Professional Documents
Culture Documents
Chapter 1
ICE PICK HEADACHE
ICD-9 CODE 784.0
ICD-10 CODE
R51
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
demyelinating disease (Figure 1-2). Magnetic resonance angiography (MRA) also may be useful in helping identify aneurysms,
which may be responsible for the patients neurological findings.
In patients who cannot undergo MRI, such as a patient with a
pacemaker, computed tomography (CT) is a reasonable second
choice. Radionuclide bone scanning and plain radiography are
indicated if fracture or bony abnormality, such as metastatic disease, is considered in the differential diagnosis.
Treatment
Ice pick headache uniformly responds to treatment with indomethacin. 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 reasonable 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 function. 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 disturbance and depression are best treated with a tricyclic antidepressant compound, such as nortriptyline, which can be started at a
single bedtime dose of 25 mg.
Figure 1-2 Diffuse pachymeningeal and calvarial metastasis from carcinoma of the breast. Axial T1-weighted postgadolinium MRI shows
diffuse nodular and bandlike contrast-enhanced thickening of the dura
over the high right frontoparietal convexity. (From Haaga JR, Lanzieri
CF, Gilkeson RC, editors: CT and MR imaging of the whole body, 4th ed,
Philadelphia, 2003, Mosby, p 198.)
Failure to correctly diagnose ice pick headache may put the patient
at risk if intracranial pathological conditions or demyelinating disease, which may mimic the clinical presentation of chronic paroxysmal hemicrania, is overlooked. MRI is indicated in all patients
thought to be suffering from ice pick headache. Failure to diagnose glaucoma, which also may cause intermittent ocular pain,
may result in permanent loss of sight.
Clinical Pearls
The diagnosis of ice pick headache is made by obtaining
a thorough, targeted headache history. Patients suffering
from ice pick headache should have a normal neurological
examination. If the results of the neurological examination
are abnormal, the diagnosis of ice pick headache should be
discarded and a careful search for the cause of the neurological findings should be undertaken.
Differential Diagnosis
Ice pick headache is a clinical diagnosis supported by a combination of clinical history, normal physical examination, radiography, and MRI. Pain syndromes that may mimic ice pick headache
include trigeminal neuralgia involving the first division of the
trigeminal nerve, demyelinating disease, and chronic paroxysmal
hemicrania. Trigeminal neuralgia involving the first division 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
SUGGESTED READINGS
Cutrer FM, Boes CJ: Cough, exertional, and sex headaches, Neurol Clin 22:
133149, 2004.
Dafer RM: Neurostimulation in headache disorders, Neurol Clin 28:835841,
2010.
Mathew NT: Indomethacin responsive headache syndromes: headache, J Head
Face Pain 21:147150, 1981.
Pascual J: Other primary headaches, Neurol Clin 27:557571, 2009.
Tuba T, Serap , Esra O, etal: Features of stabbing, cough, exertional and sexual headaches in a Turkish population of headache patients, J Clin Neurosci
15:774777, 2008.
Chapter 2
SUPRAORBITAL NEURALGIA
Differential Diagnosis
Supraorbital neuralgia is a clinical diagnosis supported by a combination of clinical history, normal physical examination, radiography, CT, and MRI. Pain syndromes that may mimic supraorbital
Inflamed
supraorbital n.
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
Figure 2-1 The supraorbital nerve sends fibers all the way to the vertex
of the scalp and provides sensory innervation to the forehead, upper
eyelid, and anterior scalp. n, Nerve.
Figure 2-2 Occasionally, a patient with supraorbital neuralgia complains that the hair on the front of the head hurts. The supraorbital
nerve sends fibers all the way to the vertex of the scalp and provides
sensory innervation to the forehead, upper eyelid, and anterior scalp.
neuralgia include ice pick headache, trigeminal neuralgia involving the first division of the trigeminal nerve, demyelinating disease, and chronic paroxysmal hemicrania. Trigeminal neuralgia
involving the first division 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 lasts
much longer than the paroxysmal pain of supraorbital neuralgia
and is associated with redness and watering of the ipsilateral eye.
Treatment
The primary treatment intervention for supraorbital neuralgia is
the identification and removal of anything causing compression
of the supraorbital nerves (e.g., tight welding or swim goggles).
A brief trial of simple analgesics alone or in combination with
gabapentin also should be considered. For patients who do not
respond to these treatments, supraorbital nerve block with local
anesthetic and a steroid is a reasonable next step.
To perform supraorbital nerve block, the patient is placed in
the supine position. Using a 10-mL sterile syringe, 3 mL of local
anesthetic is drawn up. When treating supraorbital neuralgia with
2 Supraorbital Neuralgia 5
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 frontal 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.)
Fixed
semidilated
pupil
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 n.
Supraorbital notch
Chapter 3
CHRONIC PAROXYSMAL HEMICRANIA
R51
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
demyelinating disease (Figure 3-2). Magnetic resonance angiography (MRA) also may be useful in identifying aneurysms, which
may be responsible for the patients neurological findings. In
patients who cannot undergo MRI, such as a patient with a pacemaker, computed tomography (CT) is a reasonable second choice.
Radionuclide bone scanning and plain radiography are indicated
if fracture or bony abnormality such as metastatic disease is considered in the differential diagnosis.
Screening laboratory tests consisting of complete blood cell
count, erythrocyte sedimentation rate, and automated blood
chemistry testing should be performed if the diagnosis of chronic
TABLE 3-1
Cluster
Headache
Chronic
Paroxysmal
Hemicrania
Gender predominance
Male
Female
Response to indomethacin
Negative
Positive
Chronobiological pattern
Positive
Negative
Alcohol trigger
Positive
Negative
Length of attacks
Longer
Shorter
Horners syndrome
Present
Present
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 cluster headache lasts much
longer than the pain of chronic paroxysmal hemicrania, and cluster
headache has a male predominance, a chronobiological pattern of
attacks, and a lack of response to treatment with indomethacin.
Treatment
Clinical Pearls
B
Figure 3-2 Sagittal (A) and semiaxial (B) T2-weighted images of a massive prolactinoma in a 41-year-old man with chronic daily headache.
(From Benitez-Rosario MA, McDarby G, Doyle R, Fabby G. Chronic clusterlike headache secondary to prolactinoma: uncommon cephalalgia in association with brain tumors, J Pain Symptom Manage 37:271276, 2009.
Differential Diagnosis
Chronic paroxysmal hemicrania is a clinical diagnosis supported by
a combination of clinical history, abnormal physical examination
during attacks, radiography, and MRI. Pain syndromes that may
mimic chronic paroxysmal hemicrania include cluster headache,
trigeminal neuralgia involving the first division of the trigeminal
nerve, demyelinating disease, and ice pick headache. Trigeminal
neuralgia involving the first division of the trigeminal nerve is
Chapter 4
CHARLINS SYNDROME
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
demyelinating disease (Figure 4-2). Magnetic resonance angiography (MRA) also may be useful in helping identify aneurysms,
which may be responsible for the patients neurological findings.
In patients who cannot undergo MRI, such as a patient with a
pacemaker, computed tomography (CT) is a reasonable second
choice. Radionuclide bone scanning and plain radiography are
indicated if fracture or bony abnormality such as metastatic disease is considered in the differential diagnosis.
Screening laboratory tests consisting of complete blood cell
count, erythrocyte sedimentation rate, and automated blood
chemistry testing should be performed if the diagnosis of Charlins syndrome is in question. Intraocular pressure should be measured if glaucoma is suspected.
Differential Diagnosis
Charlins syndrome is a clinical diagnosis supported by a combination of clinical history, normal physical examination, radiography, and MRI. Pain syndromes that may mimic Charlins
syndrome include cluster headache, temporal arteritis, trigeminal neuralgia involving the first division of the trigeminal nerve,
demyelinating disease, and chronic paroxysmal hemicrania (see
Table 4-1). Trigeminal neuralgia involving the first division 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 lasts much longer than the pain of
Charlins syndrome.
Treatment
The treatment of Charlins syndrome is analogous to the treatment of trigeminal neuralgia. The use of anticonvulsants such as
carbamazepine and gabapentin represents a reasonable starting
point. High-dose steroids tapered over 10 days also have been
anecdotally reported to provide relief. For patients who do not
respond to the previously mentioned treatments, daily nasociliary
ganglion block with local anesthetic and steroid is a reasonable
next step. Underlying sleep disturbance and depression associated
with the pain of supraorbital neuralgia are best treated with a tricyclic antidepressant compound, such as nortriptyline, which can
be started at a single bedtime dose of 25 mg.
Cluster
Headache
Charlins
Syndrome
Yes
Yes
Unilateral
Yes
Yes
Yes
Yes
Severe intensity
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
No
No
Yes
Yes
No
Yes
No
No
Yes
Responds to sphenopalatine
ganglion block
Yes
No
No
Yes
demyelinating disease, which may mimic the clinical presentation 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 problems, including cavernous sinus thrombosis and intracranial
and retroorbital tumors, Charlins syndrome must remain a
diagnosis of exclusion. All patients suspected to have Charlins syndrome require MRI of the brain with and without
gadolinium contrast material and thorough ophthalmological and neurological evaluation. Nasociliary nerve block via
the medial orbital approach should be performed only by
clinicians familiar with the regional anatomy.
SUGGESTED READINGS
Figure 4-1 Patients suffering from Charlins syndrome present with the
complaint of severe paroxysms of ocular or retroorbital pain that radiates 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
R51
Figure 5-1 Sexual headaches show no gender predilection and are generally benign.
11
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, demyelinating disease, and hemorrhage. More important, MRI helps
identify bleeding associated with leaking intracranial aneurysms.
Magnetic resonance angiography (MRA) may be useful in helping identify aneurysms responsible for the patients neurological
symptoms. In patients who cannot undergo MRI, such as patients
with pacemakers, computed tomography (CT) is a reasonable
second choice. Even if blood is not present on MRI or CT, if
intracranial hemorrhage is suspected, lumbar puncture should be
performed.
Screening laboratory tests consisting of complete blood cell
count, erythrocyte sedimentation rate, and automated blood
chemistry testing should be performed if the diagnosis of sexual
headache is in question. Intraocular pressure should be measured
if glaucoma is suspected.
Differential Diagnosis
Sexual headache is a clinical diagnosis supported by a combination of clinical history, normal physical examination, radiography, MRI, and MRA. Pain syndromes that may mimic sexual
headache include trigeminal neuralgia involving the first division of the trigeminal nerve, demyelinating disease, cluster headache, migraine, and chronic paroxysmal hemicrania. Trigeminal
neuralgia involving the first division 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 sexual headache. Migraine headache may or may not be associated with nonpainful neurological findings known as aura, but
the patient almost always reports some systemic symptoms, such
as nausea or photophobia, not typically associated with sexual
headache.
Treatment
It is generally thought that avoiding the inciting activity for a few
weeks decreases the propensity to trigger sexual headaches. If this
avoidance technique fails or is impractical because of patient preference, a trial of propranolol is a reasonable next step. A low dose
of 20 to 40 mg as a daily dose and titrating in 20-mg increments
to 200 mg as a divided daily dose until prophylaxis occurs treats
Clinical Pearls
The diagnosis of sexual headache is made by obtaining a
thorough, targeted headache history. As mentioned earlier,
patients may not be forthcoming about the events surrounding the onset of their headache, and the clinician should be
sensitive to this fact. Patients suffering from sexual headache should have a normal neurological examination. If
the neurological examination is abnormal, the diagnosis of
sexual headache should be discarded and a careful search
for the cause of the patients neurological findings should
be undertaken.
SUGGESTED READINGS
Evans RW: Diagnostic testing for migraine and other primary headaches, Neurol
Clin 27:393415, 2009.
Hu CM, Lin YJ, Fan YK, etal: Isolated thunderclap headache during sex: orgasmic headache or reversible cerebral vasoconstriction syndrome? J Clin Neurosci
17:13491351, 2010.
Jolobe OMP: The differential diagnosis includes reversible cerebral vasoconstrictor
syndrome, Am J Emerg Med 28:637, 2010.
Kim HJ, Seo SY: Recurrent emotion-triggered headache following primary headache associated with sexual activity, J Neurol Sci 273:142143, 2008.
Tuba T, Serap , Esra O, etal: Features of stabbing, cough, exertional and sexual headaches in a Turkish population of headache patients, J Clin Neurosci
15:774777, 2008.
Chapter 6
COUGH HEADACHE
R51
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 demyelinating disease. Special attention to the foramen magnum may help identify more subtle abnormalities responsible
for posterior fossa neurological signs and symptoms. MRI helps
identify bleeding associated with leaking intracranial aneurysms,
which may mimic the symptoms of both types of cough headache. Magnetic resonance angiography (MRA) may be useful in
helping identify aneurysms responsible for the patients neurological symptoms. In patients who cannot undergo MRI, such as
patients with pacemakers, computed tomography (CT) is a reasonable second choice. Lumbar puncture should be performed if
intracranial hemorrhage is suspected, even if blood is not present
on MRI or CT. Plain radiographs of the cervical spine also may
be useful in the evaluation of Arnold-Chiari malformations and
13
Herniation of
cerebellar tonsil
Figure 6-1 Symptomatic cough headache is often
associated with structural abnormalities, such as
Arnold-Chiari malformation, and usually occurs in the
third decade of life.
Spinal cord
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 paroxysmal hemicrania. Trigeminal neuralgia involving the first division 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 findings known as aura, but the patient almost always reports some
systemic symptoms, such as nausea or photophobia, not typically
associated with cough headache.
Treatment
Figure 6-2 Low-lying cerebellar tonsils (straight arrows) of a Chiari malformation are shown deforming the medulla (curved arrow) in a sagittal
T1-weighted spin echo image. 4, Fourth ventricle. (From Stark DD, Bradley WG Jr, editors: Magnetic resonance imaging, 3rd ed, St Louis, 1999,
Mosby, p 1841.)
Indomethacin is the treatment of choice for benign cough headache. 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. Indomethacin must be used carefully, if at all, in patients with peptic
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.
Underlying sleep disturbance and depression are best treated with
a tricyclic antidepressant compound, such as nortriptyline, which
can be started at a single bedtime dose of 25 mg.
The only uniformly effective treatment for symptomatic cough
headache is surgical decompression of the foramen magnum.
6 Cough Headache 15
This surgery is usually done via suboccipital craniectomy. Surgical decompression prevents the low-lying cerebellar tonsils from
obstructing the flow of spinal fluid from the cranium to the spinal
subarachnoid space during a Valsalva maneuver.
Clinical Pearls
Any patient presenting with headaches associated with
exertion or Valsalva maneuver should be taken very seriously. Although statistically most of these headaches ultimately 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 headache history and performing a careful physical examination.
The clinician must separate patients suffering from benign
cough headache from patients suffering from symptomatic cough headache. Patients with benign cough headache
should have a normal neurological examination. If the neurological 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.
SUGGESTED READINGS
Berciano J, Poca M-A, Garca A, Sahuquillo J: Paroxysmal cervicobrachial coughinduced pain in a patient with syringomyelia extending into spinal cord posterior gray horns, J Neurol 54:678681, 2007.
Chen YY, Lirng JF, Fuh JL, etal: Primary cough headache is associated with posterior fossa crowdedness: a morphometric MRI study, Cephalalgia 24:694699,
2004.
Pascual J: Primary cough headache, Curr Pain Headache Rep 9:272276, 2005.
Pascual J, Rubn Martn A, Oterino A: Headaches precipitated by cough, prolonged exercise or sexual activity: a prospective etiological and clinical study,
JHeadache Pain 9:259266, 2008.
Waldman SD: Arnold Chiari malformation type I. In Waldman SD, Campbell
RS, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 2728.
Waldman SD: Arnold Chiari malformation type II. In Waldman SD, Campbell
RS, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 2930.
Chapter 7
SUDDEN UNILATERAL
NEURALGIFORM CONJUNCTIVAL
INJECTION TEARING HEADACHE
ICD-9 CODE 350.1
ICD-10 CODE G50.0
The Clinical Syndrome
Sudden unilateral neuralgiform conjunctival injection tearing
(SUNCT) headache is an uncommon primary headache disorder
that is one of a group of three headache syndromes known as the
trigeminal autonomic cephalgias (Table 7-1). Whether SUNCT
headache is in fact a distinct headache entity or simply a constellation of symptoms that occurs on a continuum along with
the other trigeminal autonomic cephalgias is a point of ongoing
debate among headache and pain management specialists (Figure
7-1). As with most headache syndromes, the exact cause of the
pain of SUNCT headache is unknown; however, the pathogenesis
of this uncommon cause of head and face pain is thought to be
dysfunction of the trigeminal autonomic reflex.
The pain of SUNCT headache has a rapid onset to peak, with
attacks lasting 5 seconds to 4 minutes and the frequency of attacks
ranging from 20 to 200 attacks per day. In some patients, these
attacks can be triggered by sensory stimulation of the affected
areas, such as when washing the face, brushing the teeth, and so
forth. Although in many ways similar to cluster headache (e.g.,
unilateral, periorbital and frontal location of pain, sclera injection, rapid onset to peak, short duration of attacks, and pain-free
periods between attacks), SUNCT exhibits many dissimilarities as
well. In contrast to cluster headache, alcohol consumption does
not seem to trigger attacks of SUNCT headache, and there do not
seem to be the seasonal and chronobiological patterns so characteristic of cluster headache, although SUNCT headache occurs
most frequently in the morning and afternoon (Table 7-2).
Blockade of the sphenopalatine ganglion, which is so effective in the treatment of cluster headache, is of little value in the
treatment of SUNCT headache. Patients suffering from SUNCT
headache may respond to daily trigeminal nerve blocks with local
anesthetic, as described subsequently.
Testing
Magnetic resonance imaging (MRI) of the brain provides the clinician with 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 demyelinating disease. Magnetic resonance
angiography (MRA) also may be useful in helping identify aneurysms, which may be responsible for the patients neurological
findings. In patients who cannot undergo MRI, such as patients
with pacemakers, computed tomography (CT) is a reasonable second choice. Radionuclide bone scanning and plain radiography
are indicated if fracture or bony abnormality such as metastatic
disease is considered in the differential diagnosis.
Screening laboratory tests consisting of complete blood cell
count, erythrocyte sedimentation rate, and automated blood
chemistry testing should be performed if the diagnosis of SUNCT
TABLE 7-1
SUNCT
Paroxysmal
hemicrania
Cluster
headache
5 s4 min
230 min
15180 min
Overlap
between duration
Time
Overlap
between duration
Differential Diagnosis
SUNCT headache is a clinical diagnosis supported by a combination of clinical history, normal physical examination, radiography,
and MRI. Pain syndromes that may mimic SUNCT headache
include cluster headache, temporal arteritis, trigeminal neuralgia
TABLE 7-2
Cluster
Headache
SUNCT
Headache
Yes
Yes
Unilateral
Yes
Yes
Yes
Yes
Severe intensity
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Yes
Treatment
The treatment of SUNCT headache is analogous to the treatment
of trigeminal neuralgia, although the pharmacological management of this uncommon headache disorder is disappointing. The
use of anticonvulsants such as lamotrigine and gabapentin represents a reasonable starting point. High-dose steroids tapered over
10 days also have been anecdotally reported to provide relief. For
patients who do not respond to the previously mentioned treatments, daily trigeminal nerve block with a local anesthetic and
steroid is a reasonable next step.
Occasionally, retrogasserian injection of glycerol, balloon compression of the Gasserian ganglion, and microvascular decompression of the trigeminal nerve root are required to provide palliation
of pain. Underlying sleep disturbance and depression associated
with the pain of SUNCT headache are best treated with a tricyclic antidepressant compound, such as nortriptyline, which can be
started at a single bedtime dose of 25 mg.
Yes
No
Yes
No
No
Yes
Yes
No
Yes
No
No
Yes
Yes
No
No
Yes
TABLE 7-3
Staccato-like
Neck
Paroxysmal hemicrania
TABLE 7-4
Cluster headache
Temporal arteritis
Trigeminal neuralgia
Demyelinating disease
Primary stabbing headache
Hypnic headache
Chronic paroxysmal hemicrania
Clinical Pearls
Hemicrania continua
Migraine
NVOP
Leone M, Bussone G: Pathophysiology of trigeminal autonomic cephalalgias, Lancet 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
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, Philadelphia, 2009, Saunders, pp 1517.
Waldman SD: Gasserian ganglion block. In Waldman SD, editor: Atlas of interventional 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, Philadelphia, 2009, Saunders, pp 4347.
Waldman SD: Trigeminal nerve block: coronoid approach. In Waldman SD, editor: 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
Testing
The Clinical Syndrome
Thunderclap headache is an uncommon type of headache that
may be the result of an underlying vascular or nonvascular intracranial abnormality or may represent a primary headache syndrome of unknown cause. Common and uncommon causes of
thunderclap headache are listed in Table 8-1. The more benign,
though no less painful, primary thunderclap headache occurs over
three times more frequently than the serious secondary thunderclap headache. Because of the often-threatening causes of the less
common secondary thunderclap headache (e.g., subarachnoid
hemorrhage, cerebral venous thrombosis), urgent evaluation
including computed tomography (CT) and/or magnetic resonance
imaging of the brain and cerebrospinal fluid analysis are indicated
in all patients suspected of having thunderclap headache.
One of the most severe headaches encountered in clinical
practice, thunderclap headache is characterized by a very rapid
onset to peak of less than 1 minute. The headache may last
from 1 to 10 days and, because of its intensity, almost always
provokes an urgent trip to the emergency department, where
the headache is invariably initially misdiagnosed as the sentinel
headache of acute subarachnoid hemorrhage or other potentially
catastrophic headache syndromes (Tables 8-2 and 8-3). This is
not surprising in that primary thunderclap headache is virtually
indistinguishable clinically from subarachnoid hemorrhage, one
of the most neurologically devastating forms of cerebrovascular
accident. Thus, because of the serious consequences of misdiagnosis, by necessity primary thunderclap headache is a diagnosis
of exclusion.
Rare Causes
Vascular disorders
Subarachnoid hemorrhage
Intracerebral hemorrhage
Unruptured vascular
malformation, aneurysm
Arterial hypertension
Spontaneous intracranial
hypotension
Cerebral segmental
vasoconstriction
Erve virus
Sinusitis
Cluster headache
19
Subarachnoid
Hemorrhage
Severe headache
Yes
Yes
Yes
Yes
No
Yes
Nuchal rigidity
No
Yes
Photophobia
No
Yes
Vertigo
No
Yes
No
Yes
Comparison Factors
TABLE 8-3
Meningitis
Encephalitis
Abscess
Parasitic
Hypertensive crisis
Loss of spinal fluid
Postdural puncture headache
Spontaneous spinal fluid leak
Collagen-vascular disease
Lupus cerebritis
Vasculitis
Polymyositis
Headache
Cluster headache
Primary exertional headache
Primary cough headache
Migraine
Ice pick headache
Primary sexual headache
(Figure 8-1). Modern multidetector CT scanners have a diagnostic accuracy approaching 100% for subarachnoid hemorrhage if
CT angiography of the cerebral vessels is part of the scanning
protocol. Cerebral angiography may also be required if surgical
intervention is being considered and the site of bleeding cannot
be accurately identified.
Magnetic resonance imaging (MRI) of the brain and magnetic
resonance angiography may be useful if an aneurysm is not identified on CT studies and may be more accurate in the diagnosis of
arteriovenous malformations (Figure 8-2). Screening laboratory
tests, including an erythrocyte sedimentation rate, complete blood
count, coagulation studies, and automated blood chemistry,
C
Figure 8-1 Computed tomography scan showing subarachnoid hemorrhage (SAH). Right middle cerebral artery aneurysm in a 58-year-old
man with SAH and intracranial hematoma (IH). A, Volume rendering
image from computed tomography angiography (CTA) clearly displays
the relationship of the aneurysm to bone structures, adjacent branch
vessels, and aneurysmal neck (arrow). B, Maximum intensity projection (MIP) image from CTA clearly demonstrates the relationship of the
aneurysm (arrow). C, Thin-MIP image from CTA shows the relationship
of the aneurysm to IH (arrowhead), and the ruptured aneurysm has a
small nipple (arrow). (From Chen W, Yang Y, Xing W, etal: Applications
of multislice CT angiography in the surgical clipping and endovascular coiling of intracranial aneurysms, J Biomed Res 24:467473, 2010.)
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, Preembolization 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.)
Differential Diagnosis
The differential diagnosis of primary thunderclap headache generally can be thought of as the diagnosis of the lesser of two evils
because most of the diseases that mimic primary thunderclap
headache are also associated with significant mortality and morbidity. Table 8-3 lists diseases that may be mistaken for primary
thunderclap headache. Prominent among them is subarachnoid
hemorrhage, stroke, collagen-vascular disease, infection, neoplasm, hypertensive crisis, spinal fluid leaks, and a variety of more
benign causes of headache.
Treatment
Although no generally accepted treatment for primary thunderclap headache has been defined, the following guidelines may be
useful for the clinician when faced with a patient thought to have
this uncommon headache syndrome. First and foremost, if test
results reveal no evidence of intracranial pathology or other serious, life-threatening diseases, constant reassurance that the patient
Clinical Pearls
Primary thunderclap headache is a diagnosis of exclusion.
It is frequently misdiagnosed as the sentinel headache of
subarachnoid hemorrhage, causing the treating physician
to order urgent diagnostic testing, which is associated with
its own significant mortality and morbidity. The lack of
focal neurological findings in a patient with acute headache should point the clinician toward the diagnosis of
benign primary headaches including primary thunderclap
headache, cough headache, exertional headache atypical
migraine, and headache associated with sexual activity. This
does not mean that urgent computerized scanning of the
brain and analysis of the patients cerebrospinal fluid are
not indicated.
SUGGESTED READINGS
Anderson T: Current and evolving management of subarachnoid hemorrhage,
Crit Care Nurs Clin North Am 21:529539, 2009.
Chih-Ming H, Ya-Ju L, Yang-Kai F, Shih-Pin C, Tzu-Hsien L: Isolated thunderclap headache during sex: orgasmic headache or reversible cerebral vasoconstriction syndrome? J Clin Neurosci 17:13491351, 2010.
de Bruijn SFTM, Stam J, Kappelle LJ: CVST Study Group: Thunderclap headache as
first symptom of cerebral venous sinus thrombosis, Lancet 348:16231625, 1996.
Janardhan V, Biondi A, Riina HA, etal: Vasospasm in aneurysmal subarachnoid
hemorrhage: diagnosis, prevention, and management, Neuroimaging Clin N Am
6:483496, 2006.
Linn FHH: Primary thunderclap headache. In: Aminoff MJ, editor: Handbook of
clinical neurology, vol 97, New York, 2010, Elsevier, pp 473481.
Manno EM: Subarachnoid hemorrhage, Neurol Clin 22:347366, 2004.
Newfield P: Intracranial aneurysms: vasospasm and other issues. In Atlee JL, editor:
Complications in anesthesia, ed 2, Philadelphia, 2007, Saunders, pp 719723.
Palestrant D, Connolly ES: Subarachnoid hemorrhage, Neurobiol Dis 265270,
2007.
Pouration N, Dumont AS, Kassell NF: Subarachnoid hemorrhage. In Alves W
and Skolnick B, editors: Handbook of neuroemergency clinical trials, New York,
2006, Elsevier, pp 1744.
Chapter 9
HYPNIC 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 demyelinating disease. MRI helps identify bleeding associated with leaking intracranial aneurysms, which may mimic the
symptoms of both types of hypnic headache. Magnetic resonance
angiography (MRA) may be useful in identifying aneurysms
responsible for the patients neurological symptoms. In patients
who cannot undergo MRI, such as patients with pacemakers,
computed tomography (CT) is a reasonable second choice. Lumbar puncture should be performed if intracranial hemorrhage is
23
suspected even if blood is not present on MRI or CT. Plain radiographs of the cervical spine also may be useful in the evaluation
of Arnold-Chiari malformations and should be included in the
evaluation of all patients with hypnic headache.
Screening laboratory tests consisting of complete blood cell
count, erythrocyte sedimentation rate, and automated blood
chemistry testing should be performed if the diagnosis of hypnic
headache is in question. Intraocular pressure should be measured
if glaucoma is suspected.
Differential Diagnosis
Hypnic headache is a clinical diagnosis supported by a combination of clinical history, physical examination, radiography, MRI,
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
unique same-time nocturnal occurrence should help the clinician
easily identify the patients symptoms as hypnic headache. The
clinician must consider other types of headache that occur more
frequently at night, including cluster headache and headaches
associated with sleep apnea, nocturnal arterial hypertension, analgesic rebound, and increased intracranial pressure (Table 9-1).
Less commonly, hypnic headache may be confused with trigeminal neuralgia involving the first division of the trigeminal nerve or
demyelinating disease. Trigeminal neuralgia involving the first division 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
hypnic headache. Migraine headache may or may not be associated with painless neurological findings known as aura, but patients
almost always report some systemic symptoms, such as nausea or
photophobia, not typically associated with hypnic headache.
Treatment
Indomethacin and lithium carbonate are the treatments of choice
for hypnic headache, with indomethacin being slightly more
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. Indomethacin must be used carefully, if at all, in patients with peptic 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 hypnic headache.
TABLE 9-1
Clinical Pearls
Any patient presenting with nocturnal headaches should
be taken very seriously. Although statistically most of these
headaches ultimately are proved to be of benign cause, a
few patients have potentially life-threatening disease. The
diagnosis of hypnic headache is made by obtaining a thorough, targeted headache history and performing a careful
physical examination. The clinician must separate patients
with hypnic headache from patients with headaches caused
by an intracranial pathological condition such as tumors
or systemic disease such as nocturnal arterial hypertension. Patients with hypnic headache should have a normal
neurological examination. If the neurological examination is abnormal, the diagnosis of benign hypnic headache
should be discarded and a careful search for the cause of the
patients neurological findings should be undertaken.
SUGGESTED READINGS
Alberti A: Headache and sleep, Sleep Med Rev 10:431437, 2006.
Berciano J, Poca M-A, Garca A, Sahuquillo J: Paroxysmal cervicobrachial hypnicinduced pain in a patient with syringomyelia extending into spinal cord posterior gray horns, J Neurol 254:678681, 2007.
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
Med 2:123128, 2004.
Manni R, Ghiotto N: In Aminoff M, editor: Handbook of clinical neurology, New
York, 2010, Elsevier, pp 469472.
Pascual J: Primary hypnic headache, Curr Pain Headache Rep 9:272276, 2005.
Pascual J, Gonzlez-Mandly A, Martn R, Oterino A: Headaches precipitated by
cough, prolonged exercise or sexual activity: a prospective etiological and clinical study, J Headache Pain 9:259266, 2008.
Waldman SD: Arnold Chiari malformation type I. In Waldman SD, Campbell
RS, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 2728.
Waldman SD: Arnold Chiari malformation type II. In Waldman SD, Campbell
RS, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 2930.
Chapter 10
NUMMULAR HEADACHE
R51
Differential Diagnosis
Nummular headache is a clinical diagnosis supported by a combination of clinical history, normal physical examination, radiography, and MRI. Pain syndromes that may mimic nummular
headache include chronic paroxysmal hemicranias and jolts and
jabs headache. Trigeminal neuralgia involving the first division
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 lasts much longer than the pain of
nummular headache and is associated with redness and watering
of the ipsilateral eye.
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 cannot undergo MRI, such as patients with pacemakers, computed
25
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.)
Treatment
Nummular headache uniformly responds to treatment with indomethacin. Failure to respond to indomethacin puts the diagnosis
of nummular headache in question. A starting dosage of 25 mg
daily for 2 days and titrating to 25 mg three times a day is a reasonable treatment approach. This dose may be carefully increased
to 150 mg/day. Indomethacin must be used carefully, if at all,
in patients with peptic ulcer disease or impaired renal function.
Anecdotal reports of a positive response to cyclooxygenase-2
(COX-2) inhibitors in the treatment of nummular headache have
been noted in the headache literature, as well as a successful treatment with gabapentin. Underlying sleep disturbance and depression are best treated with a tricyclic antidepressant compound,
such as nortriptyline, which can be started at a single bedtime
dose of 25 mg.
Clinical Pearls
The diagnosis of nummular headache is made by taking a
careful, targeted headache history. Patients with nummular
headache should have a normal neurological examination.
If the results of the neurological examination are abnormal,
the diagnosis of nummular headache should be discarded
and a careful search for the cause of the patients neurological findings should be undertaken.
SUGGESTED READINGS
Cohen GL: Nummular headache: what denomination? Headache 10:14171418,
2005.
Evens RW, Pareja JA: Nummular headache, Headache 45:164165, 2005.
Mathew NT: Indomethacin responsive headache syndromes, Headache J Head
Face Pain 21:147150, 1981.
Pareja JA, Caminero AB, Serra J, etal: Nummular headache: a coin-shaped cephalgia, Neurology 58:16781679, 2002.
Pareja JA, Pareja J, Barriga FJ, etal: Nummular headache: a prospective series of
14 new cases, Headache 44:611614, 2004.
Pareja JA, Pareja J, Yangela J: Nummular headache, trochleitis, supraorbital neuralgia, and other epicranial headaches and neuralgias: the epicranias, J Headache
Pain 4:125131, 2003.
Chapter 11
HEADACHE ASSOCIATED
WITHTEMPORAL ARTERITIS
Signs and Symptoms
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
Testing
Erythrocyte sedimentation rate should be obtained in all patients
suspected to have temporal arteritis. In temporal arteritis, the
erythrocyte sedimentation rate is greater than 50 mm/hr in more
than 90% of patients. Less than 2% of patients with biopsy-proved
temporal arteritis have normal erythrocyte sedimentation rates.
Ideally, the blood for the erythrocyte sedimentation rate should
be obtained before beginning corticosteroid therapy because the
initial level of elevation of this test is useful not only to help diagnose the disease but also as a mechanism to establish the efficacy of
therapy. The erythrocyte sedimentation rate is a nonspecific test,
and other diseases that may manifest clinically in a manner similar
to that of temporal arteritis, such as malignancy or infection, also
may markedly elevate the erythrocyte sedimentation rate. Confirmation of the clinical diagnosis of temporal arteritis requires a
temporal artery biopsy.
Given the simplicity and safety of temporal artery biopsy, it
probably should be performed on all patients suspected of having temporal arteritis. The presence of an inflammatory infiltrate
with giant cells in the biopsied artery is characteristic of the disease. Edema of the intima and disruption of the internal elastic
lamina strengthen the diagnosis. A small percentage of patients
with clinical signs and symptoms strongly suggestive of temporal arteritis who also exhibit a significantly elevated erythrocyte
sedimentation rate have a negative temporal artery biopsy result.
As mentioned, in the presence of a strong clinical impression that
the patient has temporal arteritis, an immediate blood sample for
erythrocyte sedimentation rate testing should be obtained and the
patient started on corticosteroids. Complete blood cell count and
automated chemistries, including thyroid testing, are indicated in
all patients with suspected temporal arteritis to help rule out other
systemic disease that may mimic the clinical presentation of temporal arteritis.
If the diagnosis of temporal arteritis is in doubt, 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 demyelinating disease. More important, MRI helps identify bleeding associated with
leaking intracranial aneurysms. Magnetic resonance angiography
(MRA) may be useful to help identify aneurysms responsible for
Differential Diagnosis
Headache associated with temporal arteritis is a clinical diagnosis
supported by a combination of clinical history, abnormal findings on physical examination of the temporal artery, normal radiography, MRI findings, an elevated erythrocyte sedimentation
rate, and a positive temporal artery biopsy result. Pain syndromes
that may mimic temporal arteritis include tension type of headache, brain tumor, other forms of arteritis, trigeminal neuralgia
involving the first division of the trigeminal nerve, demyelinating
disease, migraine headache, cluster headache, and chronic paroxysmal hemicrania. Trigeminal neuralgia involving the first division
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 sexual headache. Migraine headache may or may not
be associated with painless neurological findings known as aura,
but the patient almost always reports some systemic symptoms,
such as nausea or photophobia, not typically associated with the
headache of temporal arteritis.
Treatment
The mainstay of treatment for temporal arteritis and its associated headaches and other systemic symptoms is the immediate use
of corticosteroids. If visual symptoms are present, an initial dose
of 80 mg of prednisone is indicated. This dose should be continued until the symptoms of temporal arteritis have completely
abated. At this point, the dose may be decreased by 5 mg/wk as
long as the symptoms remain quiescent and the erythrocyte sedimentation rate does not increase. Cytoprotection of the stomach
mucosa should be considered because ulceration and gastrointestinal bleeding are possible. If the patient cannot tolerate corticosteroids, or the maintenance dose of steroids remains so high as to
produce adverse effects, azathioprine is a reasonable next choice.
Clinical Pearls
The diagnosis of headache associated with temporal arteritis
is made by obtaining a thorough, targeted headache history. As mentioned, jaw claudication is pathognomonic for
temporal arteritis, and its presence should be sought in all
elderly patients presenting with headache. Failure to recognize, diagnose, and treat temporal arteritis promptly may
result in the permanent loss of vision.
SUGGESTED READINGS
Hazelman BL: Polymyalgia rheumatica. In Waldman SD, editor: Pain management, Philadelphia, 2009, Saunders, pp 449454.
Paget SA, Spiera RF: Polymyalgia rheumatica and temporal arteritis. In Goldman L,
Ausiello D, editors: Cecil medicine, 23rd ed, Philadelphia, 2007, Saunders, pp
11231127.
Waldman SD: Connective tissue diseases. In Waldman SD, editor: Pain review,
Philadelphia, 2009, Saunders, pp 431448.
Waldman SD: Temporal arteritis. In Waldman SD, editor: Pain review, Philadelphia, 2009, Saunders, pp 222223.
Chapter 12
POSTDURAL PUNCTURE
HEADACHE
G97.1
from the horizontal to the upright position and then abates when
the patient resumes a horizontal position is the sine qua non of
postdural puncture headache (Figure 12-1). A history of intentional dural puncture, such as lumbar puncture, spinal anesthesia, 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 mentioned, a spontaneous postural headache that manifests identically
to headache after dural puncture can occur after bouts of heavy
sneezing or coughing and is thought to be due to traumatic rents
in the dura. In this setting, a diagnosis of postdural puncture
headache is one of exclusion.
Testing
Magnetic resonance imaging (MRI) with and without gadolinium
is highly accurate in helping confirm the diagnosis of postdural
puncture headache. Enhancement of the dura with low-lying
cerebellar tonsils invariably is present. Poor visualization of the
cisterns and subdural and epidural fluid collections also may be
identified.
No additional testing is indicated for a patient who has undergone dural puncture and then develops a classic postural headache, unless infection or subarachnoid hemorrhage is suspected.
In this setting, lumbar puncture, complete blood cell count, and
erythrocyte sedimentation rate are indicated on an emergent basis.
Differential Diagnosis
If the clinician is aware that the patient has undergone dural
puncture, the diagnosis of postdural puncture headache is usually made. Delayed diagnosis most often occurs in settings in
which dural puncture is not suspected. Occasionally, postdural
puncture headache is misdiagnosed as migraine headache because
of the associated nausea and vomiting coupled with visual disturbance. In any patient with dural puncture, infection remains
an ever-present possibility. If fever is present, immediate lumbar
puncture and blood cultures should be obtained and the patient
started on antibiotics that cover resistant strains of Staphylococcus. MRI to rule out epidural abscess also should be considered
if fever is present. Subarachnoid hemorrhage may mimic post
dural puncture headache, but should be identified on MRI of
the brain.
Treatment
The mainstay of treatment of postdural puncture headache is
the administration of autologous blood into the epidural space.
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.
associated with dural puncture. Failure to diagnose central nervous system infection correctly can result in significant mortality
and morbidity.
Clinical Pearls
The diagnosis of postdural puncture headache is made by
obtaining a thorough, targeted headache history and performing a careful physical examination. The postural nature
is pathognomonic for postdural puncture headache, and
its presence should lead the clinician to strongly consider
the diagnosis of postdural puncture headache. The incidence of postdural puncture headache after lumbar puncture, myelography, or spinal anesthesia can be decreased
by using needles with a smaller diameter and placing the
needle bevel parallel to the dural fibers. Special noncutting
needles may decrease further the incidence of postdural
puncture headache.
SUGGESTED READINGS
Ghaleb A, Pablo C, Mandoff VL, Albataniah J, Candido K: Postdural puncture
cephalgia, Semin Pain Med 2:215219, 2004.
Harrington BE: Postdural puncture headache, Adv Anesth 28:121146, 2010.
Neal JM: Update on postdural puncture headache, Tech Reg Anesth Pain Manage
2:202210, 1998.
Waldman SD, Feldstein GS, Allen ML: Cervical epidural blood patch for treatment
of cervical dural puncture headache, Anesth Rev 14:2325, 1987.
Chapter 13
RAMSAY HUNT SYNDROME
of the geniculate ganglion. This pain may be accompanied by flulike symptoms and generally progresses from a dull, aching sensation to dysesthetic neuritic pain in the distribution of the geniculate
ganglion. In most patients, the pain of acute herpes zoster precedes
the eruption of rash by 3 to 7 days, often leading to erroneous diagnosis (see discussion of differential diagnosis). The clinical diagnosis of shingles is readily made, however, in most patients when
the characteristic rash appears. Similar to chickenpox, the rash of
herpes zoster appears in crops of macular lesions, which rapidly
progress to papules and then to vesicles (Figure 13-1).
As the disease progresses, the vesicles coalesce, and crusting
occurs. The area affected by the disease can be extremely painful,
and the pain tends to be exacerbated by any movement or contact
(e.g., with clothing or sheets). As healing occurs, the crusts fall
away, leaving pink scars in the distribution of the rash that gradually become hypopigmented and atrophic.
Vesicles in ear
Figure 13-1 Ramsay Hunt syndrome results from infection of the geniculate ganglion by the varicella-zoster virus.
Testing
Although in most instances the diagnosis of acute herpes zoster involving the geniculate ganglion is easily made on clinical grounds, confirmatory testing is occasionally required. Such
testing may be desirable in patients with other skin lesions that
confuse the clinical picture, such as patients with acquired immunodeficiency syndrome who have Kaposis sarcoma. In such
patients, the diagnosis of acute herpes zoster may be confirmed by
obtaining a Tzanck smear from the base of a fresh vesicle, which
reveals multinucleated giant cells and eosinophilic inclusions. To
differentiate acute herpes zoster from localized herpes simplex
infection, the clinician can obtain fluid from a fresh vesicle and
submit it for immunofluorescent testing.
Figure 13-2 Neurological examination revealed a flattened right nasolabial fold (black arrows) and ptosis of the right angle of the mouth (white
arrow). (From Taguchi T, Ueda S, Kudo T, etal: Ramsay-Hunt syndrome,
J Infect 62:180181, 2011.)
Differential Diagnosis
Careful initial evaluation, including a thorough history and physical examination, is indicated in all patients suffering from acute
herpes zoster involving the geniculate ganglion to rule out occult
malignancy or systemic disease that may be responsible for the
patients immunocompromised state and allow early recognition
of changes in clinical status that may presage the development of
complications, including myelitis or dissemination of the disease.
Other causes of pain in the distribution of the geniculate ganglion
include trigeminal neuralgia, sinus disease, glaucoma, retroorbital
tumors, inflammatory diseases such as Tolosa-Hunt syndrome,
and intracranial pathology, including tumors.
Treatment
The therapeutic challenge of a patient with acute herpes zoster
involving the geniculate ganglion is twofold: (1) to provide immediate relief of acute pain and symptoms and (2) to prevent complications, including postherpetic neuralgia. It is the consensus
of most pain specialists that the earlier in the natural course of
the disease that treatment is initiated, the less likely it is that the
patient will develop postherpetic neuralgia. Because older patients
are at highest risk for developing postherpetic neuralgia, early
aggressive treatment of these patients is mandatory.
Nerve Blocks
Sympathetic neural blockade with local anesthetics and steroids
via stellate ganglion block seems to be the treatment of choice to
relieve the symptoms of acute herpes zoster involving the geniculate ganglion and to prevent the occurrence of postherpetic neuralgia. Sympathetic nerve block is thought to achieve these goals
by blocking the profound sympathetic stimulation that results
from the viral inflammation of the nerve and geniculate ganglion.
If untreated, this sympathetic hyperactivity can cause ischemia
secondary to decreased blood flow of the intraneural capillary bed.
If this ischemia is allowed to persist, endoneural edema forms,
increasing endoneural pressure and causing a further reduction of
endoneural blood flow with irreversible nerve damage.
