, 2009, heel, Clin Podiatr Med Surg 27:443462, 2010.
Saunders, pp 196238.
Lesic A, Bumbasirevic M: Disorders of the Achilles tendon, Curr Orthop 18:
6375, 2004.
Chapter 115
Posterior
talofibular Tibia
ligament
Fibula
Anterior
Lateral
talofibular
malleolus
ligament
Achilles
tendon (cut)
Peroneal
retinacula
Calcaneofibular
ligament
Calcaneus
338
115 Anterior Talofibular Pain Syndrome 339
ICD-9 CODE 733.99 accessory ossicles that may have become inflamed. Plain radio-
graphs also often identify loose bodies or joint mice, which are
frequently seen in patients with foot and ankle pain secondary to
ICD-10 CODE M89.8X9 accessory navicular pain syndrome. Based on the patients clini-
cal presentation, additional tests, including complete blood cell
count, erythrocyte sedimentation rate, and antinuclear antibody
The Clinical Syndrome testing, may be indicated. Magnetic resonance imaging (MRI)
of the foot and ankle joint is indicated if joint instability, loose
Foot and ankle pain secondary to accessory navicular pain syndrome bodies, occult mass, or tumor is suspected and to clarify the
is being seen with increasing frequency in clinical practice because diagnosis further (Figure 116-2). Radionucleotide bone scan-
of the increased interest in physical fitness and the use of exercise ning may be useful in identifying stress fractures or tumors of
machines. Accessory navicular pain syndrome is the name given to the foot and ankle and distal humerus that may be missed on
pain that has as its nidus an accessory ossicle occasionally found in plain radiographs.
relation to the medial navicular bone and posterior tibial tendon
(Table 116-1). It is thought that accessory ossicles such as the acces-
sory navicular decrease friction and pressure of tendons as they pass
Differential Diagnosis
in proximity to a joint. Similar accessory ossicles are found in the Primary pathology of the foot and ankle, including gout and
elbows, hands, wrists, and feet. occult fractures, especially of the navicular tuberosity, may mimic
Foot and ankle pain secondary to accessory navicular pain syn- the pain and disability associated with an accessory navicular
drome is characterized by tenderness and pain over the medial bone. Entrapment neuropathy of the posterior tibial nerve, bur-
foot and ankle. Patients often report irritation from a shoe, and sitis, and tendinitis also may confuse the diagnosisall of which
patients with accessory navicular pain syndrome may come to the may coexist with accessory navicular pain syndrome. Khlers
physicians office wearing a loose slipper on the affected foot. The bone disease and synovial chondromatosis may mimic the pain
pain of accessory navicular pain syndrome worsens with activi- associated with accessory navicular pain syndrome. Primary and
ties that require repeated range of motion of the foot and ankle metastatic tumors of the foot and ankle may present in a manner
or with high-impact forces on the foot and ankle, as seen with analogous to foot and ankle pain secondary to accessory navicular
jumping sports and high-impact aerobics routines (Figure 116-1). pain syndrome.
Accessory navicular pain syndrome is often associated with loose
bodies in the foot and ankle joint and may coexist with bursitis
and posterior tibial and Achilles tendinitis.
TABLE 116-1
340
116 Accessory Navicular Pain Syndrome 341
Achilles
tendon
Navicular
Accessory
navicular
ossicle
A B C
Figure 116-2 Ankle arthrography: Intra-articular osseous body. A, Initial radiograph shows an osseous dense area (arrowhead) adjacent to the talus.
B, Arthrography confirms the intra-articular location, the dense region producing a filling defect (arrowhead) in the contrast-filled joint cavity. C,
Computed tomography arthrography using air alone in a different patient shows an osseous fragment (arrowhead) in the lateral recess of the joint
on a direct coronal scan. Note the air in the posterior subtalar joint (arrow). (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed,
Philadelphia, 2002, Saunders, p 296.)
FIBULOCALCANEAL PAIN
SYNDROME
Posterior
talofibular Tibia
ligament
Fibula
Anterior
Lateral
talofibular
malleolus
ligament
Achilles
tendon (cut)
Peroneal
retinacula
Calcaneofibular
ligament
Calcaneus
343
344 SECTION 12 Ankle and Foot Pain Syndromes
Tibia
Med malleolus
Ant inf Post tibiotalar lig
tibiofibular lig Interosseous
talocalcaneal lig
Flexor retinaculum
Talus
Tibialis post t
Ant talofibular lig
Tibiocalcaneal lig
Calcaneofibular
lig Flexor digitorum
Peroneus longus t
brevis t Sustentaculum tali
Calcaneus Flexor hallucis longus t
Peroneus Med plantar a & n
longus t
Peroneal Quadratus plantae m
retinaculum
Abductor hallucis m
Long plantar lig
Lat plantar a & n
Abductor digiti
minimi m Flexor digitorum
Plantar apon, brevis m
lat cord Plantar apron
Figure 117-2 The fibulocalcaneal ligament runs from the apex of the fibular malleolus downward and slightly backward to a tubercle on the lateral
surface of the calcaneus. (From Kang A, Resnick D: MRI of the extremities: an anatomic atlas, 2nd ed, Philadelphia, 2002, Saunders, p 387.)
SUGGESTED READINGS
Amaral De Noronha M, Borges NG Jr: Lateral ankle sprain: isokinetic test reliability Joshy S, Abdulkadir U, Chaganti S, Sullivan S, Hariharanv K: Accuracy of MRI
and comparison between invertors and evertors, Clin Biomech 19:868871, 2004. scan in the diagnosis of ligamentous and chondral pathology in the ankle, Foot
Chou MC, Yeh LR, Chen CK-H, et al: Comparison of plain MRI and MR Ankle Surg 16:7880, 2010.
arthrography in the evaluation of lateral ligamentous injury of the ankle joint, J van Rijn RM, van Os AG, Bernsen RMD, etal: What is the clinical course of acute
Chin Med Assoc 69:2631, 2006. ankle sprains? A systematic literature review, Am J Med 121:324331, e7. 2008.
Hunt GC: Injuries of peripheral nerves of the leg, foot and ankle: an often unrec- Weber JM, Maleski RM: Conservative treatment of acute lateral ankle sprains,
ognized consequence of ankle sprains, Foot 13:1418, 2003. Clin Podiatr Med Surg 19:309318, 2002.
Chapter 118
that may have become inflamed. Plain radiographs also often iden-
ICD-9 CODE 733.99 tify loose bodies or joint mice that are frequently seen in patients
with foot and ankle pain secondary to os trigonum pain syndrome.
Based on the patients clinical presentation, additional tests,
ICD-10 CODE M89.8X9 including complete blood cell count, erythrocyte sedimentation
rate, and antinuclear antibody testing, may be indicated. Magnetic
resonance imaging (MRI) and computed tomography (CT) of the
The Clinical Syndrome foot and ankle joint is indicated if joint instability, loose bodies,
occult mass, or tumor is suspected and to further clarify the diag-
Foot and ankle pain secondary to os trigonum pain syndrome is nosis (Figure 118-2). Radionucleotide bone scanning may be use-
being seen with increasing frequency in clinical practice because ful in identifying stress fractures or tumors of the foot and ankle
of the increased interest in physical fitness and the use of exercise and distal humerus that may be missed on plain radiographs.
machines. Os trigonum pain syndrome, also known as posterior ankle
impingement syndrome, is the name given to pain that has as its nidus
an accessory ossicle occasionally found in relation to the medial
Differential Diagnosis
navicular bone and posterior tibial tendon. It is thought that acces- Primary pathology of the foot and ankle, including gout and occult
sory ossicles such as the os trigonum decrease friction and pressure of fractures especially of the navicular tuberosity, may mimic the pain
tendons as they pass in proximity to a joint. Similar accessory ossicles and disability associated with an os trigonum bone. Entrapment
are found in the elbows, hands, wrists, and feet (see Chapter 31). neuropathy of the posterior tibial nerve, bursitis, and tendinitis
Foot and ankle pain secondary to os trigonum pain syndrome also may confuse the diagnosisall of which may coexist with
is characterized by tenderness and pain over the medial foot and os trigonum pain syndrome. Khlers bone disease and synovial
ankle. The patient often reports irritation from a shoe, and often chondromatosis may mimic the pain associated with os trigonum
patients with os trigonum pain syndrome come to the physicians pain syndrome. Primary and metastatic tumors of the foot and
office wearing a loose slipper on the affected foot. The pain of ankle also may manifest in a manner analogous to foot and ankle
os trigonum pain syndrome worsens with activities that require pain secondary to os trigonum pain syndrome.