As vesicular crusting occurs, the addition of steroids to the
local anesthetic may decrease neural scarring and decrease further
the incidence of postherpetic neuralgia. These sympathetic blocks
should be continued aggressively until the patient is pain free and
should be reimplemented at the return of pain. Failure to use sympathetic neural blockade immediately and aggressively, especially
in elderly patients, may sentence the patient to a lifetime of suffering from postherpetic neuralgia. Occasionally, some patients suffering from acute herpes zoster involving the geniculate ganglion
may not experience pain relief from stellate ganglion block, but
they do respond to blockade of the trigeminal nerve.
Opioid Analgesics
Opioid analgesics may be useful in relieving the aching pain
that is often present during the acute stages of herpes zoster as
sympathetic nerve blocks are being implemented. They are less
effective in the relief of the neuritic pain that is often present.
Careful administration of potent, long-acting opioid analgesics
(e.g., oral morphine elixir or methadone) on a time-contingent
rather than as-needed basis may represent a beneficial adjunct to
the pain relief provided by sympathetic neural blockade. Because
many patients with acute herpes zoster are elderly or may have
severe multisystem disease, close monitoring for the potential
side effects of potent opioid analgesics (e.g., confusion or dizziness, which may cause a patient to fall) is warranted. Daily
dietary fiber supplementation and Milk of Magnesia should be
started, along with opioid analgesics to prevent the side effect of
constipation.
Adjuvant Analgesics
The anticonvulsant gabapentin represents a first-line treatment in
the palliation of neuritic pain of acute herpes zoster involving the
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
drug may be used concurrently with neural blockade, opioid analgesics, and other adjuvant analgesics, including the antidepressant
compounds if care is taken to avoid central nervous system side
effects. Gabapentin is started at a bedtime dose of 300 mg and is
titrated in 300-mg increments to a maximum dose of 3600 mg
given in divided doses as side effects allow. Carbamazepine should
be considered in patients with severe neuritic pain who have failed
to respond to nerve blocks and gabapentin. If this drug is used, rigid
monitoring for hematological parameters is indicated, especially in
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
pseudolymphoma state that is difficult to distinguish from the
actual lymphoma itself.
Antidepressants also may be useful adjuncts in the initial treatment of patients with acute herpes zoster. On an acute basis, these
drugs help alleviate the significant sleep disturbance that is commonly seen with acute herpes zoster. In addition, antidepressants
may be valuable in helping ameliorate the neuritic component of
the pain, which is treated less effectively with opioid analgesics.
After several weeks of treatment, the antidepressants may exert
a mood-elevating effect that may be desirable in some patients.
Patients must be observed closely for central nervous system side
effects. These drugs may cause urinary retention and constipation
that may be mistakenly attributed to herpes zoster myelitis.
Clinical Pearls
Because the pain of herpes zoster usually precedes the eruption of skin lesions by 5 to 7 days, erroneous diagnosis of
other painful conditions (e.g., trigeminal neuralgia, glaucoma) may be made. In this setting, the astute clinician
advises the patient to call immediately if a rash appears
because the diagnosis of acute herpes zoster is a possibility.
Some pain specialists believe that in a few immunocompetent patients, when reactivation of virus occurs, a rapid
immune response may attenuate the natural course of the
disease and the characteristic rash of acute herpes zoster may
not appear. This pain in the distribution of the geniculate
ganglion without associated rash is termed zoster sine herpete
and is, by necessity, a diagnosis of exclusion. Other causes
of head pain must be ruled out first before invoking this
diagnosis. Because of the potential for hearing loss in Ramsay Hunt syndrome, patients should be warned of this possibility to avoid erroneously blaming this complication on
a therapeutic intervention, such as stellate ganglion block.
Antiviral Agents
A few antiviral agents, including famciclovir and acyclovir, have
been shown to shorten the course of, and may help prevent the
development of, acute herpes zoster. They are probably useful
in attenuating the disease in patients with immunosuppression.
These antiviral agents can be used in conjunction with the treatment modalities mentioned earlier. Careful monitoring for side
effects is mandatory with these drugs.
SUGGESTED READINGS
Adjunctive Treatments
The application of ice packs to the lesions of acute herpes zoster
may provide relief in some patients. Application of heat increases
pain in most patients, presumably because of increased conduction of small fibers, but it is beneficial occasionally and may be
worth trying if application of cold is ineffective. Transcutaneous
electrical nerve stimulation and vibration also may be effective in
a few patients. The favorable risk-to-benefit ratio of all of these
modalities makes them reasonable alternatives for patients who
Bhagra A, Stead LG: Ramsay Hunt syndrome: a rare entity, Ann Emerg Med
47:579, 2006.
Gantz BJ, Redleaf MI, Perry BP, Gubbels SP: Management of Bells palsy and
Ramsay Hunt syndrome. In Brackmann DE, etal: Otologic surgery, ed 3, Philadelphia, 2010, Saunders, pp 335346.
Persson A, Bergstrm T, Lindh M, Namvar L, Studahl M: Varicella-zoster virus
CNS disease: viral load, clinical manifestations and sequels, J Clin Virol 46:249
253, 2009.
Taguchi T, Ueda S, Kudo T, etal: Ramsay-Hunt syndrome, J Infect 62:180181,
2011.
Ulusoy , zkan G, Bekta D, etal: Ramsay Hunt syndrome in renal transplantation recipient: a case report, Transplant Proc 42:19861988, 2010.
Chapter 14
EAGLE SYNDROME
Testing
In patients with Eagle syndrome, radiographs and computed
tomography (CT) scans of the region of the styloid process show
an elongated styloid process that is often associated with a calcified stylohyoid ligament. The diagnosis of Eagle syndrome may be
strengthened by a diagnostic injection of the attachment of the stylohyoid ligament to the styloid process with local anesthetic. Pain
relief after this injection suggests a local cause for the pain rather
than a more distant cause, such as glossopharyngeal neuralgia or
retropharyngeal tumor (Figure 14-2).
Differential Diagnosis
Eagle syndrome can be distinguished from glossopharyngeal neuralgia because the pain of glossopharyngeal neuralgia is characterized by paroxysms of shocklike pain in a manner analogous
to trigeminal neuralgia, rather than the sharp, shooting pain on
movement that is associated with Eagle syndrome. Because glossopharyngeal neuralgia may be associated with serious cardiac
bradyarrhythmias and syncope, the clinician must distinguish the
two syndromes.
The clinician should always evaluate a patient with pain in this
anatomical region for occult malignancy. Tumors of the larynx,
hypopharynx, and anterior triangle of the neck may manifest with
clinical symptoms identical to those of Eagle syndrome. Because
of the low incidence of Eagle syndrome relative to pain secondary
to malignancy in this anatomical region, Eagle syndrome must be
considered a diagnosis of exclusion.
Treatment
Many patients with Eagle syndrome respond to a series of therapeutic injections of the attachment of the stylohyoid ligament to the
styloid process with local anesthetic and steroid. To perform this
procedure, an imaginary line is visualized running from the mastoid process to the angle of the mandible (Figure 14-3). The styloid
process should lie just below the midpoint of this line. The skin
is prepared with antiseptic solution. A 22-gauge, 1-inch needle
Temporomandibular joint
Styloid process
Glossopharyngeal nerve
Tongue
Styloid ligament
Internal carotid
Mandible
35
Figure 14-2 Tumor (T) of the piriform sinus. The lesion protrudes
through the thyroarytenoid gap between thyroid cartilage and arytenoid (arrow). The tumor invades the paraglottic space (arrowhead) of
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.)
Figure 14-3 An imaginary line from the mastoid process to the angle
of the mandible is an aid in needle placement for injection in a patient
with Eagle syndrome.
Clinical Pearls
Eagle syndrome is an uncommon cause of facial pain.
Because of the low incidence of Eagle syndrome relative
to pain secondary to malignancy in this anatomical region,
Eagle syndrome must be considered a diagnosis of exclusion. The clinician should always evaluate a patient with
pain in this anatomical region for occult malignancy.
Tumors of the larynx, hypopharynx, and anterior triangle
of the neck may manifest with clinical symptoms identical
to those of Eagle syndrome.
SUGGESTED READINGS
Blythe JN, Matthews NS, Connor S: Eagles syndrome after fracture of the elongated styloid process, Br J Oral Maxillofac Surg 47:233235, 2009.
Callahan B, Kang J, Dudekula A, Eusterman V, Rabb CH: New Eagles syndrome
variant complicating management of intracranial pressure after traumatic brain
injury, Injury Extra 41:4144, 2010.
Johnson GM, Rosdy NM, Horton SJ: Manual therapy assessment findings in patients
diagnosed with Eagles syndrome: a case series, Man Ther 16:199202, 2011.
Klcha A, Hafian H, Devauchelle B, Lefvre B: A report of post-traumatic Eagles
syndrome, Int J Oral Maxillofac Surg 37:970972, 2008.
Chapter 15
ATYPICAL ODONTALGIA
Testing
Radiographs of the head are usually within normal limits in
patients suffering from atypical odontalgia, but they may be useful
Figure 15-1 Patients with atypical odontalgia often rub the affected
area; those with trigeminal neuralgia do not.
37
Pain Factor
Trigeminal Neuralgia
Temporal pattern
of pain
Sudden and
intermittent
Constant
Character of pain
Dull, aching,
cramping
Pain-free interval
Usual
Rare
Distribution
of pain
Trigger areas
Present
Uncommon
Underlying
psychopathology
Rare
Common
Differential Diagnosis
The clinical symptoms of atypical odontalgia may be confused
with pain of dental or sinus origin or may be erroneously characterized as trigeminal neuralgia. Careful questioning and physical examination usually allow the clinician to distinguish these
overlapping pain syndromes. Tumors of the zygoma, maxilla, and
mandible, as well as posterior fossa and retropharyngeal tumors,
may produce ill-defined pain that is attributed to atypical odontalgia. These potentially life-threatening diseases must be excluded in
any patient with odontalgia (see Figure 15-2). Reflex sympathetic
dystrophy of the face should also be considered in any patient with
ill-defined odontalgia after trauma, infection, or central nervous
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
TABLE 15-2
Treatment
The mainstay of therapy is a combination of drug treatment with
tricyclic antidepressants and physical modalities such as oral orthotic
devices and physical therapy. Trigeminal nerve block and intraarticular injection of the temporomandibular joint with small amounts
of local anesthetic and steroid also may be of value. Antidepressants
such as nortriptyline at a single bedtime dose of 25 mg can help
alleviate sleep disturbance and treat any underlying myofascial pain
syndrome. Orthotic devices help the patient avoid jaw clenching
and bruxism, which may exacerbate the clinical syndrome. Management of underlying depression and anxiety is also mandatory.
Clinical Pearls
Atypical odontalgia requires careful evaluation to design
an appropriate treatment plan. Infection and inflammatory
causes, including collagen-vascular diseases, must be ruled
out. Stress and anxiety often accompany atypical odontalgia, and these factors must be addressed and treated. The
myofascial pain component of atypical odontalgia is best
treated with tricyclic antidepressants such as amitriptyline.
Dental malocclusion and nighttime bruxism should be
treated with an acrylic bite appliance. Opioid analgesics and
benzodiazepines should be avoided in patients with atypical
odontalgia.
SUGGESTED READINGS
Clark GT: Persistent orodental pain, atypical odontalgia, and phantom tooth pain:
when are they neuropathic disorders? J Calif Dent Assoc 34:599609, 2006.
Marbach JJ: Is phantom tooth pain a deafferentation (neuropathic) pain syndrome? Oral Surg Oral Med Oral Pahtol 75:95-105, 1993.
Marbach JJ: Orofacial phantom pain: theory and phenomenology, JADA
127:221229, 1996.
Marbach JJ, Raphael KG: Phantom tooth pain: a new look at an old dilemma,
Pain Med 1:6877, 2000.
Matwychuk MJ: Diagnostic challenges of neuropathic tooth pain, J Can Dent
Assoc 70:542546, 2004.
McQuay HJ, Tramr M, Nye BA, etal: A systematic review of antidepressants in
neuropathic pain, Pain 68:217227, 1996.
Melis M, Lobo SL, Ceneviz C, etal: Atypical odontalgia: a review of the literature, Headache 43:10601074, 2003.
Pertes RA, Bailey DR, Milone AS: Atypical odontalgia: a nondental toothache,
J N J Dent Assoc 66:2931, 33, 1995.
Chapter 16
BURNING MOUTH SYNDROME
Testing
No specific test exists for burning mouth syndrome, and a presumptive diagnosis can be made only if (1) the clinical examination is normal and (2) a workup for all underlying pathological findings fails
to identify a specific cause for the patients pain symptomatology. A
suggested workup based on the experience at the Mayo Clinic is outlined in Table 16-1 and should always include laboratory testing for
vitamin deficiencies and diabetes and a culture for candida infection.
Differential Diagnosis
Myriad causes of burning mouth and tongue pain have been
identified, many of which are readily treatable (Table 16-2). It is
therefore imperative that the clinician faced with a patient with
burning mouth and tongue pain obtain an extremely thorough
history and perform an oral examination with these diseases in
mind. It should be kept in mind that more often than not the
patient with burning mouth syndrome has more than one pathological condition contributing to the pain, and the possibility of
multiple diagnosis should always be considered.
Treatment
The successful treatment of burning mouth syndrome requires
the clinician to endeavor to identify the underlying pathology
responsible for the patients pain. All underlying medical conditions (e.g., diabetes, deficiency syndromes) must be treated, along
with the removal of any local irritants such as mouth washes,
spicy foods, and cinnamon and mint products. Providing the
patient with a supportive and positive emotional environment
and reassurance that cancer is not the cause of the pain is paramount if symptom relief is to be achieved. Coexistent behavioral
and psychiatric abnormalities also must be addressed in a positive
therapeutic milieu. Empirical treatments, including anticandiadal
agents, vitamin B complex supplementation, and low-dose antidepressants, are also worthy of consideration.
Treatment often involves some combination of elimination of
any local irritants, treatment of underlying medical conditions,
pharmacological therapy, and behavioral therapy.
First, any nidus of tissue trauma that is contributing to the
ongoing sympathetic dysfunction responsible for the symptoms
must be identified and removed. Second, interruption of the sympathetic innervation of the face by stellate ganglion block with
local anesthetic must be implemented. This may require daily stellate ganglion block for a considerable period. Occupational therapy consisting of tactile desensitization of the affected mucosa also
may be of value. Underlying depression and sleep disturbance are
best treated with a tricyclic antidepressant such as nortriptyline,
given as a single 25-mg dose at bedtime. Gabapentin may help palliate any neuritic pain component and is best started slowly with
TABLE 161
Local
Psychogenic,
Psychiatric,
and Idiopathic
Deficiencies
Denture factors
Psychiatric
Iron
Dental work
Depression
Vitamin B12
Mechanical
Anxiety
Folate
Obsessivecompulsive
disorder
Zinc
Clenching
Somatoform
disorder
B complex vitamins
Bruxism
Cancerphobia
Endocrine
Tongue thrusting
Psychosocial
stressors
Diabetes mellitus
Myofasical pain
Hypothyroidism
Menopause or
hormonal
Dental restoration or
denture materials
Foods
Xerostomia
Preservative, additives,
flavorings
Connective tissue
disease
Neurologic
Oral examination
Sjgrens syndrome
Sicca syndrome
Drug related
Glossopharyngeal
neuropathy
Anxiety or stress
Acoustic neuroma
Medication
Infection
Candidiasis
Angiotensinconverting enzyme
inhibitor
Esophageal reflux
Antibiotic related
Anemia
Denture related
Local trauma
Corticosteroid
Diabetes mellitus
Fusospirochetal
Dentistry
Xerostomia
Neurology
Irradiation
Otorhinolaryngology
Local disease
From Drage LA, Rogers RSR III: Burning mouth syndrome, Dermatol Clin
21:135145, 2003.
From Drage LA, Rogers RSR III: Burning mouth syndrome, Dermatol Clin
21:135145, 2003.
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.
SUGGESTED READINGS
Drage LA, Rogers RSR III: Burning mouth syndrome, Dermatol Clin 21:135145,
2003.
Miziara ID, Arajo Filho BC, Oliveira R, Rodrigues dos Santos RM: Group psychotherapy: an additional approach to burning mouth syndrome, Psychosom Res
67:443448, 2009.
Mock D: Burning tongue/mouth syndrome, J Oral Maxillofac Surg 67(Suppl 1):5,
2009.
Moore PA, Guggenheimer J, Orchard T: Burning mouth syndrome and peripheral
neuropathy in patients with type 1 diabetes mellitus, J Diabetes Complications
21:397402, 2007.
Chapter 17
NERVUS INTERMEDIUS NEURALGIA
Testing
All patients with a new diagnosis of nervus intermedius neuralgia
should undergo magnetic resonance imaging (MRI) of the brain
and brainstem, with and without gadolinium contrast medium,
to rule out posterior fossa or brainstem lesions and demyelinating disease (Figure 17-2). Magnetic resonance angiography
is also useful to confirm vascular compression of the nervus
43
Treatment
Axial
Coronal
Figure 17-2 Gadolinium-enhanced magnetic resonance imaging (MRI).
Images show a centrally enhancing lesion in the geniculate ganglion
(arrow), measuring 5 mm 10 mm in diameter. (From Miyashita T,
Hoshikawa H, Kagawa M, Mori N: A case report of facial nerve hemangioma, Auris Nasus Larynx 34:519522, 2007.)
Differential Diagnosis
Nervus intermedius neuralgia is generally a diagnosis of exclusion, although the clinical presentation makes it a straightforward
clinical diagnosis that can be made on the basis of a targeted history and physical examination. Diseases of the eyes, ears, nose,
throat, and teeth may mimic nervus intermedius neuralgia or
may coexist and confuse the diagnosis. Atypical facial pain or
temporomandibular joint dysfunction is sometimes confused
with nervus intermedius neuralgia, but it can be distinguished by
the character of the painatypical facial pain is dull and aching,
whereas the pain of nervus intermedius neuralgia is sharp and
neuritic. Additionally, the pain of nervus intermedius neuralgia
occurs in the distribution of the nervus intermedius, whereas the
pain of atypical facial pain does not follow a specific nerve distribution. Multiple sclerosis should be considered in all patients
who present with nervus intermedius neuralgia before the fifth
decade of life.
Drug Therapy
Carbamazepine
Carbamazepine is considered first-line treatment for nervus intermedius neuralgia. In fact, a rapid response to this drug helps confirms
the clinical diagnosis. Despite the safety and efficacy of carbamazepine, some confusion and anxiety exist surrounding its use. This
medication, which may be the patients best chance for pain control, is sometimes discontinued because of laboratory abnormalities 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.
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 possibility 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
patient should be kept at that dosage of carbamazepine for at least
6 months before tapering of the medication is considered. The
patient should be informed that under no circumstances should
the drug dosage be changed or the drug refilled or discontinued
without the physicians knowledge.
Gabapentin
In the uncommon event that carbamazepine does not adequately
control a patients pain, gabapentin may be considered. As with
carbamazepine, baseline blood tests should be obtained before
starting therapy and the patient should be cautioned about potential side effects, including dizziness, sedation, confusion, and rash.
The initial dose is 300 mg at bedtime for 2 nights. The drug is
then increased in 300-mg increments given in equally divided
doses over 2 days, as side effects allow, until pain relief is obtained
or a total dose of 2400 mg per day is reached. At this point, if the
patient has experienced only partial pain relief, blood values are
measured and the drug is carefully titrated upward using 100-mg
tablets. Rarely is a dosage greater than 3600 mg per day required.
Pregabalin
Pregablin represents a reasonable alternative to gabapentin and
is better tolerated in some patients. Pregablin is started at 50 mg
three times per day and may be titrated upward to 100 mg three
times per day as side effects allow. Pregablin is excreted primarily
by the kidneys, and thus the dosage should be decreased in patients
with compromised renal function.
Baclofen
Baclofen may be of value in some patients who fail to obtain relief
from carbamazepine, gabapentin, or pregabalin. As with those
drugs, baseline laboratory tests should be obtained before beginning baclofen therapy and the patient should be warned about the
same potential adverse effects. Start with a 10-mg dose at bedtime
for 2 nights, then increase the drug in 10-mg increments given in
equally divided doses over 7 days, as side effects allow, until pain
relief is obtained or a total dose of 100 mg per day is reached. This
drug has significant hepatic and central nervous system side effects,
including weakness and sedation. As with carbamazepine, careful
monitoring of laboratory values is indicated when using baclofen.
When treating individuals with any of these drugs, the physician should make sure the patient knows that premature tapering
or discontinuation of the medication may lead to the recurrence
of pain, which will be more difficult to control.
Invasive Therapy
Section of the Nervus Intermedius
This neurosurgical technique is the invasive treatment of choice
for those patients with nervus intermedius neuralgia who have
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
is sectioned in two places. Some surgeons also advocate extirpation of the geniculate ganglion. Section of the nervus intermedius
alone provides excellent palliation of pain in 75% to 90% of cases.
Clinical Pearls
Nervus intermedius neuralgia is an uncommon cause of otalgia. Because of the potential for disastrous clinical outcome
should a more common cause of otic pain be overlooked
(e.g., tumor or the temporal bone, brainstem, or nasopharynx), 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 pharmacological management in an inpatient setting may be required.
Surgical treatment consisting of the sectioning of the nervus
intermedius is often the patients best option for complete
and long-lasting pain relief.
SUGGESTED READINGS
Alcaraz N, King WA, Wackym PA: Endoscopy during neurotomy of the nervus
intermedius for geniculate neuralgia, Otolaryngol Head Neck Surg 121:334336,
1999.
Bhagra A, Stead LG: Nervus intermedius neuralgia: a rare entity, Ann Emerg Med
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,
editors:Otologic surgery, ed 3, Philadelphia, 2010, Elsevier, pp 335346.
Persson A, Bergstrm T, Lindh M, Namvar L, Studahl M: Varicella-zoster
virus CNS disease: viral load, clinical manifestations and sequels, J Clin Virol
46:249253, 2009.
Taguchi T, Ueda S, Kudo T, etal: Ramsay-Hunt syndrome, J Infect 62:180181,
2011.
Ulusoy , zkan G, Bekta D, etal: Nervus intermedius neuralgia in renal transplantation recipient: a case report, Transplant Proc 42:19861988, 2010.
Chapter 18
RED EAR SYNDROME
Testing
Magnetic resonance imaging (MRI) of the brain provides the clinician with 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 pathology, including tumors and
demyelinating disease. Magnetic resonance angiography (MRA)
also may be useful in helping identify aneurysms that may be
responsible for the patients neurological findings. In patients who
cannot undergo MRI, such as patients with pacemakers, computed tomography (CT) is a reasonable second choice. Radionuclide bone scan and plain radiography are indicated if a fracture or
TABLE 18-1
46
Differential Diagnosis
Red ear syndrome is a clinical diagnosis supported by a combination of clinical history, normal physical examination, radiography, and MRI. Pain syndromes that may mimic red ear syndrome
include erythromelalgia of the ear, polychondritis, cluster headache, temporal arteritis, trigeminal neuralgia, demyelinating
disease, primary stabbing headache, SUNCT, and chronic paroxysmal hemicranias. However, because of the overlapping features
of all headache and facial pain syndromes, red ear syndrome easily
can be mistaken for another type of headache or facial pain. Trigeminal neuralgia is more common 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 lasts much longer than the pain of
red ear syndrome.
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
anticonvulsants such as lamotrigine and gabapentin represents a
reasonable starting point. High-dose steroids tapered over 10 days
also have been anecdotally reported to provide relief. For patients
who do not respond to these treatments, a few case reports suggest
that daily ipsilateral C2-C3 facet joint blocks with local anesthetic
and steroid may provide relief of both the pain and the autonomic
dysfunction. Underlying sleep disturbance and depression associated with the pain of red ear syndrome are best treated with a
tricyclic antidepressant compound, such as nortriptyline, which
can be started at a single bedtime dose of 25 mg.
Clinical Pearls
Given the poor response to treatment with drugs traditionally used to treat trigeminal neuralgia, facet block of
the ipsilateral C2-C3 facet joints with local anesthetic and
steroids should be considered in patients thought to have
red ear syndrome. Given the uncommon nature of this
headache syndrome and its overlap with the other trigeminal autonomic cephalgias and other more serious forms of
intracranial pathological conditions such as tumors and
vascular abnormalities, red ear syndrome must remain
a diagnosis of exclusion. All patients thought to have red
ear syndrome require MRI of the brain with and without
gadolinium contrast material and thorough otic and neurological evaluation. Cervical facet block should be performed
only by clinicians familiar with the regional anatomy.
SUGGESTED READINGS
Kumar N, Swanson JW: The red ear syndrome revisited: two cases and a review
of literature, Cephalalgia 24:305308, 2004.
Lance JW: The red ear syndrome, Neurology 47:617620, 1996.
Leone M, Bussone G: Pathophysiology of trigeminal autonomic cephalalgias, Lancet
Neurol 8:18551884, 2009.
Purdy RA, Dodick DW: Red ear syndrome, Curr Pain Headache Rep 11:313316,
2007.
Waldman SD: Cervical facet block. In Waldman SD, editor: Atlas of interventional
pain management, ed 3, Philadelphia, 2009, Saunders, pp 165168.
Chapter 19
GLOSSOPHARYNGEAL NEURALGIA
Differential Diagnosis
Glossopharyngeal neuralgia is generally a straightforward clinical
diagnosis that can be made on the basis of a targeted history and
physical examination. Diseases of the eye, ears, nose, throat, and
teeth may mimic trigeminal neuralgia or may coexist and confuse
the diagnosis. Tumors of the hypopharynx, including the tonsillar
Palatine tonsil
Posterior of
tongue
Testing
Magnetic resonance imaging (MRI) of the brain and brainstem
should be performed in all patients thought to have glossopharyngeal neuralgia. 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
48
19 Glossopharyngeal Neuralgia 49
fossa and piriform sinuses, may mimic the pain of glossopharyngeal neuralgia, as may tumors at the cerebellopontine angle. Occasionally, demyelinating disease may produce a clinical syndrome
identical to glossopharyngeal neuralgia. The jaw claudication associated with temporal arteritis also sometimes confuses the clinical
picture, as does trigeminal neuralgia.
Treatment
Pharmacological Treatment
Carbamazepine
Carbamazepine is considered first-line treatment for glossopharyngeal neuralgia. Rapid response to this drug essentially confirms a clinical diagnosis of glossopharyngeal neuralgia. Despite
the safety and efficacy of carbamazepine compared with other
treatments for glossopharyngeal neuralgia, much confusion and
unfounded anxiety surround its use. This medication, which may
be the patients best chance for pain control, is sometimes discontinued because of laboratory abnormalities erroneously attributed
to it. Baseline screening laboratory tests, consisting of a complete
blood cell count, urinalysis, and automated chemistry profile,
should be obtained before starting the drug.
Carbamazepine should be started slowly, if the pain is not out
of control, at a starting dose of 100 to 200 mg at bedtime for
2 nights; the patient should be cautioned regarding 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
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 characteristic 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.)
Styloid
process
Glossopharyngeal
nerve
Figure 19-3 Proper needle placement for glossopharyngeal nerve
block. (From Waldman SD: In Waldman SD, editor: Atlas of interventional
pain management techniques, 3rd ed, Philadelphia, 2009, Saunders.)
19 Glossopharyngeal Neuralgia 51
glossopharyngeal nerve can result in dysphagia secondary to weakness of the stylopharyngeus muscle. If the vagus nerve is inadvertently blocked, as it often is during glossopharyngeal nerve block,
dysphonia secondary to paralysis of the ipsilateral vocal cord may
occur. Reflex tachycardia secondary to vagal nerve block is also
observed in some patients. Inadvertent block of the hypoglossal
and spinal accessory nerves during glossopharyngeal nerve block
will result in weakness of the tongue and trapezius muscle.
The glossopharyngeal nerve is susceptible to trauma from the
needle, hematoma, or compression during injection procedures.
Such complications, although usually transitory, can be quite
upsetting to the patient. Although uncommon, risk for infection
is ever present, especially in patients who have cancer and are
immunocompromised. Early detection of infection is crucial to
avoiding potentially life-threatening sequelae.
Clinical Pearls
The pain of glossopharyngeal neuralgia is among the most
severe pain that humans can experience and must be considered a medical emergency. The uncontrolled pain of
glossopharyngeal neuralgia has led to suicide, and hospitalization 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 compression of the nerve by a structural lesion, such as a brainstem 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.
SUGGESTED READINGS
Benoliel R, Eliav E: Neuropathic orofacial pain, Oral Maxillofac Surg Clin North
Am 20:237254, 2008.
Franzini A, Ferroli P, Messina G, Broggi G: Surgical treatment of cranial neuralgias. In Bruyn G, Vinken P, editors: Handbook of clinical neurology, vol 97,
New York, 2010, Elsevier, pp 679692.
Khan NU, Iyer A: Glossopharyngeal neuralgia associated with anomalous glossopharyngeal nerve, Otolaryngol Head Neck Surg 136:502503, 2007.
Waldman SD: Glossopharyngeal nerve block. In Waldman SD, editor: Atlas of
interventional pain management, ed 3, Philadelphia, 2009, Saunders, pp 9397.
The surgical treatment of microvascular compression syndromes, Operative Tech
Neurosurg 4:137141, 2001.
Chapter 20
CLIVAL CHORDOMA SYNDROME
Testing
Magnetic resonance imaging (MRI) of the brain and brainstem
should be performed in all patients thought to have clival chordoma
(see Figure 20-1). 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 demyelinating disease
(Figure 20-2). Magnetic resonance angiography (MRA) may be helpful in identifying aneurysms responsible for neurological symptoms.
In patients who cannot undergo MRI, such as patients with pacemakers, computed tomography (CT) is a reasonable second choice.
Clinical laboratory tests consisting of a complete blood cell
count, automated chemistry profile, and erythrocyte sedimentation rate are indicated to rule out infection, temporal arteritis, and
other malignancies that may mimic clival chordoma. Endoscopy
of the nasopharynx and hypopharynx with special attention to the
piriform sinuses also is indicated to rule out occult malignancy.
Differential Diagnosis
Clival chordoma is generally a straightforward clinical diagnosis in retrospect. Given that the time between the onset of
TABLE 20-1
Headache
52
Facial numbness
Facial pain
Facial paresthesias
Diplopia
Dysarthria
Dysphagia
Ataxia
Extremity weakness
Hoarseness
Visual disturbance
Treatment
Treatment of clival chordoma requires surgery, radiation therapy, or both. Although clival chordomas are almost always
benign and rarely metastasize, the critical location of clival chordomas relative to adjacent neural structures makes both forms
of treatment challenging. Often, complete tumor resection is
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.
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.)
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.
SUGGESTED READINGS
Aminoff M, Boller F, Swaab D: Cytogenetic analysis of three variants of clival
chordoma, Cancer Genet Cytogenet 154:124130, 2004.
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.
Chugh R, Tawbi H, Lucas DR, etal: Chordoma: the nonsarcoma primary bone
tumor, Oncologist 12:13441350, 2007.
Feng K, Qiuhang Z, Qiuyi Q: Transclival cerebrospinal fluid rhinorrhea as the
initial presenting symptom of a tiny intradural chordoma, J Clin Neurosci
17:10831085, 2010.
Chapter 21
SPASMODIC TORTICOLLIS
Spasmodic torticollis is a rare condition characterized by involuntary movement of the head. It is classified as a focal or segmental dystonia and occurs in approximately 3 in 10,000 people. It
begins in early adult life. The three varieties of spasmodic torticollis are as follows:
Tonic, which involves involuntary turning of the head to
one side
Clonic, which involves involuntary shaking of the head
Tonic/clonic, which involves both types of involuntary
movement
Spasmodic torticollis also can be subclassified based on the
specific movement of the head: (1) rotation, which involves the
turning of the head to the side; (2) laterocollis, which involves
the leaning of the head against the shoulder; (3) retrocollis, which
involves the leaning of the head toward the back; and (4) anterocollis, which involves the leaning of the head toward the chest.
The disease occurs more commonly in women and often is initially diagnosed as a hysterical reaction or tic.
Thought to be due to dysfunction centrally, rather than a disease of the affected muscles, spasmodic torticollis often begins as a
subtle involuntary movement of the head. Early in the disease, the
dystonia is often intermittent. As the disease progresses, the symptoms become more severe and harder for the patient to hide. The
dystonic movements may become more sustained and associated
with constant, aching pain in the affected muscles. The pain often
becomes the primary reason for the patient to seek medical attention, with the patient almost indifferent to the dystonic movements. The dystonia often disappears with sleep and becomes less
pronounced on first awakening, with the dystonic movements
and pain worsening as the day progresses. Spontaneous recovery
has been reported, but, overall, treatment is difficult and of limited success.
Testing
Treatment
Differential Diagnosis
Spasmodic torticollis is generally a straightforward clinical diagnosis that can be made on the basis of a targeted history and physical
examination. The involuntary nature of this movement disorder
is the hallmark of the disease and helps distinguish it from tics
and habit spasms that are voluntary and worsen when the patient
is tense. Tics and habit spasms resemble volitional movement.
Behavioral abnormalities, such as hysterical conversion reactions,
also must be considered. Acute spasm and pain of the muscles
of the neck or wry neck can mimic spasmodic torticollis, but its
onset is acute, and the symptoms usually resolve within days to a
week. Occasionally, patients with clonic spasmodic torticollis are
initially diagnosed as having Parkinson disease.
55
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. Trihexyphenidyl and diazepam also have been advocated.
In patients for whom pharmacological treatment fails, injection of the affected muscles with botulinum toxin is a reasonable
next step. Frequent injections may result in the development of
antibodies against the toxin, which makes the toxin less effective. By changing to different subtypes of toxin, efficacy may be
restored. For intractable cases, bilateral thalamotomy has been
advocated. The results of this radical treatment are variable at best.
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.
SUGGESTED READINGS
Maia FM, Kanashiro AK, Chien HF, Gonalves LR, Barbosa ER: Clinical changes
of cervical dystonia pattern in long-term botulinum toxin treated patients, Parkinsonism Relat Disord 16:811, 2010.
Ochudo S, Drzyzga K, Drzyzga LR, Opala G: Various patterns of gestes antagonistes in cervical dystonia, Parkinsonism Relat Disord 13:417420, 2007.
Takeuchi N, Chuma T, Mano Y: Phenol block for cervical dystonia: effects and
side effects, Arch Phys Med Rehabil 85:11171120, 2004.
Truong D, Brodsky M, Lew M, etal: Global Dysport Cervical Dystonia Study
Group: Long-term efficacy and safety of botulinum toxin type A (Dysport) in
cervical dystonia, Parkinsonism Relat Disord 16:316323, 2010.
Chapter 22
CERVICOTHORACIC INTERSPINOUS
BURSITIS
Testing
MRI of the lower cervical and upper thoracic spine should be
performed in all patients thought to have cervicothoracic bursitis (Figure 22-2). Electromyography of the brachial plexus and
upper extremities is indicated if neurological findings or pain
that radiates into the arms are present. Clinical laboratory tests,
including a complete blood cell count, automated chemistry profile, antinuclear antibody testing, and erythrocyte sedimentation
rate, are indicated to rule out infection; collagen-vascular disease,
including ankylosing spondylitis; and malignancy that may mimic
the clinical presentation of cervicothoracic bursitis. Injection of
the affected interspinous bursae with local anesthetic and steroid
may serve as a diagnostic and therapeutic maneuver and may help
strengthen the diagnosis of cervicothoracic bursitis. Plain radiography of the sacroiliac joints is indicated if ankylosing spondylitis
is being considered in the differential diagnosis.
Differential Diagnosis
The diagnosis of cervicothoracic bursitis is usually made on clinical grounds as a diagnosis of exclusion. The clinician needs to rule
out intrinsic disease of the spinal cord, including syringomyelia
and tumor, which may mimic the clinical presentation of cervicothoracic bursitis. Ankylosing spondylitis also may manifest in a
manner similar to that of cervicothoracic bursitis. Fibromyalgia
may coexist with cervicothoracic bursitis and should be identifiable by its characteristic trigger points and positive jump sign.
Treatment
Initial treatment of the pain and functional disability associated with
cervicothoracic bursitis should include a combination of nonsteroidal
antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2)
inhibitors and physical therapy. The local application of heat and
cold also may be beneficial. For patients who do not respond to
these treatment modalities, the following injection technique with a
local anesthetic and steroid may be a reasonable next step.
The skin overlying the C7-T1 interspace is prepared with
antiseptic solution. A syringe containing 20 mL of 0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is
attached to a 25-gauge, 1-inch needle. The needle is carefully
advanced through the supraspinal ligament into the interspinous
ligament (Figure 22-3). Care must be taken to keep the needle
in the midline and not to advance it too deeply, or inadvertent
epidural, subdural, or subarachnoid injection could occur. After
careful aspiration, a volume of 2 to 3 mL is gently injected into
the ligament. The patient should be informed that two to five
treatment sessions may be required to abolish the symptoms of
cervicothoracic bursitis completely.
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 performing injection techniques. The proximity to the vertebral artery
combined with the vascular nature of this anatomical region
makes the potential for intravascular injection high. Even small
amounts of a local anesthetic injected into the vertebral arteries
result in seizures. Given the proximity of the brain and brainstem,
ataxia after trigger point injection as a result of vascular uptake
of local anesthetic is common. Many patients also complain of a
transient increase in pain after injection in this anatomical area. If
long needles are used, pneumothorax also may occur.
Because of the proximity of the epidural, subdural, and subarachnoid space, placement of a needle too deeply could result
in inadvertent neuraxial block. Failure to recognize inadvertent
epidural, subdural, or dural puncture can result in significant
motor and sensory block with the potential for associated loss of
consciousness, hypotension, and apnea. If subdural placement is
unrecognized, and the previously mentioned doses of local anesthetics are administered, the signs and symptoms are similar to
those of subarachnoid injection, although the resulting motor and
sensory block may be spotty.
Clinical Pearls
The aforementioned injection technique is extremely effective in the treatment of cervicothoracic bursitis. 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. Most
side effects of the injection technique for cervicothoracic
bursitis 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 injection.
The avoidance of overly long needles helps decrease the
incidence of trauma to underlying structures. Special care
must be taken to avoid pneumothorax given the proximity
to the underlying pleural space.
The use of physical modalities, including local heat and
gentle stretching exercises, should be introduced several
days after the patient undergoes this injection technique
for cervicothoracic bursitis. Vigorous exercises should be
avoided because they would exacerbate the symptoms.
Simple analgesics, NSAIDs, and antimyotonic agents such
as tizanidine may be used concurrently with this injection
technique.
AR
Kyphosis
Figure 22-3 Proper needle placement for injection for treatment of cervicothoracic interspinous bursitis pain. (From Waldman SD: Atlas of pain
management injection techniques, Philadelphia, 2000, Saunders, p 33.)
SUGGESTED READINGS
Hull JJ, Tomaski SM: Osteomyelitis of the cervical spine: case report and literature
review, Otolaryngol Head Neck Surg 113:193, 1995.
Perka C, Schneider SV, Buttgereit F, Matziolis G: Development of cervical interspinous bursitis after prolonged sports trauma: a case report, Joint Bone Spine
73:118120, 2006.
Reckelhoff KE, Green MN, Kettner NW: Cervical spine osteochondroma: rare
presentation of a common lesion, J Manipulative Physiol Ther 33:711715,
2010.
Waldman SD: Cervicothoracic interspinous bursitis. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 238239.
Chapter 23
SCAPULOCOSTAL SYNDROME
Testing
Plain radiographs are indicated in all patients with scapulocostal syndrome. Based on the clinical presentation, additional tests,
including complete blood cell count, erythrocyte sedimentation
rate, and antinuclear antibody level, may be indicated. Magnetic
resonance imaging (MRI) of the shoulder is indicated if rotator
cuff tear is suspected. Radionuclide bone scanning is indicated
if metastatic disease or primary tumor involving the shoulder is
60
Differential Diagnosis
Scapulocostal syndrome is most commonly misdiagnosed as cervical radiculopathy. In contrast to cervical radiculopathy, however,
which is associated with numbness and weakness in the affected
dermatomes, the upper extremity neurological examination in
scapulocostal syndrome is normal. Osteoarthritis, rheumatoid
arthritis, posttraumatic arthritis, and rotator cuff tear arthropathy
also are common causes of shoulder pain secondary to arthritis
that may be confused with scapulocostal syndrome. Less common
causes of arthritis-induced shoulder pain include the collagenvascular diseases, infection, villonodular synovitis, and Lyme
disease. Acute infectious arthritis usually is accompanied by significant systemic symptoms, including fever and malaise, and should
be easily recognized by an astute clinician and treated appropriately with culture and antibiotics, rather than injection therapy.
The collagen-vascular diseases generally manifest as a polyarthropathy rather than a monarthropathy limited to the shoulder joint,
and the pain does not radiate into the upper extremity. Pancoast
tumor and brachial plexopathy also may mimic the clinical presentation of scapulocostal syndrome.
Treatment
Initial treatment of the pain and functional disability associated
with scapulocostal syndrome should include a combination of
nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. The local application of heat and cold also may be beneficial. Repetitive movements
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 reasonable next step.
23 Scapulocostal Syndrome 61
SUGGESTED READINGS
Supraspinatus
Levator
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 commonly. 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 steroid. Trigger point injections are 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. 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 concurrently with an injection technique.
Chapter 24
PARSONAGE-TURNER SYNDROME
(e.g., Parsonage-Turner syndrome), and postradiation plexopathy. Cervical radiculopathy is a much more common cause of
upper extremity pain and weakness relative to Parsonage-Turner
syndrome. Table 24-1 differentiates these two painful conditions.
In patients in whom Parsonage-Turner syndrome affects only an
Weakness in:
Supraspinatus
Deltoid
Infraspinatus
Biceps
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 plexopathy include compression of the plexus by cervical ribs or abnormal muscles (e.g., thoracic outlet syndrome), invasion of the
plexus by tumor (e.g., Pancoast syndrome), direct trauma to the
plexus (e.g., stretch injuries and avulsions), inflammatory causes
62
24 Parsonage-Turner Syndrome 63
Testing
All patients presenting with Parsonage-Turner syndrome must
undergo MRI of the cervical spine and the brachial plexus (Figure
24-2). Computed tomography (CT) is a reasonable second choice
if MRI is contraindicated. Electromyography and nerve conduction velocity testing are extremely sensitive, and a skilled electromyographer can help delineate the specific portion of the plexus
that is abnormal. If an inflammatory basis for the plexopathy is
suspected, serial electromyography is indicated. If Pancoast tumor
or other tumors of the brachial plexus are suspected, chest radiographs with apical lordotic views may be helpful.
Screening laboratory tests consisting of complete blood cell
count, erythrocyte sedimentation rate, antinuclear antibody testing, and automated blood chemistry testing should be performed
if the diagnosis of brachial plexopathy is in question, to help rule
out other causes of pain.
Treatment
Pharmacological Therapy
Gabapentin
Gabapentin is the first-line treatment for the neuritic pain of
Parsonage-Turner syndrome. The drug is started with a 300-mg
dose at bedtime for 2 nights; the patient should be cautioned about
potential side effects, including dizziness, sedation, confusion,
TABLE 24-1
History
Examination
Test Results
Parsonage-Turner
syndrome
Cervical
radiculopathy
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.)
Clinical Pearls
Brachial plexus block with a local anesthetic and steroid
represents an excellent stop-gap measure for patients with
the uncontrolled pain of Parsonage-Turner syndrome while
waiting for pharmacological treatments to take effect. As
mentioned, correct diagnosis is paramount to allow the clinician to design a logical treatment plan.
24 Parsonage-Turner Syndrome 65
SUGGESTED READINGS
Marshall GB, McKenna E, Mahallati H: ParsonageTurner syndrome, Eur J
Radiol Extra 6:5153, 2005.
Mileto A, Gaeta M: Calcific tendonitis of supraspinatus simulating acute brachial
neuritis (Parsonage-Turner syndrome), Clin Radiol 66:578581, 2011.
Chapter 25
HYOID SYNDROME
Treatment
Nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors represent a reasonable first step in the
treatment of hyoid syndrome. The use of tricyclic antidepressants,
such as nortriptyline, at a single bedtime dose of 25 mg titrating
as side effects allow also is useful, especially if sleep disturbance is
present. If symptoms persist, injection of the caudad attachment
of the stylohyoid ligament is a reasonable next step.
To perform this injection, the patient is placed in the supine
position. The angle of the mandible on the affected side is identified. The greater cornu of the hyoid bone should lie approximately
1 inch inferior to the angle of the mandible. Gentle pressure at the
same point on the contralateral side of the neck steadies the hyoid
bone and makes identification of the greater cornu and subsequent
injection easier (Figure 25-2). The skin is prepared with antiseptic
solution. A 22-gauge, 112-inch needle attached to a 10-mL syringe
is advanced at this point 1 inch inferior to the angle of the mandible in a plane perpendicular to the skin. The greater cornu of
the hyoid bone should be encountered within 2.5 to 3 cm (Figure 25-3). After contact is made, the needle is withdrawn slightly
out of the periosteum or substance of the calcified ligament. After
careful aspiration reveals no blood or cerebrospinal fluid, 5 mL of
0.5% preservative-free lidocaine combined with 80 mg of methylprednisolone is injected in incremental doses. Subsequent daily
nerve blocks are done in a similar manner, substituting 40 mg of
methylprednisolone for the initial 80-mg dose.
Differential Diagnosis
Testing
66
25 Hyoid Syndrome 67
Styloid process
Hyoid bone
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
bone
Gentle pressure
on greater cornu
Internal External
carotid carotid
artery artery
Trachea
Internal
jugular
vein
Carrico & Shavell
Figure 25-3 Injection technique for relieving the pain of hyoid syndrome. (From Waldman SD: Atlas of pain management injection techniques, 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.)
for tumors of the neck, apex of the lung, anterior triangle of the
neck, and hypopharynx is indicated. If a significant history of vomiting is ascertained, esophageal tear should be considered.
Although the injection technique for hyoid syndrome is safe,
complications can occur. In addition to the potential for complications involving the vasculature, if the needle is placed too
laterally, the proximity of the brachial plexus, the central neuraxial
structures, and the phrenic nerve can result in side effects and complications. Although these complications should be rare if proper
technique is observed, the potential for inadvertent epidural, subdural, or subarachnoid injection remains. Phrenic nerve block also
can occur when using this injection technique to treat hyoid syndrome 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 possibility, 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 seizures. Incremental dosing while carefully monitoring the
patient for signs of local anesthetic toxicity helps avoid this
complication.
SUGGESTED READINGS
Auvenshine RC: Anatomy of the airway: an overview, Sleep Med Clin 5:4557,
2010.
Ernest EA III, Salter EG: Hyoid bone syndrome: a degenerative injury of the middle pharyngeal constrictor muscle with photomicroscopic evidence of insertion
tendinosis, J Prosthet Dentist 66:7883, 1991.
Nir D, Hefer T, Joachims HZ: Hyoid bone syndrome and its treatment with nonsteroidal anti-inflammatory drugs, Am J Otolaryngol 19:296300, 1998.
Waldman SD: Hyoid syndrome. In Atlas of pain management injection techniques,
2nd ed, Philadelphia, 2007, Saunders. pp 1619.
Chapter 26
OMOHYOID SYNDROME
Differential Diagnosis
Soft tissue injuries to the region may mimic omohyoid syndrome.
Because trauma is invariably involved in the evolution of the painful
condition, strain and sprain of other soft tissues often exist concurrently with omohyoid syndrome. Primary or metastatic tumors of
the neck and hypopharynx also may mimic the clinical presentation
of omohyoid syndrome and should be high on the list of diagnostic
possibilities if the history of trauma is weak or absent.
Treatment
Nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase2 (COX-2) inhibitors represent a reasonable first step in the treatment
of omohyoid syndrome. The use of tricyclic antidepressants, such
as nortriptyline, at a single bedtime dose of 25 mg, titrating upward
as side effects allow also is helpful, especially if sleep disturbance
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
anesthetic can serve as a diagnostic maneuver to help strengthen
the diagnosis.
Figure 26-1 The pain of omohyoid syndrome is localized in the supraclavicular region at a point just lateral and superior to the attachment of
the sternocleidomastoid muscle to the clavicle.
69
Site of
injection
Omohyoid muscle
(superior belly)
Sternocleidomastoid
muscle:
Sternal head
1"
Clavicular head
Clavicle
Omohyoid muscle
(inferior belly)
Figure 26-2 Injection site for the treatment of omohyoid syndrome.
Clinical Pearls
Although an uncommon cause of pain, omohyoid syndrome
is a clinically distinct and easily recognizable pain syndrome.
Because of its excellent response to the injection technique
described, the diagnosis of omohyoid syndrome should be
considered in the presence of a history of trauma or after
prolonged or forceful vomiting. If the patient has severe,
acute pain after vomiting, esophageal tear is a more likely
diagnosis. More chronic pain after a significant episode of
vomiting is more likely to indicate omohyoid syndrome.
The key to performing this injection technique safely is a
clear understanding of the anatomy and careful identification
of the anatomical landmarks necessary to perform the block.
The brachial plexus is quite superficial at the level at which
this block is performed. The needle should rarely be inserted
deeper than of an inch in all but the most obese patients.
If strict adherence to technique is observed, and the needle is
never advanced medially from the lateral border of the insertion of the sternocleidomastoid muscle on the clavicle, the
incidence of pneumothorax should be less than 0.5%.
In the absence of well-documented trauma to the anterior neck, omohyoid syndrome is a diagnosis of exclusion.
The clinician should always evaluate a patient with pain in
this anatomical region for occult malignancy. Tumors of
the larynx, hypopharynx, and anterior triangle of the neck
may manifest with clinical symptoms identical to omohyoid syndrome. In the setting of flexion/extension injuries or
other forceful trauma to the soft tissues of the neck, cervical
spine, or both, the clinician also should evaluate the patient
for trauma to the brachial plexus by careful physical examination and electromyography.
26 Omohyoid Syndrome 71
SUGGESTED READINGS
Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30,
2009.
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.
Waldman SD: Omohyoid syndrome. In Waldman SD, editor: Atlas of pain management injection techniques, ed 2, Philadelphia, 2007, Saunders, pp 2931.
Wong DSY, Li HJC: The omohyoid sling syndrome, Am J Otolaryngol 21:318322,
2000.
Chapter 27
NECK-TONGUE SYNDROME
Testing
Magnetic resonance imaging (MRI) of the brain and brainstem
should be performed in all patients thought to have neck-tongue
syndrome. 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
pathology, including tumors and demyelinating disease. Magnetic
resonance angiography (MRA) may be useful to help identify
72
Differential Diagnosis
Neck-tongue syndrome is a clinical diagnosis that can be made on
the basis of a targeted history and physical examination. Because
of the rarity of this syndrome, the clinician must consider necktongue syndrome to be a diagnosis of exclusion. Diseases of the
eyes, ears, nose, throat, and teeth may coexist and confuse the
diagnosis. Tumors of the hypopharynx, including the tonsillar
fossa and piriform sinus, may mimic the pain of neck-tongue
syndrome, as may tumors at the cerebellopontine angle. Occasionally, demyelinating disease may produce a clinical syndrome
identical to neck-tongue syndrome. The jaw claudication associated with temporal arteritis also may confuse the clinical picture,
as may glossopharyngeal neuralgia.
Treatment
The initial treatment of neck-tongue syndrome should consist
of immobilization of the cervical spine with a soft cervical collar. A trial of nonsteroidal antiinflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors represents a reasonable next
step. Blockade of the atlantoaxial joint and C2 nerve root with a
local anesthetic and steroid also should be considered. For refractory cases, cervical fusion of the upper cervical segments may be
required.
27 Neck-Tongue Syndrome 73
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
Neck-tongue syndrome is a unique and uncommon cause
of neck pain. The associated ipsilateral tongue numbness is
pathognomonic for the syndrome and is unusual in character. An analogous type of proprioceptive numbness is seen
in patients with Bells palsy. Given the rarity of this painful condition, the clinician should search carefully for other
causes of the symptoms before attributing them to necktongue syndrome.
SUGGESTED READINGS
Bogduk N: An anatomical basis for the neck-tongue syndrome, J Neurol Neurosurg
Psychiatry 44:202208, 1981.
Borody C: Neck-tongue syndrome, J Manipulative Physiol Ther 27:367, 2004.
Chedrawi AK, Fishman MA, Miller G: Neck-tongue syndrome, Pediatr Neurol
22:397399, 2000.
Orrell RW, Marsden CD: The neck-tongue syndrome, J Neurol Neurosurg Psychiatry 57:348352, 1994.
Chapter 28
SUPRASPINATUS TENDINITIS
motion, making simple everyday tasks, such as combing hair, fastening a brassiere, or reaching overhead, quite difficult. With continued
disuse, muscle wasting may occur and a frozen shoulder may develop.
Testing
Plain radiographs are indicated in all patients who present with
shoulder pain. Based on the patients clinical presentation, additional testing, including complete blood cell count, sedimentation rate, and antinuclear antibody testing, may be indicated.
Magnetic resonance imaging (MRI) of the shoulder is indicated
if rotator cuff tear is suspected and to confirm the diagnosis of
supraspinatus tendinitis (Figure 28-2). The injection technique
described here serves as a diagnostic and therapeutic maneuver.
Differential Diagnosis
Because supraspinatus tendinitis may occur after seemingly minor
trauma or develop gradually over time, the diagnosis often is
delayed. Tendinitis of the musculotendinous unit of the shoulder
frequently coexists with bursitis of the associated bursae of the
shoulder joint, creating additional pain and functional disability.
This ongoing pain and functional disability can cause the patient
to splint the shoulder group with resultant abnormal movement
of the shoulder, which puts additional stress on the rotator cuff.
This stress can lead to further trauma to the entire rotator cuff.
With rotator cuff tears, passive range of motion is normal but
active range of motion is limited, in contrast to frozen shoulder,
in which passive and active range of motion are limited. Rotator
cuff tear rarely occurs before age 40 except in cases of severe acute
trauma to the shoulder. Cervical radiculopathy rarely may cause
pain limited to the shoulder, although in most instances, associated neck and upper extremity pain and numbness are present.
Treatment
Initial treatment of the pain and functional disability associated
with supraspinatus tendinitis should include a combination of
nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. The local
28 Supraspinatus Tendinitis 75
Supraspinatus
tendon
Figure 28-1 Patients with supraspinatus tendinitis exhibit point tenderness of the greater tuberosity and a painful arc of abduction.
of the acromion marks the point of insertion of the supraspinatus tendon into the upper facet of the greater tuberosity of the
humerus. The point is marked with a sterile marker.
Proper preparation with antiseptic solution of the skin overlying the shoulder, subacromial region, and joint space is carried
out. A sterile syringe containing 1 mL of 0.25% preservative-free
bupivacaine and 40 mg of methylprednisolone is attached to a
25-gauge, 1-inch needle using strict aseptic technique. With
strict aseptic technique, the previously marked point is palpated,
and the indentation indicating the insertion of the supraspinatus
tendon is identified again with the gloved finger. The needle is
carefully advanced perpendicularly at this point through the skin
and subcutaneous tissues and through the joint capsule until it
impinges on bone (Figure 28-3). The needle is withdrawn 1 to
2 mm out of the periosteum of the humerus, and the contents
of the syringe are gently injected. Slight resistance to injection
should be felt. If no resistance is encountered, either the needle tip
is in the joint space itself or the supraspinatus tendon is ruptured.
If significant resistance to injection is detected, the needle tip is
probably in the substance of a ligament or tendon and should
be advanced or withdrawn slightly until the injection proceeds
without significant resistance. The needle is removed, and a sterile
pressure dressing and ice pack are placed at the injection site.
Supraspinatus
tendon
Deltoid muscle
Head of humerus
Periosteum
Posterior
Anterior
Figure 28-3 Correct needle placement for injection into the supraspinatus tendon.
Clinical Pearls
The musculotendinous unit of the shoulder joint is susceptible 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 musculotendinous 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 microtrauma 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 associated 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 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.
Chen SK, Chou PH, Lue YL, Lu YM: Treatment for frozen shoulder combined
with calcific tendinitis of the supraspinatus, Kaohsiung J Med Sci 2880;24:
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.
Waldman SD: Supraspinatus tendinitis. In Waldman SD, editor: Atlas of
pain management injection techniques, ed 3, Philadelphia, 2007, Saunders,
pp 6467.
Waldman SD: Functional anatomy of the shoulder joint. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 8081.
Chapter 29
INFRASPINATUS TENDINITIS
Differential Diagnosis
Infraspinatus tendinitis can manifest as an acute or chronic painful condition of the shoulder. Acute infraspinatus tendinitis usually occurs in a younger group of patients after overuse or misuse
of the shoulder joint. Inciting factors include activities that require
repeated abduction and lateral rotation of the humerus, such as
installing brake pads during assembly line work. The vigorous use
of exercise equipment also has been implicated. The pain of infraspinatus tendinitis is constant, severe, and localized to the deltoid
area. Significant sleep disturbance is often reported. Patients with
infraspinatus tendinitis exhibit pain with lateral rotation of the
humerus and on active abduction. Chronic infraspinatus tendinitis tends to occur in older patients and to manifest in a more
gradual or insidious manner, without a single specific event of
antecedent trauma. The pain of infraspinatus tendinitis may be
associated with a gradual loss of range of motion of the affected
shoulder. The patient often awakens at night when he or she rolls
over onto the affected shoulder.
Treatment
The patient may attempt to splint the inflamed infraspinatus tendon by rotating the scapula anteriorly to remove tension from the
tendon (Figure 29-1). Point tenderness is usually present over the
greater tuberosity. The patient exhibits a painful arc of abduction
and complains of a catch or sudden onset of pain in the midrange of the arc. Early in the course of the disease, passive range
of motion is full and painless. As the disease progresses, patients
with infraspinatus tendinitis often experience a gradual decrease
in functional ability with decreasing shoulder range of motion,
making simple everyday tasks, such as combing hair, fastening a
brassiere, or reaching overhead, quite difficult. With continued
disuse, muscle wasting may occur and a frozen shoulder may
develop.
Testing
Plain radiographs are indicated in all patients with shoulder
pain. Based on the patients clinical presentation, additional
testing, including complete blood cell count, erythrocyte
77
Figure 29-1 Patients with infraspinatus tendinitis exhibit posterior point tenderness and a painful arc of abduction.
29 Infraspinatus Tendinitis 79
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 outline these same calcifications (arrows, arrowhead). (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders.)
Infraspinatus
tendon
Synovial bursa
Deltoid muscle
Head of humerus
Periosteum
Posterior
Anterior
Figure 29-3 Correct needle placement for injection into the infraspinatus tendon.
Clinical Pearls
The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of often
repetitive motions. Second, the space in which the musculotendinous 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
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 associated 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. Coexistent bursitis and arthritis also
may contribute to shoulder pain and may require additional
treatment with a more localized injection of a local anesthetic 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
ICD-9 CODE 719.41
ICD-10 CODE M25.519
The Clinical Syndrome
The subacromial space lies directly inferior to the acromion,
coracoid process, acromioclavicular joint, and coracoacromial
ligament (Figure 30-1). Lubricated by the subacromial bursa, the
subacromial space in health is narrow, and the anatomical structures surrounding it are responsible for maintaining static and
dynamic shoulder stability. The space between the acromion and
the superior aspect of the humeral head is called the impingement
interval, and abduction of the arm narrows the space further (Figure 30-2). Any pathological condition that further narrows this
space (e.g., osteophyte, abnormal acromial anatomy, ligamentous
calcification, or congenital defects of the acromion) increases the
incidence of impingement (Figure 30-3). The most common
causes of subacromial impingement are listed in Table 30-1.
Similar to the congenital anatomical variant of the trefoil spinal
canal being associated with a statistically significantly higher incidence of spinal stenosis, several common normal anatomical variants
of the acromion often contribute to development of subacromial
Coracoid process
Subacromial space
Acromion
Clavicle
Greater tuberosity
Lesser tuberosity
Scapula
Humerus
Figure 30-1 The subacromial space lies directly inferior to the acromion, the coracoid process, the acromioclavicular joint, and the coracoacromial ligament.
Testing
MRI of the shoulder provides the best information regarding any
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 conditions that may harm the patient, such as primary and metastatic tumors of the shoulder joint and surrounding structures.
In patients who cannot undergo MRI, such as patients with
pacemakers, computed tomography (CT) is a reasonable second
81
Coraco-clavicular ligament
Subacromial
bursa
Acromioclavicular ligament
Coracoacromial ligament
Inflamed supraspinatus
tendon
Biceps
brachii m.
Subacromial
bursa
impinged
Long head
Short head
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.
Differential Diagnosis
Subacromial impingement syndrome is a clinical diagnosis supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic
subacromial impingement syndrome include subacromial bursitis, tendinopathy and tendinitis of the rotator cuff, calcification
and thickening of coracoacromial ligament, and arthritis affecting
any of the shoulder joints. Adhesive capsulitis or frozen shoulder
may confuse the diagnosis, as may idiopathic brachial plexopathy
(Parsonage-Turner syndrome; see Chapter 24). Primary and metastatic tumors of the shoulder and surrounding structures remain
an ever-present possibility and should always be part of the differential diagnosis of patients presenting with shoulder pain.
Treatment
Initial treatment of the pain and functional disability associated with subacromial impingement syndrome should include a
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 osteophytosis (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.)
LD
Type I
Type II
Type III
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 susceptible to the development of tendinitis for several reasons. First, the joint is subjected to a wide range of often
repetitive motions. Second, the space in which the musculotendinous 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
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 associated bursae of the shoulder joint, creating additional pain
and functional disability. Patients with untreated subacromial impingement syndrome continue to experience pain
and functional disability and may continue to cause ongoing 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 mechanisms 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 PAIN SYNDROME
Testing
The Clinical Syndrome
The subacromial space lies directly inferior to the acromion,
the coracoid process, the acromioclavicular joint, and the coracoacromial ligament (see Figure 30-1). Lubricated by the subacromial bursa, the subacromial space in health is narrow and
the anatomical structures surrounding it are responsible for
maintaining static and dynamic shoulder stability. 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 (see Figure 30-2). Any pathological condition that further narrows this space (e.g., osteophyte,
abnormal acromial anatomy, ligamentous calcification, or
congenital defects of the acromion) increases the incidence of
impingement (see Figure 30-3 and Table 30-1).
One such congenital defect is caused by failure of the distal
ossification center of the acromion to fuse (Figure 31-1). This
failure to fuse is termed os acromiale and essentially results in a
second acromial joint. This second joint can lead to impingement syndromes and exacerbate shoulder instability.
Patients suffering from os acromiale have diffuse shoulder
pain, with an associated feeling of weakness combined with loss
of range of motion. Pain is often worse at night, and patients
often complain that they are unable to sleep on the affected
shoulder. The clinical presentation is usually insidious, without
a clear-cut history of trauma to the affected shoulder. Affected
patients tend to be younger than those with other causes of
shoulder impingement syndromes. Untreated, os acromiale can
lead to progressive tendinopathy of the rotator cuff and gradually increasing shoulder instability and functional disability. In
patients older than 50 years, progression of impingement often
leads to rotator cuff tear.
Differential Diagnosis
Os acromiale is a clinical diagnosis supported by a combination
of clinical history, physical examination, radiography, and MRI.
Pain syndromes that may mimic os acromiale include subacromial
impingement syndrome, subacromial bursitis, tendinopathy and
tendinitis of the rotator cuff, calcification and thickening of the
coracoacromial ligament, and arthritis affecting any of the shoulder joints. Adhesive capsulitis or frozen shoulder may confuse
the diagnosis, as may idiopathic brachial plexopathy (ParsonageTurner syndrome; see Chapter 24). Acromial stress fractures and
undiagnosed clavicular fractures also may mimic the clinical presentation of os acromiale, as may impingement syndromes caused
by aberrant subacromial blood vessels. Primary and metastatic
tumors of the shoulder and surrounding structures are an everpresent possibility and should remain as part of the differential
diagnosis of patients with shoulder pain.
Treatment
Initial treatment of the pain and functional disability associated
with os acromiale should include a combination of nonsteroidal
Os acromiale
Figure 31-1 Os acromiale is a congenital defect caused by failure of the distal ossification center of the acromion to fuse.
Clinical Pearls
The acromion has three distinct ossification centers: (1) the
basiacromion-metacromion, which is most proximal; (2)
the metacromion-mesoacromion, which is in the middle;
and (3) the mesoacromion-preacromion, which is most
distal. Lack of fusion of the mesoacromion-preacromion is
responsible for the development of os acromiale.
The musculotendinous unit of the shoulder joint is susceptible to the development of tendinitis for several reasons.
First, the joint is subjected to a wide range of often repetitive motions. Second, the space in which the musculotendinous 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 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 associated bursae of
the shoulder joint, creating additional pain and functional
disability. Patients with untreated os acromiale continue to
experience pain and functional disability and may continue
to cause ongoing irreversible shoulder damage culminating
in damage to the humeral head and rotator cuff tear.
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.)
Nissen CW: The acromion: fractures and os acromiale, Oper Tech Sports Med
12:3234, 2004.
Pagnani MJ, Mathis CE, Solman CG: Painful os acromiale (or unfused acromial
apophysis) in athletes, J Shoulder Elbow Surg 15:432435, 2006.
Chapter 32
GLOMUS TUMOR OF THE
SHOULDER
Differential Diagnosis
The triad of localized, intermittent, lancinating excruciating
pain, tenderness to palpation, and cold intolerance makes the
diagnosis apparent to an astute clinician. Glomus tumor of the
shoulder must be distinguished from other causes of localized
shoulder pain. If a history of trauma is present, fracture, osteomyelitis, tenosynovitis, and foreign body synovitis should be
Testing
Magnetic resonance imaging (MRI) of the affected area often
reveals the actual glomus tumor and may reveal erosion or a perforating lesion of the phalanx beneath the tumor. The tumor
90
Figure 32-1 Frontal T1 MRI shows the calcification at the distal insertion
of the deltoid muscle in the area of the glomus tumor. (From Boretto J-G,
Lazerges C, Coulet B, Baldet P, Chammas M: Calcified glomus tumor of the
shoulder: a case report, Chir Main 4:183186, 2008.)
Treatment
The mainstay of treatment of glomus tumor is surgical removal.
Medication management is uniformly disappointing. Injection of the affected area in the point of maximal tenderness
may provide temporary relief of the pain of glomus tumor and
blocks Posners cold induction test response, further strengthening the diagnosis.
Clinical Pearls
The diagnosis of glomus tumor of the shoulder 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.
tendencies, making complete excision of the tumor and careful
follow-up mandatory.
SUGGESTED READINGS
Abela M, Cole AS, Hill GA, Carr AJ: Glomus tumor of the scapular region,
JShoulder Elbow Surg 9:532533, 2000.
Boretto JG, Lazerges C, Coulet B, Baldet P, Chammas M: Calcified glomus tumor
of the shoulder: a case report, Chir Main 27:183186, 2008.
Ghaly RF, Ring AM: Supraclavicular glomus tumor, 20-year history of undiagnosed shoulder pain: a case report, Pain 83:379382, 1999.
Nebreda CL, Urban BJ, Taylor AE: Upper extremity pain of 10 years duration
caused by a glomus tumor, Reg Anesth Pain Med 25:6971, 2000.
Roberts SN, Carter C, Brown JN, Hayes MG, Saies A: Enormous glomus tumor
of the shoulder, J Shoulder Elbow Surg 8:365366, 1999.
Yoshikawa I, Murakami M, Ishizawa M, Matsumoto K, Hukuda S: Glomus
tumor of the musculotendinous junction of the rotator cuff, Clin Orthop
326:250253, 1996.
Chapter 33
PECTORALIS MAJOR TEAR
SYNDROME
Testing
MRI of the shoulder, proximal humerus, and anterior chest
wall provides the best information regarding pathological processes of these anatomical regions. MRI is highly accurate and
helps identify abnormalities that may require urgent surgical
repair, such as large complete muscle tears, tendon rupture,
or both. MRI of the affected anatomy also helps the clinician
rule out unsuspected pathological conditions that may harm
the patient, such as primary and metastatic tumors. In patients
who cannot undergo MRI, such as patients with pacemakers,
computed tomography (CT) is a reasonable second choice.
Radionuclide bone scanning and plain radiography are indicated if fracture or bony abnormality such as metastatic disease
of the proximal humerus, shoulder, or anterior chest wall is
being considered in the differential diagnosis. Screening laboratory tests consisting of complete blood cell count, erythrocyte
sedimentation rate, and automated blood chemistry testing
should be performed if the diagnosis of pectoralis major tear
syndrome is in question.
Figure 33-1 Microscopic tear of the pectoralis muscle with mild bleeding and slight edema.
Differential Diagnosis
Pectoralis major tear syndrome is a clinical diagnosis supported
by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic pectoralis
major tear syndrome include injuries to the pectoralis minor, subscapularis, or latissimus dorsi muscles and inferior glenohumeral
ligament injuries. Dislocation of the manubrium from the body of
the sternum after acceleration/deceleration injuries also may confuse the diagnosis. Fractures of all of the bony origins of the pectoralis major muscles (e.g., the sternum and ribs and fractures of the
anatomical or surgical neck of the humerus) may mimic the clinical presentation of pectoralis major tear syndrome. Primary and
metastatic tumors of the shoulder, humerus, and anterior chest
wall and their surrounding structures remain an ever-present possibility and should be included as part of the differential diagnosis
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.
Treatment
Although the pain and functional disability associated with mild
microscopic tears of the pectoralis major muscle may be treated
conservatively with a combination of the nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors
and gentle physical therapy, more extensive tears and rupture of
the pectoralis major tendon require urgent surgical repair if permanent cosmetic deformity and functional disability are to be
avoided.
Figure 33-8 Active internal rotation of the humerus may reveal weakness. If significant disruption of the muscle or rupture of the tendon
occurs, the patient is unable to reach behind his or her back. (From
Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms,
Philadelphia, 2006, Saunders, p 50.)
B
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
maximal contraction of the injured muscle shows a prominent bulge
in the medial aspect of the left pectoralis major muscle (arrow). (From
EdelmanRR, Hesselink JR, Zlatkin MB, etal, editors: Clinical magnetic resonance imaging, 3rd ed, Philadelphia, 2006, Saunders, p 3468.)
Biceps m.
Clinical Pearls
Pectoralis major tear syndrome is an uncommon but easily
recognized cause of anterior chest wall and shoulder pain. A
patient with complete pectoralis major muscle tear, tendon
rupture, or both may present with hematoma and ecchymosis 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
Figure 33-7 Popeyes sign associated with rupture of the biceps tendon. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and
symptoms, Philadelphia, 2006, Saunders, p 83.)
Beloosesky Y, Grinblat J, Katz M, Hendel D, Sommer R: Pectoralis major rupture in the elderly: clinical and sonographic findings, Clin Imaging 27:261264,
2003.
ElMaraghy AR, Devereaux MW: A systematic review and comprehensive classification 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
Sports Med 13:162168, 2005.
Weaver JS, Jacobson JA, Jamadar DA, etal: Sonography of the pectoralis major
tear, Ultrasound Med Biol 29:S15, 374383, 2003.
Chapter 34
SUPRASCAPULAR NERVE
ENTRAPMENT
to the ipsilateral shoulder. Tenderness over the suprascapular
notch is usually present. Shoulder movement, especially reaching
across the chest, may increase the pain. Untreated, weakness and
atrophy of the supraspinatus and infraspinatus muscles occur.
Testing
Electromyography helps to distinguish cervical radiculopathy and
Parsonage-Turner syndrome from 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
Trapezius
Supraspinatus
Suprascapular
nerve
Infraspinatus m.
Suprascapular
notch
Transverse
suprascapular
ligament
Suprascapular
nerve
Differential Diagnosis
Suprascapular nerve entrapment syndrome is often misdiagnosed as
bursitis, tendinitis, or arthritis of the shoulder. Cervical radiculopathy of the C5 nerve root also may mimic the clinical presentation
of suprascapular nerve entrapment syndrome. Parsonage-Turner
syndrome, also known as idiopathic brachial neuritis, may manifest as sudden onset of shoulder pain and can be confused with
suprascapular nerve entrapment. Tumor involving the superior
scapular nerve, shoulder, or both also should be considered in the
differential diagnosis of suprascapular nerve entrapment syndrome.
Treatment
Nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors represent a reasonable first step in the
treatment of suprascapular nerve entrapment syndrome. The use
of tricyclic antidepressants, such as nortriptyline, at a single bedtime dose of 25 mg titrating upward as side effects allow also is
useful, especially if sleep disturbance also is present. Avoidance of
Infraspinatus m.
Clinical Pearls
Avoidance techniques of the repetitive movements responsible for suprascapular nerve entrapment are often forgotten in the rush to treatment. The use of rolling briefcases
instead of backpacks may help avoid continued trauma to
the nerve. This injection technique renders the shoulder
joint insensate. It is important that the clinician ensure that
the physical and occupational therapists caring for a patient
who has undergone suprascapular nerve block understand
that the shoulder girdle as well as the shoulder joint have
been rendered insensate after this injection technique.
Deep heat modalities and range-of-motion exercises must
be monitored carefully to avoid burns or damage to the
shoulder.
Toussaint CP, Zager EL: Whats new in common upper extremity entrapment
neuropathies, Neurosurg Clin North Am 19:573581, 2008.
Waldman SD: Suprascapular nerve block. In Waldman SD, editor: Pain review,
Philadelphia, 2009, Saunders, pp 439440.
Chapter 35
QUADRILATERAL SPACE SYNDROME
Testing
Electromyography may help identify entrapment of the axillary nerve, although the test may be normal in mild cases even
though significant neurapraxia is present. Electromyography
helps distinguish cervical radiculopathy and Parsonage-Turner
syndrome from quadrilateral space syndrome. Plain radiographs
are indicated in all patients who present with quadrilateral
space syndrome to rule out occult bony pathological processes.
Based on the patients clinical presentation, additional testing,
including complete blood cell count, uric acid level, erythrocyte sedimentation rate, and antinuclear antibody testing, may
be indicated. MRI of the shoulder is indicated in all patients
thought to have quadrilateral space syndrome because this test
is highly specific for this disorder. In the rare patient in whom
MRI is nondiagnostic, subclavian arteriography to show occlusion of the posterior humeral circumflex artery may be considered because this finding is highly suggestive of a diagnosis of
quadrilateral space syndrome.
Differential Diagnosis
Quadrilateral space syndrome is often initially misdiagnosed as
bursitis, tendinitis, or arthritis of the shoulder. Cervical radiculopathy of the lower nerve roots also may mimic the clinical presentation of quadrilateral space syndrome.
Parsonage-Turner syndrome, or idiopathic brachial neuritis,
also may manifest as sudden onset of shoulder pain and can be
confused with quadrilateral space syndrome. Tumor involving
this anatomical region also should be considered in the differential diagnosis of quadrilateral space syndrome, as should occult
fractures of the proximal humerus and other mass lesions, such
as cysts and lipomas, that may compress the axillary nerve as it
traverses the quadrilateral space.
Treatment
Nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors represent a reasonable first step in the
treatment of mild, self-limited quadrilateral space syndrome. The
use of tricyclic antidepressants, such as nortriptyline, at a single
bedtime dose of 25 mg, titrating upward as side effects allow also
is useful, especially if sleep disturbance is present. Gabapentin or
carbamazepine also can be considered. Avoidance of repetitive
trauma thought to be contributing to this entrapment neuropathy also is important, especially in professional athletes. If these
maneuvers fail to produce rapid symptomatic relief, surgical
exploration and release of the axillary nerve are indicated.
99
Figure 35-1 Anatomy of axillary nerve as it travels through the quadrilateral space.
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.)
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.
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.)
Clinical Pearls
Avoidance techniques of the repetitive movements responsible for quadrilateral space syndrome often are forgotten in
the rush to treatment. Mild cases of quadrilateral space syndrome are usually self-limited, but more severe cases require
urgent surgical intervention. As with other uncommon pain
syndromes, quadrilateral space syndrome should be considered a diagnosis of exclusion and the clinician should ensure
that no potentially harmful occult space-occupying lesions
are present before attributing symptoms to other benign
causes.
SUGGESTED READINGS
Chautems RC, Glauser T, Waeber-Fey MC, Rostan O, Barraud GE: Quadrilateral space syndrome: case report and review of the literature, Ann Vasc Surg
14:673676, 2000.
McClelland D, Paxinos A: The anatomy of the quadrilateral space with reference
to quadrilateral space syndrome, J Shoulder Elbow Surg 17:162164, 2008.
Nishimura M, Kobayashi M, Hamagashira K, etal: Quadrilateral space syndrome:
a rare complication of thoracic surgery, Ann Thorac Surg 86:13501351, 2008.
Sanders TG, Tirman PFJ: Paralabral cyst: an unusual cause of quadrilateral space
syndrome, Arthroscopy 15:632637, 1999.
Chapter 36
PRONATOR SYNDROME
Median nerve
Pronator teres
muscle (cut):
Pronator teres
muscle (cut)
Humeral head
Ulnar head
Flexor digitorum
superficialis muscle
Figure 36-1 The symptoms of pronator syndrome are due to compression of the median nerve by the pronator teres muscle.
103
Testing
Electromyography helps to distinguish cervical radiculopathy,
thoracic outlet syndrome, and carpal tunnel syndrome from pronator syndrome. Plain radiographs are indicated in all patients
who present with pronator syndrome to rule out occult bony
pathological processes. Based on the patients clinical presentation, additional testing, including complete blood cell count,
uric acid level, erythrocyte sedimentation rate, and antinuclear
antibody testing, may be indicated. Magnetic resonance imaging
(MRI) of the forearm is indicated if a primary elbow pathological
condition or space-occupying lesion is suspected. The injection
of the median nerve at the elbow may serve as a diagnostic and
therapeutic maneuver.
Differential Diagnosis
Median nerve entrapment 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. Clinically,
it is difficult to distinguish from pronator syndrome. The diagnosis
is made by electromyography and nerve conduction velocity testing
that show compression of the median nerve at the elbow combined
with the radiographic finding of a supracondylar process.
Treatment
Nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors represent a reasonable first step in the
treatment of pronator syndrome. The use of tricyclic antidepressants, such as nortriptyline, at a single bedtime dose of 25 mg,
titrating upward as side effects allow, also is useful, especially
if sleep disturbance is present. Avoidance of repetitive trauma
thought to be contributing to this entrapment neuropathy also is
important. If these maneuvers fail to produce rapid symptomatic
relief, injection of the median nerve at the elbow with a local anesthetic and steroid is a reasonable next step. If symptoms persist,
surgical exploration and release of the median nerve are indicated.
Clinical Pearls
Avoidance techniques of the repetitive movements responsible 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 electromyography and nerve conduction velocity testing that show
compression of the median nerve at the elbow combined
SUGGESTED READINGS
Horak BT, Kuz JT: An unusual case of pronator syndrome with ipsilateral supracondylar process and abnormal muscle mass, J Hand Surg 33:7982, 2008.
Lacey SH, Soldatis JJ: Bilateral pronator syndrome associated with anomalous
heads of the pronator teres muscle: a case report, J Hand Surg 18:349351,
1993.
Presciutti S, Rodner CM: Pronator syndrome, J Hand Surg 36:907909, 2011.
Rehak DC: Pronator syndrome, Clin Sports Med 20:531540, 2001.
Chapter 37
CUBITAL BURSITIS
Differential Diagnosis
The most common causes of elbow pain are arthritis of the elbow
joint, tennis elbow, golfers elbow, and olecranon bursitis. Arthritis of the elbow joint may mimic cubital bursitis because both
painful conditions are associated with movement of the joint.
The anterior point tenderness seen in cubital bursitis is absent in
arthritis of the elbow, however. Tennis elbow and golfers elbow
are distinct clinical entities that should not be confused with
cubital bursitis because the point tenderness seen in these painful
conditions is identified over the lateral and medial epicondyles,
rather than at the midline, as is seen with cubital bursitis. Acute
gout affecting the elbow manifests as a diffuse acute inflammatory condition that may be difficult to distinguish from infection of the joint, rather than as a localized musculoskeletal pain
syndrome.
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 pathological 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 collagenvascular disease also should be considered in appropriate patients.
Electromyography and nerve conduction velocity testing rule out
106
Figure 37-1 A patient with cubital bursitis reports pain and swelling on
any movement of the elbow.
Treatment
Initial treatment of the pain and functional disability associated
with cubital bursitis should include a combination of nonsteroidal
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
syndrome should be avoided. For patients who do not respond to
these treatment modalities, injection of the cubital bursa with a local
anesthetic and steroid may be a reasonable next step (Figure 37-3).
To inject the cubital bursa, the patient is placed in the supine
position, with the arm fully adducted at the patients side and the
elbow extended and the dorsum of the hand resting on a folded
towel. Using a 5-mL sterile syringe, 2 mL of local anesthetic and
40 mg of methylprednisolone is drawn.
After sterile preparation of skin overlying the anterior aspect
of the joint, the clinician identifies the pulsations of the brachial
artery at the crease of the elbow. After preparation of the skin
with antiseptic solution, a 25-gauge, 1-inch needle is inserted just
lateral to the brachial artery at the crease and slowly advanced in a
slightly medial and cephalad trajectory through the skin and subcutaneous tissues. If bone is encountered, the needle is withdrawn
back into the subcutaneous tissue. The contents of the syringe
are gently injected. Little resistance to injection should be felt. If
resistance is encountered, the needle is probably in the tendon and
should be withdrawn back until the injection proceeds without
significant resistance. The needle is removed, and a sterile pressure
dressing and ice pack are placed at the injection site.
Cubital bursa
Clinical Pearls
Bursae are formed from synovial sacs whose purpose is
to allow easy sliding of muscles and tendons across one
another at areas of repeated movement. These synovial sacs
are lined with a synovial membrane invested with a network
of blood vessels that secrete synovial fluid. Inflammation of
the bursa results in an increase in the production of synovial fluid with swelling of the bursal sac. With overuse or
misuse, these bursae may become inflamed, enlarged, and,
rarely, infected. Coexistent tendinitis and epicondylitis also
may contribute to elbow pain and may require additional
treatment with more localized injection of local anesthetic
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, in particular avoiding the median
nerve by keeping the needle lateral to the brachial artery.
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 this injection technique for elbow pain. Vigorous
exercises should be avoided because they exacerbate the
patients symptoms. Simple analgesics and NSAIDs may be
used concurrently with this injection technique.
SUGGESTED READINGS
Chung CB, Kim HJ: Sports injuries of the elbow, Magn Res Imaging Clin N Am
11:239253, 2003.
Hayter CL, Giuffre BM: Overuse and traumatic injuries of the elbow, Magn Res
Imaging Clin N Am 17:617638, 2009.
Howard TM, Shaw JL, Phillips J: Physical examination of the elbow. In Seidenberg PH, Beutler AI, editors: The sports medicine resource manual. Philadelphia,
2008, Saunders, pp 7178.
Sellards R, Kuebrich C: The elbow: diagnosis and treatment of common injuriesprimary care, Clin Office Pract 32:116, 2005.
Waldman SD: Injection technique for cubital bursitis pain. In Waldman SD,
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
Figure 38-2 Eliciting Froments sign. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms, Philadelphia, 2006, Saunders, p 126.)
Testing
Electromyography helps to distinguish cervical radiculopathy and
anconeus epitrochlearis from golfers elbow. Plain radiographs are
indicated in all patients who present with anconeus epitrochlearis
to rule out occult bony pathology, such as osteophytes impinging
on the ulnar nerve. Based on the patients clinical presentation,
additional testing, including complete blood cell count, uric acid
level, erythrocyte sedimentation rate, and antinuclear antibody
testing, may be indicated. Magnetic resonance imaging (MRI) of
the elbow is indicated if joint instability is suspected and clearly
identifies whether the compression of the ulnar nerve is caused by
an accessory anconeus muscle (see Figure 38-3). Injection of the
ulnar nerve serves as a diagnostic and therapeutic maneuver.
Differential Diagnosis
Anconeus epitrochlearis is often misdiagnosed as golfers elbow,
and this fact accounts for the many patients with golfers elbow
who fail to respond to conservative measures. In anconeus epitrochlearis, the maximal tenderness to palpation is over the ulnar
nerve 1 inch below the medial epicondyle, whereas in golfers
elbow, the maximal tenderness to palpation is directly over the
medial epicondyle. Anconeus epitrochlearis also should be differentiated from cervical radiculopathy involving the C7 or C8
roots and golfers elbow. Cervical radiculopathy and ulnar nerve
entrapment may coexist as the double crush syndrome. The
double crush syndrome is seen most commonly with median
nerve entrapment at the wrist or carpal tunnel syndrome.
Treatment
Initial treatment of the pain and functional disability associated
with anconeus epitrochlearis should include a combination of
Figure 38-3 Anconeus epitrochlearis muscle replacing the cubital tunnel retinaculum. A T2-weighted axial image reveals the ulnar nerve
(white arrow) deep to an anomalous anconeus epitrochlearis muscle
(black arrow) and superficial to the posterior bundle of the medial collateral ligament (curved arrow). (From Edelman RR, Hesselink JR, Zlatkin MB,
etal, editors: Clinical magnetic resonance imaging, 3rd ed, Philadelphia,
2006, Saunders, p 3303.)
nonsteroidal 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 syndrome should be avoided. For patients who do
not respond to these treatment modalities, injection of the ulnar
nerve at the elbow with a local anesthetic and steroid may be a
reasonable next step. If the symptoms of anconeus epitrochlearis
persist, surgical exploration, resection of the accessory anconeus
muscle, and decompression of the ulnar nerve are indicated.
Clinical Pearls
An accessory anconeus muscle is present in approximately
11% of the adult population. Anconeus epitrochlearis is a
distinct clinical entity that is often misdiagnosed as golfers
elbow, and this fact accounts for the many patients with
golfers elbow who fail to respond to conservative measures. With anconeus epitrochlearis, 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 anconeus epitrochlearis is suspected, injection
SUGGESTED READINGS
Dellon AL: Musculotendinous variations about the medial humeral epicondyle,
JHand Surg 11:175181, 1985.
Kojima T: Ulnar compression neuropathy secondary to the anconeus epitrochlearis muscle, J Hand Surg 14:918919, 1989.
Masear VR, Hill JJ Jr, Cohen SM: Ulnar compression neuropathy secondary to
the anconeus epitrochlearis muscle, J Hand Surg 13:720724, 1988.
Waldman SD: The ulnar nerve. In Waldman SD, editor: Pain review, Philadelphia, 2009, Saunders, pp 7677.
Chapter 39
OS SUPRATROCHLEARE-RELATED
ELBOW PAIN
Testing
Plain radiographs are indicated in all patients with os supratrochleare to rule out fractures and identify accessory ossicles that may
have become inflamed. Plain radiographs also often identify loose
bodies or joint mice frequently seen in patients with elbow pain
secondary to os supratrochleare. Based on the patients clinical presentation, additional testing, including complete blood cell count,
erythrocyte sedimentation rate, and antinuclear antibody testing, may be indicated. Magnetic resonance imaging (MRI) of the
elbow joint is indicated if joint instability, occult mass, or tumor
is suspected and to clarify the diagnosis further (Figure 39-2).
Radionucleotide bone scanning may be useful in identifying stress
fractures or tumors of the elbow and distal humerus that may be
missed on plain radiographs.
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
Figure 39-1 Elbow pain secondary to os supratrochleare is characterized by tenderness and pain over the posterior elbow.
Figure 39-2 Accessory ossicles. A, Os vesalianum. B, Os intermetatarseum. C, Os supratrochleare posterius (dorsale). (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 4570.)
Clinical Pearls
Pain emanating from the elbow is a common problem
encountered in clinical practice. Os supratrochleare must be
distinguished from fractures of the elbow, fractures of the os
supratrochleare itself, entrapment neuropathies of the ulnar
nerve, bursitis, tendinitis, and epicondylitis. Less common
causes of posterior elbow pain are osteochondritis dissecans,
Panners disease, and synovial chondromatosis.
SUGGESTED READINGS
Gudmundsen E, stensen H: Accessory ossicles in the elbow, Acta Orthop Scand
58:130132, 1987.
McFarland EG, Gill HS, Laporte DM, Streiff M: Miscellaneous conditions about
the elbow in athletes [review], Clin Sports Med 23:743763, 2004.
Waldman SD: Functional anatomy of the elbow. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 7677.
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
Testing
Plain radiographs are indicated in all patients with osteonecrosis
of the elbow joint to rule out underlying occult bony pathological processes and identify sclerosis and fragmentation of
the osseous support of the articular surface. However, early in
TABLE 40-1
Figure 40-1 The blood supply to the elbow is easily disrupted, often
leaving the proximal portion of the bone without nutrition and leading
to osteonecrosis.