repeated range of motion of the foot and ankle or with high-
impact forces on the foot and ankle, as seen with jumping sports
and high-impact aerobics routines (Figure 118-1). Os trigonum
Treatment
pain syndrome is often associated with loose bodies in the foot Initial treatment of the pain and functional disability associ-
and ankle joint and may coexist with bursitis and posterior tibial ated with os trigonum pain syndrome should include a combi-
and Achilles tendinitis. nation of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local
Signs and Symptoms application of heat and cold may be beneficial. Avoidance of
repetitive activities that aggravate the symptoms also may provide
On physical examination, pain can be reproduced by pressure relief. For patients who do not respond to these treatment modali-
on the os trigonum bone and medial navicular. Some pes planus ties, injection of the os trigonum ossicle with a local anesthetic
deformity may be evident if serious compromise of the posterior and steroid may be a reasonable next step. For pain that persists,
tibial tendon has occurred. In contradistinction to Achilles bur- or if the os trigonum pain syndrome is causing damage to the foot
sitis, in which the tender area remains posteriorly over the area and ankle joint, surgical removal is indicated.
of the Achilles bursa, with os trigonum pain syndrome, the area
of maximal tenderness is just above the accessory ossicle itself. A
creaking or grating sensation over the posterior tibial tendon may
Complications and Pitfalls
be appreciated by the examiner with range of motion of the ankle The major complication of injection of an os trigonum ossicle is
if serious posterior tibial tendinitis is present. infection. This complication should be exceedingly rare if strict
aseptic technique is followed. Approximately 25% of patients
Testing report a transient increase in pain after injection of an os trigonum
ossicle, and patients should be warned of this possibility. Another
Plain radiographs are indicated in all patients with os trigonum potential risk of this injection technique is trauma to the extensor
pain syndrome to rule out fractures and identify accessory ossicles tendons from the injection.
346
118 Os Trigonum Pain Syndrome 347
Inflamed
accessory bone
Navicular Achilles
tendon
Tibialis posterior
tendon and sheath
Figure 118-1 The pain of os trigonum pain syndrome is often associated with high-impact force on the foot.
SP SP
A B C
Figure 118-2 A, Lateral radiograph of the ankle in a patient with posterior impingement. The os trigonum (arrow) is compressed between the pos-
terior tibia and calcaneus. B, Corresponding sagittal T1-weighted magnetic resonance imaging (MRI) shows the fatty marrow within the os trigonum
(arrow). C, On the fast spin T2-weighted MRI, high-signal intensity fluid around the os trigonum, with reactive high-signal intensity marrow edema in
the ossicle and posterior talus (broken arrows). (From Waldman SD: Os trigonum. In Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia,
2010, Saunders, pp 449450.)
BUNIONETTE PAIN
deformity is the fact that bursitis and tendinitis of the foot and
ICD-9 CODE 727.1 ankle frequently coexist with the bunion pain. Stress fractures of
the metatarsals, phalanges, or sesamoid bones also may confuse
the clinical diagnosis and require specific treatment.
ICD-10 CODE M20.10
Treatment
The Clinical Syndrome Initial treatment of the pain and functional disability associated
with bunionette deformity should include a combination of non-
Occurring less commonly than the common bunion, bunionette is steroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
a common cause of lateral foot pain. The term bunionette refers to (COX-2) inhibitors and physical therapy. Local application of
a constellation of symptoms, including soft tissue swelling over the heat and cold may be beneficial. Avoidance of repetitive activities
fifth metatarsophalangeal joint associated with abnormal angulation that aggravate the symptoms and narrow-toed or high-heeled
of the joint resulting in a prominent fifth metatarsal head with asso- shoes combined with short-term immobilization of the affected
ciated medial angulation (Figure 119-1). Bunionette also is known toes also may provide relief. For patients who do not respond to
as tailors bunion. This deformity is analogous to the hallux valgus these treatment modalities, an injection with a local anesthetic
deformity and occurs more commonly in women. The develop- and steroid may be a reasonable next step.
ment of an inflamed adventitious bursa may accompany bunionette
formation and contribute to the patients pain. A corn overlying
the fifth metatarsal head also is usually present. The most common
Complications and Pitfalls
cause of bunionette formation is the wearing of tight, narrow-toed Failure to identify primary or metastatic tumor of the foot that
shoes (Figure 119-2). High heels may exacerbate the problem. is responsible for the patients pain may yield disastrous results.
Testing
Plain radiographs are indicated in all patients with bunionette
pain. Based on the patients clinical presentation, additional tests,
including complete blood cell count, erythrocyte sedimentation
rate, and antinuclear antibody testing, may be indicated. Magnetic
A B
resonance imaging (MRI) of the fifth metatarsophalangeal joint is
indicated if joint instability, occult mass, or tumor is suspected. Figure 119-1 A, Tailors bunion deformity may be assessed radiograph-
ically with a lateral splaying in the distal fifth metatarsal. B, Clinically,
the patient generally presents with symptoms occurring laterally or
Differential Diagnosis plantarlaterally, often with an adduction of the fifth toe. (From Clinical
Practice Guideline Forefoot Disorders Panel; Thomas JL, Blitch EL IV, Chaney
The diagnosis of bunionette is usually obvious on clinical grounds DM, etal: Diagnosis and treatment of forefoot disorders. IV. Tailors bunion.
alone. Complicating the care of a patient with a typical bunion J Foot Ankle Surg 2009;48:257263.)
348
119 Bunionette Pain 349
Clinical Pearls
Pain from bunionette can be debilitating, and the defor-
mity is cosmetically unacceptable for many patients. Injec-
tion of the bunionette with a local anesthetic and steroid is
extremely effective in treating pain secondary to bunionette.
Coexistent arthritis, bursitis, and tendinitis may contribute
to bunionette pain and may require additional treatment
with more localized injection of a local anesthetic and depot
steroid.
Patients with bunionette should be advised to avoid
tight, narrow-toed shoes. The use of physical modalities,
including local heat and gentle range-of-motion exercises,
should be introduced several days after the patient under-
goes this injection technique for toe pain. Vigorous exer-
cises should be avoided because they would exacerbate the
patients symptoms. Simple analgesics and NSAIDs may be
used concurrently with this injection technique.
Fifth metatarsal
SESAMOIDITIS
Distal phalanx
2 1
3 Proximal phalanx
4
5 Medial sesamoid
Lateral sesamoid
Figure 120-1 Sesamoiditis is characterized by tenderness and pain over the metatarsal heads. The patient often feels as if he or she is walking with
a stone in the shoe.
Figure 120-2 Radiograph of a patient with an asymptomatic bipartite medial sesamoid (white arrows) and a normal lateral sesamoid (black arrow).
(From Waldman SD: Sesamoiditis. In Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2010, Saunders, pp 455456.)
352 SECTION 12 Ankle and Foot Pain Syndromes
A B
Figure 120-3 Sesamoid stress fractures. In a 26-year-old runner, sagittal T1-weighted (TR/TE, 600/14) spin echo (A) and fat-suppressed fast spin
echo (TR/TE, 4000/68) (B) magnetic resonance imaging reveal a stress fracture of the medial sesamoid bone of the first metatarsophalangeal joint.
The fracture line (arrows) and marrow edema are evident. (From Waldman SD: Sesamoiditis In Resnick D, editor: Diagnosis of bone and joint disorders,
4th ed, Philadelphia, 2002, Saunders, p 2671.)
METATARSALGIA
Testing
Plain radiographs are indicated in all patients with metatarsalgia
to rule out fractures and to identify sesamoid bones that may
have become inflamed. Based on the patients clinical presen-
tation, additional tests, including complete blood cell count,
erythrocyte sedimentation rate, and antinuclear antibody testing,
may be indicated. Magnetic resonance imaging (MRI) of the
metatarsal bones is indicated if joint instability, occult mass,
or tumor is suspected. Radionucleotide bone scanning may be
useful in identifying stress fractures that may be missed on plain Figure 121-1 On physical examination, pain can be reproduced by
radiographs of the foot. pressure on the metatarsal heads.
353
354 SECTION 12 Ankle and Foot Pain Syndromes
Clinical Pearls
Pain emanating from the forefoot is a common problem
encountered in clinical practice. Metatarsalgia must be
distinguished from stress fractures of the metatarsal bones,
Mortons neuroma, and sesamoiditis. Although the previ-
ously mentioned injection technique provides palliation
of the pain of metatarsalgia, the patient often also requires
shoe orthoses, including metatarsal bars and padded insoles,
to help remove pressure from the metatarsal heads. Coex-
istent bursitis and tendinitis may contribute to metatar-
sal pain and may require additional treatment with more
localized injection of a local anesthetic and depot steroid.