Radiation therapy
Sickle cell disease
113
Differential Diagnosis
Coexistent arthritis and gout of the elbow joint, bursitis, and
tendinitis may coexist with osteonecrosis of the elbow joints and
exacerbate the pain and disability. Tears of the ligaments, bone
cysts, bone contusions, and fractures may mimic the pain of osteonecrosis of the elbow joint, as can occult metastatic disease.
Treatment
Initial treatment of the pain and functional disability associated
with osteonecrosis of the elbow joint should include a combination of the nonsteroidal antiinflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and decreased weight bearing of the affected elbow joint or joints. 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 elbow joint may be a reasonable next step to provide palliation
of acute pain. Vigorous exercises should be avoided because they
will exacerbate the symptoms. Ultimately, surgical repair in the
form of total joint arthroplasty is the treatment of choice.
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.)
Po
255/128
255/128
Figure 40-3 Multifocal aspect of elbow osteonecrosis. A, Anterior; P, posterior. (From Mukaza MM, Manicom O, Fillipini P, Hernigou P: Elbow osteonecrosis in sickle cells anemia: a study of six cases, Orthop Traumatol 95:8284, 2009.)
Clinical Pearls
Osteonecrosis of the elbow joint is a diagnosis that is often
missed, leading to considerable unnecessary pain and disability. The clinician should include osteonecrosis of the
elbow joint in the differential diagnosis in all patients with
shoulder joint pain, especially if any of the predisposing factors listed in Table 40-1 are present. Coexistent arthritis,
tendinitis, and gout may contribute to the pain and may
require additional treatment. The use of physical modalities, including local heat and cold and decreased weight
bearing may provide symptomatic relief. Vigorous exercises
should be avoided because they will exacerbate the symptoms and may cause further damage to the wrist. Simple
analgesics and NSAIDs may be used concurrently with this
injection technique.
SUGGESTED READINGS
Henderson AB: Sickle cell anemia: clinical study of fifty-four cases (review), Am J
Med 9:757765, 1950.
Mukaza MM, Manicom O, Fillipini P, Hernigou P: Elbow osteonecrosis in sickle
cells anemia: a study of six cases, Orthop Traumatol 95:8284, 2009.
Savini CJ, James CW: HIV infection and osteonecrosis, J Assoc Nurse AIDS Care
12:8385, 2001.
Waldman SD: Functional anatomy of the elbow. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 7677.
Waldman SD: Osteonecrosis of the elbow. In Waldman SD, Campbell RSD, editors: Imaging of pain, New York, 2011, Elsevier, pp 281283.
Watanabe R, Sato K, Nakamura T, etal: Steroid-induced osteonecrosis of bilateral distal humerus treated by arthroplasty using costal osteochondral graft: case
report, J Hand Surg 36:816819, 2011.
Chapter 41
TRICEPS TENDINITIS
Testing
Plain radiographs and magnetic resonance imaging (MRI) are
indicated for all patients who present with posterior elbow pain
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
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 antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors 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.
Figure 41-3 The pain of triceps tendinitis is constant and severe and is
localized in the posterior elbow.
(see Figures 41-1 and 41-2). Based on the patients clinical presentation, additional tests, including complete blood count, erythrocyte sedimentation rate, and antinuclear antibody testing, may be
indicated. MRI of the elbow is indicated if joint instability is suspected and to confirm the diagnosis. Radionuclide bone scanning
Clinical Pearls
The triceps tendon is a very strong tendon, but it is also very
susceptible to rupture. Coexistent bursitis and arthritis also
may contribute to posterior elbow pain and may require
additional treatment with a more localized injection of local
anesthetic and methylprednisolone acetate.
Injection of the triceps tendon 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 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.
SUGGESTED READINGS
Badia A, Stennett C: Sports-related injuries of the elbow, J Hand Ther 19:
206227, 2006.
Jafarnia K, Gabel GT, Morrey BF: Triceps tendinitis, Oper Tech Sports Med
9:217221, 2001.
Potter HG, Schachar J, Jawetz S: Imaging of the elbow, Oper Tech Orthop 19:
199208, 2009.
Waldman SD: Functional anatomy of the elbow. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 7677.
Chapter 42
RADIAL TUNNEL SYNDROME
include aberrant fibrous bands in front of the radial head, anomalous blood vessels that compress the nerve, extrinsic masses, or a
sharp tendinous margin of the extensor carpi radialis brevis. These
entrapments may exist alone or in combination.
TABLE 42-1
Frequency
Cause
Characteristic patient
Tennis players
Pain location
Pain over the neck of the radius and lateral aspect of the
proximal forearm over the extensor muscles themselves
(distal to where the pain is located in LE)
Pain and tenderness over the lateral epicondyle and immediately distal to it (at the
origin of the extensor muscles)
Pain radiation
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
Differential Diagnosis
Radial nerve
Cervical radiculopathy and tennis elbow can mimic radial tunnel 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
may be difficult to distinguish from infection of the joint, rather
than a localized nerve entrapment.
Treatment
Extensor carpi
radialis brevis
muscle
Figure 42-1 The pain of radial tunnel syndrome is localized to the deep
extensor muscle mass and may radiate proximally and distally into the
upper arm and forearm.
and (3) a positive result on the middle finger test. The middle
finger test is performed by having the patient extend the forearm,
wrist, and middle finger and sustain this action against resistance.
Patients with radial tunnel syndrome exhibit increased lateral
elbow pain secondary to fixation and compression of the radial
nerve by the extensor carpi radialis brevis muscle.
Testing
Because of the ambiguity and confusion surrounding this clinical syndrome, testing is important to help confirm the diagnosis
of radial tunnel syndrome. Electromyography helps to distinguish cervical radiculopathy and radial tunnel syndrome from
tennis elbow. Plain radiographs are indicated in all patients who
present with radial tunnel syndrome to rule out occult bony
pathology. Based on the patients clinical presentation, additional testing, including complete blood cell count, uric acid,
erythrocyte sedimentation rate, and antinuclear antibody testing, may be indicated.
Magnetic resonance imaging (MRI) of the elbow is indicated
if internal derangement of the joint is suspected and may help
identify the factors responsible for the nerve entrapment, such as
ganglion cysts or lipomas (Figure 42-2). The injection technique
of the radial nerve at the elbow with a local anesthetic and steroid
may help confirm the diagnosis and treat the syndrome.
Clinical Pearls
Radial tunnel syndrome is a distinct clinical entity that is
often misdiagnosed as tennis elbow, and this fact accounts
for the many patients with tennis elbow who fail to
respond to conservative measures. Radial tunnel syndrome
can be distinguished from tennis elbow because with radial
tunnel syndrome, the maximal tenderness to palpation is
over the radial nerve, whereas with tennis elbow, the maximal tenderness to palpation is over the lateral epicondyle.
If radial tunnel syndrome is suspected, injection of the
radial nerve at the humerus with a local anesthetic and steroid gives almost instantaneous relief. Careful neurological
examination to identify preexisting neurological deficits
that may later be attributed to the nerve block should be
performed on all patients before beginning radial nerve
block at the humerus.
Post-op
Pre-op
Pre-op
C
Pre-op
Post-op
E
Post-op
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
Clavert P, Lutz JC, Adam P: Frohses arcade is not the exclusive compression site
of the radial nerve in its tunnel, Orthop Traumatol Surg Res 95:114118, 2009.
Lee JT, Azari K: Ford Jones N: Long term results of radial tunnel release: the effect
of co-existing tennis elbow, multiple compression syndromes and workers
compensation, J Plast Reconstr Aesthet Surg 61:10951099, 2008.
Huisstede B, Miedema HS, van Opstal T: Interventions for treating the radial tunnel syndrome: a systematic review of observational studies, J Hand Surg 33:72,
2008, e1-72.e10.
Chapter 43
CUBITAL TUNNEL SYNDROME
Testing
Electromyography helps distinguish cervical radiculopathy and
cubital tunnel syndrome from golfers elbow. Plain radiographs are
indicated in all patients with cubital tunnel syndrome to rule out
occult bony pathological processes, such as osteophytes impinging
on the ulnar nerve. Based on the patients clinical presentation,
122
Differential Diagnosis
Cubital tunnel syndrome 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 syndrome, the maximal 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. Cubital tunnel syndrome also should
be differentiated from cervical radiculopathy involving the C7
or C8 roots and golfers elbow. Cervical radiculopathy and ulnar
nerve entrapment may coexist as the double crush syndrome.
The double crush syndrome is seen most commonly with median
nerve entrapment at the wrist or carpal tunnel syndrome.
Treatment
Initial treatment of the pain and functional disability associated
with cubital tunnel syndrome should include a combination of
nonsteroidal anti-inflammatory 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 syndrome should be avoided. For patients who do not
respond to these treatment modalities, injection of the ulnar nerve
at the elbow with a local anesthetic and steroid may be a reasonable
next step. If the symptoms of cubital tunnel syndrome persist, surgical exploration and decompression of the ulnar nerve are indicated.
Ulnar nerve
Medial epicondyle
Ulnar
nerve
Flexor carpi
ulnaris muscle
Ulnar collateral
ligament
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 tunnel syndrome. (From Waldman SD: Physical diagnosis of pain: an atlas of
signs and symptoms, Philadelphia, 2006, Saunders, p 127.)
Examiner
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.)
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
ME
Tunnel
Figure 43-6 In this patient with UCT the ulnar nerve has a cross sectional anatomy (CSA) of 0.29 cm2. The cross-section of the ulnar nerve is
depicted by arrows outlining its periphery. The nerve also is hypoechoic,
a finding that can be seen with increased edema. ME, Medial epicondyle; Tunnel, ulnar tunnel. (From Wiesler ER, Chloros GD, Cartwright MS,
Shin HW, Walker FO: Ultrasound in the diagnosis of ulnar neuropathy at the
cubital tunnel, J Hand Surg 31:10881093, 2006.)
Clinical Pearls
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
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
a local anesthetic and steroid gives almost instantaneous
relief. Careful neurological examination to identify preexisting neurological deficits that may later be attributed to
the nerve block should be performed on all patients before
beginning ulnar nerve block at the elbow.
Palmer BA, Hughes TB: Cubital tunnel syndrome, J Hand Surg 35:153163,
2010.
Rich BC, McKay MP: The cubital tunnel syndrome: a case report and discussion,
J Emerg Med 23:347350, 2002.
Chapter 44
DRIVERS ELBOW
and hand that are innervated by the ulnar nerve may be identified 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
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
syndrome. The double crush syndrome is seen most commonly
with median nerve entrapment at the wrist or with carpal tunnel
syndrome. The clinician should be aware that early in the course
of the evolution of drivers elbow the only physical finding other
than tenderness over the nerve may be the loss of sensation on the
ulnar side of the little finger.
Testing
Drivers elbow should be differentiated from cervical radiculopathy involving the C7 or C8 roots and golfers elbow. Electromyography helps distinguish cervical radiculopathy and drivers
elbow from golfers elbow. Ultrasound imaging of the elbow
may be useful in assessing the status of the ulnar nerve and can
provide important anatomic information when combined with
the neurophysiological data obtained from electromyography.
Plain radiographs and magnetic resonance imaging (MRI) are
indicated in all patients with drivers elbow to rule out intrinsic
pathological conditions of the elbow joint (Figure 44-2). Based
on the patients clinical presentation, additional testing, including complete blood count, uric acid level, sedimentation rate,
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 external 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 distinguished from golfers elbow in that in drivers elbow, the maximal 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 management injection techniques, 3rd ed, Philadelphia, 2013, Saunders, p 129.)
126
Summary of Ulnar Nerve Motor Signs and Tests Grouped by Affected Musculature
Test Name
Description
Positive Result
Jeannes sign
Egawas sign
Andr-Thomas sign
Masses sign
Observe the metacarpal arch as compared with the uninvolved side. The convex nature of the ulnar aspect of the
hand is altered by hypothenar atrophy.
Pitres-Testut sign
The sparing of the palmaris brevis muscle in contrast to the uninvolved side.
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.
anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX2) 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 not
respond to these treatment modalities, injection of the ulnar
nerve at the elbow with a local anesthetic and steroid may be a
reasonable next step. If the symptoms of cubital tunnel syndrome
persist, surgical exploration and decompression of the ulnar nerve
are indicated.
LE
ME
O
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.)
Clinical Pearls
Drivers elbow is a distinct clinical entity often misdiagnosed as golfers elbow, which accounts for the many
patients with golfers elbow who fail to respond to conservative measures. Drivers elbow can be distinguished
from golfers elbow because, with cubital 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. Drivers elbow also should be differentiated from cervical radiculopathy involving the C8 spinal
root, which may at times mimic ulnar nerve compression.
Furthermore, it should be remembered that cervical radiculopathy and ulnar nerve entrapment may coexist in double
crush syndrome. The double crush syndrome is seen most
commonly with median nerve entrapment at the wrist or
with carpal tunnel syndrome. Pancoasts tumor invading
the medial cord of the brachial plexus may also mimic an
isolated ulnar nerve entrapment and should be ruled out by
apical lordotic chest radiograph.
Careful neurological examination to identify preexisting neurological deficits that may later be attributed to
the nerve block should be performed on all patients before
beginning ulnar nerve block at the elbow.
Ulnar nerve entrapment at the elbow is often misdiagnosed as golfers elbow, and this fact accounts for the many
patients whose golfers elbow fails to respond to conservative measures. Drivers elbow can be distinguished from
golfers elbow in that in drivers elbow, the maximal 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. If cubital tunnel syndrome is suspected, injection
of the ulnar nerve at the elbow with local anesthetic and
steroid gives almost instantaneous relief.
SUGGESTED READINGS
Abdel-Salam A, Eyres KS, Cleary J: Drivers elbow: a cause of ulnar neuropathy,
JHand Surg 16:436437, 1991.
Palmer BA, Hughes TB: Cubital tunnel syndrome, J Hand Surg 35:153163,
2010.
Szabo RM, Kwak C: Natural history and conservative management of cubital tunnel syndrome, Hand Clin 23:311318, 2007.
Waldman SD: Golfers elbow. In Waldman SD, editor: Pain review, Philadelphia,
2009, Saunders, pp 267268.
Waldman SD: The ulnar nerve. In Waldman SD, editor: Pain review, Philadelphia, 2009, Saunders, pp 76.
Waldman SD: Ulnar nerve entrapment at the elbow. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 270271.
Chapter 45
ANTERIOR INTEROSSEOUS
SYNDROME
ICD-9 CODE 354.9
ICD-10 CODE G56.90
Differential Diagnosis
Anterior interosseous syndrome is an uncommon cause of forearm and wrist pain. The onset of symptoms in patients with
anterior interosseous syndrome is usually after acute trauma to
the forearm or after repetitive forearm and elbow motions, such
as using an ice pick. In this setting, the pain and muscle weakness
of anterior interosseous syndrome are thought to be secondary
to median nerve compression of the nerve just below the elbow
by the tendinous origins of the pronator teres muscle and flexor
digitorum superficialis muscle of the long finger or by aberrant
blood vessels. In some patients, no antecedent trauma is identified, and an inflammatory cause analogous to Parsonage-Turner
syndrome has been suggested as the cause of anterior interosseous syndrome in the absence of trauma.
Clinically, anterior interosseous syndrome manifests as acute
pain in the proximal forearm and deep in the wrist. As the syndrome progresses, patients with anterior interosseous syndrome
may report a tired or heavy sensation in the forearm with minimal
activity and the inability to pinch items between the thumb and
index finger because of paralysis of the flexor pollicis longus and
the flexor digitorum profundus (Figure 45-1).
Testing
Electromyography helps distinguish cervical radiculopathy, thoracic outlet syndrome, and carpal tunnel syndrome from anterior interosseous syndrome. Plain radiographs are indicated in all
patients who present with anterior interosseous syndrome to rule
out occult bony pathology. Based on the patients clinical presentation, additional tests, including complete blood cell count,
130
Treatment
Nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors represent a reasonable first step in
the treatment of anterior interosseous syndrome. The use of the
tricyclic antidepressants, such as nortriptyline, at a single bedtime
dose of 25 mg, titrating upward as side effects allow, also is useful, especially if sleep disturbance is present. It is important for
the patient to avoid repetitive trauma thought to be contributing
to this entrapment neuropathy. If these maneuvers fail to produce rapid symptomatic relief, injection of the median nerve at
the elbow with a local anesthetic and steroid is a reasonable next
step. If symptoms persist, surgical exploration and release of the
anterior interosseous branch of the median nerve are indicated.
Muscle paralysis:
Nerve compression:
Normal
Pronator teres
muscle
Median nerve
Muscle paralysis
Pronator digitorum
superficialis muscle
Anterior interosseous
branch of median nerve
Flexor pollicis
longus muscle
Flexor digitorum
profundus muscle
Figure 45-1 Patients with anterior interosseous syndrome exhibit acute forearm pain and progressive weakness of pinch.
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 significantly 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)
Clinical Pearls
Avoidance techniques for the repetitive movements responsible 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.
SUGGESTED READINGS
Chi Y, Harness NG: Anterior interosseous nerve syndrome, J Hand Surg 35:2078
2080, 2010.
Douglas H, Chin CL, Meals RA: Anterior interosseous nerve syndrome, J Am Soc
Surg Hand 1:249257, 2001.
Feldman MI, Muhammad K, Beltran J: Preoperative diagnosis of anterior interosseous nerve syndrome resulting in complete recovery, Eur J Radiol Extra
69:e73e76, 2009.
Waldman SD: Anterior interosseous syndrome. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 271272.
Waldman SD: Anterior interosseous syndrome. In Waldman SD, Campbell RSD,
editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 291293.
Chapter 46
ULNAR TUNNEL SYNDROME
ICD-9 CODE 354.2
ery
Ar t
Moto
Sens
ory
Figure 46-1 The ulnar nerve can be divided into sensory (palmar) and
motor (dorsal) branches. Note the fibrous arch of the hypothenar muscles under which the deep motor branch passes on its way out of the
ulnar tunnel. The ulnar artery travels along the radial side of the nerve
through the tunnel, after which it splits and becomes the deep and
superficial palmar arches. Blue tag, Sensory branch; black tag, motor
branch; red tag, ulnar artery. (From Waugh RP, Pellegrini Jr VD: Ulnar tunnel syndrome, Hand Clin 23:301310, 2007.)
133
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, Anomalous 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.)
Testing
Electromyography helps distinguish cervical radiculopathy, diabetic
polyneuropathy, and Pancoasts tumor from ulnar tunnel syndrome.
Plain radiographs are indicated in all patients who present with ulnar
tunnel syndrome to rule out occult bony pathological processes.
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 to help confirm
the diagnosis and whether joint instability or a space-occupying
lesion is suspected (Figures 46-2 and 46-3). The injection technique
described here serves as a diagnostic and therapeutic maneuver.
Differential Diagnosis
Ulnar tunnel syndrome often is misdiagnosed as arthritis of the
carpometacarpal joints, cervical radiculopathy, Pancoasts tumor,
and diabetic neuropathy. Patients with arthritis of the carpometacarpal joint usually have radiographic evidence and physical findings suggestive of arthritis. Most patients with a cervical
radiculopathy have reflex, motor, and sensory changes associated
with neck pain, whereas patients with ulnar tunnel syndrome have
no reflex changes, and motor and sensory changes are limited to
the distal ulnar nerve.
Diabetic polyneuropathy generally manifests as symmetrical
sensory deficit involving the entire hand, rather than limited in the
distribution of the ulnar nerve. Cervical radiculopathy and ulnar
nerve entrapment may coexist as the double crush syndrome.
Because ulnar tunnel syndrome is commonly seen in patients with
diabetes, diabetic polyneuropathy usually occurs in patients with
diabetes with ulnar tunnel syndrome. Pancoasts tumor invading
the medial cord of the brachial plexus also may mimic an isolated
ulnar nerve entrapment and should be ruled out by apical lordotic
chest radiographs.
P
S
T
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. (Reproduced with permission from Spratt JD, etal: The role of diagnostic radiology in compressive and entrapment neuropathies, Eur Radiol 12:23522364, 2002.)
Treatment
Initial treatment of the pain and functional disability associated
with ulnar tunnel syndrome should include a combination of
nonsteroidal anti-inflammatory 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 syndrome should be avoided. For patients who do
not respond to these treatment modalities, injection of the ulnar
nerve at the ulnar tunnel with a local anesthetic and steroid may
be a reasonable next step. If the symptoms of ulnar tunnel syndrome persist, surgical exploration and decompression of the
ulnar nerve are indicated.
Clinical Pearls
Ulnar tunnel syndrome should be differentiated from cervical radiculopathy involving the C8 spinal root, which
sometimes may mimic ulnar nerve compression. Cervical
radiculopathy and ulnar nerve entrapment may coexist in
the double crush syndrome. The double crush syndrome is
seen most commonly with ulnar nerve entrapment at the
wrist or carpal tunnel syndrome. Pancoasts tumor invading the medial cord of the brachial plexus also may mimic
isolated ulnar nerve entrapment and should be ruled out by
apical lordotic chest radiographs.
SUGGESTED READINGS
Chapter 47
CHEIRALGIA PARESTHETICA
Differential Diagnosis
Cheiralgia paresthetica is often misdiagnosed as lateral antebrachial cutaneous nerve syndrome. Cheiralgia paresthetica also
should be differentiated from cervical radiculopathy involving the C6 or C7 roots, although patients with cervical radiculopathy generally present not only with pain and numbness
but also with reflex and motor changes. Cervical radiculopathy
and radial nerve entrapment may coexist as the double crush
syndrome. The double crush syndrome is seen most commonly
Superficial radial nerve
Testing
Electromyography can help identify the exact source of neurological dysfunction and clarify the differential diagnosis; this should
be the starting point of the evaluation of all patients thought to
136
Figure 47-2 A positive Tinels sign over the radial nerve at the distal
forearm is usually present in patients with cheiralgia paresthetica. (From
Waldman SD: Physical diagnosis of pain: an atlas of signs and symptoms,
Philadelphia, 2006, Saunders, p 168.)
with median nerve entrapment at the wrist or carpal tunnel syndrome. It should be remembered that radial nerve compression
has many causes and the nerve can be compressed anywhere
along its path (Table 47-1).
Treatment
The first step in the treatment of cheiralgia paresthetica is the
removal of the cause of pressure on the radial nerve. A trial of
nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors represents a reasonable next step.
For patients for whom these treatment modalities fail, injection of the sensory branch of the radial nerve at the wrist with a
local anesthetic and steroid should be considered. For persistent
Cause
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
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.
Clinical Pearls
Radial nerve block at the wrist is an effective treatment for
the symptoms of cheiralgia paresthetica. 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 radial nerve
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 anesthetic and steroid should lead to marked improvement in
most patients.
SUGGESTED READINGS
Markiewitz AD, Merryman J: Radial nerve compression in the upper extremity,
JAm Soc Surg Hand 5:8799, 2005.
Massey EW, Pleet AB: Handcuffs and cheiralgia paresthetica, Neurology 28:1312
1313, 1978.
Smith MS: Handcuff neuropathy, Ann Emerg Med 10:668, 1981.
Waldman SD: Cheiralgia paresthetica. In Waldman SD, editor: Pain review, Philadelphia, 2009, Saunders, pp 275276.
Chapter 48
SECRETANS SYNDROME
Testing
Plain radiographs are indicated in all patients who present with
Secretans syndrome to rule out underlying occult bony pathological processes. 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 hand
will help confirm the diagnosis and is also indicated if joint instability, infection, or tumor is suspected. Electromyography is indicated if coexistent ulnar or carpal tunnel syndrome is suspected.
Injection of the areas of fibrosis provides improvement of the pain
and disability of this disease if implemented early.
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
Clinical Pearls
This injection technique is extremely effective in the treatment of pain and dysfunction secondary to Secretans syndrome. 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 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, massage, 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 patients symptoms. Simple analgesics and
NSAIDs may be used concurrently with this injection technique.
SUGGESTED READINGS
Moretta DN, Cooley RD Jr: Secretans disease: a unique case report and literature
review, Am J Orthop 31:524527, 2002.
Reading G: Secretans syndrome: hard edema of the dorsum of the hand, Plast
Reconstr Surg 65:182187, 1980.
Whitney TM, Jones NF: Magnetic resonance imaging findings in Secretans disease, J Hand Surg 20:464466, 1995.
Winkelmann RK, Barker SM: Factitial traumatic panniculitis, J Am Acad Dermatol
13:988994, 1985.
Chapter 49
FOREIGN BODY SYNOVITIS
Testing
Magnetic resonance imaging (MRI) of the affected joint often
reveals the offending foreign body. Vegetable matter such as plant
thorns, wood, and glass are not radiopaque and do not show up
on plain radiographs; failure to obtain MRI results in a missed
diagnosis (Figures 49-2 and 49-3). Sea urchin spines have a high
calcium content and may appear on plain radiographs. 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.
Electromyography is indicated if coexistent ulnar or carpal tunnel syndrome is suspected. Joint aspiration and synovial biopsy
may be required to make the diagnosis of foreign body synovitis.
Arthroscopy or arthrotomy may be the mechanism by which the
diagnosis is finally made.
Differential Diagnosis
The recognition of the possibility of antecedent trauma with the
introduction of a foreign body makes the diagnosis apparent. Foreign body synovitis must be distinguished from other causes of
monarthritis and synovitis. Table 49-1 lists common causes of
monarthritis. The ultimate differential diagnosis usually requires a
careful targeted history and physical examination combined with
appropriate laboratory and radiographic testing.
Treatment
Initial treatment of the pain and functional disability associated
with foreign body synovitis should include a combination of
nonsteroidal 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 into
the affected area with a local anesthetic and steroid 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. Vigorous
exercises should be avoided because they would exacerbate the
patients symptoms. Surgical removal of the offending foreign
body often is the only intervention that successfully treats foreign
body synovitis.
Middle phalanx
Joint cavity
Thorn
Inflamed synovial
membrane
Proximal phalanx
Figure 49-1 Foreign body synovitis manifests as a monarthritis without apparent cause.
Clinical Pearls
The diagnosis of foreign body synovitis is easy if the clinician thinks of it. By including foreign body synovitis in
the differential diagnosis of patients with monarthritis or
tenosynovitis, the diagnosis is more easily recognized. The
early use of MRI of the affected area also helps increase the
diagnostic accuracy of the clinician.
Sarcoidosis
Amyloidosis
SUGGESTED READINGS
Osteoarthritis
Bode KS, Haggerty CJ, Krause J: Latent foreign body synovitis, J Foot Ankle Surg
46:291296, 2007.
Kandel L, Friedman A, Chaimski G, etal: Foreign-body synovitis mimicking septic arthritis of the knee, Arthroscopy 17:993996, 2001.
Olenginski TP, Bush DC, Harrington TM: Plant thorn synovitis: an uncommon
cause of monoarthritis, Semin Arthritis Rheum 21:4046, 1991.
Yewlett A, Oakley J, Makwana N, Patel HJ: Retained blackthorn causing peroneal
tendonitis: a case report, Foot Ankle Surg 15:205206, 2009.
Osteonecrosis
Villonodular synovitis
Neoplasm
Foreign body synovitis
Chapter 50
GLOMUS TUMOR OF THE HAND
Testing
Magnetic resonance imaging (MRI) of the affected digit often
reveals the actual glomus tumor and may reveal erosion or a
144
Differential Diagnosis
The triad of localized excruciating distal digit pain, tenderness to
palpation, and cold intolerance makes the diagnosis apparent to
an astute clinician. Glomus tumor of the hand must be distinguished from other causes of localized hand pain, including subungual melanoma and osteoid osteoma. If a history of trauma is
present, fracture, osteomyelitis, tenosynovitis, and foreign body
synovitis should be considered. If there is no history of trauma,
gout, other crystal monarthropathies, tumors, and diseases of the
nail and nail bed should be considered. Reflex sympathetic dystrophy should be distinguishable from glomus tumor of the hand
because the pain of reflex sympathetic dystrophy is less localized
and is associated with trophic skin and nail changes and vasomotor and sudomotor abnormalities. Raynauds syndrome usually
involves the entire hand, and the ice water test mentioned typically triggers pain if the unaffected finger is tested.
Figure 50-1 The classic bluish discoloration of the nail plate is seen on
the right proximal corner of the nail. (From McDermott EM, Weiss A-P C:
Glomus tumors, J Hand Surg Am 31:13971400, 2006.)
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 positive 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.
B
Figure 50-2 Glomus tumor: MRI abnormalities. A, On a sagittal
T1-weighted (TR/TE, 350/25) spin echo magnetic resonance image, a
glomus tumor (arrows) led to subtle erosion of the dorsal surface of
the distal phalanx. Its signal intensity is identical to that of the nail bed
(arrowhead). B, After intravenous gadolinium administration, a sagittal fat-suppressed T1-weighted (TR/TE, 500/25) spin echo image shows
the glomus tumor (arrows) and nail bed (arrowhead) as regions of high
signal intensity. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3999.)
SUGGESTED READINGS
Abou Jaoude JF, Roula Farah A, Sargi Z, Khairallah S, Fakih C: Glomus tumors:
report on eleven cases and a review of the literature, Chirurg Main 19:243252,
2000.
Constantinesco A, Arbogast S, Foucher G, etal: Detection of glomus tumor of the
finger by dedicated MRI at 0.1 T, Magn Reson Imaging 12:11311134, 1994.
Gandon F, Legaillard Ph, Brueton R, Le Viet D, Foucher G: Forty-eight glomus
tumours of the hand: retrospective study and four-year follow-up, Ann Chir
Main Memb Super 11:401405, 1992.
Gombos Z, Fogt F, Zhang PJ: Intraosseous glomus tumor of the great toe: a case
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
Testing
Plain radiographs are indicated in all patients with boxers knuckle
to rule out fractures and identify subchondral cysts, which are
often associated with osteochondral fracture (Figure 51-3). Based
on the patients clinical presentation, additional testing may be
warranted to rule out inflammatory arthritis, including a complete blood count, erythrocyte sedimentation rate, uric acid level,
and antinuclear antibody testing. Magnetic resonance imaging
(MRI) of the fingers and wrist is indicated if joint instability,
occult mass, occult fracture, infection, or tumor is suspected.
Radionuclide bone scanning may be useful to identify stress
fractures.
Differential Diagnosis
The tentative diagnosis of boxers knuckle is made on clinical
grounds and confirmed by radiographic testing. Arthritis, tenosynovitis, or gout of the affected digits may accompany boxers
knuckle and exacerbate the patients pain. Occult fractures
occasionally confuse the clinical presentation.
Treatment
146
Central
extensor tendon
Metacarpal
Torn capsule
Boxers knuckle
Injured joint
cartilage
Torn sagittal
band
Clinical Pearls
Posner MA, Ambrose L: Boxers knuckle: dorsal capsular rupture of the metacarpophalangeal joint of a finger, J Hand Surg Am 14:229236, 1989.
Waldman SD: Painful conditions of the wrist and hand. Physical diagnosis of pain:
an atlas of signs and symptoms, ed 2, Philadelphia, 2010, Saunders, pp 153154.
Chapter 52
TRIANGULAR FIBROCARTILAGE TEAR
SYNDROME
Triangular fibrocartilage
complex
149
TABLE 52-2
Differential Diagnosis
Coexistent arthritis, gout of the radioulnar joint, carpometacarpal
and interphalangeal joints, and tendinitis also may coexist with triangular fibrocartilage tear syndrome and exacerbate the patients
pain and disability. Ulnocarpal abutment syndrome, Kienbcks
disease, and extensor carpi ulnaris tendinitis also may mimic the
pain of triangular fibrocartilage tear syndrome.
Treatment
were a piano key. If the ulnar styloid readily depresses, the test is
considered positive (Figure 52-3).
Testing
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 ulnaris 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.)
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.)
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.)
Clinical Pearls
Triangular fibrocartilage tear syndrome is a straightforward
diagnosis in the presence of obvious antecedent trauma. The
diagnosis is less obvious in the absence of trauma, however,
unless the clinician includes it in the differential diagnosis with all patients with ulnar-sided wrist pain. 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. The
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.
SUGGESTED READINGS
Buterbaugh GA, Brown TR, Horn PC: Ulnar-sided wrist pain in athletes, Clin
Sports Med 17:567583, 1998.
Coggins CA: Imaging of ulnar-sided wrist pain, Clin Sports Med 25:505526,
2006.
Kovachevich R, Elhassan BT: Arthroscopic and open repair of the TFCC,
Hand Clin 26:485494, 2010.
Sachar K: Ulnar-sided wrist pain: evaluation and treatment of triangular fibrocartilage complex tears, ulnocarpal impaction syndrome, and lunotriquetral
ligament tears, J Hand Surg Br 33:16691679, 2008.
Chapter 53
SCAPHOLUNATE LIGAMENT TEAR
SYNDROME
Testing
Plain radiographs are indicated in all patients who present with
scapholunate ligament tear syndrome to rule out underlying
occult bony pathological conditions and identify widening of
the scapholunate gap (also known as a positive Terry Thomas or
David Lettermans sign after the space between the teeth of these
Differential Diagnosis
Coexistent arthritis and gout of the radioulnar, carpal, metacarpal,
and interphalangeal joints; dorsal wrist ganglion; de Quervains
stenosing tenosynovitis; and tendinitis may coexist with scapholunate ligament tear syndrome and exacerbate the patients pain and
disability. Kienbcks disease, avascular necrosis of the scaphoid,
and scaphoid fractures also may mimic the pain of scapholunate
ligament tear.
Treatment
Initial treatment of the pain and functional disability associated
with scapholunate ligament tear syndrome should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and short-term immobilization 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 scapholunate joint may be a reasonable next step. Vigorous
exercises should be avoided because they would exacerbate the
patients symptoms. Ultimately, surgical repair is the treatment
of choice.
Scapholunate
ligament
complex
Figure 53-2 Common injuries that lead to scapholunate ligament tear include falls onto a hyperextended wrist.
Figure 53-3 Watsons test (scaphoid displacement test) for the diagnosis of scapholunate dissociation is performed by pushing upward on
the scaphoid tuberosity while the hand is in ulnar deviation. This action
tends to cause the scaphoid to ride out of the radial fossa over the dorsal rim, at times producing a painful snap. The test might be positive
in loose-jointed individuals and should always be compared with the
contralateral side. (From Manuel J, Moran SL: The diagnosis and treatment
of scapholunate instability, Hand Clin 26:129144, 2010.)
Figure 53-5 Intercarpal ligaments: three-dimensional Fourier transform gradient recalled magnetic resonance imaging. Normal and abnormal scapholunate 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 scapholunate interosseous ligament. (From Resnick D, editor: Diagnosis of bone and Joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3039.)
Clinical Pearls
Scapholunate ligament tear and other disorders of the
scaphoid are a straightforward diagnosis in the presence
of obvious antecedent trauma. The diagnosis is less obvious in the absence of trauma, however, unless the clinician
includes it in the differential diagnosis with all patients
reporting radial-sided wrist pain. 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. The 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.
SUGGESTED READINGS
Goldberg SH, Riansuwan K, Rosenwasser MP: Arthroscopic treatment of
scapholunate ligament tears, In Slutsky DJ, Osterman AL (eds) Fractures and
Injuries of the Distal Radius and Carpus 463474, 2009.
Manuel J, Moran SL: The diagnosis and treatment of scapholunate instability,
Orthop Clin North Am 38:261277, 2007.
Manuel J, Moran SL: The diagnosis and treatment of scapholunate instability,
Hand Clin 26:129144, 2010.
OMeeghan CJ, Stuart W, Mamo V, Stanley JK, Trail IA: The natural history of
an untreated isolated scapholunate interosseus ligament injury, J Hand Surg Br
28:307310, 2003.
Chapter 54
LUNOTRIQUETRAL INSTABILITY
PAIN SYNDROME
Differential Diagnosis
Testing
Plain radiographs are indicated in all patients who present with
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
Lunotriquetral
ligament complex
159
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 immobilization 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 exercises should be avoided because they would exacerbate the patients
symptoms. Ultimately, surgical repair is the treatment of choice.
Torn lunotriquetral
ligament
Right
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.)
Clinical Pearls
Lunotriquetral instability pain syndrome and other disorders of the lunate and triquetrum are a straightforward
diagnosis in the present of obvious antecedent trauma. The
diagnosis is less obvious in the absence of trauma, however,
unless the clinician included it in the differential diagnosis with all patients with ulnar-sided wrist pain. 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. The
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.
SUGGESTED READINGS
Butterfield WL, Joshi AB, Lichtman D: Lunotriquetral injuries, J Am Soc Surg
Hand 2:195203, 2002.
Goldberg SH, Strauch RE, Rosenwasser MP: Scapholunate and lunotriquetral
instability in the athlete: diagnosis and management, Oper Tech Sports Med
14:108121, 2006.
Lunotriquetral instability pain syndrome. In Waldman SD, Campbell RSD,
editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 307308.
Sachar K: Ulnar-sided wrist pain: evaluation and treatment of triangular fibrocartilage complex tears, ulnocarpal impaction syndrome, and lunotriquetral
ligament tears, J Hand Surg Am 33:16691679, 2008.
Chapter 55
KIENBCKS DISEASE
Differential Diagnosis
Coexistent arthritis and gout of the radioulnar, carpometacarpal,
and interphalangeal joints; dorsal wrist ganglion; and tendinitis
may coexist with Kienbcks disease and exacerbate the pain and
disability of the patient. Lunate cysts, contusions, and fractures
also may mimic the pain of Kienbcks disease, as can tear of the
triangular fibrocartilage complex and ulnar impaction syndrome
(Figure 55-3).
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
other causes of joint instability, infection, or tumor are suspected
(Figure 55-2). Electromyography is indicated if coexistent ulnar
or carpal tunnel syndrome is suspected. A very gentle injection of
162
Figure 55-1 Repetitive microtrauma to the wrist from repetitive compressive loading and unloading and recurrent compression of the lunate by the
capitate and distal radius owing to extreme wrist positions have been implicated in the evolution of this painful condition of the wrist and forearm.
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.)
Treatment
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.)
Clinical Pearls
Kienbcks disease and other disorders of the lunate are a
relatively straightforward diagnosis in the present of obvious antecedent trauma. The diagnosis is less obvious in the
absence of trauma, however, unless the clinician included it
in the differential diagnosis with all patients with dorsoulnar wrist pain that radiated into the forearm. 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. The
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.
SUGGESTED READINGS
Beredjiklian PK: Kienbcks disease, J Hand Surg Am 34:167175, 2009.
Innes L, Strauch RJ: Systematic review of the treatment of Kienbcks disease in its
early and late stages, J Hand Surg Am 35:713717, 2010.
Taniguchi Y, Yoshida M, Iwasaki H, Otakara H, Iwata S: Kienbcks disease in
elderly patients, J Hand Surg Am 28:779783, 2003.
Wagner JP, Chung KC: A historical report on Robert Kienbck (18711953) and
Kienbcks disease, J Hand Surg Am 30:11171121, 2005.
Yazaki N, Nakamura R, Nakao E, etal: Bilateral Kienbcks disease, J Hand Surg
Br 30:133136, 2005.
Chapter 56
AVASCULAR NECROSIS OF THE
SCAPHOID
Differential Diagnosis
Coexistent arthritis and gout of the radioulnar, carpometacarpal,
and interphalangeal joints; dorsal wrist ganglion; and tendinitis
may coexist with avascular necrosis of the scaphoid and exacerbate the patients pain and disability. Distal fractures of the radius,
Testing
Plain radiographs are indicated in all patients who present with
avascular necrosis of the scaphoid to rule out underlying occult
bony pathological conditions and identify sclerosis and fragmentation of the scaphoid, although early in the course of the disease,
plain radiographs can be notoriously unreliable (Figure 56-3).
Based on the patients clinical presentation, additional tests,
including complete blood cell count, uric acid level, erythrocyte
Fractured
scaphoid
165
Treatment
Initial treatment of the pain and functional disability associated
with avascular necrosis of the scaphoid should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and short-term immobilization 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.
Failure to treat significant avascular necrosis of the scaphoid surgically usually results in continued pain and disability and in some
patients leads to ongoing damage to the wrist. Injection of the joint
with local anesthetic and steroid is a safe technique if the clinician
is attentive to detail, specifically using small amounts of local anesthetic and steroid and avoiding high injection pressures, which may
damage the joint further. Another complication of this injection
technique 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 this injection technique, and patients should be warned of this possibility.
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 computed tomography scan, however, confirms fracture nonunion. (From In Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011,
Saunders, pp 313-315.
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 enhancement 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 fractures 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.)
Clinical Pearls
Avascular necrosis of the scaphoid is a diagnosis that is
often missed, leading to much unnecessary pain and disability. The clinician should include avascular necrosis of
the scaphoid in the differential diagnosis in all patients with
radial-sided wrist pain after trauma to the wrist. 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. The
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.
SUGGESTED READINGS
Adey L, Souer JS, Lozano-Calderon S: Computed tomography of suspected
scaphoid fractures, J Hand Surg Am 32:6166, 2007.
Kawamura K, Chung KC: Treatment of scaphoid fractures and nonunions,
J Hand Surg Am 33:988997, 2008.
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.
Chapter 57
EXTENSOR CARPI ULNARIS
TENDINITIS
Differential Diagnosis
Extensor carpi ulnaris tendinitis is generally easily identified on clinical grounds; however, coexistent bursitis may confuse the diagnosis.
Fractures of the ulnar styloid and lunate and tears of the triangular
fibrocartilage complex, ulnocarpal abutment syndrome, and Kienbcks disease also may mimic extensor carpi ulnaris tendinitis.
Treatment
Initial treatment of the pain and functional disability associated
with extensor carpi ulnaris tendinitis should include a combination
Inflamed extensor
carpi ulnaris tendon
Testing
Plain radiographs and magnetic resonance imaging (MRI) are indicated for all patients who present with ulnar-sided wrist pain. Based
Figure 57-1 Improper grip of golf clubs and tennis racquets is often
implicated as the inciting cause of acute extensor carpi ulnaris tendinitis.
169
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 tendon in the sixth extensor compartment. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 3048.)
*
Triquetrum
Ulna
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 Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 329330.)
of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local application of
heat and cold also may be beneficial. Repetitive activities responsible
for the evolution of the tendinitis should be avoided. For patients
who do not respond to these treatment modalities, injection with
local anesthetic and steroid may be a reasonable next step.
Clinical Pearls
The extensor carpi ulnaris is a very strong tendon, but it
is also very susceptible to rupture. Coexistent bursitis and
arthritis also may contribute to wrist pain and may require
additional treatment with a more localized injection of local
anesthetic and methylprednisolone acetate.
Injection of the extensor carpi ulnaris tendon 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 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.
Waldman SD: Extensor carpi ulnaris tendinitis. In Waldman SD, Campbell RSD,
editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 329330.
Watanabe A, Souza F, Vezeridis PS, Blazar P, Yoshioka H: Ulnar-sided wrist pain.
II. Clinical imaging and treatment, Skeletal Radiol 39:837857, 2010.
Chapter 58
FLEXOR CARPI RADIALIS TENDINITIS
Differential Diagnosis
Flexor carpi radialis tendinitis is generally easily identified on
clinical grounds; however, coexistent bursitis may confuse the
diagnosis. Fractures of the distal radius and scaphoid and tears of
the triangular fibrocartilage complex and avascular necrosis of the
scaphoid also may mimic flexor carpi radialis tendinitis.
Testing
Plain radiographs and magnetic resonance imaging (MRI) are
indicated for all patients who present with ulnar-sided wrist
172
Inflamed
flexor carpi
radialis tendon
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
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 diastasis 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.)
Treatment
Initial treatment of the pain and functional disability associated
with flexor carpi radialis tendinitis should include a combination
of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local application of heat and cold also may be beneficial. Repetitive activities
responsible for the evolution of the tendinitis should be avoided.
For patients who do not respond to these treatment modalities,
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 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 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.
SUGGESTED READINGS
Bishop AT, Gabel G, Carmichael SW: Flexor carpi radialis tendinitis. I. Operative
anatomy, J Bone Joint Surg Am 76:10091014, 1994.
Cowey AJ, Carmont MR, Tins B, Ford DJ: Flexor carpi radialis rupture reined in!,
Injury Extra 38:9093, 2007.
Fitton JM, Shea FW, Goldie W: Lesions of flexor carpi radialis tendon and sheath
causing pain at the wrist, J Bone Joint Surg Br 50:359363, 1968.
Gabel G, Bishop AT, Wood MB: Flexor carpi radialis tendinitis. II. Results of
operative treatment, J Bone Joint Surg Am 76:10151018, 1994.
Kosiyatrakul A, Luenam S, Prachaporn S: Symptomatic flexor carpi radialis brevis:
case report, J Hand Surg 35:633635, 2010.
Chapter 59
TRIGGER WRIST
Testing
Plain radiographs are indicated in all patients who present with
trigger wrist to rule out occult bony pathological processes. Based
on the patients clinical presentation, additional testing, including
a complete blood count, uric acid level, erythrocyte sedimentation
rate, and antinuclear antibody testing, may be indicated. Magnetic
resonance imaging (MRI) of the hand is indicated if joint instability, mass, tumor, or some other abnormality is suspected. The
injection technique described later serves as both a diagnostic and
therapeutic maneuver. Occasionally, surgical exploration is required
to accurately ascertain the cause of trigger wrist (Figure 59-3).
Differential Diagnosis
The diagnosis of trigger wrist is usually made on clinical grounds.
Arthritis or gout of the carpal or radioulnar joint may accompany
trigger wrist and exacerbate the patients pain. Occult fractures
occasionally confuse the clinical presentation. Trigger finger and
carpal tunnel syndrome frequently coexist with the much less
commonly occurring trigger wrist.
Treatment
Initial treatment of the pain and functional disability associated
with trigger wrist includes a combination of nonsteroidal antiinflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2)
175
B
Figure 59-2 The catching tendon sign for trigger wrist. A, The patient is
asked to actively flex the affected wrist for 30 seconds. B, The examiner
passively extends the affected wrist while palpating the flexor tendons.
Clinical Pearls
Figure 59-3 Giant cell tumour of the flexor sheath compressing the
median nerve. (From Chalmers RL, Mandalia M, Contreras R, Schreuder F:
Acute trigger wrist and carpal tunnel syndrome due to giant-cell tumour of
the flexor sheath, J Plast Reconstr Aesthet Surg 61:1557, 2008.)
Chapter 60
DEVILS GRIP
ICD-9 CODE 074.1
ICD-10 CODE R07.81
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
178
Figure 60-1 Deep inspiration markedly increases the pain of devils grip.
*
*
A
D
*
B
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 pneumonia (*) 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.)
Differential Diagnosis
As is the case with costochondritis, costosternal joint pain, Tietzes syndrome, and rib fractures, many patients with devils
grip first seek medical attention because they believe they are
having a heart attack. If the area innervated by the subcostal
nerve is involved, patients may believe they have gallbladder
disease. Statistically, children with devils grip have abdominal
pain more often than do adults, and such pain may be attributed to appendicitis, leading to unnecessary surgery. In contradistinction to most other causes of pain involving the chest
wall, which are musculoskeletal or neuropathic, the pain of
devils grip is infectious. The constitutional symptoms associated with devils grip may lead the clinician to consider pneumonia, empyema, and occasionally pulmonary embolus as the
most likely diagnosis.
As mentioned earlier, the pain of devils grip is often mistaken for pain of cardiac or gallbladder origin and can lead to
visits to the emergency department and unnecessary cardiac
and gastrointestinal workups. If trauma has occurred, devils
grip may coexist with fractured ribs or fractures of the sternum
itself, which can be missed on plain radiographs and may require
radionucleotide bone scanning for proper identification. Tietzes
syndrome, which is painful enlargement of the upper costochondral cartilage associated with viral infection, can be confused
with devils grip.
Neuropathic pain involving the chest wall also may be confused
or coexist with costosternal syndrome. Examples of such neuropathic pain include diabetic polyneuropathies and acute herpes
zoster involving the thoracic nerves. The possibility of diseases of
the structures of the mediastinum is ever present, and such disease
sometimes can be difficult to diagnose. Pathological processes that
Intercostal a.
Intercostal n.
Intercostal v.
Rib
Figure 60-3 Injection technique to relieve the pain of devils grip. a, Artery; n, nerve; v, vertebra.
Treatment
Initial treatment of devils grip should include a combination
of simple analgesics and nonsteroidal anti-inflammatory drugs
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. If these medications do not control the patients symptoms adequately, opioid
analgesics may be added during the period of acute pain. Local
application of heat and cold also may be beneficial to provide
symptomatic relief of the pain of devils grip. The use of an elastic
rib belt may help provide symptomatic relief in some patients.
For patients who do not respond to the aforementioned treatment modalities, the following injection technique using a local
anesthetic and steroid may be a reasonable next step. The patient
is placed in the prone position with the patients arms hanging
loosely off the side of the cart. Alternatively, this block can be
done with the patient in the sitting or lateral position. The rib
are done in a similar manner, substituting 40 mg of methylprednisolone for the initial 80-mg dose. Because of the overlapping
innervation of the chest and upper abdominal wall, the intercostal nerves above and below the nerve suspected of subserving the
painful condition need to be blocked.
Clinical Pearls
Devils grip is an uncommon cause of chest pain that is
frequently misdiagnosed. Correct diagnosis is necessary to
treat this painful condition properly and to avoid overlooking serious intrathoracic or intra-abdominal pathology.
Intercostal nerve block is a simple technique that can produce dramatic relief for patients with devils grip. As mentioned, the proximity of the intercostal nerve to the pleural
space makes careful attention to technique mandatory.
SUGGESTED READINGS
Connolly JH, ONeill HJ: Bornholm disease associated with coxsackie A9 virus
infection, Lancet 298:1035, 1971.
Cotterill JA: The devils grip, Lancet 301:13081309, 1973.
Ikeda RM, Kondracki SF, Drabkin PD, Birkhead GS, Morse DL: Pleurodynia
among football players at a high school: an outbreak associated with coxsackievirus B1, JAMA 270:22052206, 1993.
Stalkup JR, Chilukuri S: Enterovirus infections: a review of clinical presentation,
diagnosis, and treatment, Dermatol Clin 20:217223, 2002.
Chapter 61
STERNOCLAVICULAR SYNDROME
Testing
Plain radiographs are indicated in all patients who have pain
thought to emanate from the sternoclavicular joint to rule out
occult bony pathological processes, including tumor. Based on
Sternoclavicular
joint
Figure 61-1 Acute protraction or retraction of the shoulder reproduces the pain of sternoclavicular syndrome.
182
B
Figure 61-2 A, Anterior view shows anterior dislocation of the right
sternoclavicular joint. B, Superior view shows posterior dislocation of
the acromioclavicular joint. (From Schemitsch LA, Schemitsch EH, McKee
MD: Bipolar clavicle injury: posterior dislocation of the acromioclavicular
joint with anterior dislocation of the sternoclavicular jointa report of two
cases, J Shoulder Elbow Surg 20:e18e22, 2011.)
the patients clinical presentation, additional tests, including complete blood cell count, prostate-specific antigen level, erythrocyte
sedimentation rate, and antinuclear antibody testing, may be
indicated. Computed tomography (CT) or magnetic resonance
imaging (MRI) of the joint is indicated if joint instability, tumor,
or infection is suspected (Figure 61-3). Injection of the sternoclavicular joint with a local anesthetic, steroid, or both serves as a
diagnostic and therapeutic maneuver.
Differential Diagnosis
As mentioned earlier, the pain of sternoclavicular syndrome is
often mistaken for pain of cardiac origin and can lead to visits
to the emergency department and unnecessary cardiac workups.
If trauma has occurred, sternoclavicular syndrome may coexist
with fractured ribs or fractures of the sternum itself, which can
be missed on plain radiographs and may require radionucleotide bone scanning for proper identification. Tietzes syndrome,
which is painful enlargement of the upper costochondral cartilage
B
Figure 61-3 Three-dimensional computed tomography images show
bipolar dislocation of the clavicle. (From Schemitsch LA, Schemitsch EH,
McKee MD: Bipolar clavicle injury: posterior dislocation of the acromioclavicular joint with anterior dislocation of the sternoclavicular jointa report
of two cases, J Shoulder Elbow Surg 20:e18e22, 2011.)
Treatment
Initial treatment of the pain and functional disability associated with
sternoclavicular syndrome should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
(COX-2) inhibitors. Local application of heat and cold also may
be beneficial. The use of an elastic clavicle splint may help provide symptomatic relief and help protect the sternoclavicular joints
from additional trauma. For patients who do not respond to these
treatment modalities, injection of the sternoclavicular joint using a
local anesthetic and steroid may be a reasonable next step.
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 remembered that this musculoskeletal pain syndrome and coronary artery disease can coexist. Tietzes syndrome, which
is painful enlargement of the upper costochondral cartilage
associated with viral infections, can be confused with sternoclavicular 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 several days after the patient undergoes 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 technique. Laboratory evaluation for collagen-vascular disease
is indicated in patients with sternoclavicular joint pain in
whom other joints are involved.
SUGGESTED READINGS
Bicos J, Nicholson GP: Treatment and results of sternoclavicular joint injuries,
Clin Sports Med 22:359370, 2003.
Crisostomo RA, Laskowski ER, Bond JR, Agerter DC: Septic sternoclavicular
joint: a case report, Arch Physical Med Rehabil 89:884886, 2008.
Puri V, Meyers BF, Kreisel D, etal: Sternoclavicular joint infection: a comparison
of two surgical approaches, Ann Thorac Surg 91:257261, 2011.
Schemitsch LA, Schemitsch EH, McKee MD: Bipolar clavicle injury: posterior
dislocation of the acromioclavicular joint with anterior dislocation of the sternoclavicular jointa report of two cases, J Shoulder Elbow Surg 20:e18e22, 2011.
Chapter 62
POSTMASTECTOMY PAIN
Testing
Plain radiographs are indicated in all patients who present with
pain thought to be due to postmastectomy syndrome to rule out
occult bony pathology, including tumor. Electromyography helps
rule out damage to the intercostobrachial nerve or plexopathy
that may be contributing to the patients pain. Radionucleotide
185
Breast
ICBN
LTV
AV
Fibrofatty
tissue
bone scanning may be useful to rule out occult pathological fractures of the ribs, sternum, or both. Based on the patients clinical presentation, additional tests, including complete blood cell
count, prostate-specific antigen level, erythrocyte sedimentation
rate, and antinuclear antibody testing, may be indicated. Computed tomography (CT) scan of the thoracic contents is indicated
if occult mass is suspected. Magnetic resonance imaging (MRI)
of the brachial plexus also should be considered if plexopathy
secondary to tumor involvement is a consideration.
Differential Diagnosis
As mentioned earlier, the pain of postmastectomy syndrome is
often mistaken for postoperative pain. If the breast surgery was
performed for malignancy, a careful search for metastatic disease
or tumor invasion of the chest wall is mandatory. Postmastectomy
syndrome 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 also may be confused
or coexist with postmastectomy syndrome. Examples of such neuropathic pain include diabetic polyneuropathies and acute herpes
zoster involving the thoracic nerves. The possibility of diseases of
the structures of the mediastinum is ever present, and these diseases
sometimes can be difficult to diagnose. Pathological processes that
inflame the pleura, such as pulmonary embolus, infection, and
Bornholms disease, also may mimic the pain of postmastectomy
syndrome.
Treatment
Initial treatment of postmastectomy syndrome should include a combination of simple analgesics and nonsteroidal anti-inflammatory
Clinical Pearls
Postmastectomy syndrome is a cause of chest wall and thoracic pain that should not be overlooked in patients after
breast surgery. Correct diagnosis is necessary to treat this
painful condition properly and to avoid overlooking serious intrathoracic or intra-abdominal pathological processes.
The use of the pharmacological agents mentioned, including gabapentin, allows the clinician to control the pain of
postmastectomy syndrome adequately. Intercostal nerve
block is a simple technique that can produce dramatic relief
for patients with postmastectomy syndrome. As mentioned,
the proximity of the intercostal nerve to the pleural space
makes careful attention to technique mandatory.
SUGGESTED READINGS
Bjrkman B, Arnr S, Hydn L-C: Phantom breast and other syndromes after
mastectomy: eight breast cancer patients describe their experiences over time a
2-year follow-up study, J Pain 9:10181025, 2008.
Chang SH, Mehta V, Langford RM: Acute and chronic pain following breast
surgery, Acute Pain 11:114, 2009.
Katz J, Poleshuck EL, Andrus CH, etal: Risk factors for acute pain and its persistence following breast cancer surgery, Pain 119:1625, 2005.
Watson CP, Evans RJ, Watt VR: The post-mastectomy pain syndrome and the
effect of topical capsaicin, Pain 38:177186, 1989.
Chapter 63
STERNALIS SYNDROME
Differential Diagnosis
As mentioned earlier, the pain of sternalis syndrome is often
mistaken for pain of cardiac origin and can lead to visits to the
emergency department and unnecessary cardiac workups. If
Myofascial
trigger points
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 presentation, additional tests, including complete blood cell count,
prostate-specific antigen level, erythrocyte sedimentation rate,
188
trauma has occurred, sternalis syndrome may coexist with fractured ribs or fractures of the sternum itself, which can be missed
on plain radiographs and may require radionucleotide bone scanning for proper identification. Tietzes syndrome, which is painful
enlargement of the upper costochondral cartilage associated with
viral infections, can be confused with sternalis syndrome, as can
costosternal syndrome.
Neuropathic pain involving the chest wall also may be confused or coexist with costosternal syndrome. Examples of such
neuropathic pain include diabetic polyneuropathies and acute
herpes zoster involving the thoracic nerves. The possibility of
diseases of the structures of the mediastinum is ever present, and
these diseases sometimes can be difficult to diagnose. Pathological
processes that inflame the pleura, such as pulmonary embolus,
infection, and tumor, also should be considered.
Treatment
Initial treatment of sternalis syndrome should include a combination of simple analgesics and nonsteroidal anti-inflammatory
drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. Local
application of heat and cold also may be beneficial to provide
symptomatic relief of the pain of sternalis syndrome. The use of
an elastic rib belt may help provide symptomatic relief in some
patients. For patients who do not respond to these treatment
modalities, injection of the trigger areas located in the sternalis
muscle using a local anesthetic and steroid may be a reasonable
next step.
Clinical Pearls
Patients with sternalis syndrome often present to the emergency department fearing they are having a heart attack. The
syndrome also is misdiagnosed frequently as cervical radiculopathy secondary to the referred arm pain. Electromyography
helps delineate the cause and extent of neural compromise.
The injection technique is extremely effective in the treatment of sternalis syndrome. Coexistent costosternal or manubriosternal arthritis also may contribute to anterior chest wall
pain and may require additional treatment with a more localized injection of a local anesthetic 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. Pneumothorax can be avoided if shorter needles are used, and the
needle is not advanced too deeply. 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 this injection technique for shoulder pain. Vigorous exercises should be avoided because they
would exacerbate symptoms. Simple analgesics and NSAIDs
may be used concurrently with this injection technique.
SUGGESTED READINGS
Alpert JB, Naidich DP: Imaging of incidental findings on thoracic computed
tomography, Radiol Clin North Am 49:267289, 2011.
Baldry P: The chest wall. In Baldry P, editor: Myofascial pain fibromyalgia
syndromes, London, 2001, Churchill Livingstone, pp 303327.
Bennett R: Myofascial pain syndromes and their evaluation, Best Pract Res Clin
Rheumatol 21:427445, 2007.
Baldry PE, Thompson JW, editors: Acupuncture, trigger points and musculoskeletal
pain, ed 3, London, 2005, Churchill Livingstone, pp 165185.
Chapter 64
MANUBRIOSTERNAL JOINT PAIN
Testing
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 resonance 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
190
As mentioned earlier, manubriosternal joint pain is often mistaken 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 polyneuropathies and acute herpes zoster involving the thoracic nerves. The
possibility of diseases of the structures of the mediastinum is ever
present, and these diseases sometimes can be difficult to diagnose.
Pathological processes that inflame the pleura, such as pulmonary
embolus, infection, and Bornholms disease, also may mimic the
pain emanating from the manubriosternal joint.
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
combination of simple analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. If these medications do not control the patients symptoms
adequately, or if considerable sleep disturbance exists, a tricyclic
antidepressant should be added.
Traditionally, tricyclic antidepressants have been a mainstay
in the palliation of sleep disturbance associated with painful
conditions. Controlled studies have shown the efficacy of amitriptyline for this indication. Other tricyclic antidepressants,
including nortriptyline and desipramine, also have been shown
to be clinically useful. This class of drugs is associated with
considerable anticholinergic side effects, including dry mouth,
constipation, sedation, and urinary retention. These drugs
should be used with caution in patients with glaucoma, cardiac arrhythmia, and prostatism. To minimize side effects and
Clinical Pearls
Patients with pain emanating from the manubriosternal
joint often attribute their pain symptoms to a heart attack.
Reassurance is required, although it should be remembered
that this musculoskeletal pain syndrome and coronary
artery disease can coexist. 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 rangeof-motion exercises, should be introduced several days after
the patient undergoes this injection technique for manubriosternal joint pain. Vigorous exercise should be avoided
because it exacerbates the symptoms. Simple analgesics and
NSAIDs may be used concurrently with this injection technique. Laboratory evaluation for collagen-vascular disease is
indicated for patients who have manubriosternal joint pain
with other joints involved.
SUGGESTED READINGS
Al-Dahiri A, Pallister I: Arthrodesis for osteoarthritis of the manubriosternal joint,
Eur J Cardiothorac Surg 29:119121, 2006.
Ellis H: The superior mediastinum, Anaesth Intens Care Med 10:360361, 2009.
Lyons I, Saha S, Arulampalam T: Manubriosternal joint dislocation: an unusual
risk of trampolining, J Emerg Med 39:596598, 2010.
Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders,
Med Clin North Am 94:259273, 2010.
Waldman SD: Manubriosternal joint syndrome. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 247248.
Chapter 65
XIPHODYNIA
Differential Diagnosis
The Clinical Syndrome
An uncommon cause of anterior chest wall pain, xiphodynia is
often misdiagnosed as pain of cardiac or upper abdominal origin.
Xiphodynia syndrome is a constellation of symptoms consisting
of severe intermittent anterior chest wall pain in the region of
the xiphoid process that worsens with overeating, stooping, and
bending. The patient may report a nauseated feeling associated
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/
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 osteoarthritis, 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.
As with costochondritis, costosternal joint pain, devils grip, Tietzes syndrome, and rib fractures, many patients with xiphodynia
first seek medical attention because they believe they are having a
heart attack. Patients also may believe they have ulcer or gallbladder disease. In contrast to most other causes of pain involving
the chest wall that are musculoskeletal or neuropathic in origin,
the pain of devils grip results from infection. The constitutional
symptoms associated with devils grip may lead the clinician to
Xiphisternal joint
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 sedimentation rate, and antinuclear antibody testing, may be indicated.
Computed tomography (CT) or magnetic resonance imaging
193
The major problem in the care of patients thought to have xiphodynia is the failure to identify potentially serious pathology of the
thorax or upper abdomen. The major complication of injection
of the xiphisternal joint is pneumothorax if the needle is placed
too laterally or deeply and invades the pleural space. Infection,
although rare, can occur if strict aseptic technique is not followed.
Trauma to the contents of the mediastinum is an ever-present
possibility. This complication can be greatly decreased if the
clinician pays close attention to accurate needle placement.
Clinical Pearls
Figure 65-3 The xiphosternal angle was 105 degrees. The curved shape
of the xyphoid process hindered the measurement of the angle. (From
Maigne J-Y, Vareli M, Rousset P, Cornelis P: Xiphodynia and prominence of
the xyphoid process: value of xiphosternal angle measurementthree case
reports, Joint Bone Spine 77:474476, 2010.)
Treatment
Initial treatment of xiphodynia should include a combination
of simple analgesics and nonsteroidal anti-inflammatory drugs
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. If these
SUGGESTED READINGS
Howell J: Xiphodynia: an uncommon cause of exertional chest pain, Am J Emerg
Med 8:176, 1990.
Howell JM: Xiphodynia: a report of three cases, J Emerg Med 10:435438, 1992.
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
cul-de-sac, Am J Emerg Med 16:177178, 1998.
Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders,
Med Clin North Am 94:259273, 2010.
Chapter 66
SERRATUS ANTERIOR MUSCLE
SYNDROME
Testing
Plain radiographs are indicated in all patients with suspected
serratus anterior muscle syndrome to rule out occult bony
pathological processes, including metastatic lesions. Based on
the patients clinical presentation, additional testing may be
Differential Diagnosis
As mentioned, the pain of serratus anterior muscle syndrome is
often mistaken for pain of cardiac origin and can lead to visits
to the emergency department and unnecessary cardiac workups.
If trauma has occurred, serratus anterior muscle syndrome may
coexist with fractured ribs or fractures of the sternum itself, which
can be missed on plain radiographs and may require radionucleotide bone scanning for proper identification. Tietzes syndrome,
which is painful enlargement of the upper costochondral cartilage
associated with viral infections, can be confused with sternalis
syndrome, as can costosternal syndrome.
Neuropathic pain involving the chest wall may be confused or
coexist with costosternal syndrome. Examples of such neuropathic
pain include diabetic polyneuropathies and acute herpes zoster
involving the thoracic nerves. The possibility of diseases of the
structures of the mediastinum remains ever present and at times
can be difficult to diagnose. Pathological processes that inflame
the pleura, such as pulmonary embolus, infection, and tumor, also
should be considered.
Treatment
Initial treatment of serratus anterior muscle syndrome should
include a combination of simple analgesics and the nonsteroidal
anti-inflammatory agents or the cyclooxygenase-2 (COX-2)
inhibitors. The local application of heat and cold may be beneficial to provide symptomatic relief of the pain of serratus anterior
muscle syndrome. The use of an elastic rib belt may help provide
symptomatic relief in some patients. For patients who do not
respond to these treatment modalities, injection of the trigger
areas located in the sternalis muscle using a local anesthetic and
steroid may be a reasonable next step.
195
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.
*
A
Clinical Pearls
Patients with serratus anterior muscle syndrome will often
go the emergency department, fearing they are having a
heart attack. The syndrome is also frequently misdiagnosed
as a cervical radiculopathy because of the referred arm pain.
Electromyography will help delineate the cause and extent
of neural compromise.
This injection technique is extremely effective in the
treatment of serratus anterior muscle syndrome. Coexistent
costosternal or manubriosternal arthritis may contribute to
anterior chest wall pain and may require additional treatment with a more localized injection of an anesthetic 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. Pneumothorax can be avoided if
shorter needles are used and the needle is not advanced
too deeply. Care must be taken to use sterile technique to
avoid infection, and universal precautions must be used 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 rangeof-motion exercises, should be introduced several days after
the patient undergoes this injection technique for shoulder
pain. Vigorous exercises should be avoided because they will
exacerbate the symptoms. Simple analgesics and nonsteroidal anti-inflammatory agents may be used concurrently
with this injection technique.
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Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30,
2009.
Ge H-Y, Nie H, Madeleine P, etal: Contribution of the local and referred pain from
active myofascial trigger points in fibromyalgia syndrome, Pain 147:233240,
2009.
Son MBF, Sundel RP: Musculoskeletal causes of pediatric chest pain, Pediatr Clin
North Am 57:13851395, 2010.
Yurtsever I, Topal U, Yalin R, Adm B, Bayram S: Desmoid tumor of the chest
wall, Eur J Radiol Extra 46:119121, 2003.
Chapter 67
SLIPPING RIB SYNDROME
Differential Diagnosis
As mentioned earlier, the pain of slipping rib syndrome is often
mistaken for pain of cardiac or gallbladder origin and can lead
to visits to the emergency department and unnecessary cardiac
and gastrointestinal workups. If trauma has occurred, slipping rib
syndrome may coexist with rib fractures or fractures of the sternum, which can be missed on plain radiographs and may require
radionucleotide bone scanning for proper identification. Tietzes
syndrome, which is painful enlargement of the upper costochondral cartilage associated with viral infections, can be confused with
8th rib
9th rib
10th rib
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, prostatespecific antigen level, erythrocyte sedimentation rate, and antinuclear antibody testing, may be indicated. Magnetic resonance
198
Figure 67-1 Patients with slipping rib syndrome exhibit pain on hooking of the affected costochondral cartilage.
Treatment
Initial treatment of the pain and functional disability associated
with slipping rib syndrome should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
(COX-2) inhibitors and physical therapy. The local application of
heat and cold may be beneficial. The repetitive movements that
incite the syndrome should be avoided. For patients who do not
respond to these treatment modalities, injection of the affected
costochondral cartilages with a local anesthetic and steroid may be
a reasonable next step.
To inject the slipping ribs, the patient is placed in the supine
position, and proper preparation with antiseptic solution of the skin
overlying the affected costal cartilage and rib is done. A sterile syringe
containing 1 mL of 0.25% preservative-free bupivacaine for each
joint to be injected and 40 mg of methylprednisolone is attached to
a 25-gauge, 1-inch needle using strict aseptic technique.
With strict aseptic technique, the distal rib and costal cartilage
are identified. The lower margin of each affected distal rib is identified and marked with a sterile marker. The needle is carefully
advanced at the point marked through the skin and subcutaneous
tissues until the needle tip impinges on the periosteum of the
underlying rib. The needle is withdrawn back into the subcutaneous tissues and walked inferiorly off the inferior rib margin. The
needle should be advanced just beyond the inferior rib margin,
but no farther, or pneumothorax or damage to the abdominal
viscera could result. After careful aspiration to ensure that the
needle tip is not in an intercostal vein or artery, 1 mL of solution
is gently injected. There should be limited resistance to injection. If significant resistance is encountered, the needle should be
withdrawn slightly until the injection proceeds with only limited
resistance. This procedure is repeated for each affected rib and
associated cartilage. The needle is removed, and a sterile pressure
dressing and ice pack are placed at the injection site.
Clinical Pearls
Patients with pain from slipping rib syndrome often attribute their pain symptoms to a gallbladder attack or ulcer
disease. Reassurance is required, although it should be
remembered that this musculoskeletal pain syndrome and
intra-abdominal pathological conditions can coexist. 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 this
injection technique for slipping rib syndrome. Vigorous
exercises should be avoided because they would exacerbate
the symptoms. Simple analgesics and NSAIDs may be used
concurrently with this injection technique. Laboratory evaluation for collagen-vascular disease is indicated in patients
with costal cartilage pain in whom other joints are involved.
SUGGESTED READINGS
Brunse MH, Stochkendahl MJ, Vach W, etal: Examination of musculoskeletal
chest pain: an inter-observer reliability study, Manual Ther 15:167172, 2010.
Cranfield KAW, Buist RJ, Nandi PR, Baranowski AP: The twelfth rib syndrome,
J Pain Symptom Manage 13:172175, 1997.
Fam AG, Smythe HA: Musculoskeletal chest wall pain, CMAJ 133:379389,
1985.
Stochkendahl MJ, Christensen HW: Chest pain in focal musculoskeletal disorders,
Med Clin North Am 94:259273, 2010.
Verdon F, Herzig L, Burnand B, etal: Chest pain in daily practice: occurrence,
causes and management, Swiss Med Wkly 138:340347, 2008.
Wright JT: Slipping-rib syndrome, Lancet 316:632634, 1980.
Chapter 68
WINGED SCAPULA SYNDROME
Testing
Owing to the ambiguity and confusion surrounding this clinical
syndrome, testing is important to help confirm the diagnosis of
winged scapula syndrome. Electromyography helps distinguish
isolated damage to the long thoracic nerve of Bell associated
with winged scapula syndrome from brachial plexopathy. Plain
radiographs are indicated in all patients who present with winged
scapula syndrome to rule out occult bony pathological processes.
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 brachial plexus,
cervical spine, or both is indicated if the patient exhibits other
neurological deficits.
Differential Diagnosis
Lesions of the cervical spinal cord, brachial plexus, and cervical
nerve roots can produce clinical symptoms that include winging
of the scapula. Such lesions also should produce additional neurological findings that allow the clinician to distinguish these pathological conditions from the isolated neurological findings seen in
winged scapula syndrome. Pathology of the scapula or shoulder
group also may confuse the clinical diagnosis.
Treatment
No specific treatment for winged scapula syndrome exists other than
removal of the cause of nerve entrapment (e.g., heavy backpacks
or tumor compressing a nerve) and use of an orthotic device to
help stabilize the scapula to allow normal shoulder function. Initial
symptomatic relief of the pain and functional disability associated
with winged scapula should include a combination of nonsteroidal
anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2)
inhibitors and physical therapy. Local application of heat and cold
also may be beneficial. Repetitive movements or movements that
incite the syndrome should be avoided.
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
rather a part of a larger neurological problem.
Clinical Pearls
Winged scapula syndrome is a distinct clinical entity that
is difficult to treat. Early removal of the offending cause
of nerve entrapment should allow rapid recovery of nerve
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 neurological finding to winged scapula syndrome.
SUGGESTED READINGS
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
report and review, J Emerg Med 29:279282, 2005.
Nakatsuchi Y, Saitoh S, Hosaka M, Uchiyama S: Long thoracic nerve paralysis
associated with thoracic outlet syndrome, J Shoulder Elbow Surg 3:2833, 1994.
Sherman SC, OConnor M: An unusual cause of shoulder pain: winged scapula,
J Emerg Med 28:329331, 2005.
Chapter 69
ANTERIOR CUTANEOUS NERVE
ENTRAPMENT
Testing
Plain radiographs are indicated in all patients with pain thought
to be emanating from the lower costal cartilage and ribs to rule
out occult bony pathological conditions, including rib fracture
and tumor. Radiographic evaluation of the gallbladder is indicated if cholelithiasis is suspected. Based on the patients clinical presentation, additional tests, including complete blood cell
count, rectal examination with stool guaiac, erythrocyte sedimentation rate, and antinuclear antibody testing, may be indicated. Ultrasonography and computed tomography (CT) scan
of the abdomen are indicated if intra-abdominal pathological
process or occult mass is suspected. Injection of the anterior
cutaneous nerve with or without ultrasound guidance at the
point at which it pierces the fascia serves as a diagnostic and
therapeutic maneuver (Figure 69-4).
Differential Diagnosis
The differential diagnosis of anterior cutaneous nerve entrapment
syndrome should consider ventral hernia, peptic ulcer disease,
cholecystitis, intermittent bowel obstruction, renal calculi,
angina, mesenteric vascular insufficiency, diabetic polyneuropathy, and pneumonia (Table 69-1). Rarely, the collagen-vascular
diseases, including systemic lupus erythematosus and polyarteritis nodosa, may cause intermittent abdominal pain; porphyria
also may cause intermittent abdominal pain. Because the pain of
acute herpes zoster may precede the rash by 24 to 72 hours, the
pain may be attributed erroneously to anterior cutaneous nerve
entrapment.
Linea alba
Rectus
abdominis
Entrapped anterior
cutaneous nerve
Transverse
abdominis
Figure 69-1 The course of the anterior cutaneous nerve within the abdominal wall.
A
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
with anterior cutaneous entrapment syndrome should include a
combination of nonsteroidal anti-inflammatory drugs (NSAIDs)
or the cyclooxygenase-2 (COX-2) inhibitors and physical
therapy. Local application of heat and cold may be beneficial.
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
at which the nerve pierces the fascia with a local anesthetic and
steroid may be a reasonable next step. If the symptoms of anterior
cutaneous entrapment syndrome persist, surgical exploration and
decompression of the anterior cutaneous nerve are indicated.
B
Figure 69-3 A, The patient is asked to completely relax the abdominal
muscles and point with one finger to the most painful area. B, The
patient is then asked to maximally tense the abdominal muscles. The
Carnetts test is positive if the localized pain increases at the previously
identified painful area.
Figure 69-4 Transverse ultrasound image demonstrating the linea alba, rectus muscles, and the skin and subcutaneous tissues.
TABLE 69-1
Endometriosis
Diabetic radiculopathy
Herpes zoster
Hernia
Clinical Pearls
Patients with pain from anterior cutaneous nerve entrapment syndrome often attribute their pain symptoms to a
gallbladder attack or ulcer disease. Reassurance is required,
although it should be remembered that this musculoskeletal
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 introduced several days after the patient undergoes this injection 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 intraabdominal pathological conditions is indicated in patients
with anterior abdominal pain of unclear origin.
SUGGESTED READINGS
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 ultrasoundguided abdominal cutaneous nerve infiltration: a case series, Pain Med 12:
382386, 2011.
Kuan L-C, Li Y-T, Chen F-M, etal: Efficacy of treating abdominal wall pain by
local injection, Taiwan J Obstet Gynecol 45:239243, 2006.
Srinivasan R, Greenbaum DS: Chronic abdominal wall pain: a frequently overlooked
problem: practical approach to diagnosis and management, Am J Gastroenterol
97:824830, 2002.
Chapter 70
ACUTE INTERMITTENT PORPHYRIA
Testing
Given the usual delay in the diagnosis of acute intermittent porphyria, a considerable amount of testing is done. Most standard
laboratory testing does not point the clinician toward a diagnosis
of acute intermittent porphyria, however. Specifically, liver function tests are normal. A mild normocytic, normochromic anemia
is sometimes present. Freshly passed urine is colorless, but it turns
a port wine color if exposed to light. Given the low incidence of
porphyria, qualitative urine screening tests, such as the WatsonSchwartz test, is a reasonable first step in diagnosing porphyria. If
the qualitative tests are positive, quantitative testing, such as gas
chromatographic measurements for aminolevulinic acid, should
be performed.
205
Differential Diagnosis
Essentially all causes of acute intermittent abdominal pain must
be included in the differential diagnosis. The clinician needs to
take a detailed history and perform a careful physical examination to rule out life-threatening causes of acute, intermittent
abdominal pain, such as ischemic bowel, volvulus, and acute
appendicitis. The key distinguishing factor in acute intermittent
porphyria is that the patients report of severe abdominal pain
and the benign abdominal examination do not correlate. Given
the high incidence of psychiatric abnormalities in patients with
acute intermittent porphyria, psychogenic causes of abdominal
pain must be included in the differential diagnosis.
Treatment
Attacks of acute intermittent porphyria can be aborted by the
intravenous administration of large quantities of carbohydrates,
such as glucose. Hematin can be given intravenously and seems to
be well tolerated. Cimetidine, a histamine-2 inhibitor, also may
be useful in ameliorating acute attacks. Avoidance of barbiturates,
anticonvulsants, and alcohol is imperative to avoid exacerbating
the symptoms of acute intermittent porphyria attacks. Careful attention to fluid and electrolyte balance also is important.
Despite careful treatment, fatalities during attacks do occur.
Clinical Pearls
The cause of abdominal pain in acute intermittent porphyria is thought to be the result of intermittent autonomic
dysfunction causing abnormal gut motility with alternating
spasm and obstruction. The incidence of psychiatric abnormalities in patients with acute intermittent porphyria often
confounds the clinician and complicates treatment. It has
been said that to make a diagnosis, the clinician must think
of it first. Nowhere is this statement more true than in the
case of acute intermittent porphyria.
SUGGESTED READINGS
Crimlisk HL: The little imitator: porphyriaa neuropsychiatric disorder, J Neurol
Neurosurg Psychiatry 62:319328, 1997.
Herrick AL, McColl KEL: Acute intermittent porphyria, Best Pract Res Clin
Gastroenterol 19:235249, 2005.
Kuo H-C, Lee M-J, Chuang W-L, Huang C-C: Acute intermittent porphyria with
peripheral neuropathy: a follow-up study after hematin treatment, J Neurol Sci
260:231235, 2007.
Peters TJ, Deacon AC: International air travel: a risk factor for attacks in acute
intermittent porphyria, Clin Chim Acta 335:5963, 2003.
Shen FC, Hsieh CH, Huang CR: Acute intermittent porphyria presenting as acute
pancreatitis and posterior reversible encephalopathy syndrome, Acta Neurol
Taiwan 17:177183, 2008.
Chapter 71
RADIATION ENTERITIS
Differential Diagnosis
A history of previous radiation therapy is necessary to consider the
diagnosis of radiation enteritis. The very problem that necessitated
radiation therapy in the first placemalignancy can recur, however, and produce clinical symptoms indistinguishable from those
of radiation enteritis. Given the immunocompromised state of
most patients who have received radiation therapy, the possibility
of infectious enteritis or intra-abdominal abscess always must be
included in the differential diagnosis. Other causes of abdominal
pain, including diverticulitis, bowel obstruction, and appendicitis,
also may occur in conjunction with radiation enteritis.
Treatment
Symptom management is the primary thrust of the treatment of
radiation enteritis. Careful attention to the patients fluid and
metabolic status during the acute phases of the disease is crucial to
avoid complications. Psyllium helps the patient with diarrhea and
with mucoid stools and may decrease the sensations of needing to
move the bowels frequently. Anticholinergics such as dicyclomine
and antiperistaltics such as loperamide can help decrease diarrhea.
Zinc oxide ointment and sitz baths with aluminum acetate soaks
help with the symptoms of tenesmus and rectal pain. Steroid and
sucralfate enemas also have been reported to provide symptomatic
relief in difficult cases of radiation enteritis.
Testing
Patient Factors
Treatment Factors
Smoking
Radiotherapy technique
Modified from Theis VS, Sripadam R, Ramani V, etal: Chronic radiation enteritis,
Clin Oncol 2:7083, 2010.
207
Clinical Pearls
Treatment of the symptoms associated with radiation enteritis 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 suffering. Vigilance for life-threatening complications of radiation 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.
Chapter 72
LIVER PAIN
Testing
The Clinical Syndrome
Liver pain is a common clinical occurrence, but it is often poorly
diagnosed and treated. The liver can serve as a source of pain in and
of itself through the sympathetic nervous system and via referred
pain secondary to peritoneal irritation through the intercostal and
subcostal nerves. Pain that emanates from the liver itself tends to
be ill defined and may be referred primarily to the epigastrium. It
is dull and aching and is mild to moderate in severity. The pain
can be related to swelling of the liver and concomitant stretching
of the liver capsule or distention of the veins, as is seen with portal
obstruction. This pain is carried via sympathetic fibers from the
celiac ganglion that enter the liver along with the hepatic artery and
vein. This type of liver pain responds poorly to adjuvant analgesics.
Occasionally, hepatic enlargement causes diaphragmatic irritation,
which produces pain that is referred to the ipsilateral supraclavicular
and shoulder region. This referred pain is known as Kehrs sign and
is transmitted via the phrenic nerve and is often misdiagnosed.
Referred liver pain is caused by mechanical irritation and
inflammation of the inferior pleura and peritoneum. This pain is
somatic and carried primarily by the lower intercostal and subcostal
nerves. This somatic pain is sharp and pleuritic and is moderate to
severe in intensity. It responds more favorably to nonsteroidal antiinflammatory drugs (NSAIDs) and opioid analgesics in contrast to
sympathetically mediated liver pain.
Clavicle
Liver
Figure 72-1 Patients with liver pain may report ill-defined pain in the
supraclavicular region.
209
Differential Diagnosis
Pain of hepatic origin must be taken seriously. It is often the result
of an underlying serious disease, such as biliary malignancy, portal
Treatment
Initial treatment of liver pain should include a combination of simple 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 sympathetically 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 thickening of the gallbladder wall with a gallstone (large arrow) and metastasis to
lymph nodes (n). (From Haaga JR, Lanzieri CF, Sartoris UJ, etal: Computed
tomography and magnetic resonance imaging of the whole body, 3rd ed,
St Louis, 1994, Mosby, p 1359.)
Clinical Pearls
Chapter 73
ABDOMINAL ANGINA
15 to 30 minutes
after eating
Testing
The diagnosis of abdominal angina is based on clinical history.
Angiography of the celiac artery provides proof of vascular insufficiency 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
stool and blood cultures for infectious enteritis, may be indicated.
Given the possibility that the patients abdominal angina is due to
212
A
Figure 73-2 Thumbprinting in acute ischemic colitis at the splenic flexure. (From Grainger RG, Allison D: Grainger and Allisons diagnostic radiology: a textbook of medical imaging, 3rd ed, New York, 1997, Churchill
Livingstone, p 1036.)
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 thickening (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: Clinical ultrasound, vol 1, ed 3, New York, 2011, Churchill Livingstone, p 402.)
Treatment
occult mass or abscess is suspected. Magnetic resonance angiography (MRA) of the celiac and mesenteric vessels also can help clarify
the diagnosis and aid in planning a treatment strategy, as can ultrasonogrpahic and Doppler flow studies (Figures 73-3 and 73-4).
Differential Diagnosis
Any disease process that can produce ischemic bowel can mimic
the pain of abdominal angina. The vasculitides, including polyarteritis nodosum and Henoch-Schnlein purpura, also can cause
the symptoms of abdominal angina. Embolic disease that may
cause occlusion of the vascular supply to the gut also should be
considered. The possibility of infectious enteritis always must be
Clinical Pearls
Treatment of the symptoms associated with abdominal
angina is difficult, and, ultimately, correction of the vascular insufficiency is required. Vigilance for life-threatening
complications of abdominal angina, including bowel infarction, is mandatory to avoid disaster.
SUGGESTED READINGS
Cho JS, Carr JA, Jacobsen G, etal: Long-term outcome after mesenteric artery
reconstruction: a 37-year experience, J Vasc Surg 35:453460, 2002.
Cognet F, Ben Salem D, Dranssart M, etal: Chronic mesenteric ischemia: imaging
and percutaneous treatment, Radiographics 22:863879, 2002.
Hamed RMA, Ghandour K: Abdominal angina and intestinal gangrene: a catastrophic presentation of arterial fibromuscular dysplasiacase report and
review of the literature, J Pediatr Surg 32:13791380, 1997.
Rha SE, Ha HK, Lee SH, etal: CT and MR imaging findings of bowel ischemia
from various primary causes, RadioGraphics 20:2942, 2000.
Chapter 74
EPIDURAL ABSCESS
ICD-9 CODE 324.1
ICD-10 CODE G06.1
The Clinical Syndrome
Epidural abscess is an uncommon cause of spine pain that, if undiagnosed, can result in paralysis and life-threatening complications.
Epidural abscess can occur anywhere in the spine and intracranially.
It can occur spontaneously via hematogeneous seeding, most frequently as a result of urinary tract infections that spread to the spinal
epidural space via Batsons plexus. More commonly, epidural abscess
occurs after instrumentation of the spine, including surgery and epidural nerve blocks. The literature suggests that the administration of
steroids into the epidural space results in immunosuppression, with
a resultant increase in the incidence of epidural abscess. Although
theoretically plausible, the statistical evidencegiven the thousands
of epidural steroid injections performed around the United States on
a daily basiscalls this belief into question.
A patient with epidural abscess initially presents with ill-defined
pain in the segment of the spine affected (e.g., cervical, thoracic,
or lumbar) (Figure 74-1). This pain becomes more intense and
localized as the abscess increases in size and compresses neural
structures. Low-grade fever and vague constitutional symptoms,
including malaise and anorexia, progress to frank sepsis with
a high-grade fever, rigors, and chills. At this point, the patient
begins to experience sensory and motor deficits and bowel and
bladder symptoms as the result of neural compromise. As the
abscess continues to expand, compromise of the vascular supply to
the affected spinal cord and nerve occurs with resultant ischemia
and, if untreated, infarction and permanent neurological deficits.
Testing
Myelography is still considered the best test to ascertain compromise of the spinal cord and exiting nerve roots by an extrinsic
mass such as an epidural abscess. In this era of readily available
magnetic resonance imaging (MRI) and high-speed computed
tomography (CT), it may be more prudent to perform this noninvasive testing first, rather than wait for a radiologist or spine
surgeon to perform a myelogram (Figure 74-2). MRI and CT are
highly accurate in the diagnosis of epidural abscess and are probably more accurate than myelography in the diagnosis of intrinsic
disease of the spinal cord and spinal tumor. All patients suspected
to have epidural abscess should undergo laboratory testing consisting of complete blood cell count, erythrocyte sedimentation
rate, and automated blood chemistries. Blood and urine cultures
should be performed immediately in all patients thought to have
epidural abscess to allow immediate implementation of antibiotic
therapy while the workup is in progress. Gram stains and cultures
of the abscess material also should be performed, but antibiotic
treatment should not be delayed waiting for this information.
Differential Diagnosis
The diagnosis of epidural abscess should be strongly considered
in any patient with spine pain and fever, especially if the patient
has undergone spinal instrumentation or epidural nerve blocks for
either surgical anesthesia or pain control. Other pathological processes that must be considered in the differential diagnosis include
intrinsic disease of the spinal cord, such as demyelinating disease
and syringomyelia, and other processes that can result in compression of the spinal cord and exiting nerve roots, such as metastatic
215
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.