Injection of the metatarsal heads with a local anesthetic and
steroid is a safe procedure if careful attention is paid to the
clinically relevant anatomy in the areas to be injected. The
use of physical modalities, including local heat and gentle
Figure 121-2 Stress fracture of the metatarsal (march fracture). range-of-motion exercises, should be introduced several
Anteroposterior radiograph shows fluffy periosteal new bone along the days after the patient undergoes this injection technique for
distal shaft of the third metatarsal (arrow); the patient had foot pain for
16 days. (From Grainger RG, Allison D: Grainger and Allisons diagnostic metatarsalgia pain. Vigorous exercises should be avoided
radiology: a textbook of medical imaging, 3rd ed, New York, 1997, because they would exacerbate the patients symptoms.
Churchill Livingstone, 1997, p 1610.) Simple analgesics and NSAIDs may be used concurrently
with this injection technique.
forefoot pain. Primary and metastatic tumors of the foot also
may manifest in a manner analogous to that of arthritis of the SUGGESTED READINGS
midtarsal joints. Armagan OE, Shereff MJ: Injuries to the toes and metatarsals, Orthop Clin North
Am 32:110, 2001.
Treatment Bardelli M, Turelli L, Scoccianti G: Definition and classification of metatarsalgia,
Foot Ankle Surg 9:7985, 2003.
Initial treatment of the pain and functional disability associated Gregg JM, Schneider T, Marks P: MR imaging and ultrasound of metatarsalgia:
the lesser metatarsals, Radiol Clin North Am 46:10611078, 2008.
with metatarsalgia should include a combination of nonsteroidal Umans HR: Imaging sports medicine injuries of the foot and toes, Clin Sports Med
anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) 25:763780, 2006.
inhibitors and physical therapy. Local application of heat and cold Waldman SD: Metatarsalgia. In Waldman SD, editor: Pain review, Philadelphia,
may be beneficial. Avoidance of repetitive activities that aggravate 2009, Saunders, p 326.
Chapter 122
SUBMETATARSAL ADVENTITIAL
BURSITIS
A B
Figure 122-1 Adventitial bursitis. A, Clinically proven adventitial bursitis. Coronal T1 fat-suppressed scans with contrast shows a large cystic lesion
with enhancing walls prolapsing from the first web space to plantar tissues. B, A 22-year-old who had rheumatoid arthritis. Longitudinal sonogram
of fifth metatarsophalangeal joint shows severe adventitial bursitis. (From Gregg JM, Schneider T, Marks P: MR imaging and ultrasound of metatarsalgia:
the lesser metatarsals, Radiol Clin North Am 46:10611078, 2008.)
355
356 SECTION 12 Ankle and Foot Pain Syndromes
* *
A B
* *
C D
*
*
E F
G
Figure 122-2 A, Sagittal sonogram of a large partial tear in the plantar plate (asterisk). B, Transverse sonogram of a central tear in the plantar plate
(asterisk). C, Longitudinal image demonstrating moderate adventitial bursitis (arrowhead) at the level of the second metatarsophalangeal joint and a
full-thickness tear in the plantar plate (asterisk). D, Longitudinal sonogram of the fourth metatarsophalangeal joint demonstrating plantar plate rupture
(asterisk) and associated flexor tenosynovitis (arrow). E, Transverse image of plantar plate rupture (asterisks), flexor tendon lateral subluxation (arrow),
and tenosynovitis. F, Hypervascularity of an acute tear of the plantar plate with overlying adventitial bursitis (arrows). G, Longitudinal sonogram of
the lateral fibers of the second plantar plate with osteophytic change (arrow). (From Gregg JM, Schneider T, Marks P: MR imaging and ultrasound of
metatarsalgia: the lesser metatarsals, Radiol Clin North Am 46:10611078, 2008.)
122 Submetatarsal Adventitial Bursitis 357
iii
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Printed in China
It has been said that the three most dangerous things in medi- often than we would care to admit, though, when dealing with
cine are (1) a medical student with a sharp object, (2) a resident a patient with a perplexing constellation of signs and symptoms,
with a recently published study from the New England Journal of it can provide the wrong one. In fact, overreliance on Occams
Medicine, and (3) an attending physician with an anecdote. One razor can be downright dangerous for patient and physician alike.
must suspect that point 2 was at play when in the 1940s while Often, the simplest, or in the case of medical diagnosis, the most
on rounds at the University of Maryland Hospital in Baltimore, common, illness is exactly what is causing the patients symptoms.
Maryland, Theodore Woodward, MD, stated, If you hear hoof But sometimes, in our almost obsessive desire to make the diag-
beats out on Green Street, dont look for zebras! How this admoni- nosis, simplicity is our enemy. In our haste to make the patient
tion to aspiring physicians morphed into when you hear hoof beats, fit the diagnosis, we get it wrong. Uncommon diseases are called
look for horses, not zebras is anybodys guess. (My son, an ophthal- uncommon diseases because they are uncommonthey are not
mology resident in Baltimore, suggests that it was also just as likely called unknown diseases. Since the beginning of time, healers have
that this sage piece of advice was accompanied by a long-winded recognized that the correct diagnosis is the key to getting the
and confusing anecdotesee point 3.) patient well, and, as a corollary, they also realized that the wrong
On the surface, most of us would agree with Dr. Woodwards diagnosis is not a practice builder. Which brings us to country
logic that the most common things are the most common. Occam music legend Mickey Gilley.
agreed, when in the fourteenth century he put forth the philo- In 1976, Mickey Gilley recorded the classic country ballad
sophical tenant of parsimony, which proposes that simpler expla- Dont the Girls All Get Prettier at Closing Time, a plaintive lament
nations are, all things being equal, almost always better than more about loneliness and late-night desperation and how ones percep-
complex ones. He used a razor to shave away unnecessary or tion of things can change as circumstances change. What turns an
extraneous data to get to the simplest solution. The razor was all unknown disease into an uncommon disease is knowledge. What
the rage as a medical instrument in the fourteenth century, so it is changes our perception of what a constellation of symptoms and
not surprising that Occam chose it as his preferred medical device. physical findings mean when confronted with a perplexing diag-
Occams razor certainly has a nice ring to itbetter than Occams nosis is knowledge. As we gain more clinical experience, things
MRI, which would no doubt be the name of his maxim if he had that were once unknown become known, even commonplace.
lived in the twenty-first century, given that currently the MRI The more we hone our clinical acumen, the easier it is to put
is certainly our most popular medical device for shaving away the pieces together. Our perception of the diagnostic information
extraneous data. our patients present us with changes from a jumble of disparate
Which brings us to KISSnot the Gene Simmons rock band signs and symptoms to the certain diagnosis of an uncommon
KISS, but the admonition Keep it simple, stupid. KISS was set diseaseone that we will never miss again! Atlas of Uncommon
forth by Lockheed aeronautical engineer, Kelly Johnson, when he Pain Syndromes, Third Edition, seeks to accomplish three things:
handed his design team a few simple tools and challenged them to The first is to familiarize the clinician with a group of uncommon
design combat jets that could be easily fixed with the simple tools pain syndromes that occur with enough frequency that they merit
that were available in combat situations. It is still not exactly clear serious studynot rare or orphan diseases, just uncommon ones
to me who was stupid, but I certainly hope it is not the guys that are often misdiagnosed. Second, this text is written with the
who fix the jets I fly on. KISS makes sense when designing jet goal of helping clinicians reinforce their knowledge of common
engines, but what does this have to do with the individual patient? pain syndromes to help in those situations when Occam is sort of
The sick one? The scared one? The one you worry about in the correctwhen the pieces of the puzzle do not quite fit the simple
middle of the night? Unfortunately, very little. Because for the diagnosis. The third goal is more about the clinician and a little
individual patient with a difficult diagnosis, Hickam was probably less about the patient. It is about what attracted many of us to
more correct than Occam. medicine to begin with. It is the irresistible charm of being pre-
Harry Hickam, MD, while on teaching rounds at Duke Uni- sented with a difficult clinical problem and getting it right. And
versity, admonished his students and residents that Patients can what a great feeling that is! I hope you enjoy reading the third
have as many diseases as they damn well please! (also see point 3). edition of Atlas of Uncommon Pain Syndromes as much as I did
He correctly posited that when diagnosing the individual patient, writing it.