Treatment
The rapid initiation of treatment of epidural abscess is mandatory if the patient is to avoid the sequelae of permanent neurological deficit or death. The treatment of epidural abscess has
two goals: (1) treatment of the infection with antibiotics and (2)
drainage of the abscess to relieve compression on neural structures. Because most epidural abscesses are caused by Staphylococcus
aureus, antibiotics such as vancomycin that treat staphylococcal
infection should be started immediately after blood and urine culture samples are taken. Antibiotic therapy can be tailored to the
culture and sensitivity reports as they become available. As mentioned, antibiotic therapy should not be delayed while waiting for
definitive diagnosis if epidural abscess is being considered as part
of the differential diagnosis.
Antibiotics alone rarely treat an epidural abscess successfully
unless the diagnosis is made very early in the course of the disease;
drainage of the abscess is required to effect full recovery. Drainage
of the epidural abscess is usually accomplished via decompression
laminectomy and evacuation of the abscess. More recently, interventional radiologists have been successful in draining epidural
abscesses percutaneously using drainage catheters placed with the
Clinical Pearls
Delay in diagnosis puts the patient and clinician at tremendous risk for a poor outcome. The clinician should assume
that all patients who present with fever and back pain have
an epidural abscess until proved otherwise and should treat
accordingly. Overreliance on a single negative or equivocal imaging test is a mistake. Serial CT or MRI scans are
indicated should there be any deterioration in the patients
neurological status.
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 highsignal-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
Chapter 75
MULTIPLE MYELOMA
secondary to hypercalcemia also may be elicited. Anasarca resulting from renal failure, if present, is an ominous prognostic sign.
Testing
The presence of Bence Jones protein in the urine, anemia, and
increased M protein on serum protein electrophoresis point
Rib pain
Spine pain
Figure 75-1 Pain is the most common clinical symptom that ultimately
leads to the diagnosis of multiple myeloma.
219
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.)
Differential Diagnosis
Treatment
Clinical Pearls
SUGGESTED READINGS
Kaufman J, Lonial S: Multiple myeloma: the role of transplant and novel treatment
strategies, Semin Oncol 31(Suppl 4):99105, 2004.
Mahindra A, Hideshima T, Anderson KC: Multiple myeloma: biology of the
disease, Blood Rev 24(Suppl 1):S5S11, 2010.
Mitsiades CS, Hayden PJ, Anderson KC, Richardson PG: From the bench to the
bedside: emerging new treatments in multiple myeloma, Best Pract Res Clin
Haematol 20:797816, 2007.
Reece DE: Management of multiple myeloma: the changing landscape, Blood Rev
21:301314, 2007.
San Miguel JF, Gutirrez NC, Mateo G, Orfao A: Conventional diagnostics in
multiple myeloma, Eur J Cancer 42:15101519, 2006.
Chapter 76
PAGETS DISEASE
renal calculi and gout may occur, especially in men with Pagets
disease. In less than 1% of patients, a pagetic bone lesion may
transform into a malignant osteosarcoma.
Testing
As mentioned previously, Pagets disease is often fortuitously
diagnosed when the patient is undergoing radiographic testing
for an unrelated problem, such as intravenous pyelography for
renal calculi. The classic radiographic appearance of areas of bone
resorption with surrounding areas of dense, chaotic bone points
strongly to the diagnosis of Pagets disease. In patients with Pagets
disease, radionucleotide bone scanning can be used to assess the
extent of the disease because many bone lesions are clinically silent
(Figure 76-2). Magnetic resonance imaging (MRI) is indicated in
any patient thought to have Pagets disease who exhibits signs of
spinal cord compression. Serum creatine testing and automated
blood chemistries, including serum calcium determinations, are
indicated in all patients with Pagets disease. Alkaline phosphatase
levels are elevated, especially during the resorption phase of the
disease. Given the increased incidence of hearing loss in patients
with Pagets disease, audiometric testing is indicated.
Differential Diagnosis
Numerous other diseases of the bone, including osteoporosis, multiple myeloma, osteopetrosis, and primary and metastatic bone
tumors, can mimic the clinical presentation of Pagets disease.
Acromegaly also shares many common clinical signs and symptoms.
Metastatic disease from prostate and breast cancer can produce
Spine pain
Thickening of
long bones
Treatment
mentioned earlier, pagetic lesions undergo malignant transformation in approximately 1% of patients with Pagets disease.
Clinical Pearls
Careful evaluation of patients with Pagets disease is mandatory to help avoid the potential complications of the disease.
The clinician must look carefully for subtle signs of brainstem or spinal cord compression. Epidural and intercostal
injection of local anesthetics and steroids can provide excellent palliation of the pain associated with Pagets disease
that fails to respond to pharmacological treatment.
SUGGESTED READINGS
Ralston SH: Pathogenesis of Pagets disease of bone, Bone 43:819825, 2008.
Rousire M, Michou L, Cornlis F, Orcel P: Pagets disease of bone, Best Pract Res
Clin Rheumatol 17:10191041, 2003.
Rousire M, Michou L, Cornlis F, Orcel P: Pagets disease. In Waldman SD,
Campbell RSD, editors: Imaging of pain, Philadelphia, 2010, Saunders.
Walsh JP, Attewell R, Stuckey BGA, et al: Eisman treatment of Pagets disease
of bone: a survey of clinical practice in Australia, Bone 42:12191225, 2008.
Whitten CR, Saifuddin A: MRI of Pagets disease of bone, Clin Radiol 58:
763769, 2003.
Chapter 77
DIFFUSE IDIOPATHIC SKELETAL
HYPEROSTOSIS
ICD-9 CODE 733.99
ICD-10 CODE M89.30
The Clinical Syndrome
Diffuse idiopathic skeletal hyperostosis (DISH) is a disease of
the ligamentous structures of the spine. The cause of DISH is
unknown. The hallmark of this disease is confluent ossification of
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,
and bones of the pelvis.
DISH causes stiffness and pain of the cervical and thoracolumbar spine. The symptoms are worse on wakening and at night.
When the disease affects the cervical spine, cervical myelopathy
may result. If anterior spurring of the cervical spine occurs, dysphagia may result. DISH is a disease of the late fifth and early
sixth decades. It also can cause a relative spinal stenosis with
intermittent claudication. It affects men twice as commonly as
women. DISH is a disease that affects primarily whites. Patients
with DISH have a higher incidence of diabetes mellitus, hypertension, and obesity than the general population. DISH usually is
diagnosed by plain radiographs of the spine.
TABLE 77-1
numbness, weakness, and lack of coordination in the extremities subserved by the spinal segments affected by DISH. Muscle
spasms, back pain, and pain referred to the buttocks are common
(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
second most common cause of cervical myelopathy after cervical
spondylosis. Patients with lumbar myelopathy or cauda equina
syndrome experience varying degrees of lower extremity weakness
and bowel and bladder symptoms; this represents a neurosurgical
emergency and should be treated as such.
Testing
DISH is diagnosed by plain radiographs. Confluent ossification of
the spinal ligamentous structures spanning at least three interspaces
is pathognomonic for the disease. Disk space height is preserved
in patients with DISH. If myelopathy is suspected, magnetic resonance imaging (MRI) of the spine provides the best information
regarding the status of the spinal cord and nerve roots. MRI is
highly accurate and helps identify other abnormalities that may
put the patient at risk for the development of permanent spinal
cord injury (Figure 77-2). In patients who cannot undergo MRI,
such as a patient with a pacemaker, computed tomography (CT)
or myelography is a reasonable second choice. Radionucleotide
bone scanning and plain radiographs are indicated if fracture or
bony abnormality, such as metastatic disease, is being considered.
Although this testing provides useful neuroanatomical information, electromyography and nerve conduction velocity testing provide neurophysiological information that can delineate
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
chemistry testing, should be performed if the diagnosis of DISH
is in question.
Differential Diagnosis
DISH is a radiographic diagnosis that is supported by a combination of clinical history, physical examination, and MRI. Pain syndromes that may mimic DISH include neck and low back strain;
bursitis; fibromyositis; inflammatory arthritis; ankylosing spondylitis; and disorders of the spinal cord, roots, plexus, and nerves.
Thirty percent of patients with multiple myeloma or Pagets
disease also have DISH. Screening laboratory tests consisting of
complete blood cell count, erythrocyte sedimentation rate, antinuclear antibody testing, human leukocyte antigen (HLA) B-27
antigen screening, and automated blood chemistry testing should
225
Treatment
DISH is best treated with a multimodality approach. Physical
therapy, including heat modalities, range-of-motion exercises,
and deep sedative massage, combined with nonsteroidal antiinflammatory drugs (NSAIDs) and skeletal muscle relaxants
represents a reasonable starting point. The addition of steroid
epidural nerve blocks is a reasonable next step if pain remains a
problem. Underlying sleep disturbance and depression are best
treated with a tricyclic antidepressant compound, such as nortriptyline, which can be started at a single bedtime dose of 25 mg.
Clinical Pearls
Given the association of DISH with multiple myeloma and
Pagets disease, these potentially life-threatening diseases
must always be included in the differential diagnosis. DISH
and degenerative arthritis and discogenic disease may coexist.
Each disease process may require its own specific course of
treatment.
SUGGESTED READINGS
Hannallah D, White AP, Goldberg G, Albert TJ: Diffuse idiopathic skeletal
hyperostosis, Operat Techn Orthop 17:174177, 2007.
Kasper D, Hermichen H, Koster R, Schultz-Coulon HJ: Clinical manifestations
of diffuse idiopathic skeletal hyperostosis (DISH), HNO 50:978983, 2002.
Mader R: Diffuse idiopathic skeletal hyperostosis: a distinct clinical entity, Isr Med
Assoc J 5:506508, 2003.
Mader R: Current therapeutic options in the management of diffuse idiopathic
skeletal hyperostosis, Exp Opin Pharmacother 6:13131318, 2005.
Chapter 78
SPONDYLOLISTHESIS
Testing
Plain radiographs of the lumbar spine usually are sufficient to
diagnose spondylolisthesis (Figure 78-2). The lateral view shows
the slippage of one vertebra onto another. Magnetic resonance
Figure 78-1 Patients with spondylolisthesis often report back pain with
motion of the lumbar spine. Rising from a sitting to a standing position
often reproduces the pain.
227
L4
Differential Diagnosis
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
lumbar radiculopathy; low back strain; lumbar bursitis; lumbar fibromyositis; 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
laboratory tests consisting of complete blood cell count, erythrocyte
sedimentation rate, antinuclear antibody testing, human leukocyte
antigen (HLA) B-27 antigen screening, and automated blood chemistry testing should be performed if the diagnosis of spondylolisthesis
is in question to help rule out other causes of pain.
Treatment
Spondylolisthesis is best treated with a multimodality approach.
Physical therapy, including flexion exercises, heat modalities,
and deep sedative massage, combined with nonsteroidal anti-
inflammatory drugs (NSAIDs) and skeletal muscle relaxants represents a reasonable starting point. The addition of steroid epidural
nerve blocks is a reasonable next step. Caudal or lumbar epidural
blocks with a local anesthetic and steroid have been shown to be
extremely effective in the treatment of pain secondary to spondylolisthesis. Underlying sleep disturbance and depression are best
L5
treated with a tricyclic antidepressant compound, such as nortriptyline, which can be started at a single bedtime dose of 25 mg.
Clinical Pearls
The diagnosis of spondylolisthesis should be considered in
any patient reporting back pain, radicular pain, or both or
symptoms of pseudoclaudication. Patients with symptoms
of myelopathy should undergo MRI on an urgent basis.
Physical therapy may help prevent recurrent episodes of
pain, but, ultimately, surgical stabilization of the affected
segments may be required.
78 Spondylolisthesis 229
SUGGESTED READINGS
Agabegi SA, Fischgrund JS: Contemporary management of isthmic spondylolisthesis: 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 relation 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 sagittal dimension of the lumbar spinal canal from the upper to lower levels. 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
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 acuity, and excessive lacrimation and represents an ophthalmological
emergency.
Testing
Plain radiographs of the sacroiliac joints usually allow the clinician to diagnose ankylosing spondylitis. Erosion of the sacroiliac
joints produces a characteristic symmetrical pseudowidening
that is diagnostic of the disease (Figure 79-2), as is squaring of
the vertebral bodies, sclerosis of the anterior margins of the vertebral bodies (so-called shiny corners), and the classic trolley track
sign resulting from ankylosis of the facet joints (Figure 79-3).
Magnetic resonance imaging (MRI) of the spine provides the
best information regarding the contents of the lumbar spine and
sacroiliac joints. MRI is highly accurate and helps identify abnormalities that may put the patient at risk for the development of
myelopathy (Figure 79-4). In patients who cannot undergo MRI,
such as patients with pacemakers, computed tomography (CT)
or myelography is a reasonable second choice. Radionucleotide
bone scanning and plain radiography are indicated if fracture or
bony abnormality, such as metastatic disease, is being considered
in the differential diagnosis.
Although no test is diagnostic for ankylosing spondylitis, finding of the HLA B-27 antigen is highly suggestive of the disease
in patients with the previously mentioned clinical findings. This
antigen is present in 90% of patients with ankylosing spondylitis.
Complete blood cell count may reveal normocytic normochromic
anemia. The erythrocyte sedimentation rate is usually elevated, as
is the serum immunoglobulin A level.
Differential Diagnosis
Ankylosing spondylitis is a radiographic diagnosis that is supported by a combination of clinical history, physical examination,
and laboratory testing. Pain syndromes that may mimic ankylosing spondylitis include low back strain; lumbar bursitis; lumbar
fibromyositis; inflammatory arthritis; Reiters syndrome; collagenvascular diseases; and disorders of the lumbar spinal cord, roots,
plexus, and nerves as well as the sacroiliac joints. The clinician
should be aware that many other causes of sacroiliitis-related pain
exist (Table 79-1). Screening laboratory tests, consisting of complete blood cell count, erythrocyte sedimentation rate, antinuclear
antibody testing, HLA B-27 antigen screening, and automated
blood chemistry testing, should be performed if the diagnosis of
ankylosing spondylitis is in question to help rule out other causes
of the patients pain.
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 function, heat modalities, and deep sedative massage, combined with
nonsteroidal anti-inflammatory drugs (NSAIDs) and skeletal muscle relaxants represents a reasonable starting point. Sulfasalazine
may be useful in managing the arthritis associated with the disease.
The addition of steroid epidural nerve blocks is a reasonable next
step. Caudal or lumbar epidural blocks with a local anesthetic and
steroid have been shown to be extremely effective in the treatment
of pain secondary to ankylosing spondylitis. Underlying sleep disturbance and depression are best treated with a tricyclic antidepressant compound, such as nortriptyline, which can be started at
Figure 79-3 Lateral radiograph of the lumbar spine with squaring of the
vertebral bodies, which is typical of early ankylosing spondylitis. Generalized osteopenia and early inflammatory arthropathy of the lower facet
joints are seen. (From Waldman SD: Seronegative spondyloarthropathy. In
Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2011,
Saunders, pp 141144.)
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 quadriplegia, is a serious problem if diagnosis is delayed. Electromyography helps distinguish plexopathy from radiculopathy and helps
identify coexistent entrapment neuropathy, such as tarsal tunnel
syndrome, which confuse the diagnosis.
Septic arthritis
Ulcerative colitis
Crohns disease
Synovitis-acne-pustulosis hyperostosis-osteomyelitis (SAPHO)
syndrome
Seronegative arthropathies, including ankylosing spondylitis
Tuberculosis
Intestinal bypassinduced arthritis
Sarcoidosis
Whipples disease
Clinical Pearls
The diagnosis of ankylosing spondylitis should be considered in any patient reporting back or sacroiliac pain and
stiffness that are worse in the morning or after prolonged
periods of inactivity. Patients with symptoms of myelopathy
should undergo MRI on an urgent basis. Physical therapy
combined with NSAIDs may help prevent recurrent episodes of pain and help preserve function.
Brucellosis
Hyperparathyroidism
SUGGESTED READINGS
Joseph A, Brasington R, Kahl L, etal: Immunologic rheumatic disorders, J Allergy
Clin Immunol 125(Suppl 2):S204S215, 2010.
Mansour M, Cheema GS, Naguwa SM, et al: Ankylosing spondylitis: a contemporary perspective on diagnosis and treatment, Semin Arthritis Rheum
36:210223, 2007.
Reveille JD, Arnett FC: Spondyloarthritis: update on pathogenesis and management,
Am J Med 118:592603, 2005.
Waldman SD: Seronegative spondyloarthropathy. In Waldman SD, Campbell
RSD, editors: Imaging of pain, Philadelphia, 2011, Saunders, pp 141144.
Chapter 80
SUPERIOR CLUNEAL NERVE
ENTRAPMENT SYNDROME
ICD-9 CODE 355.9
ICD-10 CODE G58.9
The Clinical Syndrome
Entrapment of the superior cluneal nerve is an uncommon cause
of low back and buttocks pain. Comprising the terminal branches
of the posterior rami of L1, L2, and L3 nerve roots, the superior
cluneal nerves provide cutaneous innervation to the upper part of
the buttocks and are susceptible to entrapment as it passes over
the iliac crest through a tunnel formed by the thoracolumbar fascia and the superior rim of the iliac crest in a manner analogous
to compression of the median nerve as it passes through the carpal tunnel (Figure 80-1). The middle branch is most commonly
affected.
This entrapment neuropathy presents as pain, numbness, and
dysesthesias in the distribution of the superior cluneal nerve. The
symptoms often begin as a burning pain in the upper buttocks
with associated cutaneous sensitivity. Patients with superior cluneal
nerve entrapment note that sitting, squatting, or wearing tight jeans
with a low rise causes the symptoms to worsen. Although traumatic
lesions to the superior cluneal nerve during bone harvesting procedures and pelvic fractures have been implicated in superior cluneal
nerve entrapment, in most patients, no obvious antecedent trauma
can be identified.
Testing
Electromyography can distinguish lumbar radiculopathy and
plexopathy from superior cluneal nerve entrapment. Plain radiographs of the back, hip, and pelvis are indicated in all patients who
present with superior cluneal nerve entrapment to rule out occult
bony pathological processes. Based on the patients clinical presentation, additional testing may be warranted, including a complete
blood count, uric acid level, erythrocyte sedimentation rate, and
antinuclear antibody testing. Magnetic resonance imaging (MRI)
of the back is indicated if herniated disk, spinal stenosis, or spaceoccupying lesion is suspected. The injection technique described
later serves as both a diagnostic and therapeutic maneuver.
Differential Diagnosis
Superior cluneal nerve entrapment is often misdiagnosed as lumbar
radiculopathy, sacroiliac joint pain, gluteal bursitis, or primary hip
pathological conditions. Radiographs of the hip and electromyography can distinguish superior cluneal nerve entrapment from
radiculopathy or pain emanating from the hip. In addition, most
patients with lumbar radiculopathy have back pain associated with
reflex, motor, and sensory changes, whereas patients with superior cluneal nerve entrapment have no back pain and no motor
or reflex changes. The sensory changes of superior cluneal nerve
entrapment are limited to the distribution of the superior cluneal
nerve and should not extend below the upper buttocks. It should
be remembered that lumbar radiculopathy and superior cluneal
nerve entrapment may coexist as the double crush syndrome.
Occasionally, lumbar plexopathy produces buttocks pain, which
may confuse the diagnosis.
Treatment
Patients with superior cluneal nerve entrapment should be
instructed in avoidance techniques to reduce the symptoms and
pain associated with this entrapment neuropathy. A short course
of conservative therapy consisting of simple analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), or cyclooxygenase-2
(COX-2) inhibitors is a reasonable first step in the treatment of
superior cluneal nerve entrapment. If patients do not experience
rapid improvement, injection is the next step.
To treat the pain of superior cluneal nerve entrapment, the
patient is placed in the prone position. The posterior iliac crest is
identified by palpation, as are the spinous processes of the adjacent
lumbar vertebra. A point 7 cm lateral to midline, along the posterior iliac crest, is identified and prepared with antiseptic solution.
A 112-inch, 25-gauge needle is slowly advanced perpendicular to
the skin until the needle is felt to pop through the fascia. A paresthesia is often elicited. After careful aspiration, a solution of 5 to 7
mL of 1% preservative-free lidocaine and 40 mg methylprednisolone is injected in a fanlike pattern as the needle pierces the fascia
gluteal muscle. After injection of the solution, pressure is applied
to the injection site to decrease the incidence of ecchymosis and
233
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.
Clinical Pearls
Superior cluneal nerve entrapment is a common condition
that is often misdiagnosed as lumbar radiculopathy, sacroiliac
pain, or gluteal bursitis. The injection technique described
can produce dramatic pain relief; however, if a patient has
pain suggestive of superior cluneal nerve entrapment but
does not respond to superior cluneal nerve block, a lesion
more proximal in the lumbar plexus or an L1-3 radiculopathy should be considered. Such patients often respond to
epidural block with steroid. Electromyography and MRI of
the lumbar plexus are indicated in this patient population to
rule out other causes of pain, including malignancy invading
the lumbar plexus or epidural or vertebral metastatic disease
at L1-3.
SUGGESTED READINGS
Akbas M, Yegin A, Karsli B: Superior cluneal nerve entrapment eight years after
decubitus surgery, Pain Pract 5:364366, 2005.
Aly TA, Tanaka Y, Aizawa T, Ozawa H, Kokubun S: Medial superior cluneal
nerve entrapment neuropathy in teenagers: a report of two cases, Tohoku J Exp
Med 197:229231, 2002.
Herring A, Price DD, Nagdev A, Simon B: Superior cluneal nerve block for
treatment of buttock abscesses in the emergency department, J Emerg Med
39:8385, 2010.
Lu J, Ebraheim NA, Huntoon M, Heck BE, Yeasting RA: Anatomic considerations of superior cluneal nerve at posterior iliac crest region, Clin Orthop Relat
Res 347:224228, 1998.
Maigne JY, Doursounian L: Entrapment neuropathy of the medial superior cluneal
nerve: nineteen cases surgically treated, with a minimum of 2 years follow-up,
Spine 22:11561159, 1997.
Talu GK, zyalin S, Talu U: Superior cluneal nerve entrapment, Reg Anesth Pain
Med 25:648650, 2000.
Chapter 81
LUMBAR MYOFASCIAL PAIN
SYNDROME
Multifidus m.
Figure 81-1 Myofascial pain syndrome is a chronic pain syndrome that affects a focal or regional portion of the body.
235
muscle often occurs that is called a jump sign. This jump sign also
is characteristic of myofascial pain syndrome.
Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. Despite this consistent 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 repetitive microtrauma or chronic deconditioning of the agonist and
antagonist muscle unit.
In addition to muscle trauma, a variety of other factors seem
to predispose to development of myofascial pain syndrome. The
weekend athlete who subjects his or her body to unaccustomed
physical activity often develops myofascial pain syndrome. Poor
posture while sitting at a computer keyboard or watching television
has been implicated as a predisposing factor to the development of
myofascial pain syndrome. Previous injuries 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 muscles of the low back seem to be particularly susceptible to stress-induced myofascial pain syndrome.
Stiffness and fatigue often coexist with the pain of myofascial
pain syndrome, increasing the functional disability associated with
this disease and complicating its treatment. Myofascial pain syndrome may occur as a primary disease state or may occur in conjunction with other painful conditions, including radiculopathy
and chronic regional pain syndromes. Psychological or behavioral
abnormalities, including depression, frequently coexist with the
muscle abnormalities associated with myofascial pain syndrome.
Treatment of these psychological and behavioral abnormalities
must be an integral part of any successful treatment plan for myofascial pain syndrome.
spondylolisthesis also may mimic the clinical presentation of lumbar myofascial pain syndrome.
Treatment
Lumbar myofascial pain syndrome is best treated with a multimodality approach. Physical therapy, including correction of
functional abnormalities (e.g., poor posture, improper chair or
computer height) and the use of heat modalities and deep sedative
massage, combined with nonsteroidal anti-inflammatory drugs
(NSAIDs) and skeletal muscle relaxants represents a reasonable
starting point. If these treatments fail to provide rapid symptomatic
relief, local trigger point injection of anesthetic and steroid into the
myofascial trigger point area is a reasonable next step. Underlying
diffuse muscle pain and sleep disturbance and depression are best
treated with a tricyclic antidepressant compound, such as nortriptyline, which can be started at a single bedtime dose of 25 mg.
When performing trigger point injections, careful preparation of the patient before injection helps optimize results. Trigger
point injections are directed at the primary trigger point, rather
than the area of referred pain. It should be explained to the patient
that the goal of trigger point injection is to block the trigger of the
persistent pain and, it is hoped, provide long-lasting relief. It is
important that the patient understand that for most patients with
myofascial pain syndrome, more than one treatment modality is
required to provide optimal pain relief. The use of the prone or
lateral position when identifying and marking trigger points and
when performing the actual trigger point injection helps decrease
the incidence of vasovagal reactions. The skin overlying the trigger point to be injected should always be prepared with antiseptic
solution before injection to avoid infection.
After the goals of trigger point injection are explained to the
patient and proper preparation of the patient has been carried out,
the trigger point to be injected is reidentified by palpation with a
sterile gloved finger (Figure 81-2). A syringe containing 10 mL of
Testing
No specific test exists for lumbar myofascial pain syndrome. Testing is aimed primarily at identifying occult pathology or other
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 sedimentation rate, antinuclear antibody testing, and automated blood
chemistry testing, should be performed to rule out occult inflammatory arthritis, infection, and tumor.
Trapezius m.
Erector spinae m.
Latissimus dorsi m.
Serratus posterior m.
Trigger points
Differential Diagnosis
Lumbar myofascial pain syndrome is a clinical diagnosis of exclusion that is supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that
may mimic lumbar myofascial pain syndrome include lumbar
strain, inflammatory arthritis, and disorders of the lumbar spinal cord, roots, plexus, and nerves. Congenital abnormalities,
such as arteriovenous malformations and trefoil spinal canal, and
0.25% preservative-free bupivacaine and 40 mg of methylprednisolone to be injected is attached to a 25-gauge needle of a length
adequate to reach the trigger point. For the deeper muscles of
posture in the low back, a 312-inch needle is required. A volume
of 0.5 to 1 mL of solution is injected into each trigger point. The
patient should be informed that a series of two to five treatment
sessions may be required to abolish the trigger point completely.
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 technique to avoid infection and universal precautions to avoid
risk to the operator. Most side effects of trigger 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 pressure is placed
on the injection site immediately after trigger point injection. 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 trigger points in proximity to the underlying pleural space.
Antidepressant compounds are the primary pharmacological treatment for myofascial pain syndrome. Tricyclic
antidepressants are thought to be more effective than selective serotonin reuptake inhibitors in the treatment of this
painful condition. The precise mechanism of action of antidepressant 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 nortriptyline 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.
SUGGESTED READINGS
Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122:S22S30, 2009.
Ge H-Y, Nie HL, Madeleine P, et al: Contribution of the local and referred
pain from active myofascial trigger points in fibromyalgia syndrome, Pain
147:233240, 2009.
Krismer M, van Tulder M: The Low Back Pain Group of the Bone and Joint
Health Strategies for Europe Project: Low back pain (non-specific), Best Pract
Res Clin Rheumatol 21:7791, 2007.
Mens JMA: The use of medication in low back pain, Best Pract Res Clin Rheumatol
19:609621, 2005.
Stanos SP, PM, Harden RN: The physiatric approach to low back pain, Semin
Pain Med 2:186196, 2004.
Chapter 82
PROCTALGIA FUGAX
Testing
Similar to the physical examination, testing in patients with proctalgia fugax is usually normal. Because of the risk for overlooking rectal malignancy that may be responsible for pain that may
be attributed to a benign cause, by necessity proctalgia fugax is
238
Differential Diagnosis
As mentioned previously, because of the risk for overlooking serious pathology of the anus and rectum, proctalgia fugax must be
a diagnosis of exclusion. The clinician first must rule out rectal
malignancy to avoid disaster. Proctitis can mimic the pain of proctalgia fugax and can be diagnosed on sigmoidoscopy or colonoscopy. Hemorrhoids usually manifest with bleeding associated with
pain and can be distinguished from proctalgia fugax on physical
examination. Prostadynia sometimes may be confused with proctalgia fugax, but the pain is more constant, more dull, and aching.
Treatment
Initial treatment of proctalgia fugax should include a combination of simple analgesics and nonsteroidal anti-inflammatory drugs
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. If these medications do not control the symptoms adequately, a tricyclic antidepressant or gabapentin should be added. Traditionally, tricyclic
antidepressants have been a mainstay in the palliation of pain secondary to proctalgia fugax. Controlled studies have shown the efficacy
of amitriptyline for this indication. Other tricyclic antidepressants,
including nortriptyline and desipramine, also have been shown to be
clinically useful. This class of drugs is associated with significant anticholinergic side effects, including dry mouth, constipation, sedation,
and urinary retention. These drugs should be used with caution in
patients with glaucoma, cardiac arrhythmia, and prostatism.
To minimize side effects and encourage compliance, the primary care physician should start amitriptyline or nortriptyline at
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.
Figure 82-2 Ulcerative colitis. The bowel wall of the rectum and sigmoid colon is minimally thickened with a target appearance (arrowheads). (From Haaga JR, Lanzieri CF, Gilkeson RC, editors: CT and MR
imaging of the whole body, 4th ed, Philadelphia, 2003, Mosby, p 1245.)
Clinical Pearls
Proctalgia fugax is a distressing disease for patients. The
paroxysms of pain may occur without warning and make
the patient afraid to leave the house. The main focus of
the clinician caring for a patient with proctalgia fugax is
to ensure that occult malignancy has not been overlooked.
Given the psychological implications of pain involving the
genitals and rectum, the clinician should not overlook the
possibility of psychological abnormality in patients with
pain in the rectum.
SUGGESTED READINGS
Bharucha AE, Wald A, Enck P, Rao A: Functional anorectal disorders, Gastroenterology 130:15101518, 2006.
Karras JD, Angelo G: Proctalgia fugax, Am J Surg 82:616625, 1951.
Vincent C: Anorectal pain and irritation: anal fissure, levator syndrome, proctalgia
fugax, and pruritus ani, Prim Care 26:5368, 1999.
Waldman SD: Proctalgia fugax. In Waldman SD, editor: Pain review, Philadelphia,
2009, Saunders, pp 307308.
Weizman Z, Binsztok M: Proctalgia fugax in teenagers, J Pediatr 114:813814,
1989.
Chapter 83
PROSTATODYNIA
Testing
Prostatodynia is an uncommon cause of perineal pain in men.
Also known as chronic nonbacterial prostatitis and chronic pelvic pain syndrome, prostatodynia probably is not a single clinical entity, but rather the conglomeration of a variety of disorders
that can cause pain in this anatomical region. Included in these
disorders are chronic infections of the prostate, chronic inflammation of the prostate without demonstrable infection, bladder
outflow abnormalities, pelvic floor muscle disorders, reflex sympathetic dystrophy, and psychogenic causes. All have in common
the ability to cause chronic, ill-defined perineal pain, which is the
hallmark of prostatodynia.
The pain of prostatodynia is characterized by dull, aching,
or burning pain of the perineum and underlying structures
(Figure 83-1). The intensity of pain is mild to moderate and
may worsen with urination or sexual activity. The pain may be
referred to the penis, testicles, scrotum, or inner thigh. Irritative
urinary outflow symptoms and sexual dysfunction often coexist with the pain of prostatodynia. The history of all patients
with chronic prostatodynia should include specific questioning
regarding a history of sexual abuse.
Differential Diagnosis
Treatment
Initial treatment of the pain associated with prostatodynia should
include a combination of nonsteroidal anti-inflammatory drugs
(NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors. The local
application of heat and cold with sitz baths also may be beneficial.
241
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 normal 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
resonance imaging, 3rd ed, St Louis, 1999, Mosby, p 626.)
83 Prostatodynia 243
TABLE 83-1
Syndrome
Confirmed UTI
Prostate
Examination
WBC
Culture
Response to
Antibiotics
Impaired
Urinary Flow
Acute bacterial
prostatitis
Yes
Tender, warm
Yes
Yes
Yes
Yes
Chronic bacterial
prostatitis
Usually
Varied
Yes
Yes
Slow
Nonbacterial
prostatitis
No
Varied
Yes
No
Poor
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.
Clinical Pearls
The clinician should be aware that the relationship of the
genitalia to the male psyche presents some unique challenges 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.
SUGGESTED READINGS
Lummus WE, Thompson I: Prostatitis, Emerg Med Clin North Am 19:691707,
2001.
Rarbalias GA: Prostatodynia or painful male urethral syndrome? Urology
36:146153, 1990.
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
167:17681773, 2002.
Wesselmann U, Burnett AL, Heinberg LJ: The urogenital and rectal pain
syndromes, Pain 73:269294, 1997.
Chapter 84
GLUTEUS MAXIMUS PAIN
SYNDROME
Gluteus maximus m.
244
Testing
No specific test exists for gluteus maximus pain syndrome. Testing
is aimed primarily at identifying occult pathological conditions or
other diseases that may mimic myofascial pain syndrome (see discussion of differential diagnosis). Plain radiographs help delineate
bony abnormality of the pelvis and hip, including arthritis, avascular necrosis of the hip, fracture, congenital abnormalities, and
tumor. All patients with the recent onset of myofascial pain syndrome should undergo magnetic resonance imaging (MRI) of the
lumbar spine and pelvis to rule out occult pathological processes
(Figure 84-3). Screening laboratory tests, consisting of complete
blood count, erythrocyte sedimentation rate, antinuclear antibody
testing, and automated blood chemistry testing, should be performed to rule out occult inflammatory arthritis, infection, and
tumor.
Differential Diagnosis
Gluteus maximus pain syndrome is a clinical diagnosis of exclusion supported by a combination of clinical history, physical
examination, radiography, and MRI. Pain syndromes that may
mimic gluteus maximus pain syndrome include lumbosacral
radiculopathy and plexopathy, stress fractures of the pelvis and
hip, muscle strain, inflammatory arthritis, and disorders of the
lumbar spinal cord, roots, plexus, and nerves. Intrapelvic tumors
also may mimic the clinical presentation of gluteus maximus pain
syndrome.
Treatment
Gluteus maximus pain syndrome is best treated with a multimodality approach. Physical therapy, including correction of
functional abnormalities (e.g., poor posture, improper chair or
computer height) and the use of heat modalities and deep sedative
massage, combined with nonsteroidal anti-inflammatory drugs
(NSAIDs) and skeletal muscle relaxants, represents a reasonable
starting point. If these treatments fail to provide rapid symptomatic relief, local trigger point injection of local anesthetic and steroid into the myofascial trigger point area is a reasonable next step.
Underlying diffuse muscle pain and sleep disturbance and depression are best treated with a tricyclic antidepressant compound,
such as nortriptyline, which can be started at a single bedtime
dose of 25 mg.
When performing trigger point injections, careful preparation of the patient before trigger point injection helps optimize
results. Trigger point injections are directed at the primary trigger point, rather than in the area of referred pain. It should be
explained to the patient that the goal of trigger point injection is
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, Philadelphia, 2007, Saunders, p 379.)
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 hyperintense signal pattern. (From Edelman RR, Hesselink JR, Zlatkin MB, et al, editors: Clinical magnetic resonance imaging, 3rd ed, Philadelphia, 2006,
Saunders, p 3387.)
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
technique to avoid infection; universal precautions should
be used to avoid risk to the operator. Most side effects of
trigger 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 pressure is placed on the injection site immediately after
trigger point injection. 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 trigger points in proximity to the underlying pleural space. The antidepressant compounds represent
the primary pharmacological treatment for myofascial pain
syndrome. Tricyclic antidepressants are thought to be more
effective than selective serotonin reuptake inhibitors in the
treatment of this painful condition. The precise mechanism
of action of the antidepressant 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 present in many patients
with myofascial pain syndrome. Drugs such as amitriptyline
and nortriptyline 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.
Chapter 85
GLUTEUS MEDIUS SYNDROME
248
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 attributed
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
posterior iliac crest that is referred down the buttocks across the
sacroiliac joint and into the posterior lower extremity.
The trigger point is the pathognomonic lesion of myofascial
pain and is thought to be the result of microtrauma to the affected
muscles. This pathological lesion is characterized by a local point
of exquisite tenderness in affected muscle. Mechanical stimulation
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, often an involuntary withdrawal of the stimulated muscle, termed a jump sign, occurs. The jump sign also is
characteristic of myofascial pain syndrome. Patients with gluteus
medius syndrome will exhibit a trigger point along the posterior
iliac crest.
Taut bands of muscle fibers often are identified when myofascial trigger points are palpated. In spite of this consistent
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 repetitive 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 watching television also has been implicated as a predisposing factor
to the development of myofascial pain syndrome. Previous injuries 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 gluteus medius muscle seems to be particularly susceptible to stressinduced myofascial pain syndrome.
Stiffness and fatigue often coexist with the pain of myofascial pain syndrome, increasing the functional disability associated with this disease and complicating its treatment. Myofascial
pain syndrome may occur as a primary disease state or in conjunction with other painful conditions, including radiculopathy
Testing
Biopsies of clinically identified trigger points have not revealed
consistently abnormal histological findings. The muscle hosting
the trigger points has been described as moth eaten and as containing waxy degeneration. Increased plasma myoglobin has
been reported in some patients with gluteus medius syndrome, but
this finding has not been corroborated by other investigators. Electrodiagnostic testing has revealed an increase in muscle tension in
some patients, but again, this finding has not been reproducible.
Because of the lack of objective diagnostic testing, the clinician
must rule out other coexisting disease processes that may mimic
gluteus medius syndrome (see discussion of differential diagnosis).
Differential Diagnosis
The diagnosis of gluteus medius syndrome is based on clinical
findings rather than specific laboratory, electrodiagnostic, or
radiographic testing. For this reason, a targeted history and physical examination, with a systematic search for trigger points and
identification of a positive jump sign, must be carried out in every
Treatment
Treatment is focused on eliminating the myofascial trigger and
achieving relaxation of the affected muscle. It is hoped that interrupting 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
error is involved in developing a treatment plan.
Conservative therapy consisting of trigger point injection with
local anesthetic or saline is the initial treatment of gluteus medius
syndrome. Because underlying depression and anxiety are present
in many patients, antidepressants are an integral part of most treatment plans. Other methods, including physical therapy, therapeutic heat and cold, transcutaneous nerve stimulation, and electrical
stimulation, may be helpful on a case-by-case basis. For patients
who do not respond to these traditional measures, consideration
should be given to the use of botulinum toxin type A. Although
not currently approved by the Food and Drug Administration for
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.
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.)
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.
SUGGESTED READINGS
Arnold LM: The pathophysiology, diagnosis and treatment of fibromyalgia, Psychiatr
Clin North Am 33:375408, 2010.
Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30,
2009.
Imamura M, Cassius DA, Fregni F: Fibromyalgia: from treatment to rehabilitation,
Eur J Pain Suppl 3:117122, 2009.
Marsh M: Milnacipran, The comprehensive pharmacology reference, Philadelphia, 2008,
Elsevier, pp 14.
Waldman SD: Atlas of pain management injection techniques, Philadelphia, 2007,
Saunders, pp 378380.
Chapter 86
ORCHIALGIA
tapping over the ilioinguinal nerve at the point it pierces the transverse abdominis muscle. A patient with ilioinguinal or genitofemoral neuralgia may assume a bent-forward novice skiers position
to eliminate pressure on the affected nerve.
Testing
Ultrasound examination of the scrotal contents is indicated in all
patients with orchialgia. Radionucleotide and Doppler studies are
indicated if vascular compromise is suspected. Transillumination
of the scrotal contents also can help identify varicocele. Electromyography helps distinguish ilioinguinal nerve entrapment from
lumbar plexopathy, lumbar radiculopathy, and diabetic polyneuropathy. 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 lumbar
plexus and pelvis is indicated if tumor or hematoma is suspected
(Figure 86-2).
Differential Diagnosis
Extrascrotal pathology, including inguinal hernia, ilioinguinal neuralgia, and lesions of the lumbar plexus, nerve roots, and spinal cord,
can mimic the pain of orchialgia and must be included in the differential diagnosis, as can a variety of systemic diseases (Table 86-1).
Considerable intrapatient variability exists in the anatomy of the
ilioinguinal and genitofemoral nerves, which can result in variation
in patients clinical presentation. The ilioinguinal nerve is a branch
of the L1 nerve root with contribution from T12 in some patients.
The nerve follows a curvilinear course that takes it from its origin of
the L1 and occasionally T12 somatic nerves to inside the concavity
of the ilium. The ilioinguinal nerve continues anteriorly to perforate
the transverse abdominis muscle at the level of the anterior superior iliac spine. The nerve may interconnect with the iliohypogastric
nerve as it continues along its course medially and inferiorly, where
it accompanies the spermatic cord through the inguinal ring and
into the inguinal canal. The distribution of the sensory innervation
of the ilioinguinal nerves varies among patients because considerable
overlap may occur with the iliohypogastric nerve. In general, the
ilioinguinal nerve provides sensory innervation to the upper portion
of the skin of the inner thigh and the root of the penis and upper
scrotum in men.
Treatment
Many treatments have been advocated for orchialgia, with varying degrees of success (Table 86-2). Initial treatment of the pain
251
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
Diabetic neuropathy
Epididymal cyst/spermatocele
Epididymitis
Infectious (e.g., Chlamydia trachomatis, Neisseria gonorrhea, Ureaplasma 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
genitofemoral or ilioinguinal nerve roots (T10-L1), with or without
a history of surgery
Testicular torsion or torsion of the appendix testis (intermittent)
Testicular vasocongestion from sexual arousal without ejaculation
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
TABLE 86-2
Clinical Pearls
The clinician should be aware that the relationship of the
genitalia to the male psyche presents some unique challenges when treating patients suffering from orchialgia.
The behavioral and psychological issues must be addressed
concurrently with the medical issues if treatment is to be
successful. The possibility for testicular malignancy is ever
present and should be carefully sought in all patients with
orchialgia.
associated with orchialgia should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
(COX-2) inhibitors and physical therapy. Local application of
heat and cold may be beneficial. The use of supportive undergarments or an athletic supporter may provide symptomatic relief.
For patients who do not respond to these treatment modalities,
injection of the spermatic cord or ilioinguinal and genitofemoral
nerves with a local anesthetic and steroid may be a reasonable next
step. If the symptoms of orchialgia persist, surgical exploration of
the scrotal contents should be considered. Psychological evaluation and interventions should take place concurrently with the
previously mentioned treatment modalities.
SUGGESTED READINGS
Christiansen CG, Sandlow JI: Testicular pain following vasectomy: a review of
postvasectomy pain syndrome, J Androl 24:293298, 2003.
Heidelbaugh JJ: Academic mens health: case studies in clinical practice: chronic
orchialgia, J Mens Health 6:220225, 2009.
Linnebur S, Hiatt WH: Probable statin-induced testicular pain, Ann Pharmacother
41:138142, 2007.
Masarani M, Cox R: The aetiology, pathophysiology and management of chronic
orchialgia, BJU Int 91:435437, 2003.
Waldman SD: Orchialgia. In Waldman SD, editor: Pain review, Philadelphia,
2009, Saunders, pp 304305.
Wampler SM, Llanes M: Common scrotal and testicular problems primary care,
Clin Office Pract 37:613626, 2010.
Wesselman U, Burnett AL, Heinburg LJ: The urogenital and rectal pain syndromes,
Pain 73:269294, 1997.
Chapter 87
VULVODYNIA
Extravulvar pathological processes can manifest with the primary symptom of vulvodynia. One of the most common causes
of vulvodynia of extravulvar origin is malignancy involving the
pelvic contents other than the vulva. Tumor involving the lumbar plexus, cauda equina, or hypogastric plexus rarely can manifest as pain localized to the vulva and perineum. Postradiation
neuropathy can occur after radiation therapy for the treatment of
malignancy of the vulva and rectum and can mimic the pain of
vulvodynia. Ilioinguinal or genitofemoral entrapment neuropathy
also can manifest clinically as vulvodynia.
Testing
Pelvic examination is the cornerstone of the diagnosis of patients
with vulvodynia. Careful examination for infection, cutaneous or
mucosal abnormalities, tenderness, muscle spasm, or tumor is crucial to avoid overlooking vulvar malignancy. Ultrasound examination of the pelvis is indicated in all patients with vulvodynia. If any
question of occult malignancy of the vulva or pelvic contents exists,
magnetic resonance imaging (MRI) or computed tomography
(CT) of the pelvis is mandatory to rule out malignancy or disease of
the pelvic organs, such as endometriosis, which may be responsible
for the pain symptoms (Figure 87-2). Urinalysis to rule out urinary
tract infection also is indicated in all patients with vulvodynia. Culture for sexually transmitted diseases, including herpes, is indicated
in the evaluation of all patients thought to have vulvodynia.
Electromyography helps distinguish entrapment neuropathy of
the genitofemoral or ilioinguinal nerves from lumbar plexopathy or
lumbar radiculopathy. Based on the patients clinical presentation,
additional tests, including complete blood cell count, erythrocyte
sedimentation rate, and antinuclear antibody testing, may be indicated. MRI of the lumbar plexus is indicated if tumor or hematoma
is suspected.
Differential Diagnosis
Extravulvar pathological findings, including reflex sympathetic dystrophy and lesions of the lumbar plexus, nerve roots, and spinal
cord, can mimic the pain of vulvodynia and must be included in
the differential diagnosis. As mentioned earlier, because of the disastrous results of missing a diagnosis of pelvic or vulvar malignancy
when evaluating and treating patients thought to have vulvodynia,
it is mandatory that malignancy be high on the list of differential
diagnostic possibilities.
Treatment
A variety of treatments have been advocated in the treatment of
vulvodynia with varying degrees of success (Tables 87-1 and 87-2).
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.
Clinical Pearls
The clinician should be aware that the relationship of
the genitalia to the female psyche presents some unique
challenges when treating patients with vulvodynia. The
behavioral and psychological issues must be addressed
concurrently with the medical issues if treatment is to be
successful. The possibility for vulvar or pelvic malignancy
is ever present and should be carefully sought out in all
patients with vulvodynia.
*
C
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, Fatsuppressed 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
87 Vulvodynia 257
TABLE 87-2
SUGGESTED READINGS
Chapter 88
CLITORAL PRIAPISM
(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
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.
Often, the patient may report a painful swelling of her vagina
and attribute her symptoms to an insect bite, urinary tract or
vaginal infection, or allergic reaction. On physical examination,
the examiner will note that the clitoris is erect and firm, with the
glans of the clitoris retracted beneath the engorged clitoral hood.
Rubor is often present, as well as significant allodynia. Vaginal
transudation, which is seen as part of female sexual arousal, is
usually absent. It should be noted that enlargement of the clitoris
has other causes, some of which are painful and some not, such
as infiltrative tumors (Table 88-2).
Testing
Pelvic examination is the cornerstone of the diagnosis of patients
with vulvodynia. Careful examination for infection, cutaneous
or mucosal abnormalities, tenderness, muscle spasm, or tumor
is crucial to avoid overlooking clitoral, vulvar, or pelvic malignancy. Ultrasound examination of the pelvis is indicated in all
patients with clitoral priapism. If any question exists regarding occult malignancy of the vulva or pelvic contents, magnetic
TABLE 88-1
258
TABLE 88-2
Causes of Clitoromegaly
Congenital
Congenital adrenal hyperplasia, classical
Ambiguous genitalia, isolated or in syndromic conditions
Acquired
Hormonal
Congenital adrenal hyperplasia, late onset
Ovarian or adrenal tumors (androgen secreting)
Iatrogenic androgen exposure
Nonhormonal
Neurofibromatosis
Epidermoid cyst (spontaneous or traumatic, female genital
mutilation)
Hemangioma of the clitoris or the prepuce
Metastatic infiltration
Idiopatic
Modified from Bruni V, Pontello V, Dei M, etal: Hemangioma of the clitoris
presenting as clitoromegaly: a case report, J Pediatr Adolesc Gynecol
22:el37e138, 2009.
Differential Diagnosis
Extravulvar pathological findings, including reflex sympathetic
dystrophy and lesions of the lumbar plexus, nerve roots, and spinal cord, can mimic the pain of vulvodynia and must be included
in the differential diagnosis. As mentioned earlier, because of the
disastrous results of missing a diagnosis of pelvic or vulvar malignancy when evaluating and treating patients thought to have vulvodynia, it is mandatory that malignancy be high on the list of
differential diagnostic possibilities.
Treatment
The foundation of treatment of clitoral priapism is to first identify the factor responsible for the symptoms and then immediately
remove it. Because the vast majority of cases of both male and
female priapism are drug induced, a careful drug history looking at
both legal and illegal drugs is mandatory (see Table 88-1). A history of spider bite or painful insect stings also should be ascertained
because the venom of both black widow spiders and scorpions can
cause priapism. Empiric treatment with alpha-adrenergic drugs
such as phenylephrine and phenylpropanolamine should be initiated with careful monitoring of the patients cardiovascular status.
Clinical Pearls
The most common cause of clitoral priapism is drug-induced
clitoral dysfunction. The clinician should be aware that the
relationship of the genitalia to the female psyche presents
some unique challenges when treating patients with clitoral
priapism. The behavioral and psychological issues must be
addressed concurrently with the medical issues if treatment
is to be successful. The possibility for vulvar or pelvic malignancy is ever present and should be carefully sought in all
patients thought to have clitoral priapism.
SUGGESTED READINGS
Figure 88-2 Clitoral carcinoma. (From Matsuo K, Hew KE, Im DD, Rosenshein NB: Clitoral metastasis of anal adenocarcinoma associated with rectovaginal fistula in long standing Crohns disease, Eur J Obstet Gynecol
Reprod Biol 144:182183, 2009.)
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 clitoromegaly, 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,
2007.
Rosenberg I, Aniskin D, Bernay L: Psychiatric treatment of patients predisposed to
priapism induced by quetiapine, trazodone and risperidone: a case report, Gen
Hosp Psychiatry 31:98, 2009.
Chapter 89
GLUTEAL BURSITIS
Testing
Plain radiographs of the hip may reveal calcification of the bursa
and associated structures consistent with chronic inflammation.
Magnetic resonance imaging (MRI) is indicated if occult mass or
tumor of the hip is suspected. Electromyography should be performed if neurological findings are present to rule out plexopathy, radiculopathy, or nerve entrapment syndromes of the lower
extremity. Based on the patients clinical presentation, additional
tests, including complete blood cell count; human leukocyte antigen (HLA) B-27 testing; automated serum chemistries, including
uric acid; erythrocyte sedimentation rate; and antinuclear antibody
testing, may be indicated. The injection technique described here
serves as a diagnostic and therapeutic maneuver for patients with
gluteal bursitis.
Differential Diagnosis
Gluteal bursitis is often misdiagnosed as sciatica or attributed to
primary hip pathological processes. Radiographs of the hip and
electromyography help distinguish gluteal bursitis from radiculopathy of pain emanating from the hip. Most patients with a lumbar
radiculopathy have back pain associated with reflex, motor, and
sensory changes, whereas patients with gluteal bursitis have only
secondary back pain and no neurological changes. Piriformis syndrome sometimes may be confused with gluteal bursitis, but can
Figure 89-1 The action of the gluteus maximus muscle includes the
flexion of trunk on thigh when maintaining a sitting position when
riding a horse.
Treatment
Initial treatment of the pain and functional disability associated
with gluteal bursitis should include a combination of nonsteroidal
anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2)
inhibitors and physical therapy. Local application of heat and cold
may be beneficial. The repetitive movements that incite the syndrome should be avoided. For patients who do not respond to
these treatment modalities, injection of gluteal bursa with a local
anesthetic and steroid may be a reasonable next step.
To inject the gluteal bursae, the patient is placed in the lateral
position with the affected side up and the affected leg flexed at the
knee. Preparation with antiseptic solution of the skin overlying
the upper outer quadrant of the buttocks is carried out. A syringe
containing 4 mL of 0.25% preservative-free bupivacaine and 40
mg of methylprednisolone is attached to a 25-gauge, 112-inch
needle. The point of maximal tenderness within the upper, outer
quadrant of the buttocks is identified with a sterile gloved finger.
Before needle placement, the patient should be advised to say
There! immediately if he or she feels a paresthesia into the lower
Gluteal
medius
Ilium
Gluteal
maximus
Gluteal
minimus
Gluteal
bursae
Sciatic
nerve
Figure 89-2 Injection technique to relieve the pain resulting from gluteal
bursitis.
Clinical Pearls
This injection technique is extremely effective in the treatment of gluteal bursitis. It 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. Most side effects of this injection technique
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 injection. The avoidance of overly long needles helps decrease the incidence of
trauma to underlying structures. Special care must be taken
to avoid trauma to the sciatic nerve.
The use of physical modalities, including local heat and
gentle stretching exercises, should be introduced several
days after the patient undergoes this injection technique.
Vigorous exercises should be avoided because they would
exacerbate the symptoms. Simple analgesics, NSAIDs, and
antimyotonic agents such as tizanidine may be used concurrently with this injection technique.
SUGGESTED READINGS
Bancroft LW, Peterson JJ, Kransdorf MJ: Cysts, geodes, and erosions, Radiol Clin
North Am 42:7387, 2004.
Hodnett PA, Shelly MJ, MacMahon PJ, Kavanagh EC, Eustace SJ: MR imaging of
overuse injuries of the hip, MRI Clin North Am 17:667679, 2009.
Tibor LM, Sekiya JK: Differential diagnosis of pain around the hip joint, Arthroscopy
24:14071421, 2008.
Waldman SD: Injection technique for gluteal bursitis. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 549551.
Waldman SD: The gluteal bursa. In Waldman SD, editor: Pain review, Philadelphia, 2009, Saunders, pp 139140.
Chapter 90
LEVATOR ANI PAIN SYNDROME
attributed to other organ systems, leading to extensive evaluations and ineffective treatment. Patients with levator ani syndrome
exhibit a trigger point along the rectum or perineum (Figure 90-2).
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 pathophysiology of the myofascial trigger point remains elusive, although many
theories have been advanced. Common to all of these theories is
the thought 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 may occur as the result of repetitive 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 develops myofascial pain syndrome. Poor
posture while sitting at a computer keyboard or while watching
television also has been implicated as a predisposing factor to the
Trigger point
Referred pain
Levator ani m.
Figure 90-1 The levator ani muscle originates at the posterior surface of
the body of the pubis, the fascia of the obturator internus muscle, and
the ischial spine.
262
Figure 90-2 Patients with levator ani syndrome exhibit a trigger point
along the rectum or perineum. (From Waldman SD: Atlas of pain management injection techniques, 2nd ed, Philadelphia, 2007, Saunders, p 385.)
Testing
No specific test exists for levator ani pain syndrome. Testing
is aimed primarily at identifying occult pathological conditions
or other diseases that may mimic myofascial pain syndrome
(see discussion of differential diagnosis). Plain radiographs
help delineate bony abnormality of the pelvis and hip, including arthritis, avascular necrosis of the hip, fracture, congenital
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
pathological processes. Screening laboratory tests, consisting of
complete blood count, erythrocyte sedimentation rate, antinuclear antibody testing, and automated blood chemistry testing,
C
Figure 90-3 Crohns disease with enterorectal fistula. A, Small-bowel follow-through examination shows an enterorectal fistula (arrow). B, Computed 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.)
Differential Diagnosis
Levator ani pain syndrome is a clinical diagnosis of exclusion
supported by a combination of clinical history, physical examination, radiography, and MRI. Pain syndromes that may mimic
levator ani pain syndrome include lumbosacral radiculopathy and
plexopathy; stress fractures of the pelvis and hip; myofascial pain
syndromes such as gluteus medius pain syndrome; pelvic floor
muscle strain; inflammatory arthritis; and disorders of the lumbar
spinal cord, roots, plexus, and nerves. Intrapelvic tumors also may
mimic the clinical presentation of gluteus medius pain syndrome
(Figure 90-3).
Treatment
Levator ani pain syndrome is best treated with a multimodality
approach. Physical therapy, including correction of functional
abnormalities (e.g., poor posture, improper chair or computer
height) and use of heat modalities and deep sedative massage,
combined with nonsteroidal anti-inflammatory drugs (NSAIDs)
and skeletal muscle relaxants is a reasonable starting point. If these
treatments fail to provide rapid symptomatic relief, local trigger
point injection of local anesthetic and steroid into the myofascial trigger point area is a reasonable next step. Underlying diffuse
muscle pain, sleep disturbance, and depression are best treated
with a tricyclic antidepressant compound, such as nortriptyline,
which can be started at a single bedtime dose of 25 mg.
When performing trigger point injections, careful preparation
of the patient before trigger point injection helps optimize results.
Trigger point injections are directed at the primary trigger point,
rather than in the area of referred pain. It should be explained
to the patient that the goal of trigger point injection is to block
the trigger of the persistent pain and, it is hoped, provide longlasting 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
use of the prone or lateral position when identifying and marking
trigger points and when performing the actual trigger point injection helps decrease the incidence of vasovagal reactions. The skin
overlying the trigger point to be injected always should be prepared with antiseptic solution before injection to avoid infection.
well versed in the regional anatomy and experienced in performing interventional pain management techniques. Many patients
also report a transient increase in pain after injection of trigger
points. If long needles are used, damage to the retroperitoneal
organs also may occur.
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 technique to avoid infection and universal precautions
to avoid risk to the operator. Most side effects of trigger
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
pressure is placed on the injection site immediately after
trigger point injection. 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 trigger points in proximity to the
underlying pleural space. The antidepressant compounds
represent the primary pharmacological treatment for
myofascial pain syndrome. Tricyclic antidepressants are
thought to be more effective than selective serotonin reuptake inhibitors in the treatment of this painful condition.
The precise mechanism of action of the antidepressant
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 who have myofascial pain syndrome. Drugs such as amitriptyline and
nortriptyline 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.
SUGGESTED READINGS
Arnold LM: The pathophysiology, diagnosis and treatment of fibromyalgia,
Psychiatr Clin North Am 33:375408, 2010.
Bradley LA: Pathophysiology of fibromyalgia, Am J Med 122(Suppl 1):S22S30,
2009.
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
the human female levator ani muscle, Am J Obstet Gynecol 199:686.e1686.e6,
2008.
Singh K, Reid WMN, Berger LA: Magnetic resonance imaging of normal levator
ani anatomy and function, Obstet Gynecol 99:433438, 2002.
Chapter 91
AVASCULAR NECROSIS OF THE HIP
ICD-9 CODE 733.40
ICD-10 CODE M87.00
The Clinical Syndrome
Avascular necrosis of the hip is an often missed diagnosis. It is
also known as osteonecrosis. Similar to the scaphoid, the hip is
extremely susceptible to this disease because of its tenuous blood
supply. The blood supply of the hip is easily disrupted, often leaving the proximal portion of the bone without nutrition, thereby
leading to osteonecrosis. Avascular necrosis of the hip is a disease
of the fourth and fifth decades of life and is more common in
men, with an 8:1 male-to-female preponderance (Figure 91-1),
except for patients with avascular necrosis of the hip secondary to
Pregnancy
Radiation therapy
265
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.)
Testing
Plain radiographs are indicated in all patients with avascular
necrosis of the hip to rule out underlying occult bony pathological
processes and identify sclerosis and fragmentation of the femoral
head, although early in the course of the disease, plain radiographs are unreliable. Based on the patients clinical presentation,
additional tests, including complete blood cell count, uric acid,
Treatment
Clinical Pearls
B
Figure 91-3 Osteonecrosis of the left hip with subchondral osseous collapse and osteoarthritis. A, Coronal T1-weighted magnetic resonance
imaging. Decreased marrow signal intensity is identified within the
superior lateral aspect of the left femoral head and the adjacent lateral
aspect of the acetabulum. Lateral subluxation of the femoral head also is
present. B, Coronal fat-saturated T2-weighted image. Flattening of the
articular surface of the superior lateral portion of the left femoral head
is evident, indicating subchondral osseous collapse. Increased marrow
signal intensity involving the lateral acetabulum and the proximal femur
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.)
Differential Diagnosis
Coexistent arthritis and gout of the hip joints, bursitis, and tendinitis may coexist with avascular necrosis of the hips and exacerbate the pain and disability of the patient. Tears of the labrum,
ligament tears, bone cysts, bone contusions, bone fractures, and
SUGGESTED READINGS
Israelite CL, Garino JP: Osteonecrosis of the hip, Semin Arthroplasty 16:2732,
2005.
Malizos KN, Karantanas AH, Varitimidis SE, etal: Osteonecrosis of the femoral
head: etiology, imaging and treatment, Eur J Radiol 63:1628, 2007.
Waldman SD: Osteonecrosis of the hip. In Waldman SD, Campbell RSD, editors:
Imaging of pain, Philadelphia, 2011, Saunders, pp 339341.
Zibis AH, Karantanas AH, Roidis NT, etal: The role of MR imaging in staging
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
nerve. These motor and sensory changes are limited to the distribution of the femoral nerve below the inguinal ligament. Ilioinguinal and genitofemoral neuropathy also can be confused with
psoas bursitis. Lumbar radiculopathy and these nerve entrapments
may coexist as the double crush syndrome. The pain of psoas
bursitis also may cause alteration of gait, which may result in secondary back and radicular symptoms that may coexist with this
entrapment neuropathy.
Testing
Plain radiographs of the hip may reveal calcification of the bursa
and associated structures consistent with chronic inflammation
(Figure 92-2). Magnetic resonance imaging (MRI) is indicated
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 antinuclear antibody testing, are indicated if collagen-vascular disease
is suspected. Injection of the psoas bursa with a local anesthetic
and steroid serves as a diagnostic maneuver and a therapeutic
maneuver.
Treatment
Initial treatment of the pain and functional disability associated
with psoas bursitis should include a combination of nonsteroidal anti-inflammatory 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 syndrome should be avoided. For patients who do
not respond to these treatment modalities, injection of the psoas
bursa with a local anesthetic and steroid may be a reasonable
next step.
Differential Diagnosis
Psoas bursitis is often misdiagnosed as an inguinal hernia or
attributed to a primary hip pathological process. Radiographs of
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,
motor, and sensory changes, whereas patients with psoas bursitis have only secondary back pain as a result of altered gait and
no neurological changes. Femoral diabetic neuropathy sometimes
may be confused with psoas bursitis, but can be distinguished by
the presence of motor and sensory changes involving the femoral
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.)
Clinical Pearls
It is important to rule out other causes of groin pain, including inguinal hernia and entrapment neuropathies of the
ilioinguinal, genitofemoral, and femoral nerves. Injection
of the psoas bursa is extremely effective in the treatment of
psoas bursitis. Special care must be taken to avoid trauma
to the femoral nerve.
The use of physical modalities, including local heat and
gentle stretching exercises, should be introduced several
days after the patient undergoes this injection technique.
Vigorous exercises should be avoided because they would
exacerbate the symptoms. Simple analgesics, NSAIDs, and
antimyotonic agents such as tizanidine may be used concurrently with injection of the bursa.
SUGGESTED READINGS
Ilizaliturri VM Jr, Camacho-Galindo J, Evia Ramirez AN, etal: Soft tissue pathology around the hip, Clin Sports Med 30:391415, 2011.
Patel K, Wallace R, Busconi BD: Radiology, Clin Sports Med 30:239283, 2011.
Valeriano-Marcet J, Carter JD, Vasey FB: Soft tissue disease, Rheum Dis Clin
North Am 29:7788, 2003.
Waldman SD: Injection technique for psoas bursitis. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 551552.
Chapter 93
FEMORAL NEUROPATHY
Differential Diagnosis
It is difficult to separate femoral neuropathy from an L4 radiculopathy on purely clinical grounds. Subtle differences may exist because
the L4 radiculopathy may manifest with sensory changes into the
foot and weakness of the dorsiflexors of the foot. Intrapelvic or retroperitoneal tumor or hematoma may compress the lumbar plexus
and mimic the clinical presentation of femoral neuropathy.
Treatment
Mild cases of femoral neuropathy usually respond to conservative therapy, and surgery should be reserved for more severe cases.
Femoral
nerve
Inguinal
ligament
Quadriceps
muscles
Testing
Electromyography can help identify the exact source of neurological 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
antibody testing, may be indicated. Magnetic resonance imaging
Figure 93-1 Patients with femoral neuropathy present with pain that
radiates into the anterior thigh and medial calf.
271
Initial treatment of femoral neuropathy should consist of treatment with simple analgesics, nonsteroidal anti-inflammatory
drugs (NSAIDs), or cyclooxygenase-2 (COX-2) inhibitors and
avoidance of repetitive activities that exacerbate the symptoms.
If diabetes is thought to be the cause of the patients femoral
neuropathy, tight control of blood glucose levels is mandatory.
Avoidance of repetitive activities thought to be responsible for the
exacerbation of femoral neuropathy (e.g., repetitive hip extension
and flexion) also helps ameliorate the symptoms. If the patient
fails to respond to these conservative measures, a next reasonable
step is injection of the femoral nerve with a local anesthetic and
steroid.
Clinical Pearls
Figure 93-2 Amyotrophy of the left quadriceps femoris. (From Jellad A,
Boudokhane S, Ezzine S, etal: Femoral neuropathy caused by compressive
iliopsoas hydatid cyst: a case report and review of the literature, Joint Bone
Spine 77:371372, 2010.)
SUGGESTED READINGS
Figure 93-3 T2-Weighted coronal magnetic resonance imaging showing the hematoma as an area of increased signal intensity in the muscle belly (arrowhead). Fascial edema/hemorrhage is depicted as linear
hyperintensity. An ill-defined area of high signal intensity can be seen
at the distal myotendinous junction of the left psoasiliacus complex,
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.)
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 retroperitoneal hemorrhage: case series and review of the literature, Ann Vasc Surg
20:536540, 2006.
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
Testing
Electromyography can help identify the exact source of neurological dysfunction and clarify the differential diagnosis and should
be the starting point of the evaluation of all patients suspected
to have saphenous neuralgia. Plain radiographs of the spine, hip,
pelvis, and femur are indicated in all patients who present with
saphenous neuralgia to rule out occult bony pathological processes. 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 spine, pelvis,
and proximal lower extremity is indicated if tumor or hematoma
is suspected. Injection of the saphenous nerve with a local anesthetic and steroid as it exits Hunters canal serves as a diagnostic
and therapeutic maneuver.
Differential Diagnosis
It is difficult to separate saphenous neuralgia from a lumbar radiculopathy on purely clinical grounds, and electromyography is
strongly recommended. Electromyography and nerve conduction
testing also help rule out the presence of peripheral neuropathy.
Intrapelvic or retroperitoneal tumor or hematoma may compress
the lumbar plexus and mimic the clinical presentation of saphenous neuralgia.
Treatment
Mild cases of saphenous neuralgia usually respond to conservative
therapy, and surgery should be reserved for more severe cases. Initial treatment of saphenous neuralgia should consist of treatment
with simple analgesics, nonsteroidal anti-inflammatory drugs
(NSAIDs), or cyclooxygenase-2 (COX-2) inhibitors and avoidance of repetitive activities that exacerbate the symptoms. If diabetes is thought to be the cause of the patients saphenous neuralgia,
tight control of blood glucose levels is mandatory. Avoidance of
repetitive activities thought to be responsible for the exacerbation
of saphenous neuralgia helps ameliorate the symptoms. The use
of gabapentin or a tricyclic antidepressant such as nortriptyline
as an adjuvant analgesic also may help ameliorate the symptoms
of saphenous neuralgia. If the patient fails to respond to these
conservative measures, a next reasonable step is injection of the
saphenous nerve with a local anesthetic and steroid. Ultrasound
guidance may be useful in patients in whom anatomical landmarks are difficult to identify (Figure 94-3).
Sartorius
Gracilis
SSV
GSV
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.)
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.
Local anesthetic
Anterior
Posterior
Sartorius muscle
A
Vastus medialis
muscle
Needle
tip
Femoral
artery
Subsartorial plexus
Anterior
Posterior
Sartorius muscle
Subsartorial
plexus
B
Vastus medialis
muscle
Local
anesthetic
Femoral
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.)
Clinical Pearls
Saphenous neuralgia always should be differentiated from
lumbar plexopathy and radiculopathy of the nerve roots,
which may sometimes mimic saphenous nerve compression.
Lumbar radiculopathy and saphenous 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 saphenous nerve 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 later
may be attributed to the nerve block should be performed
on all patients before beginning saphenous nerve block,
especially in patients with clinical symptoms of diabetes or
clinically significant saphenous neuralgia.
SUGGESTED READINGS
Dayan V, Cura L, Cubas S, Carriquiry G: Surgical anatomy of the saphenous
nerve, Ann Thorac Surg 85:896900, 2008.
Iizuka M, Yao R, Wainapel S: Saphenous nerve injury following medial knee joint
injection: a case report, Arch Phys Med Rehabil 86:20622065, 2005.
Kalenak A: Saphenous nerve entrapment, Oper Tech Sports Med 4045, 1996.
Mountney J, Wilkinson GAL: Saphenous neuralgia after coronary artery bypass
grafting, Eur J Cardiothorac Surg 16:440443, 1999.
Waldman SD: Saphenous nerve block at the knee. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 573574.
Chapter 95
OBTURATOR NEURALGIA
Differential Diagnosis
It is sometimes difficult to separate obturator neuralgia from a
lumbar plexopathy or radiculopathy on purely clinical grounds,
and electromyography is strongly recommended. Electromyography and nerve conduction testing also help rule out the presence
of peripheral neuropathy. Intrapelvic or retroperitoneal tumor or
hematoma may compress the lumbar plexus and mimic the clinical presentation of obturator neuralgia (Figure 95-3).
Treatment
Mild cases of obturator neuralgia usually respond to conservative
therapy, and surgery should be reserved for more severe cases. Initial treatment of obturator neuralgia should consist of treatment
with simple analgesics, nonsteroidal anti-inflammatory drugs
(NSAIDs), or cyclooxygenase-2 (COX-2) inhibitors and avoidance
Obturator
nerve
Testing
Electromyography can help identify the exact source of neurological 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, pelvis, and proximal femur are indicated in all patients with obturator neuralgia to rule out occult bony pathology. 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 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 anesthetic and steroid serves as a diagnostic and therapeutic maneuver.
Figure 95-1 Patients with obturator neuralgia have pain that radiates
into the medial thigh and does not extend below the knee.
277
Sigmoid colon
Endometriosis tumor in
right obturator fossae
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.)
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 medulloblastoma, 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.)
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 examination 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.
SUGGESTED READINGS
Cardosi RJ, Cox CS, Hoffman MS: Postoperative neuropathies after major pelvic
surgery, Obstet Gynecol 100:240244, 2002.
Langebrekke A, Qvigstad E: Endometriosis entrapment of the obturator nerve
after previous cervical cancer surgery, Fertil Steril 91:622623, 2009.
Toth C: Peripheral nerve injuries attributable to sport and recreation, Phys Med
Rehabil Clin North Am 20:77100, 2009.
Toussaint CP, Perry EC III, Pisansky MT, Anderson DE: Whats new in the
diagnosis and treatment of peripheral nerve entrapment, Neuropath Neurol Clin
28:9791004, 2010.
Waldman SD: Obturator nerve block. In Waldman SD, editor: Pain review, Philadelphia, 2009, Saunders, pp 565566.
Chapter 96
ADDUCTOR TENDINITIS
hip joint, creating additional pain and functional disability. Neurological examination of the hip and lower extremity is normal,
unless there has been concomitant stretch injury to the plexus or
obturator nerve.
Testing
Plain radiographs are indicated in all patients with hip, thigh, and
groin 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 resonance imaging (MRI) and ultrasound imaging of
the hip and pelvis are indicated if aseptic necrosis or occult mass
is suspected and to help confirm the diagnosis. Radionucleotide
bone scanning should be considered if the possibility of occult
fracture of the pelvis is being considered. Electromyography can
help rule out compression neuropathy or trauma of the obturator
nerve and rule out plexopathy and radiculopathy. Injection of the
insertion of the adductor tendons serves as a diagnostic maneuver
and a therapeutic maneuver.
Adductor longus
Gracilis
Sartorius
Vastus medialis
Adductor magnus
Figure 96-1 The patient with adductor tendinitis reports pain on palpation of the origins of the adductor tendons. Active resisted adduction
and passive abduction reproduce the pain.
Tennis
ball
Figure 96-2 Patients with adductor tendinitis also exhibit a positive Waldman knee squeeze test for adductor tendinitis. A, The patient places a tennis 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.)
Differential Diagnosis
Internal derangement of the hip may mimic the clinical presentation of adductor tendinitis. Occasionally, indirect inguinal hernia
can produce pain that can be confused with adductor tendinitis. If
trauma has occurred, consideration of the possibility of occult pelvic fracture, especially in individuals with osteopenia or osteoporosis, should be entertained, and radionucleotide bone scanning
should be obtained. Avascular necrosis of the hip also may produce hip pain that can mimic the clinical presentation of adductor
tendinitis. Entrapment neuropathy or stretch injury to the ilioinguinal, genitofemoral, and obturator nerves and plexopathy and
radiculopathy should be considered if the physical finding of neurological deficit is identified in patients thought to have adductor
tendinitis, because all of these clinical entities may coexist.
Treatment
Initial treatment of the pain and functional disability associated with
adductor tendinitis should include a combination of nonsteroidal
Clinical Pearls
The proper use of exercise equipment can greatly reduce
the incidence of adductor tendinitis. Injection of the adductor tendons is extremely effective in the treatment of pain
secondary to the previously mentioned causes of hip pain.
Gentle injection technique decreases the incidence of traumatic rupture of the tendons owing to injection. Coexistent
bursitis and arthritis may contribute to hip pain and may
require additional treatment with a more localized injection
of a local anesthetic and depot steroid. 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 hip pain. Vigorous
exercises should be avoided because they would exacerbate
the symptoms. Simple analgesics and NSAIDs may be used
concurrently with this injection technique.
SUGGESTED READINGS
Jrvinen M, Orava S, Kujala UM: Groin pain (adductor syndrome), Oper Techn
Sports Med 5:133137, 1997.
Morelli V, Weaver V: Groin injuries and groin pain in athletes, part 1, Prim Care
32:163183, 2005.
Morelli V, Espinoza L: Groin injuries and groin pain in athletes, part 2, Prim Care
32:185200, 2005.
Noesberger B, Eichenberger AR: Overuse injuries of the hip and snapping hip
syndrome, Oper Techn Sports Med 5:138142, 1997.
Waldman SD: Adductor tendinitis. In Waldman SD, Campbell RSD, editors:
Imaging of pain, Philadelphia, 2011, Saunders, pp 355356.
Chapter 97
ILIOPECTINATE BURSITIS
the point at which the ilium and the pubis bone merge. The psoas
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
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 (Figure 97-1). The iliacus muscle is innervated by
the femoral nerve.
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
Testing
Plain radiographs of the hip may reveal calcification of the bursa
and associated structures consistent with chronic inflammation. Magnetic resonance imaging (MRI) is indicated if occult
mass or tumor of the hip or groin is suspected and help confirm
the diagnosis (Figure 97-2). The injection technique described
subsequently serves as a diagnostic maneuver and a therapeutic
maneuver.
Differential Diagnosis
Iliopectinate bursitis is often attributed to primary hip or groin
pathological conditions. Radiographs of the hip and pelvis combined with electromyography help distinguish iliopectinate bursitis from radiculopathy or plexopathy from pain emanating from
the hip. Most patients with a lumbar radiculopathy have back
pain associated with reflex, motor, and sensory changes, whereas
patients with iliopectinate bursitis have only secondary back pain
and no neurological changes. Ilioinguinal or genitofemoral neuralgia sometimes may be confused with iliopectinate bursitis,
but can be distinguished by the presence of motor and sensory
changes involving these nerves. Lumbar radiculopathy and ilioinguinal nerve entrapment may coexist as the double crush syndrome. The pain of iliopectinate bursitis may cause alteration of
gait, which may result in secondary back and radicular symptoms
that may coexist with less common forms of bursitis.
Treatment
Initial treatment of the pain and functional disability associated
with iliopectinate bursitis should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
(COX-2) inhibitors and physical therapy. Local application of
Psoas major m.
Femoral n.
Femoral a.
inflamed iliopectineal bursa
Psoas major m.
Femoral v.
Figure 97-2 Skeletal metastasis: Pelvisloss of supra-acetabular line.
Loss of the supra-acetabular line (arrow) on the right side confirms the
presence of an adjacent osteolytic lesion. Compare with the opposite
uninvolved hip. (From Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia, 2002, Saunders, p 4299.)
Figure 97-3 Injection technique to relieve the pain resulting from iliopectinate bursitis. (From Waldman SD: Atlas of pain management injection techniques, 2nd ed, Philadelphia, 2007, Saunders, p 359.)
Clinical Pearls
This injection technique is extremely effective in the treatment of iliopectinate bursitis. The 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 techniques to avoid infection and universal
precautions to avoid risk to the operator. Most side effects
of this injection technique 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 injection. The avoidance of overly long needles
helps decrease the incidence of trauma to underlying structures. Special care must be taken to avoid trauma to the
sciatic nerve.
The use of physical modalities, including local heat and
gentle stretching exercises, should be introduced several
days after the patient undergoes this injection technique.
Vigorous exercises should be avoided because they would
exacerbate the symptoms. Simple analgesics, NSAIDs, and
antimyotonic agents such as tizanidine may be used concurrently with this injection technique.
SUGGESTED READINGS
Morelli V, Weaver V: Groin injuries and groin pain in athletes, part 1, Prim Care
32:163183, 2005.
Morelli V, Espinoza L: Groin injuries and groin pain in athletes, part 2, Prim Care
32:185200, 2005.
Noesberger B, Eichenberger AR: Overuse injuries of the hip and snapping hip
syndrome, Oper Techn Sports Med 51385142, 1997.
Waldman SD: Injection technique for iliopectineal bursitis. In Waldman SD,
editor: Pain review, Philadelphia, 2009, Saunders, pp 553554.
Chapter 98
SNAPPING HIP SYNDROME
Testing
Plain radiographs are indicated in all patients with pain thought
to be emanating from the hip to rule out occult bony pathological processes and tumor. Based on the patients clinical presentation, additional tests may be indicated, including complete blood
count, prostate-specific antigen, erythrocyte sedimentation rate,
and antinuclear antibody testing. Magnetic resonance imaging
(MRI) and ultrasound imaging of the affected hip are indicated
286
Differential Diagnosis
Snapping hip syndrome frequently coexists with trochanteric
bursitis and arthritis of the hip, which may require specific treatment to provide palliation of pain and return of function. Occasionally, snapping hip syndrome can be confused with meralgia
paresthetica because both manifest with pain in the lateral thigh.
The two syndromes can be distinguished by the fact that patients
with meralgia paresthetica do not have any of the previously mentioned physical findings associated with snapping hip syndrome
and have decreased sensation in the distribution of the lateral femoral cutaneous nerve (Figure 98-6). Electromyography helps sort
out confusing clinical presentations. The clinician must consider
the potential for primary or secondary tumors of the hip in the
differential diagnosis of snapping hip syndrome.
Treatment
A short course of conservative therapy consisting of simple analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), or
cyclooxygenase-2 (COX-2) inhibitors is a reasonable first step
in the treatment of patients with snapping hip syndrome. The
patient should be instructed to avoid repetitive activity that may
be responsible for the development of snapping hip syndrome,
such as running on sand. If the patient does not experience rapid
improvement, the following injection technique is a reasonable
next step.
The patient is placed in the lateral decubitus position with
the affected side up. The midpoint of the greater trochanter is
identified. Proper preparation with antiseptic solution of the skin
overlying this point is carried out. A syringe containing 2 mL of
0.25% preservative-free bupivacaine and 40 mg of methylprednisolone is attached to a 25-gauge, 312-inch needle.
Before needle placement, the patient should be advised to
say There! as soon as a paresthesia into the lower extremity
is felt, indicating that the needle has impinged on the sciatic
nerve. If a paresthesia occurs, the needle should be withdrawn
immediately and repositioned more laterally. The needle is
advanced carefully through the previously identified point at a
right angle to the skin, directly toward the center of the greater
trochanter. The needle is advanced slowly to avoid trauma to
the sciatic nerve until it hits the bone (Figure 98-7). The needle
is withdrawn out of the periosteum, and after careful aspiration
for blood and, if no paresthesia is present, the contents of the
Iliopsoas m.
Gluteus medius m.
Tensor fasciae
latae m.
Deep trochanteric
bursa
Superficial
trochanteric
bursa
Iliotibial tract
Iliopsoas bursa
Inflamed superficial
trochanteric bursa
Gluteus medius m.
Tensor fasciae
latae m.
Iliotibial tract
Superficial
trochanteric
bursa
Figure 98-1 The snapping sensation and pain are the result of the iliopsoas tendon subluxing over the greater trochanter or iliopectinate eminence.
Gluteus medius
muscle
Gluteus maximus
muscle
Trochanteric bursa
Greater trochanter
Gluteus
medius m
Piriformis m & t
Coccygeus m
Sciatic n
Ischium, spine
Sup gemellus m
Obturator internus
m&t
Iliotibial tract
Greater trochanter
Inf gemellus m
Ischium
Semimembranosus t
Vastus lateralis m
Quadratus femoris m
Sciatic n
Gluteus minimus m
Gluteus medius m
Iliotibial tract
Greater trochanter
Piriformis m
Sciatic n
Ischium, spine
Sup gemellus m
Inf gemellus m
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.)
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.)
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, Philadelphia, 2006, Saunders, p 316.)
Lat. femoral
cutaneous n.
Greater trochanter
Inguinal ligament
Iliotibial band
Clinical Pearls
Snapping hip syndrome frequently coexists with trochanteric bursitis and arthritis of the hip, which may require
specific treatment to provide palliation of pain and return
of function. This injection technique is extremely effective
in the treatment of snapping hip syndrome. It is a safe procedure if careful attention is paid to the clinically relevant
anatomy in the areas to be injected. Most side effects of this
injection technique are related to needle-induced trauma to
the injection site and underlying tissues. Special care must
be taken to avoid trauma to the sciatic nerve.
The use of physical modalities, including local heat and
gentle stretching exercises, should be introduced several
days after the patient undergoes this injection technique.
Vigorous exercises should be avoided because they would
exacerbate the symptoms. Simple analgesics, NSAIDs, and
antimyotonic agents may be used concurrently with this
injection technique.
Figure 98-7 Injection technique to relieve the pain of snapping hip syndrome. (From Waldman SD: Atlas of pain management injection techniques, 2nd ed, Philadelphia, 2007, Saunders, p 368.)
SUGGESTED READINGS
Allen WC, Cope R: Coxa saltans: the snapping hip revisited, J Am Acad Orthop
Surg 3:303308, 1995.
Byrd WT: Snapping hip, Oper Techn Sports Med 13:4654, 2005.
Fery A, Sommelet J: The snapping hip: late results of 24 surgical cases, Int Orthop
12:277282, 1988.
Ilizaliturri VM Jr, Camacho-Galindo J, Ramirez ANE, Lizette Y, etal: Soft tissue
pathology around the hip, Clin Sports Med 30:391415, 2011.
Waldman SD: Snapping hip. In Waldman SD, Campbell RSD, editors: Imaging
of pain, Philadelphia, 2011, Saunders, pp 365366.
Chapter 99
TIBIOFIBULAR PAIN SYNDROME
ICD-9 CODE 715.96
ICD-10 CODE M17.9
The Clinical Syndrome
Tibiofibular joint pain is most often the result of arthritis of
the joint. Osteoarthritis of the joint is the most common form
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 arthritisinduced tibiofibular pain include collagen-vascular diseases,
infection, villonodular synovitis, and Lyme disease. In addition
to arthritis, the tibiofibular joint is susceptible to the development of tendinitis, bursitis, and disruption of the ligaments, cartilage, 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 tibiofibular 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.
Testing
Plain radiographs of the knee are indicated in all patients with
tibiofibular joint pain. Based on the patients clinical presentation,
additional tests, including complete blood cell count, erythrocyte
Posterior knee
Osteoarthritis of
tibiofibular joint
Fibula
Tibia
291
sedimentation rate, and antinuclear antibody testing, may be indicated. Magnetic resonance imaging (MRI) of the tibiofibular joint
is indicated if aseptic necrosis or occult mass or tumor is suspected
and to help confirm the diagnosis. Bone scan may be useful to
identify occult stress fractures involving the joint, especially if
trauma has occurred.
Differential Diagnosis
The tibiofibular joint is susceptible to the development of arthritis from a variety of conditions that have in common the ability
to damage the joint cartilage. Acute infectious arthritis usually is
accompanied by significant systemic symptoms, including fever
and malaise, and should be easily recognized by an astute clinician and treated appropriately with culture and antibiotics, rather
than with injection therapy. The collagen-vascular diseases generally manifest as a polyarthropathy rather than a monarthropathy
limited to the tibiofibular joint, although tibiofibular pain secondary to collagen-vascular disease responds well to the intra-articular
injection technique described subsequently. Lumbar radiculopathy may mimic the pain and disability associated with arthritis of
the tibiofibular joint. In patients with lumbar radiculopathy, the
knee examination should be negative. Entrapment neuropathies,
such as meralgia paresthetica, and bursitis of the knee also may
confuse the diagnosis; both may coexist with arthritis of the tibiofibular joint. Primary and metastatic tumors of the femur and
spine also may manifest clinically in a manner analogous to arthritis of the knee.
Treatment
Initial treatment of the pain and functional disability associated with arthritis of the knee should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy.
Local application of heat and cold may be beneficial. For
patients who do not respond to these treatment modalities, an
intra-articular injection of a local anesthetic and steroid may be
a reasonable next step.
Clinical Pearls
Coexistent bursitis and tendinitis may contribute to tibiofibular pain and may require additional treatment with
more localized injection of a local anesthetic and depot steroid. Injection of the tibiofibular joint is extremely effective
in the treatment of pain secondary to the previously mentioned causes of arthritis of the knee joint. 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 use of
physical modalities, including local heat and gentle rangeof-motion exercises, should be introduced several days after
the patient undergoes this injection technique for knee
pain. Vigorous exercises should be avoided because they
would exacerbate the symptoms.
SUGGESTED READINGS
Bozkurt M, Ylmaz E, Akseki D, Havtcolu H: Gnal : The evaluation of
the proximal tibiofibular joint for patients with lateral knee pain, Knee 11:
307312, 2004.
ztuna V, Yldz A, zer C, etal: Involvement of the proximal tibiofibular joint
in osteoarthritis of the knee, Knee 10:347349, 2003.
Rethnam U, Sinha A: Instability of the proximal tibiofibular joint, an unusual
cause for knee pain, Injury Extra 37:190192, 2006.
Waldman SD: Arthritis pain of the knee. In Waldman SD, editor: Pain review,
Philadelphia, 2009, Saunders, p 316.
Waldman SD: Functional anatomy of the knee. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 144149.
Chapter 100
JUMPERS KNEE
Testing
Plain radiographs are indicated in all patients with knee pain.
Based on the patients clinical presentation, additional tests may
be indicated, including complete blood count, erythrocyte sedimentation rate, and antinuclear antibody testing. Magnetic resonance imaging (MRI) and ultrasound imaging of the knee are
indicated if jumpers knee is suspected, because they readily show
the tendinosis of the quadriceps or patellar tendons responsible
for this common pain syndrome (Figure 100-3). Bone scan may
be useful to identify occult stress fractures involving the joint,
especially if trauma has occurred.
Differential Diagnosis
The most common cause of anterior knee pain is arthritis of the
knee; this should be readily identifiable on plain radiographs of
the knee and may coexist with jumpers knee. Another common cause of anterior knee pain that may mimic or coexist with
jumpers knee is suprapatellar or superficial and deep patellar
bursitis. Internal derangement of the knee or torn medial meniscus also may confuse the clinical diagnosis, but should be readily
identifiable on MRI of the knee.
Treatment
Initial treatment of the pain and functional disability associated with
jumpers knee should include a combination of nonsteroidal antiinflammatory 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, injection of the suprapatellar and infrapatellar space
with a local anesthetic and steroid may be a reasonable next step.
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 steroid 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 technique to avoid infection; universal precautions should be
used 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 this injection technique for tibiofibular pain. Vigorous exercises should be
avoided because they would exacerbate the symptoms. Simple analgesics and NSAIDs may be used concurrently with
this injection technique.
SUGGESTED READINGS
Figure 100-3 Chronic patellar tendinosis. Sagittal intermediateweighted (TR/TE, 2200/30) (A) and T2-weighted (TR/TE, 2200/80) (B)
spin echo magnetic resonance imaging show marked thickening of the
entire patellar tendon, more pronounced in the middle and distal segments, and indistinctness of the anterior margin of the tendon. (From
Resnick D, editor: Diagnosis of bone and joint disorders, 4th ed, Philadelphia,
2002, Saunders, p 3236.)