using Occams razor often provides the correct diagnosis. More Steven D. Waldman, MD, JD
vii
INDEX
359
360 Index
Chordoma, clival, 5254, 52t, 53f Computed tomography (CT) (Continued) Cyclooxygenase-2 (COX-2) inhibitors (Continued)
Chronic paroxysmal hemicrania, 78, 7f, 8f, 7t. See of thunderclap headache, 1920, 20f for pronator syndrome, 104
also Hemicrania, chronic paroxysmal. of vulvodynia, 254 for prostatodynia, 241243
Chvosteks sign, in multiple myeloma, 219 of xiphodynia, 193, 194f for psoas bursitis, 269
Cimetidine, for acute intermittent porphyria, 206 Contusions, vs. avascular necrosis of scaphoid, for quadriceps expansion syndrome, 307
Claudication, jaw. See Jaw claudication. 165166 for quadrilateral space syndrome, 99
Clavicular fractures, vs. os acromial pain syndrome, Coracoacromial ligament, calcification and for radial tunnel syndrome, 120
86 thickening of for runners knee, 308309
Clitoral priapism, 258259, 258f259f, 258t259t vs. os acromial pain syndrome, 86 for saphenous neuralgia, 273
Clitoromegaly, causes of, 259t vs. subacromial impingement syndrome, 82 for scapholunate ligament tear syndrome, 155
Clival chordoma syndrome, 5254, 52t, 53f Coronary ligament strain, 301302, 301f for scapulocostal syndrome, 60
Cluster headache vs. pes anserine bursitis, 320 for Secretans syndrome, 139
pain location in, 18f Corticosteroids. See also Steroids. for semimembranosus insertion syndrome, 297
vs. Charlins syndrome, 9, 10t for headache associated with temporal arteritis, 28 for serratus anterior muscle syndrome, 195
vs. chronic paroxysmal hemicrania, 78, 7t Costosternal syndrome, vs. devils grip, 179180 for sesamoiditis, 350
vs. cough headache, 14 Cough headache, 1315, 14f for slipping rib syndrome, 199
vs. headache associated with temporal arteritis, 28 Cox sultans, 286. See also Snapping hip syndrome. for snapping hip syndrome, 286
vs. ice pick headache, 1 Crossed finger test, 127t for sternalis syndrome, 189
vs. red ear syndrome, 47 Cubital bursitis, 106107, 106f107f for sternoclavicular syndrome, 183
vs. sexual headache, 12 Cubital tunnel syndrome, 122125, 123f124f for subacromial impingement syndrome, 82
vs. SUNCT headache, 1617, 17t Cyclooxygenase-2 (COX-2) inhibitors for submetatarsal adventitial bursitis, 357
Coin-shaped headache, 25 for accessory navicular pain syndrome, 341 for subtalar joint pain, 324325
Colitis, ischemic, 213, 213f for Achilles bursitis, 335 for superior cluneal nerve entrapment syndrome,
Collagen-vascular diseases for adductor tendinitis, 281 233
vs. ankylosing spondylitis, 230 for anconeus epitrochlearis, 109 for suprascapular nerve entrapment, 97
vs. anterior cutaneous nerve entrapment, 202 for anterior cutaneous nerve entrapment, 203 for supraspinatus tendinitis, 7475
vs. midtarsal joint pain, 327 for anterior interosseous syndrome, 130 for tibiofibular pain syndrome, 292
vs. scapulocostal syndrome, 60 for anterior talofibular pain syndrome, 339 for triangular fibrocartilage tear syndrome, 150
vs. subtalar joint pain, 324 for avascular necrosis of hip, 267 for triceps tendinitis, 117
vs. tibiofibular pain syndrome, 292 for avascular necrosis of scaphoid, 166 for trigger wrist, 175176
Colonoscopy for boxers knuckle, 146 for ulnar tunnel syndrome, 135
for proctalgia fugax, 238 for breaststrokers knee, 304305 for vulvodynia, 254255
for radiation enteritis, 207 for bunionette pain, 348 for winged scapula syndrome, 200
Computed tomography (CT) for cervicothoracic interspinous bursitis, 57 for xiphodynia, 194
of accessory navicular pain syndrome, 341f for cheiralgia paresthetica, 137 Cyst(s)
of ankylosing spondylitis, 230 for coronary ligament strain, 302 Bakers. See Bakers cyst
of anterior cutaneous nerve entrapment, 202 for cubital bursitis, 107 lunate, vs. Kienbcks disease, 162
of atypical odontalgia, 38f for cubital tunnel syndrome, 122 scaphoid, vs. avascular necrosis of scaphoid,
of avascular necrosis of scaphoid, 165 for devils grip, 180 165166
of Charlins syndrome, 9 for drivers elbow, 126127 thyroglossal duct, vs. hyoid syndrome, 66
of chronic paroxysmal hemicrania, 7 for extensor carpi ulnaris tendinitis, 169170 Cytotoxic drugs, for Pagets disease, 223
of clitoral priapism, 258259 for fabella syndrome, 316
of clival chordoma syndrome, 52 for femoral neuropathy, 271272
of cough headache, 1314 for fibulocalcaneal pain syndrome, 344 D
of devils grip, 178, 179f for flexor carpi radialis tendinitis, 173 Dawbarns sign, in supraspinatus tendinitis, 74
of diffuse idiopathic skeletal hyperostosis, 225 for foreign body synovitis, 141 De Quervains stenosing tenosynovitis
of Eagles syndrome, 35, 36f for gluteal bursitis, 261 vs. avascular necrosis of scaphoid, 165166
of epidural abscess, 215 for hamstring tendinitis, 318319 vs. scapholunate ligament tear syndrome, 155
of glossopharyngeal neuralgia, 48 for hyoid syndrome, 66 Degenerative arthritis. See Arthritis, degenerative.
of hypnic headache, 2324 for iliopectinate bursitis, 284 Demyelinating disease
of levator ani pain syndrome, 263264, 263f for iliotibial band bursitis, 313 vs. chronic paroxysmal hemicrania, 8
of liver pain, 209210, 210f for infraspinatus tendinitis, 77 vs. clival chordoma syndrome, 5253
of manubriosternal joint pain, 190, 191f for jumpers knee, 293 vs. cough headache, 14
of neck-tongue syndrome, 72 for Kienbcks disease, 163 vs. epidural abscess, 215216
of nummular headache, 25 for liver pain, 210 vs. glossopharyngeal neuralgia, 49
of os acromial pain syndrome, 86, 88f for lunotriquetral instability pain syndrome, 160 vs. headache associated with temporal arteritis, 28
in os trigonum pain syndrome, 346 for manubriosternal joint pain, 191 vs. hypnic headache, 24
of osteonecrosis of elbow joint, 113114, 115f for metatarsalgia, 354 vs. ice pick headache, 2
of Parsonage-Turner syndrome, 63 for midtarsal joint pain, 327 vs. neck-tongue syndrome, 72
of pectoralis major tear syndrome, 92 for multiple myeloma, 221 vs. nummular headache, 25
of postmastectomy pain, 185186 for neck-tongue syndrome, 72 vs. red ear syndrome, 47
of proctalgia fugax, 238 for obturator neuralgia, 277279 vs. sexual headache, 12
of prostatodynia, 241 for omohyoid syndrome, 6970 vs. SUNCT headache, 17
of radiation enteritis, 207 for orchialgia, 251253 vs. supraorbital neuralgia, 34
of red ear syndrome, 4647 for os acromial pain syndrome, 8687 Desipramine, for postmastectomy pain, 186
of sexual headache, 12 for os supratrochlearerelated elbow pain, Devils grip, 178181
of spasmodic torticollis, 55 111112 clinical pearls on, 181b
of spondylolisthesis, 227 for os trigonum pain syndrome, 346 clinical syndrome of, 178
of sternalis syndrome, 188, 189f for osteonecrosis of elbow joint, 114 complications and pitfalls of, 181
of sternoclavicular syndrome, 182183, 183f for Pagets disease, 223 differential diagnosis of, 179180
of subacromial impingement syndrome, 8182 for pectoralis major tear syndrome, 94 signs and symptoms of, 178, 178f
of subtalar joint pain, 326f for pes anserine bursitis, 320 testing for, 178, 179f
of SUNCT headache, 16 for posterior tibial tendinitis, 333 treatment of, 180181, 180f
of supraorbital neuralgia, 3 for postmastectomy pain, 186 vs. slipping rib syndrome, 198199
of temporal arteritis, 28 for proctalgia fugax, 238 vs. xiphodynia, 193194
362 Index
Diabetic neuropathy, femoral, vs. psoas bursitis, 269 Electromyography (Continued) Explosive type sexual headache, 11
Diabetic polyneuropathy. See also Neuropathic pain. in femoral neuropathy, 271 Extensor carpi ulnaris tendinitis, 169171,
vs. anterior cutaneous nerve entrapment, 202, in foreign body synovitis, 141 169f170f
204t in glomus tumor of hand, 144 vs. triangular fibrocartilage tear syndrome, 150
Diffuse idiopathic skeletal hyperostosis (DISH), in glomus tumor of knee, 311312
225226, 225t, 226f in gluteal bursitis, 260
DISH (diffuse idiopathic skeletal hyperostosis), in iliotibial band bursitis, 313 F
225226, 225t, 226f in Kienbcks disease, 162 Fabella, location of, 315, 315f
Double crush syndrome in lunotriquetral instability pain syndrome, 159 Fabella syndrome, 315317, 315f317f
anconeus epitrochlearis in, 109 in obturator neuralgia, 277 Facial pain, atypical, vs. nervus intermedius neu-
anterior interosseous syndrome in, 130 in orchialgia, 251 ralgia, 44
cheiralgia paresthetica in, 136137 in osteonecrosis of elbow joint, 113114 Facial pain syndrome(s)
cubital tunnel syndrome in, 122 in Parsonage-Turner syndrome, 63 atypical odontalgia as, 3739, 37f38f, 38t39t
drivers elbow in, 126 in postmastectomy pain, 185186 burning mouth syndrome as, 4042, 40f, 41t
gluteal bursitis in, 260261 in pronator syndrome, 104 Charlins syndrome as, 10f, 910, 10f, 10t
iliopectinate bursitis in, 284 in prostatodynia, 241 chronic paroxysmal hemicrania as, 8f, 78, 7f, 7t.
pronator syndrome in, 104 in quadrilateral space syndrome, 99 See also Hemicrania, chronic paroxysmal.
psoas bursitis in, 269 in radial tunnel syndrome, 120 Eagles syndrome as, 3536, 35f36f
Drainage, of epidural abscess, 215216 in runners knee, 308 glossopharyngeal neuralgia as, 4851, 48f50f
Drivers elbow, 126129 in saphenous neuralgia, 273 nervus intermedius neuralgia as, 4345, 43f44f
clinical pearls on, 129b in scapholunate ligament tear syndrome, 155 Ramsay Hunt syndrome as, 3234, 32f33f
clinical syndrome of, 126 in Secretans syndrome, 139 red ear syndrome as, 4647, 46f
complications and pitfalls of, 127129 in serratus anterior muscle syndrome, 195 supraorbital neuralgia as, 4f, 36, 3f, 5f6f
differential diagnosis of, 126 in spondylolisthesis, 227228 Famciclovir, for Ramsay Hunt syndrome, 34
signs and symptoms of, 126, 126f, 127t in sternalis syndrome, 188 Femoral neuropathy, diabetic, vs. psoas bursitis, 269
testing for, 126, 128f in superior cluneal nerve entrapment syndrome, Fibulocalcaneal pain syndrome, 343345,
treatment of, 126127 233 343f344f
Drugs, implicated in priapism, 258t, 259 in suprascapular nerve entrapment, 9697 Finger flexion sign, 127t
Dry pleurisy, 178. See also Devils grip. in triangular fibrocartilage tear syndrome, 150 Flexor carpi radialis tendinitis, 172174, 172f174f
Duchennes sign, 127t in ulnar tunnel syndrome, 134 Fluoxetine, for proctalgia fugax, 238239
Dull type sexual headache, 11 in vulvodynia, 254 Foot pain. See Ankle and foot pain syndromes.
Dural puncture, headache after, 3031, 31f in winged scapula syndrome, 200 Foramen magnum, surgical decompression of, for
Dystonia, in spasmodic torticollis, 55 Empyema, vs. devils grip, 179 cough headache, 1415
Enemas, steroid and sucralfate, for radiation Foreign body synovitis, 141143, 142f, 143t
enteritis, 207 vs. glomus tumor of shoulder, 9091
E Enteritis Fracture(s)
Eagles syndrome, 3536, 35f36f infectious avulsion
Egawas sign, 127t vs. abdominal angina, 213 vs. anterior talofibular pain syndrome, 339
Elastic rib belt vs. radiation enteritis, 207 vs. fibulocalcaneal pain syndrome, 344
for devils grip, 180 radiation, 207t, 207208, 208f clavicular, vs. os acromial pain syndrome, 86
for liver pain, 210 Entrapment neuropathies distal radial
for manubriosternal joint pain, 192 vs. accessory navicular pain syndrome, 340 vs. avascular necrosis of scaphoid, 165166
for multiple myeloma, 221 vs. adductor tendinitis, 281 vs. flexor carpi radialis tendinitis, 172
for Pagets disease, 223 vs. coronary ligament strain, 302 elbow, vs. os supratrochlearerelated elbow pain,
for postmastectomy pain, 186 vs. iliotibial band bursitis, 313 111
for serratus anterior muscle syndrome, 195 vs. metatarsalgia, 353354 lunate
for sternalis syndrome, 189 vs. midtarsal joint pain, 327 vs. extensor carpi ulnaris tendinitis, 169
for xiphodynia, 194 vs. os supratrochlearerelated elbow pain, 111 vs. lunotriquetral instability pain syndrome, 159
Elbow pain syndromes vs. os trigonum pain syndrome, 346 occult, vs. boxers knuckle, 146
anconeus epitrochlearis as, 108110, 108f109f vs. pes anserine bursitis, 320 pelvic, vs. adductor tendinitis, 281
anterior interosseous syndrome as, 130132, vs. runners knee, 308 scaphoid
131f132f vs. semimembranosus insertion syndrome, 297 vs. flexor carpi radialis tendinitis, 172
cubital bursitis as, 106107, 106f107f vs. sesamoiditis, 350 vs. scapholunate ligament tear syndrome, 155
cubital tunnel syndrome as, 122125, vs. subtalar joint pain, 324 stress. See Stress fractures.
123f124f vs. tibiofibular pain syndrome, 292 tibial plateau, vs. semimembranosus insertion
drivers elbow as, 126129. See also Drivers Epicondylitis syndrome, 297
elbow. elbow, vs. os supratrochlearerelated elbow pain, ulnar styloid, vs. extensor carpi ulnaris tendinitis,
os supratrochlearerelated elbow pain as, 111 169
111112, 111f112f lateral. See Tennis elbow. vs. avascular necrosis of scaphoid, 165166
osteonecrosis of elbow joint as, 113115, Epidural abscess, 215218, 216f217f, 217t vs. pectoralis major tear syndrome, 9394
113f115f, 113t Epidural blood patch, for postdural puncture Froments sign, 127t
pronator syndrome as, 103105, 103f104f headache, 3031 in anconeus epitrochlearis, 108109, 109f
radial tunnel syndrome as, 119121, 119t, Epidural nerve blocks Frozen shoulder
120f121f for ankylosing spondylitis, 231232 vs. os acromial pain syndrome, 86
triceps tendinitis as, 116118, 116f117f for diffuse idiopathic skeletal hyperostosis, 226 vs. subacromial impingement syndrome, 82
Electromyography for prostatodynia, 241243
in adductor tendinitis, 280 for spondylolisthesis, 228
in anconeus epitrochlearis, 109 Erythrocyte sedimentation rate, for temporal G
in anterior interosseous syndrome, 130 arteritis, 28 Gabapentin
in avascular necrosis of hip, 266 Erythromelelgia of ear, vs. red ear syndrome, 47 for burning mouth syndrome, 41
in avascular necrosis of scaphoid, 165 Etidronate, for Pagets disease, 223 for Charlins syndrome, 9
in cheiralgia paresthetica, 136 Exertional headache, benign for Eagles syndrome, 36
in cubital tunnel syndrome, 122 vs. cough headache, 14 for glossopharyngeal neuralgia, 49
in diffuse idiopathic skeletal hyperostosis, 225 vs. hypnic headache, 24 for nervus intermedius neuralgia, 44
in drivers elbow, 126 Expansions, in quadriceps tendon, 306 for obturator neuralgia, 277279
Index 363
Gabapentin (Continued) Hand pain syndromes. See Wrist and hand pain Hip and lower extremity pain syndromes
for Parsonage-Turner syndrome, 63 syndromes. adductor tendinitis as, 280282, 280f281f
for postmastectomy pain, 186 Handcuff neuropathy, 136 avascular necrosis of hip as, 265267, 265f267f,
for proctalgia fugax, 238239 Hawkings test, for os acromial pain syndrome, 86, 265t
for quadrilateral space syndrome, 99 88f femoral neuropathy as, 271272, 271f272f
for Ramsay Hunt syndrome, 34 Headache iliopectinate bursitis in, 283285, 283f284f
for red ear syndrome, 47 associated with temporal arteritis, 2729, 27f obturator neuralgia as, 277279, 277f278f
for saphenous neuralgia, 273 from clival chordoma, 52 psoas bursitis as, 268270, 268f269f
for SUNCT headache, 17 cough, 1315, 14f saphenous neuralgia as, 273276, 274f, 275f,
for thunderclap headache, 21 hypnic, 2324, 23f, 24t 275f. See also Saphenous neuralgia.
Gallbladder attack ice pick, 12, 1f2f snapping hip syndrome as, 286290, 287f290f.
vs. devils grip, 179 migraine. See Migraine headache. See also Snapping hip syndrome.
vs. liver pain, 210 nummular, 2526, 25f26f HLA B-27 screening
Gasserian ganglion, balloon decompression of, for postdural puncture, 3031, 31f for ankylosing spondylitis, 230
SUNCT headache, 17 sexual, 1112, 11f for gluteal bursitis, 260
Geniculate ganglion, herpes zoster involvement of, sudden unilateral neuralgiform conjunctival in spondylolisthesis, 228
in Ramsay Hunt syndrome, 32, 32f injection tearing, 1618, 16f18f, 16t18t Hooking maneuver test, for slipping rib syndrome,
Geniculate neuralgia, 43 swimmers, 3f, 4f, 5f, 6f, 6f, 3. See also 198, 198f
Genitofemoral neuralgia Supraorbital neuralgia. Horners syndrome, 7
vs. iliopectinate bursitis, 284 thunderclap, primary, 1922, 19t20t, 20f21f Humerus, tumors of, vs. pectoralis major tear
vs. orchialgia, 251 Heart attack syndrome, 9394
Giant cell arteritis, 27. See also Temporal arteritis. vs. devils grip, 179 Hyoid syndrome, 6668, 67f
Glaucoma vs. manubriosternal joint pain, 190 Hypnic headache, 2324, 23f, 24t
vs. Ramsay Hunt syndrome, 33 vs. serratus anterior muscle syndrome, 195 vs. SUNCT headache, 17
vs. supraorbital neuralgia, 3, 6f vs. slipping rib syndrome, 198199 Hypopharynx, tumors of. See Tumor(s),
Glenohumeral joint, tumors of, vs. glomus tumor of vs. sternalis syndrome, 188189 hypopharyngeal.
shoulder, 9091 vs. sternoclavicular syndrome, 183 Hysterical conversion reactions, vs. spasmodic
Glomus tumor vs. xiphodynia, 193194 torticollis, 55
of hand, 144145, 144f145f Heat therapy
of knee, 311312, 311f312f for cervicothoracic interspinous bursitis, 57
of shoulder, 9091, 90f for Ramsay Hunt syndrome, 34 I
Glossopharyngeal nerve, radiofrequency destruction Heavy chain disease, vs. multiple myeloma, 221 Ice packs, for Ramsay Hunt syndrome, 34
of, for glossopharyngeal neuralgia, 50 Heel pain, in subtalar joint pain, 324 Ice pick headache, 12, 1f2f
Glossopharyngeal nerve block, for glossopharyngeal Hemarthrosis, of knee, vs. semimembranosus vs. chronic paroxysmal hemicrania, 8
neuralgia, 50, 50f insertion syndrome, 297 vs. cough headache, 14
Glossopharyngeal neuralgia, 4851, 48f50f Hematin, for acute intermittent porphyria, 206 vs. hypnic headache, 24
vs. Eagles syndrome, 35 Hemicrania, chronic paroxysmal, 78, 7f8f, 7t vs. supraorbital neuralgia, 34
vs. hyoid syndrome, 66 pain location in, 18f Ice water test, for glomus tumor of hand, 144
vs. neck-tongue syndrome, 72 vs. Charlins syndrome, 9 Ilioinguinal nerve anatomy, orchialgia and, 251
Glossopharyngeal root, microvascular decompres- vs. cough headache, 14 Ilioinguinal neuralgia
sion of, for glossopharyngeal neuralgia, 50, 50f vs. headache associated with temporal arteritis, 28 vs. iliopectinate bursitis, 284
Glucose, for acute intermittent porphyria, 206 vs. ice pick headache, 2 vs. orchialgia, 251
Gluteal bursitis, 260261, 260f261f vs. nummular headache, 25 Iliopectinate bursitis, 283285, 283f284f
vs. gluteus medius syndrome, 249 vs. red ear syndrome, 47 Iliopsoas muscle, 283, 283f
vs. superior cluneal nerve entrapment syndrome, vs. sexual headache, 12 Iliopsoas tendon subluxation, in snapping hip
233 vs. SUNCT headache, 17 syndrome, 286, 287f
Gluteal nerve entrapment, vs. gluteus medius vs. supraorbital neuralgia, 34 Iliotibial band bursitis, 313314, 314f
syndrome, 249 Hemicrania continua, pain location in, 18f Iliotibial band friction syndrome, 308310,
Gluteus maximus muscle, function of, 244, 244f Hemorrhage, subarachnoid 308f309f
Gluteus maximus pain syndrome, 244247, thunderclap headache and, 19, 19t20t Iliotibial bursitis, with runners knee, 308
244f246f vs. postdural puncture headache, 30 Impingement interval, 81, 82f
Gluteus medius pain syndrome, 248250, Hemorrhoids, vs. proctalgia fugax, 238 Impingement syndrome, subacromial, 8185,
248f249f Henoch-Schnlein purpura, vs. abdominal angina, 81f85f, 84t. See also Subacromial impinge-
vs. levator ani pain syndrome, 264 213 ment syndrome.
Golfers elbow Hernia Indomethacin
vs. anconeus epitrochlearis, 109 inguinal for chronic paroxysmal hemicrania, 8
vs. cubital bursitis, 106 vs. adductor tendinitis, 281 for cough headache, 14
vs. cubital tunnel syndrome, 122 vs. psoas bursitis, 269 for hypnic headache, 24
vs. drivers elbow, 126 ventral, vs. anterior cutaneous nerve entrapment, for ice pick headache, 2
Gout 202, 204t for nummular headache, 26
elbow Herniated cervical disc, lateral, vs. Parsonage- for sexual headache, 12
vs. cubital bursitis, 106 Turner syndrome, 63 Infection(s)
vs. os supratrochlearerelated elbow pain, 111 Herpes zoster, acute. See Neuropathic pain. vs. postdural puncture headache, 30
vs. radial tunnel syndrome, 120 vs. anterior cutaneous nerve entrapment, 202, vs. scapulocostal syndrome, 60
vs. accessory navicular pain syndrome, 340 204t Infectious arthritis, acute See. Arthritis, infectious,
Grip of the phantom, 178. See also Devils grip. Hildreths test acute.
Groin pain syndromes. See Abdominal/groin pain for glomus tumor of hand, 144 Infectious enteritis
syndromes. for glomus tumor of knee, 311 vs. abdominal angina, 213
Hip vs. radiation enteritis, 207
arthritis of, with snapping hip syndrome, 286 Inflammatory arthritis. See Arthritis,
H avascular necrosis of, 265267, 265f267f, 265t inflammatory.
Habit spasms, vs. spasmodic torticollis, 55 vs. adductor tendinitis, 281 Infraspinatus tendinitis, 7780, 78f80f
Hamstring tendinitis, 318319, 318f internal derangement of, vs. adductor tendinitis, clinical pearls on, 80b
Hand, glomus tumor of, 144145, 144f145f 281 clinical syndrome of, 77
pathologies of, vs. gluteal bursitis, 260261 complications and pitfalls of, 7880
364 Index
Magnetic resonance imaging (MRI) (Continued) Magnetic resonance imaging (MRI) (Continued) Mesenteric vascular insufficiency, vs. anterior
of anconeus epitrochlearis, 109, 109f of quadriceps expansion syndrome, 307 cutaneous nerve entrapment, 202
of ankylosing spondylitis, 230, 232f of quadrilateral space syndrome, 101f, 99, 101f Metastatic disease
of anterior interosseous syndrome, 130, 132f of radial tunnel syndrome, 120, 121f vs. manubriosternal joint pain, 190
of anterior talofibular pain syndrome, 338 of radiation enteritis, 207, 208f vs. postmastectomy pain, 186
of atypical odontalgia, 3738, 38f of red ear syndrome, 4647 Metatarsalgia, 353354, 353f354f
of avascular necrosis of hip, 266, 266f267f of runners knee, 308, 309f vs. sesamoiditis, 350
of avascular necrosis of scaphoid, 165, 167f of saphenous neuralgia, 273, 274f vs. submetatarsal adventitial bursitis, 355357
of boxers knuckle, 146 of scapholunate ligament tear syndrome, 155, Metatarsals, stress fractures of, vs. submetatarsal
of breaststrokers knee, 304, 304f 157f adventitial bursitis, 355357
of bunionette pain, 348 of scapulocostal syndrome, 60 Midtarsal joint pain, 327330
of cervicothoracic interspinous bursitis, 57, 59f of Secretans syndrome, 139 clinical pearls on, 330b
of Charlins syndrome, 9, 10f of semimembranosus insertion syndrome, 297, clinical syndrome of, 327, 328f
of cheiralgia paresthetica, 136 299f complications and pitfalls of, 327330
of chronic paroxysmal hemicrania, 7, 8f of serratus anterior muscle syndrome, 195, 196f differential diagnosis of, 327
of clitoral priapism, 258259 of sesamoiditis, 350, 352f signs and symptoms of, 327
of clival chordoma syndrome, 53f, 52 of sexual headache, 12 testing for, 327, 329f
of coronary ligament strain, 302 of slipping rib syndrome, 198 treatment of, 327
of cough headache, 1314 of snapping hip syndrome, 286 Migraine headache
of cubital bursitis, 106 of spasmodic torticollis, 55 pain location in, 18f
of cubital tunnel syndrome, 122, 124f of spondylolisthesis, 227, 228f229f vs. cough headache, 14
of diffuse idiopathic skeletal hyperostosis, 225, of sternalis syndrome, 188 vs. headache associated with temporal arteritis, 28
226f of sternoclavicular syndrome, 182183 vs. hypnic headache, 24
of drivers elbow, 126, 128f of subacromial impingement syndrome, 8182, vs. postdural puncture headache, 30
of epidural abscess, 215, 217f 83f84f vs. sexual headache, 12
of extensor carpi ulnaris tendinitis, 169, 170f of submetatarsal adventitial bursitis, 355, 355f Monoarthritis, causes of, 143t
of fabella syndrome, 315, 316f of subtalar joint pain, 324 Monoclonal gammopathy, benign, vs. multiple
of femoral neuropathy, 271, 272f of SUNCT headache, 16 myeloma, 221
of fibulocalcaneal pain syndrome, 343, 344f of superior cluneal nerve entrapment syndrome, Mortons neuroma, vs. submetatarsal adventitial
of flexor carpi radialis tendinitis, 172, 173f 233 bursitis, 355357
of foreign body synovitis, 141, 142f of supraorbital neuralgia, 3, 5f Multiple myeloma, 219221, 219f220f
of glomus tumor of hand, 144, 145f of suprascapular nerve entrapment, 9697 vs. Pagets disease, 222223
of glomus tumor of knee, 311312, 311f312f of supraspinatus tendinitis, 74, 75f Multiple sclerosis, vs. nervus intermedius neuralgia,
of glomus tumor of shoulder, 90, 90f of temporal arteritis, 28 44
of glossopharyngeal neuralgia, 48, 49f of thunderclap headache, 20, 21f Muscle, iliopsoas, 283, 283f
of gluteal bursitis, 260 of tibiofibular pain syndrome, 291292 Muscle relaxants, for levator ani pain syndrome, 264
of gluteus maximus pain syndrome, 245, 246f of triangular fibrocartilage tear syndrome, 150, Muscle strain, vs. gluteus maximus pain syndrome,
of hamstring tendinitis, 318 152f153f 245
of hyoid syndrome, 66 of triceps tendinitis, 116117, 117f Myelography
of hypnic headache, 2324 of trigger wrist, 175 for ankylosing spondylitis, 230
of ice pick headache, 1, 2f of ulnar tunnel syndrome, 134, 134f135f for epidural abscess, 215
of iliopectinate bursitis, 284 of vulvodynia, 254, 256f for spondylolisthesis, 227
of iliotibial band bursitis, 313 of winged scapula syndrome, 200 Myocardial infarction. See Heart attack.
of infraspinatus tendinitis, 77 of xiphodynia, 193 Myofascial pain syndrome
of jumpers knee, 293, 295f Malignancy gluteus maximus, 244245
of Kienbcks disease, 162, 163f164f prostatic, vs. prostatodynia, 241 gluteus medius, 248249
of levator ani pain syndrome, 263264, 263f rectal, vs. proctalgia fugax, 238 levator ani, 262263
of liver pain, 209210, 210f recurrent, vs. radiation enteritis, 207 Myofascial trigger points
of lumbar myofascial pain syndrome, 236 vs. clitoral priapism, 259 in gluteus maximus pain syndrome, 244245, 245f
of lunotriquetral instability pain syndrome, 159 Mandibular tumors, vs. atypical odontalgia, in gluteus medius syndrome, 248249
of manubriosternal joint pain, 190 3839 in levator ani pain syndrome, 262263, 262f
of metatarsalgia, 353 Manubriosternal joint pain, 190192, 190f191f lumbar, 235236, 236f
of midtarsal joint pain, 327, 329f Manubrium, dislocation of, vs. pectoralis major tear in serratus anterior muscle syndrome, 195, 196f
of multiple myeloma, 219220, 220f syndrome, 9394 in sternalis syndrome, 188, 188f
of neck-tongue syndrome, 72 Masses sign, 127t
of nervus intermedius neuralgia, 4344, 44f Mastectomy, pain after, 185187, 185f186f
of nummular headache, 25, 26f Maxillary tumors, vs. atypical odontalgia, 3839 N
of obturator neuralgia, 277 Median nerve entrapment Nail bed ridging, in glomus tumor, 144
of omohyoid syndrome, 69 in anterior interosseous syndrome, 130, 131f Nail file sign, 127t
of orchialgia, 251 by ligament of Struthers, vs. pronator syndrome, Nasociliary neuralgia, 910, 10f, 10t
of os acromiale pain syndrome, 86, 88f 104 Nasopharynx, tumors of, vs. clival chordoma
of os supratrochlearerelated elbow pain, 111 Mediastinum, diseases of syndrome, 5253
of os trigonum pain syndrome, 346, 347f vs. manubriosternal joint pain, 190 Neck
of osteonecrosis of elbow joint, 113114, 114f vs. postmastectomy pain, 186 tumors of
of Pagets disease, 222 vs. serratus anterior muscle syndrome, 195 vs. Eagles syndrome, 35
of Parsonage-Turner syndrome, 63, 64f vs. slipping rib syndrome, 199 vs. hyoid syndrome, 66
of pectoralis major tear syndrome, 92, 95f vs. sternalis syndrome, 189 vs. omohyoid syndrome, 69
of pes anserine bursitis, 320, 321f322f Melanoma, subungual, vs. glomus tumor of hand, wry, vs. spasmodic torticollis, 55
of postdural puncture headache, 30 144 Neck pain syndromes
of posterior tibial tendinitis, 331, 333f Meniscal injury clival chordoma syndrome as, 5254, 52t, 53f
of postmastectomy pain, 185186 vs. hamstring tendinitis, 318 hyoid syndrome as, 6668, 67f
of proctalgia fugax, 238, 239f vs. jumpers knee, 293 neck-tongue syndrome as, 7273, 73f
of pronator syndrome, 104 Meralgia paresthetica omohyoid syndrome as, 70f, 6971, 69f
of prostatodynia, 241 vs. snapping hip syndrome, 286, 290f spasmodic torticollis as, 5556, 56f
of psoas bursitis, 269 vs. tibiofibular pain syndrome, 292 Neck-tongue syndrome, 7273, 73f
366 Index
Parsonage-Turner syndrome, 6265, 62f, 63t, 64f Piriformis syndrome, vs. gluteal bursitis, 260261 Radiculopathy
vs. os acromial pain syndrome, 86 Pitres-Testit sign, 127t cervical. See Cervical radiculopathy.
vs. quadrilateral space syndrome, 99 Plantar fasciitis, vs. metatarsalgia, 353354 lumbar. See Lumbar radiculopathy.
vs. subacromial impingement syndrome, 82 Pleurisy, dry, 178. See also Devils grip. Radiofrequency destruction, of glossopharyngeal
vs. suprascapular nerve entrapment, 97 Pleuritis, vs. liver pain, 210 nerve, for glossopharyngeal neuralgia, 50
Patellar bursitis, vs. jumpers knee, 293 Pneumonia Radiography
Pectoralis major tear syndrome, 9295 vs. anterior cutaneous nerve entrapment, 202 in abdominal angina, 212213, 213f
clinical pearls on, 95b vs. devils grip, 179 in accessory navicular pain syndrome, 340, 341f
clinical syndrome of, 92, 93f95f Polyarteritis nodosa, vs. anterior cutaneous nerve in Achilles bursitis, 335
complications and pitfalls of, 9495 entrapment, 202 in adductor tendinitis, 280
differential diagnosis of, 9394 Polyarteritis nodosum, vs. abdominal angina, 213 in anconeus epitrochlearis, 109
signs and symptoms of, 92, 95f Polychondritis, vs. red ear syndrome, 47 in ankylosing spondylitis, 230, 231f
testing for, 92 Polyneuropathy, diabetic, vs. ulnar tunnel syn- in anterior cutaneous nerve entrapment, 202
treatment of, 94 drome, 134 in anterior interosseous syndrome, 130
Pelvic examination, for vulvodynia, 254 Popeyes sign, in pectoralis major tear syndrome, in anterior talofibular pain syndrome, 338
Pelvic floor muscle strain, vs. levator ani pain 92, 95f in atypical odontalgia, 3738
syndrome, 264 Porphyria, acute intermittent, 205206, 205f in avascular necrosis of hip, 266
Pelvic pain syndrome(s) Posner cold induction test, for glomus tumor of in avascular necrosis of scaphoid, 165, 166f
chronic, 241 knee, 311 in boxers knuckle, 146, 147f
clitoral priapism as, 258259, 258f259f, Postdural puncture headache, 3031, 31f in breaststrokers knee, 304
258t259t Posterior ankle impingement syndrome, 346 in bunionette pain, 348, 348f
distinguishing features, 242f Posterior fossa, tumors of, vs. atypical odontalgia, in cheiralgia paresthetica, 136
gluteal bursitis as, 260261, 260f261f 3839 in coronary ligament strain, 302
gluteus maximus pain syndrome as, 244247, Posterior tibial tendinitis, 331f, 331334, in cubital bursitis, 106
244f246f 331f333f in cubital tunnel syndrome, 122
gluteus medius syndrome as, 248250, 248f249f Postherpetic neuralgia, 33 in devils grip, 178, 179f
levator ani pain syndrome as, 262264, 262f263f Postmastectomy pain, 185187, 185f186f in diffuse idiopathic skeletal hyperostosis, 225
orchialgia as, 251253, 252f, 252t253t Posttraumatic arthritis in Eagles syndrome, 35
proctalgia fugax as, 238240, 239f subtalar joint pain from, 324 in extensor carpi ulnaris tendinitis, 169
prostatodynia as, 241243, 242f, 243t vs. scapulocostal syndrome, 60 in fabella syndrome, 315
vulvodynia, 254257, 255f256f, 256t257t. See Posttraumatic edema syndrome, 139 in femoral neuropathy, 271
also Vulvodynia. Postural type sexual headache, 11 in fibulocalcaneal pain syndrome, 343
Pelvis Pregabalin in flexor carpi radialis tendinitis, 172, 174f
fractures of for burning mouth syndrome, 41 in gluteal bursitis, 260
stress, vs. gluteus maximus pain syndrome, 245 for nervus intermedius neuralgia, 44 in gluteus maximus pain syndrome, 245
vs. adductor tendinitis, 281 Prepatellar bursitis, vs. quadriceps expansion in hamstring tendinitis, 318
tumors in, vs. gluteus maximus pain syndrome, 245 syndrome, 307 in iliopectinate bursitis, 284, 284f
Peptic ulcer disease, vs. anterior cutaneous nerve Priapism in iliotibial band bursitis, 313
entrapment, 202 clitoral, 258259, 258f259f, 258t259t in infraspinatus tendinitis, 77, 79f
Peripheral neuropathy, vs. obturator neuralgia, 277 drugs implicated in, 258t in jumpers knee, 293
Persistent orodental pain syndrome, 3739, Proctalgia fugax, 238240, 239f in Kienbcks disease, 162, 164f
37f38f, 38t39t Proctitis, vs. proctalgia fugax, 238 in levator ani pain syndrome, 263264
Pes anserine bursitis, 320323 Pronator syndrome, 103105, 103f104f in liver pain, 209210
clinical pearls on, 323b vs. anterior interosseous syndrome, 130 in lumbar myofascial pain syndrome, 236
clinical syndrome of, 320, 321f Propranolol, for sexual headache, 12 in lunotriquetral instability pain syndrome, 159,
complications and pitfalls of, 320323 Prostadynia, vs. proctalgia fugax, 238 161f
differential diagnosis of, 320 Prostate exam, digital, for prostatodynia, 241 in manubriosternal joint pain, 190, 190f
signs and symptoms of, 320 Prostatic malignancy, vs. prostatodynia, 241 in metatarsalgia, 353, 354f
testing for, 320, 321f322f Prostatitis, chronic nonbacterial, 241 in midtarsal joint pain, 327
treatment of, 320 Prostatodynia, 241243, 242f, 243t in multiple myeloma, 219220, 220f
Physical therapy Psoas bursitis, 268270, 268f269f in obturator neuralgia, 277
for ankylosing spondylitis, 231232 Psyllium, for radiation enteritis, 207 in os supratrochlearerelated elbow pain, 111
for cubital bursitis, 107 Pulmonary embolus in os trigonum pain syndrome, 346, 347f
for cubital tunnel syndrome, 122 vs. devils grip, 179 in osteonecrosis of elbow joint, 113114
for diffuse idiopathic skeletal hyperostosis, 226 vs. liver pain, 210 in Pagets disease, 222
for flexor carpi radialis tendinitis, 173 in pes anserine bursitis, 320, 322f
for foreign body synovitis, 141 in posterior tibial tendinitis, 331, 332f
for gluteal bursitis, 261 Q in postmastectomy pain, 185186
for gluteus maximus pain syndrome, 245 Quadriceps expansion syndrome, 306307, in pronator syndrome, 104
for gluteus medius syndrome, 249 306f307f in psoas bursitis, 269, 269f
for infraspinatus tendinitis, 77 Quadrilateral space syndrome, 99102 in quadriceps expansion syndrome, 307
for levator ani pain syndrome, 264 clinical pearls on, 102b in runners knee, 308
for lumbar myofascial pain syndrome, 236 clinical syndrome of, 99, 100f101f in saphenous neuralgia, 273
for orchialgia, 251253 complications and pitfalls of, 101102 in scapholunate ligament tear syndrome, 155,
for os acromial pain syndrome, 8687 differential diagnosis of, 99 157f
for Parsonage-Turner syndrome, 64 signs and symptoms of, 99 in scapulocostal syndrome, 60
for radial tunnel syndrome, 120 testing for, 99, 100f101f in Secretans syndrome, 139
for Secretans syndrome, 139 treatment of, 99 in semimembranosus insertion syndrome, 297
for spondylolisthesis, 228 in serratus anterior muscle syndrome, 195
for subacromial impingement syndrome, 82 in sesamoiditis, 350, 351f
for supraspinatus tendinitis, 7475 R in slipping rib syndrome, 198
Piriform sinus tumors Radial neuropathies, compressive, causes of, 138t in snapping hip syndrome, 286
vs. clival chordoma syndrome, 5253 Radial tunnel syndrome, 119121, 119t, 120f121f in spondylolisthesis, 227, 228f
vs. glossopharyngeal neuralgia, 49 Radiation enteritis, 207208, 207t, 208f in sternalis syndrome, 188
vs. neck-tongue syndrome, 72 Radiation therapy, for multiple myeloma, 221 in sternoclavicular syndrome, 182183
368 Index
Wrist and hand pain syndromes (Continued) Wrist and hand pain syndromes (Continued) Z
Kienbcks disease as, 162164, 162f164f trigger wrist as, 175177 Zinc oxide ointment
lunotriquetral instability pain syndrome as, ulnar tunnel syndrome as, 133135 for radiation enteritis, 207
159161, 159f161f Wristwatch sign, for cheiralgia paresthetica, 136, for Ramsay Hunt syndrome, 34
scapholunate ligament tear syndrome as, 137f Zygoma, tumors of, vs. atypical odontalgia, 3839
155158, 156f157f. See also Scapholu- Wry neck, vs. spasmodic torticollis, 55
nate ligament tear syndrome.
Secretans syndrome as, 139140, 139f
triangular fibrocartilage tear syndrome as, X
149154, 149f, 151f154f. See also Trian- Xiphodynia, 193194, 193f194f
gular fibrocartilage tear syndrome.