Chapter 101
SEMIMEMBRANOSUS INSERTION
SYNDROME
Semimembranosus
m&t
Vastus medialis
m
Med sup
genicular a
Adductor magnus t
Med femoral
condyle
Med patellar
retinaculum
Semitendinosus t
Gracilis t
Sartorius t
Greater
saphenous v
Gastrocnemius m,
med head
Figure 101-1 Anatomy of the knee joint. a, Artery; m, muscle; n, nerve; t, tendon; v, vein. (From Kang HS, Ahn JM, Resnick D, editors: MRI of the
extremities, 2nd ed, Philadelphia, 2002, Saunders, p 325.)
296
Semimembranosus
Femur
Tibia
Fibula
Figure 101-2 Direct trauma to the posterior knee by kicks or tackles may cause semimembranosus insertion syndrome to develop. Semimembranosus 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.)
Differential Diagnosis
Testing
Plain radiographs are indicated in all patients with pain thought
to be emanating from semimembranosus insertion syndrome to
rule out occult bony pathology, including tibial plateau fractures
and tumor. Based on the patients clinical presentation, additional tests may be indicated, including complete blood count,
prostate-specific antigen, sedimentation rate, and antinuclear
antibody testing. Magnetic resonance imaging (MRI) of the knee
is indicated if internal derangement, occult mass, or tumor is suspected as well as to confirm the diagnosis of semimembranosus
insertion syndrome (Figure 101-4). Radionucleotide bone scanning may be useful to rule out stress fractures not seen on plain
radiographs. Injection of the semimembranosus insertions with
local anesthetic and steroid may serve as a diagnostic and therapeutic maneuver.
Treatment
Initial treatment of the pain and functional disability associated with semimembranosus insertion syndrome should
include a combination of nonsteroidal anti-inflammatory
drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and
physical therapy. Local application of heat and cold may be
beneficial. For patients who do not respond to these treatment
modalities, the injection of the semimembranosus insertion
with a local anesthetic and steroid may be a reasonable next
step.
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 complete 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 semimembranosus (arrows). (From House CV, Connell DA, Saifuddin A: Posteromedial corner injuries of the knee, Clin Radiol 62:539546, 2007.)
Clinical Pearls
The proper use of exercise equipment can greatly reduce
the incidence of semimembranosus insertion syndrome.
Injection of the semimembranosus tendon insertion is
extremely effective in the treatment of pain secondary to
the previously mentioned causes of knee pain. Gentle injection technique decreases the incidence of traumatic rupture
of the tendons as a result of injection. Coexistent bursitis
and arthritis also may contribute to knee pain and may
require additional treatment with a more localized injection
of a local anesthetic and depot steroid. 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 knee pain. Vigorous
exercises should be avoided because they would exacerbate
the symptoms. Simple analgesics and NSAIDs may be used
concurrently with this injection technique.
SUGGESTED READINGS
Bencardino JT, Rosenber ZS, Brown RR, et al: Traumatic musculotendinous
injuries of the knee: diagnosis with MR imaging, Radiographics 20:S103S120,
2000.
Chan KK, Resnick D, Goodwin D, et al: Posteromedial tibial plateau injury
including avulsion fracture of the semimembranosus tendon insertion site:
ancillary sign of anterior cruciate ligament tear at MR imaging, Radiology
211:754758, 1999.
El-Dieb A, Yu JS, Huang G-S, Farooki S: Pathologic conditions of the ligaments
and tendons of the knee, Radiol Clin North Am 40:10611079, 2002.
House CV, Connell DA, Saifuddin A: Posteromedial corner injuries of the knee,
Clin Radiol 62:539546, 2007.
Waldman SD: Functional anatomy of the knee. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 144149.
Chapter 102
CORONARY LIGAMENT STRAIN
of the knee, makes the pain worse (Figure 102-1); rest and heat
provide some relief. The pain is constant and characterized as aching; it may interfere with sleep. Coexistent bursitis, tendinitis,
arthritis, or internal derangement of the knee, in particular of the
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
Testing
Plain radiographs are indicated in all patients with coronary ligament syndrome 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 resonance imaging (MRI) of the knee is indicated
to quantify the extent of internal derangement of the knee and to
rule out occult mass or tumor. Bone scan may be useful to identify
occult stress fractures involving the joint, especially if significant
trauma has occurred. Arthroscopy may ultimately be required as a
diagnostic and therapeutic maneuver.
Differential Diagnosis
The most common cause of medial knee pain is degenerative
arthritis of the knee. Other pathological processes may mimic
the pain and functional disability of coronary ligament strain.
Lumbar radiculopathy may cause pain and disability similar to
that of coronary ligament strain. In such patients, back pain is
usually present, and the knee examination should be negative.
Entrapment neuropathies of the lower extremity, such as femoral
neuropathy, and bursitis of the knee also may confuse the diagnosis; both of these conditions may coexist with coronary ligament
strain. Primary and metastatic tumors of the femur and spine also
may manifest in a manner analogous to coronary ligament strain.
Clinical Pearls
Coexistent bursitis and tendinitis may contribute to knee
pain and may require additional treatment with more localized injection of a local anesthetic and depot steroid. Injection of the coronary ligament is extremely effective in the
treatment of pain secondary to coronary ligament strain.
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 technique for knee pain. Vigorous exercises should be avoided
because they would exacerbate the patients symptoms.
Treatment
Initial treatment of the pain and functional disability associated with coronary ligament strain should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local
application of heat and cold may be beneficial. For patients who
do not respond to these treatment modalities, injection of the
coronary ligament with a local anesthetic and steroid may be a
reasonable next step.
SUGGESTED READINGS
Colletti JE, Kilgore KP, Derrick J: Traumatic knee pain, Ann Emerg Med
53(403):409, 2009.
El-Khoury GY, Usta HY, Berger RA: Meniscotibial (coronary) ligament tears, Skelet Radiol 11:191196, 1984.
Lougher L, Southgate CRW, Holt MD: Coronary ligament rupture as a cause of
medial knee pain, Arthroscopy 19:e157e158, 2003.
Parvizi J, Kim GK: Knee ligament injuries, In Parvizi J (ed) High yield orthopaedics,
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
Lat patellar
retinaculum
Med patellar
retinaculum
Vastus lateralis t
Lat femoral
condyle
Iliotibial tract
Med femoral
condyle
Common
peroneal n
Gracilis t
Semimembranosus t
Semitendinosus t
Lat sural
cutaneous n
Oblique popliteal
Tibial n
lig and joint capsule
Popliteal
a and v
Gastrocnemius
m and t, med head
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
Figure 1033 The valgus stress test for medial collateral ligament integrity. (From Waldman SD: Physical diagnosis of pain: an atlas of signs and
symptoms, 2nd ed, Philadelphia, 2006, Saunders, p 291.)
Testing
MRI is indicated in all patients with medial collateral ligament
pain, particularly if internal derangement or occult mass or tumor
is suspected. In addition, MRI should be performed in all patients
Treatment
Initial treatment of the pain and functional disability associated
with injury to the medial collateral ligament includes a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy.
The local application of heat and cold may also be beneficial.
withdrawn slightly until the injection can proceed without significant resistance. The needle is then removed, and a sterile pressure
dressing and ice pack are applied to the injection site.
Lt.
fem
tib
fem
Clinical Pearls
tib
B
Figure 1034 A, Grade 2 tear of the medial collateral ligament with
an interrupted superficial part of tibial collateral ligament (arrow). B,
A normal contralateral MCL. Fem, Femoral; Lt, left; m, meniscus; tib, tibial.
(From Wakefield SD, DAgostino MA: Essential application of musculoskeletal ultrasound in rheumatology, Philadelphia, 2010, Saunders, p 271.)
SUGGESTED READINGS
Beall DP, Googe JD, Moss JT, etal: Magnetic resonance imaging of the collateral ligaments and the anatomic quadrants of the knee, Radiol Clin North Am
45:9831002, 2007.
Jones L, Bismil Q, Alyas F, Connell D, Bell J: Persistent symptoms following nonoperative management in low grade MCL injury of the knee: the role of the
deep MCL, Knee 16:6468, 2009.
Kastelein M, Wagemakers HPA, Luijsterburg PAJ, et al: Assessing medial collateral ligament knee lesions in general practice, Am J Med 121:982988, 2008.
Kennedy JC, Hawkins R, Krissoff WB: Orthopaedic manifestations of swimming,
Am J Sports Med 6:309322, 1978.
Malone WJ, Verde F, Weiss D, Fanelli GC: MR imaging of knee instability, MRI
Clin North Am 17:61026724, 2009.
Stulberg SD, Shulman K, Stuart S, etal: Breaststrokers knee: pathology, etiology,
and treatment, Am J Sports Med 8:164171, 1980.
Vizsolyi P: Breaststrokers knee: an analysis of epidemiological and biomechanical
factors, Am J Sports Med 15:6371, 1987.
Waldman SD: Atlas of pain management injection techniques, Philadelphia, 2007,
Saunders, pp 434436.
Chapter 104
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
Rectus femoris m.
Vastus medialis m.
Vastus
lateralis m.
Testing
Plain radiographs of the knee are indicated in all patients with
quadriceps expansion syndrome 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 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.
Differential Diagnosis
Anterior knee pain most commonly is due to arthritis of the knee;
this should be readily identifiable on plain radiographs of the knee
and may coexist with quadriceps expansion syndrome. Another
common cause of anterior knee pain that may mimic or coexist
with quadriceps expansion syndrome is suprapatellar or prepatellar 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.
Treatment
Initial treatment of the pain and functional disability associated
with quadriceps expansion syndrome should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local
application of heat and cold may be beneficial. For patients who
do not respond to these treatment modalities, injection of the
quadriceps expansion with a local anesthetic and steroid may be a
reasonable next step.
To inject the quadriceps expansion, the patient is placed in the
supine position with a rolled blanket underneath the knee to flex
the joint gently. The skin overlying the medial aspect of the knee
joint is prepared with antiseptic solution. A sterile syringe containing 2 mL of 0.25% preservative-free bupivacaine and 40 mg
of methylprednisolone is attached to a 25-gauge, 112-inch needle
using strict aseptic technique. With strict aseptic technique, the
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
of the patella. The needle is withdrawn slightly out of the periosteum of the patella, and the contents of the syringe are gently
injected. There should be little resistance to injection. If resistance
is encountered, the needle is probably in a ligament or tendon
and should be advanced or withdrawn slightly until the injection
proceeds without significant resistance. The needle is removed,
and a sterile pressure dressing and ice pack are placed at the injection site.
Figure 104-2 Injection technique to relieve pain secondary to quadriceps expansion syndrome. (From Waldman SD: Atlas of pain management
injection techniques, Philadelphia, 2000, Saunders, p 266.)
Clinical Pearls
This injection technique is extremely effective in the treatment of pain secondary to the causes of quadriceps extension
syndrome mentioned earlier. 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 a local anesthetic
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 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 tibiofibular 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.
SUGGESTED READINGS
Greenhill BJ: The importance of the medial quadriceps expansion in medial ligament injury, Can J Surg 10:312317, 1967.
Heng RC, Haw CS: Patello-femoral pain syndrome: diagnosis and management
from an anatomical and biomechanical perspective, Curr Orthop 10:256266,
1996.
Waldman SD: Quadriceps expansion syndrome. In Waldman SD, editor: Atlas
of pain management injection techniques, Philadelphia, 2013, Saunders, p 364.
Waldman SD: Functional anatomy of the knee. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 144149.
Chapter 105
RUNNERS KNEE
Differential Diagnosis
The most common cause of lateral knee pain is degenerative arthritis
of the knee. Other pathological processes may mimic the pain and
functional disability of runners knee. Lumbar radiculopathy may
cause pain and disability similar to that of runners knee. In such
patients, back pain is usually present, and the knee examination
should be negative. Entrapment neuropathies of the lower extremity,
such as meralgia paresthetica, and bursitis of the knee also may confuse the diagnosis; both conditions may coexist with runners knee.
Primary and metastatic tumors of the femur and proximal tibia and
fibula may manifest in a manner analogous to runners knee.
Treatment
Initial treatment of the pain and functional disability associated
with runners knee should include a combination of nonsteroidal
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 resonance 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
radiculopathy, and plexopathy. Injection of the iliotibial band
at the friction point may serve as a diagnostic and therapeutic
maneuver.
308
Iliotibial band
Femur
Lateral
epicondyle
Clinical Pearls
Coexistent bursitis and tendinitis may contribute to knee
pain and may require additional treatment with more
localized injection of a local anesthetic and depot steroid.
Injection of the iliotibial band is extremely effective in the
treatment of pain secondary to runners knee. 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 technique
for knee pain. Vigorous exercises should be avoided because
they would exacerbate the patients symptoms.
Chapter 106
GLOMUS TUMOR OF THE KNEE
of the rarity of glomus tumor in areas other than the digits, diagnosis is often delayed.
Testing
Magnetic resonance imaging (MRI) of the affected area often
reveals the actual glomus tumor and may reveal erosion or a perforating lesion of the phalanx beneath the tumor. The tumor
appears as a very high and homogeneous signal on T2-weighted
images (Figures 106-1 and 106-2). The bony changes associated
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
with glomus tumor of the knee also may appear on plain radiographs if a careful comparison of the corresponding contralateral
knee is made. Radionuclide bone scan also may reveal localized
bony destruction. If the tumor is superficial, pain may be reproduced by placing an ice pack over the affected area. 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. Electromyography is indicated if coexistent plexopathy or radiculopathy
is suspected. Surgical exploration of the affected area bed often
is necessary to confirm the diagnosis. Ultimately arthroscopy or
arthrotomy may be required to ascertain the exact cause of the
patients persistent knee pain (Figure 106-3).
Differential Diagnosis
The triad of localized, intermittent, lancinating excruciating pain;
tenderness to palpation; and cold intolerance makes the diagnosis
apparent to an astute clinician. Glomus tumor of the knee must
be distinguished from other causes of localized knee pain. If a history of trauma is present, fracture, osteomyelitis, tenosynovitis,
and foreign body synovitis should be considered. If the patient
has no history of trauma, tumors and diseases of the glenohumoral
joint and associated soft tissues should be considered. Reflex sympathetic dystrophy should be distinguishable from glomus tumor
of the knee because the pain of reflex sympathetic dystrophy is
less localized and is associated with distal trophic skin and nail
changes and vasomotor and sudomotor abnormalities.
Treatment
The mainstay of treatment of glomus tumor is surgical removal.
Medication management is uniformly disappointing. Injection of
Figure 106-3 Arthroscopy showed the soft tissue mass beneath the plica
synovialis. (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.)
the affected area in the point of maximal tenderness may provide temporary relief of the pain of glomus tumor and blocks
the Posner cold induction test response, further strengthening the
diagnosis.
Clinical Pearls
The diagnosis of glomus tumor of the knee is usually
straightforward if the clinician identifies its unique clinical
presentation. Because of the rare potential for aggressive,
invasive behavior, complete excision and careful follow-up
are important.
SUGGESTED READINGS
Clark ML, OHara C, Dobson PJ, Smith AL: Glomus tumor and knee pain: a
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.
ztekin HH: Popliteal glomangioma mimicking Bakers cyst in a 9-year-old child:
an unusual location of a glomus tumor, Arthroscopy 19:e67e71, 2003.
Waseem M, Jari S, Paton RW: Glomus tumour, a rare cause of knee pain: a case
report, Knee 9:161163, 2002.
Chapter 107
ILIOTIBIAL BAND BURSITIS
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 resonance
Differential Diagnosis
The most common cause of lateral knee pain is degenerative
arthritis of the knee. Other pathological processes may mimic
the pain and functional disability of iliotibial band bursitis. Lumbar radiculopathy may cause pain and disability similar to that
of iliotibial band bursitis. In such patients, back pain is usually
present, and the knee examination should be negative. Entrapment neuropathies of the lower extremity, such as meralgia paresthetica, and bursitis of the knee also may confuse the diagnosis;
both conditions may coexist with iliotibial band bursitis. Primary
and metastatic tumors of the femur and spine may manifest in a
manner analogous to iliotibial band bursitis.
Treatment
Initial treatment of the pain and functional disability associated
with iliotibial band bursitis should include a combination of nonsteroidal 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, injection of the iliotibial band bursa
with a local anesthetic and steroid may be a reasonable next step.
The iliotibial band bursa is injected by placing the patient in
the supine position with a rolled blanket underneath the knee to
flex the joint gently. The skin over the lateral epicondyle of the
femur is prepared with antiseptic solution. A sterile syringe containing 2 mL of 0.25% preservative-free bupivacaine and 40 mg
of methylprednisolone is attached to a 25-gauge, 1-inch needle using strict aseptic technique. With strict aseptic technique,
the iliotibial band bursa is located by identifying the point of
maximal tenderness over the lateral condyle of the femur. The
bursa usually is identified by point tenderness at that spot. At
this point, the needle is inserted at a 45-degree angle to the
femoral condyle to pass through the skin, subcutaneous tissues,
and iliotibial band into the iliotibial band bursa (Figure 107-2).
If the needle strikes the femur, it is withdrawn slightly into the
substance of the bursa. When the needle is in position in proximity to the iliotibial band bursa, the contents of the syringe are
gently injected. Little resistance to injection should be noted. If
313
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
Inflamed iliotibial bursa
Chapter 108
FABELLA SYNDROME
sedimentation rate, and antinuclear antibody testing, may be indicated. Magnetic resonance imaging (MRI) and ultrasound imaging of the knee joint is indicated if bursitis, tendinitis, Bakers
cyst, joint instability, occult mass, or tumor is suspected and to
further clarify the diagnosis (Figures 108-3 and 108-4). Radionucleotide bone scanning may be useful in identifying stress fractures
or tumors of the knee that may be missed on plain radiographs.
Arthrocentesis of the knee joint may be indicated if septic arthritis
or crystal arthropathy is suspected.
Differential Diagnosis
Fabella pain syndrome is a clinical diagnosis supported by a combination of clinical history, physical examination, radiography,
ultrasound, radionucleotide scanning, and MRI. Pain syndromes
that may mimic fabella pain syndrome include primary pathologic
conditions of the knee, including gout and occult fractures, as
may bursitis and tendinitis of the knee, both of which may coexist
Popliteal fossa
Fabella
Medial head of
gastrocnemius
Lateral head of
gastrocnemius
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 presentation, additional testing, including complete blood cell count,
Figure 108-1 The fabella is located in the lateral head of the gastrocnemius muscle in approximately 25% of patients.
315
Lateral gastrocnemius
with fabella. Bakers cyst rupture may mimic the pain associated
with fabella. Primary and metastatic tumors of the knee may present in a manner analogous to knee pain secondary to fabella.
Treatment
Initial treatment of the pain and functional disability associated
with fabella should include a combination of nonsteroidal antiinflammatory 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, injection of the fabella with a local anesthetic and steroid may be a reasonable next step.
The goals of this injection technique are explained to the
patient. The patient is placed in the prone position with the anterior ankle resting on a folded towel to slightly flex the knee. The
Clinical Pearls
Popliteal fossa
Fabella
Medial head of
gastrocnemius
Lateral head of
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.
Chapter 109
HAMSTRING TENDINITIS
Differential Diagnosis
The most common cause of posterior joint pain is a Bakers cyst.
It is a herniation of the synovial sac of the knee. It may rupture
spontaneously and may be misdiagnosed as thrombophlebitis.
Occasionally, injury to the medial meniscus may be confused with
hamstring tendinitis. Primary or metastatic tumors in the region,
although rare, must be considered in the differential diagnosis.
Treatment
Initial treatment of the pain and functional disability associated
with hamstring tendinitis should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
(COX-2) inhibitors and physical therapy. Local application of
heat and cold may be beneficial. Patients with hamstring tendinitis
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. Magnetic resonance imaging (MRI) of the knee is indicated if internal
derangement, occult mass, Bakers cyst, or partial tendon disruption is suspected. Injection of the hamstring tendons serves as a
diagnostic and therapeutic maneuver.
318
should avoid the repetitive activities responsible for the development of this painful condition. For patients who do not respond
to these treatment modalities, injection of the hamstring tendons
with a local anesthetic and steroid may be a reasonable next step.
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 significant 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 inflammation continues, complicating subsequent treatment. Tendinitis of the musculotendinous insertion of the hamstring
frequently coexists with bursitis of the associated bursa of
the knee joint, creating additional pain and functional disability. This injection technique is extremely effective in the
treatment of pain secondary to hamstring tendinitis. Coexistent 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 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 technique.
Vigorous exercises should be avoided because they would
exacerbate the symptoms.
SUGGESTED READINGS
Bencardino JT, Mellado JM: Hamstring injuries of the hip, Magn Res Imaging Clin
North Am 13:677690, 2005.
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.
Ptasznik R: Ultrasound in acute and chronic knee injury, Radiol Clin North Am
37:797830, 1999.
Chapter 110
PES ANSERINE BURSITIS
Differential Diagnosis
Less common than prepatellar and infrapatellar bursitis, pes anserine bursitis nevertheless can cause significant knee pain and functional disability. The pes anserine bursa lies between the combined
tendinous insertion of the sartorius, gracilis, and semitendinosus
muscles and the medial tibia. Patients with pes anserine bursitis
have pain over the medial knee joint and increased pain on passive valgus and external rotation of the knee. Activity, especially
involving flexion and external rotation of the knee, makes the
pain worse; rest and heat provide some relief. Often, the patient
is unable to kneel or walk down stairs (Figure 110-1). The pain
is constant and characterized as aching. The pain may interfere
with sleep. Coexistent prepatellar or infrapatellar bursitis, tendinitis, arthritis, or internal derangement of the knee may confuse
the clinical picture after trauma to the knee joint. Frequently, the
medial collateral ligament also is involved if the patient has sustained trauma to the medial knee joint. If the inflammation of
the pes anserine bursa becomes chronic, calcification of the bursa
may occur.
Testing
Plain radiographs are indicated in all patients thought to have
pes anserine bursitis. Based on the patients clinical presentation,
additional tests, including complete blood cell count, erythrocyte
320
Treatment
Initial treatment of the pain and functional disability associated
with pes anserine bursitis should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
(COX-2) inhibitors and physical therapy. Local application of
heat and cold may be beneficial. Patients should be advised to
avoid the repetitive activities responsible for the evolution of this
painful condition. For patients who do not respond to these treatment modalities, injection of the coronary pes anserine bursa with
a local anesthetic and steroid may be a reasonable next step.
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.
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.)
Tendons
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.)
Clinical Pearls
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 a local anesthetic and depot steroid. Injection of the
pes anserine bursa is extremely effective in the treatment
of pain secondary to pes anserine 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 rangeof-motion exercises, should be introduced several days after
the patient undergoes this injection technique for prepatellar
bursitis pain. Vigorous exercises should be avoided because
they would exacerbate the symptoms. Simple analgesics
and NSAIDs may be used concurrently with this injection
technique.
SUGGESTED READINGS
Marra MD, Crema MD, Chung M, etal: MRI features of cystic lesions around the
knee, Knee 15:423438, 2008.
OKeeffe SA, Hogan BA, Eustace SJ, Kavanagh EC: Overuse injuries of the knee,
Magn Res Imaging Clin North Am 17:725739, 2009.
Waldman SD: Bursitis syndromes of the knee. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, pp 318322.
Wasserman AR, Melville LD, Birkhahn RH: Septic bursitis: a case report and
primer for the emergency clinician, J Emerg Med 37:269272, 2009.
Chapter 111
SUBTALAR JOINT PAIN
ICD-9 CODE 715.97
ICD-10 CODE M19.90
The Clinical Syndrome
Ankle and heel pain emanating from the subtalar joint is occasionally encountered in clinical practice. The subtalar joint is a
synovial planetype articulation between the talus and the calcaneus (Figure 111-1). Osteoarthritis of the subtalar joint is the
most common form of arthritis that results in subtalar joint pain,
although the joint also is susceptible to damage from rheumatoid
and posttraumatic arthritis.
Most patients with subtalar joint pain secondary to osteoarthritis and posttraumatic arthritis pain report pain localized deep
within the heel, with a secondary dull aching pain in the ankle
(Figure 111-2). Activity, especially adduction of the calcaneus,
makes the pain worse; rest and heat provide some relief. The
pain is constant and characterized as aching; it may interfere
with sleep. Some patients report a grating or popping sensation
with use of the joint, and crepitus may be present on physical
examination.
In addition to the pain described, patients with arthritis of
the subtalar joint often experience a gradual decrease in functional ability with decreasing subtalar range of motion, making
simple everyday tasks such as walking and climbing stairs quite
difficult. With continued disuse, muscle wasting may occur, and
a frozen subtalar joint secondary to adhesive capsulitis may
develop.
Testing
Plain radiographs are indicated in all patients with subtalar joint
pain. Based on the patients clinical presentation, additional tests,
including complete blood cell count, erythrocyte sedimentation
rate, and antinuclear antibody testing, may be indicated. Arthrography, magnetic resonance imaging (MRI) of the subtalar joint,
or both, is indicated if joint instability, occult mass, or tumor is
suspected (Figure 111-3).
Differential Diagnosis
The subtalar joint is susceptible to the development of arthritis
from a variety of conditions that have in common the ability
to damage the joint cartilage. Osteoarthritis is the most common cause, but rheumatoid arthritis and posttraumatic arthritis
cause subtalar pain secondary to arthritis. Less common causes of
arthritis-induced subtalar pain include collagen vascular diseases,
infection, and Lyme disease. Acute infectious arthritis usually is
accompanied by significant systemic symptoms, including fever
and malaise, and should be easily recognized by an astute clinician and treated appropriately with culture and antibiotics, rather
than with injection therapy. The collagen-vascular diseases generally manifest as polyarthropathy rather than monoarthropathy
limited to the subtalar joint, although subtalar pain secondary to
collagen-vascular disease responds well to the intra-articular injection technique described subsequently.
Lumbar radiculopathy may mimic the pain and disability associated with arthritis of the subtalar joint. In such patients, the
ankle examination findings should be negative. Entrapment neuropathies, such as tarsal tunnel syndrome, and bursitis of the ankle
also may confuse the diagnosis; both conditions may coexist with
arthritis of the subtalar joint. Primary and metastatic tumors of
the distal tibia and fibula and spine and occult fractures also may
manifest in a manner analogous to arthritis of the subtalar joint.
Treatment
Initial treatment of the pain and functional disability associated
with arthritis of the subtalar joint should include a combination
of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local application of heat and cold may be beneficial. Avoidance of repetitive
Extensor
digitorum longus t
Extensor
digitorum brevis m
Peroneus
tertius m
Tibia
Peroneus
brevis m
Lat malleolus
Lat cuneiform
Talus
Interosseous
cuneocuboid lig
Post inf
tibiofibular lig
Post
talofibular lig
Interosseous
talocalcaneal lig
3th metatarsal
4th metatarsal
Interosseous
mm
Cuboid
Calcaneus
Plantar apon,
lat cord
Peroneus
longus t
Abductor digiti
Long
minimi m
plantar lig
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.)
fluoroscopic, or ultrasound guidance may be useful when performing injection of the subtalar joint if the anatomic landmarks
are difficult to identify (Figures 111-4 and 111-5).
Talus
Subtalar joint
Clinical Pearls
Calcaneus
Figure 111-2 Most patients with subtalar joint pain secondary to osteoarthritis and posttraumatic arthritis complain of pain that is localized
deep within the heel, with a secondary dull aching pain in the ankle.
activities that aggravate the symptoms and short-term immobilization of the ankle joint also may provide relief. For patients who
do not respond to these treatment modalities, an intra-articular
injection of the subtalar joint with a local anesthetic and steroid
may be a reasonable next step. Computed tomography (CT),
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
Figure 111-4 Sonographic view of anterolateral approach. Peroneal
tendons circled. Arrows surround sural nerve. Left, Cephalad; right, caudal; top, superficial; bottom, deep; CALC, calcaneus; PSTJ (with arrow),
posterior subtalar joint; TAL, talus. (From Henning T, Finnoff JT, Smith J:
Sonographically guided posterior subtalar joint injections: anatomic study
and validation of 3 approaches. PM R 1:925931, 2009.)
SUGGESTED READINGS
Henning T, Finnoff JT, Smith J: Sonographically guided posterior subtalar joint
injections: anatomic study and validation of 3 approaches, PM R 1:925931,
2009.
Anatomy: special imaging considerations of the ankle and foot. In
Waldman SD: Functional anatomy of the ankle and foot. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 155156.
Ward ST, Williams PL, Purkayastha S: Intra-articular corticosteroid injections in
the foot and ankle: a prospective 1-year follow-up investigation, J Foot Ankle
Surg 47:138144, 2008.
Chapter 112
MIDTARSAL JOINT PAIN
Differential Diagnosis
Treatment
Initial treatment of the pain and functional disability associated with arthritis of the midtarsal joints should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs)
or cyclooxygenase-2 (COX-2) inhibitors and physical therapy.
Local application of heat and cold may be beneficial. Avoidance
of repetitive activities that aggravate the patients symptoms and
short-term immobilization of the ankle joint may provide relief.
For patients who do not respond to these treatment modalities,
an injection of the midtarsal joints with a local anesthetic and
steroid may be a reasonable next step.
Testing
Plain radiographs are indicated in all patients with midtarsal joint
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
resonance imaging (MRI) of the midtarsal is indicated if joint
instability, occult mass, or tumor is suspected and to confirm the
diagnosis (Figure 112-2).
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.
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-bearing 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.)
Clinical Pearls
Pain emanating from the midtarsal joints is commonly seen
in individuals who forcefully point their toes, such as ballet dancers and football punters. This injection technique
is extremely effective in the treatment of pain secondary to
the previously mentioned causes of arthritis of the midtarsal
joint. Coexistent bursitis and tendinitis may contribute to
midtarsal joint 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 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 this injection technique for midtarsal 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.
SUGGESTED READINGS
Reid JJ, Pinney SJ: Midfoot injuries in athletes: fundamentals of examination and
treatment, Oper Techn Sports Med 18:4649, 2010.
Waldman SD: Functional anatomy of the ankle and foot. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 155156.
Waldman SD: Anatomy: special imaging considerations of the ankle and foot. In
Waldman SD, Campbell RSD, editors: Imaging of pain, Philadelphia, 2010,
Saunders, pp 417419.
Ward ST, Williams PL, Purkayastha S: Intra-articular corticosteroid injections in
the foot and ankle: a prospective 1-year follow-up investigation, J Foot Ankle
Surg 4713847144, 2008.
Chapter 113
POSTERIOR TIBIAL TENDINITIS
331
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 associated with rupture of the posterior tibial tendon (Figures 113-3,
113-4, and 113-5). Based on the patients clinical presentation,
additional tests, including complete blood count, erythrocyte
sedimentation rate, and antinuclear antibody testing, may be
indicated. MRI of the ankle is indicated if joint instability is suspected. Radionuclide bone scanning identifies stress fractures of
the tibia not seen on plain radiographs. Injection of the posterior
tibial tendon with local anaesthetic and steroid serves as a diagnostic
and therapeutic maneuver.
Differential Diagnosis
Posterior tibial tendinitis generally is identified easily on clinical grounds. Because a bursa is located between the Achilles tendon and the base of the tibia and the upper posterior calcaneus,
B
Figure 113-3 Injuries of the tibialis posterior tendon: Complete tears.
Although a lateral radiograph obtained without weight bearing (A)
appears normal, a lateral radiograph obtained with weight bearing (B)
shows plantar flexion of the distal portion of the talus with malalignment at the talonavicular joint. (From Myerson M, Solomon G, Shereff M:
Posterior tibial tendon dysfunction: its association with seronegative inflammatory disease, Foot Ankle 9:219225, 1989.)
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.)
Talus
Treatment
Initial treatment of the pain and functional disability associated
with posterior tibial tendinitis should include a combination of
nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local application
of heat and cold may be beneficial. The patient should be encouraged to avoid repetitive activities responsible for the evolution of
the tendinitis, such as jogging. For patients with tendinitis of the
posterior tibial tendon who do not respond to these treatment
modalities, careful injection of the area underneath the deltoid
ligament just below the medial malleolus with local anesthetic
and steroid may be a reasonable next step. Surgery is required for
patients who have sustained rupture of the posterior tibial tendon.
Clinical Pearls
The posterior tibial tendon is a strong tendon but also is
very susceptible to rupture. Injection of the tendinitis is
extremely effective in the treatment of pain secondary to
the previously mentioned causes of posterior ankle pain.
Coexistent bursitis and arthritis may contribute to posterior ankle pain and may require additional treatment with a
more localized injection of local anesthetic and methylprednisolone acetate.
The described 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 technique for ankle pain. Vigorous exercises should be avoided because they would exacerbate the
symptoms. Simple analgesics and NSAIDs may be used
concurrently with this injection technique. Tendon rupture
requires surgical repair to protect the ankle and foot from
further damage.
Chapter 114
ACHILLES BURSITIS
Testing
Plain radiographs are indicated in all patients with posterior
ankle pain. Based on the patients clinical presentation, additional tests, including complete blood cell count, erythrocyte
sedimentation rate, and antinuclear antibody testing, may be
Differential Diagnosis
Achilles bursitis generally is identified easily on clinical grounds.
Because tendinitis frequently accompanies Achilles bursitis, the
specific diagnosis may be unclear. Stress fractures of the ankle also
may mimic Achilles bursitis and tendinitis and may be identified
on plain radiographs, MRI, or radionucleotide bone scanning.
Treatment
Initial treatment of the pain and functional disability associated
with Achilles bursitis should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2
(COX-2) inhibitors and physical therapy. Local application of
heat and cold may be beneficial. The patient should be encouraged to avoid repetitive activities responsible for the evolution of
the bursitis, such as jogging. For patients who do not respond to
these treatment modalities, the following injection technique with
a local anesthetic and steroid may be a reasonable next step.
For injection, the patient is placed in the prone position with
the affected foot hanging off the end of the table. The foot is
gently dorsiflexed to facilitate identification of the margin of the
tendon to aid in avoiding injection directly into the tendon. The
tender points at the tendinous insertion or at its narrowest part
approximately 5 cm above the insertion are identified and marked
with a sterile marker.
Proper preparation with antiseptic solution of the skin
overlying these points is carried out. A sterile syringe containing 2 mL of 0.25% preservative-free bupivacaine and 40 mg of
methylprednisolone is attached to a 25-gauge, 1-inch needle
using strict aseptic technique. With strict aseptic technique, the
previously marked points are palpated. The needle is carefully
advanced at this point alongside the tendon through the skin and
subcutaneous tissues, with care taken not to enter the substance
of the tendon (Figure 114-2). The contents of the syringe are
gently injected while slowly withdrawing the needle. Minimal
resistance to injection should be felt. If significant resistance to
injection is noted, the needle tip is probably in the substance of
the Achilles tendon and should be withdrawn slightly until the
injection proceeds without significant resistance. The needle is
removed, and a sterile pressure dressing and ice pack are placed
at the injection site.
335
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
Achilles tendon
Inflamed Achilles bursa
Van der Wall H, Lee A, Magee M, etal: Radionuclide bone scintigraphy in sports
injuries, Semin Nucl Med 40:1630, 2010.
Vyce SD, Addis-Thomas E, Mathews EE, Perez SL: Painful prominences of the
heel, Clin Podiatr Med Surg 27:443462, 2010.
Chapter 115
ANTERIOR TALOFIBULAR PAIN
SYNDROME
Signs and Symptoms
Testing
Plain radiographs are indicated in all patients with ankle 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 resonance imaging (MRI) of the ankle is indicated if disruption of the talofibular ligament or joint instability, occult mass, or
tumor is suspected.
Posterior
talofibular
ligament
Tibia
Anterior
talofibular
ligament
Lateral
malleolus
Fibula
Achilles
tendon (cut)
Peroneal
retinacula
Calcaneofibular
ligament
Calcaneus
Peroneus
brevis tendon
Long plantar
ligament
Peroneus
longus tendon
Figure 115-1 The talofibular ligament is susceptible to strain from acute injury from sudden inversion of the ankle or from repetitive microtrauma to
the ligament from overuse or misuse, such as long-distance running on soft or uneven surfaces.
338
Differential Diagnosis
Avulsion fractures of the calcaneus, talus, lateral malleolus, and
base of the fifth metatarsal can mimic the pain of injury to the
talofibular ligament. Bursitis, tendinitis, and gout of the midtarsal
joints may coexist with ligament strain and may confuse the diagnosis. Tarsal tunnel syndrome may occur after ankle trauma and
may further confuse the clinical picture.
Treatment
Initial treatment of the pain and functional disability associated with talofibular pain syndrome should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy.
Local application of heat and cold may be beneficial. Avoidance
of repetitive activities that aggravate the patients symptoms
and short-term immobilization of the ankle joint also may provide relief. For patients who do not respond to these treatment
modalities, the injection of the talofibular ligament may be a
reasonable next step.
Clinical Pearls
It is estimated that approximately 25,000 individuals sprain
their ankle every day. Although viewed as benign by the
lay public, ankle sprains can result in significant permanent
pain and disability. The major ligaments of the ankle joint
include the deltoid, anterior talofibular, calcaneofibular,
and posterior talofibular ligaments, which provide most of
the strength to the ankle joint. The talofibular ligament is
not as strong as the deltoid ligament and is susceptible to
strain. The talofibular ligament runs from the anterior border of the lateral malleolus to the lateral surface of the talus.
The injection technique described here is extremely effective
in the treatment of pain secondary to the talofibular ligament
strain. Coexistent arthritis, bursitis, and tendinitis may contribute to medial ankle pain and may require additional treatment
with more localized injection of a local anesthetic and depot
steroid. 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
ankle pain. Vigorous exercises should be avoided because they
would exacerbate the symptoms. Simple analgesics and NSAIDs
may be used concurrently with this injection technique.
SUGGESTED READINGS
Bonnel F, Toullec E, Mabit C, etal: Chronic ankle instability: biomechanics and
pathomechanics of ligaments injury and associated lesions, Orthop Traumatol
Surg Res 96:424432, 2010.
Haller J, Bernt R, Seeger T, etal: MR-imaging of anterior tibiotalar impingement
syndrome: agreement, sensitivity and specificity of MR-imaging and indirect
MR-arthrography, Eur J Radiol 58:450460, 2006.
Waldman SD: Anterior talofibular ligament tear. In Waldman SD, Campbell RSD,
editors: Imaging of pain, Philadelphia, 2010, Saunders, pp 437438.
Waldman SD: Functional anatomy of the ankle and foot. In Waldman SD, editor:
Pain review, Philadelphia, 2009, Saunders, pp 155156.
Waldman SD: The anterior talofibular ligament. In Waldman SD, editor: Pain
review, Philadelphia, 2009, Saunders, p 158.
Chapter 116
ACCESSORY NAVICULAR PAIN
SYNDROME
ICD-9 CODE 733.99
ICD-10 CODE M89.8X9
The Clinical Syndrome
Foot and ankle pain secondary to accessory navicular pain syndrome
is being seen with increasing frequency in clinical practice because
of the increased interest in physical fitness and the use of exercise
machines. Accessory navicular pain syndrome is the name given to
pain that has as its nidus an accessory ossicle occasionally found in
relation to the medial navicular bone and posterior tibial tendon
(Table 116-1). It is thought that accessory ossicles such as the accessory navicular decrease friction and pressure of tendons as they pass
in proximity to a joint. Similar accessory ossicles are found in the
elbows, hands, wrists, and feet.
Foot and ankle pain secondary to accessory navicular pain syndrome is characterized by tenderness and pain over the medial
foot and ankle. Patients often report irritation from a shoe, and
patients with accessory navicular pain syndrome may come to the
physicians office wearing a loose slipper on the affected foot. The
pain of accessory navicular pain syndrome worsens with activities that require 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 116-1).
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.
accessory ossicles that may have become inflamed. Plain radiographs also often identify loose bodies or joint mice, which are
frequently seen in patients with foot and ankle pain secondary to
accessory navicular pain syndrome. Based on the patients clinical presentation, additional tests, including complete blood cell
count, erythrocyte sedimentation rate, and antinuclear antibody
testing, may be indicated. Magnetic resonance imaging (MRI)
of the foot and ankle joint is indicated if joint instability, loose
bodies, occult mass, or tumor is suspected and to clarify the
diagnosis further (Figure 116-2). Radionucleotide bone scanning may be useful in identifying stress fractures or tumors of
the foot and ankle and distal humerus that may be missed on
plain radiographs.
Differential Diagnosis
Primary pathology of the foot and ankle, including gout and
occult fractures, especially of the navicular tuberosity, may mimic
the pain and disability associated with an accessory navicular
bone. Entrapment neuropathy of the posterior tibial nerve, bursitis, and tendinitis also may confuse the diagnosisall of which
may coexist with accessory navicular pain syndrome. Khlers
bone disease and synovial chondromatosis may mimic the pain
associated with accessory navicular pain syndrome. Primary and
metastatic tumors of the foot and ankle may present in a manner
analogous to foot and ankle pain secondary to accessory navicular
pain syndrome.
TABLE 116-1
Description
Type I
Type Ia
Type IIa
Type IIb
Type III
Testing
Plain radiographs are indicated in all patients with accessory
navicular pain syndrome to rule out fractures and identify
340
Achilles
tendon
Navicular
Accessory
navicular
ossicle
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.)
Treatment
Initial treatment of the pain and functional disability associated
with accessory navicular pain syndrome should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local
application of heat and cold may be beneficial. Avoidance of repetitive activities that aggravate the symptoms may provide relief.
For patients who do not respond to these treatment modalities,
Clinical Pearls
Pain emanating from the foot and ankle is a common problem encountered in clinical practice. Accessory navicular
pain syndrome must be distinguished from fractures of the
foot and ankle, fractures of the accessory navicular bone
itself, entrapment neuropathies of the tibial nerves, bursitis,
and tendinitis. Less common causes of posterior foot and
ankle pain, including Khlers bone disease, should be considered when evaluating patients thought to have accessory
navicular pain syndrome.
SUGGESTED READINGS
Emms NM, Walsh HPJ: Stress fracture of accessory navicular: a rare cause of foot
pain, Foot Ankle Surg 7:241243, 2001.
Jasiewicz B, Potaczek T, Kcki W, Tsiorowski M, Lipik E: Results of simple
excision technique in the surgical treatment of symptomatic accessory navicular
bones, Foot Ankle Surg 14:5761, 2008.
Kiter E, Gnal I, Karatosun V, Korman E: The relationship between the tibialis
posterior tendon and the accessory navicular, Ann Anat 182:6568, 2000.
Leonard Z, Fortin PT: Adolescent accessory navicular, Foot Ankle Clin North Am
15:337347, 2010.
Ugolini PA, Raikin SM: The accessory navicular, Foot Ankle Clin North Am
9:165180, 2004.
Chapter 117
FIBULOCALCANEAL PAIN
SYNDROME
Testing
Plain radiographs are indicated in all patients with ankle 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
resonance imaging (MRI) of the ankle is indicated if disruption
of the fibulocalcaneal ligament, joint instability, occult mass, or
tumor is suspected.
Posterior
talofibular
ligament
Tibia
Anterior
talofibular
ligament
Lateral
malleolus
Fibula
Achilles
tendon (cut)
Peroneal
retinacula
Calcaneofibular
ligament
Calcaneus
Peroneus
brevis tendon
Long plantar
ligament
Peroneus
longus tendon
Figure 117-1 Fibulocalcaneal pain syndrome is the result of injury to the fibulocalcaneal ligament, usually caused by sudden inversion of the ankle
as when stepping off a high curb.
343
Ant inf
tibiofibular lig
Talus
Ant talofibular lig
Calcaneofibular
lig
Peroneus
brevis t
Calcaneus
Peroneus
longus t
Peroneal
retinaculum
Long plantar lig
Abductor digiti
minimi m
Plantar apon,
lat cord
Tibia
Med malleolus
Post tibiotalar lig
Interosseous
talocalcaneal lig
Flexor retinaculum
Tibialis post t
Tibiocalcaneal lig
Flexor digitorum
longus t
Sustentaculum tali
Flexor hallucis longus t
Med plantar a & n
Quadratus plantae m
Abductor hallucis m
Lat plantar a & n
Flexor digitorum
brevis m
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.)
Differential Diagnosis
Avulsion fractures of the calcaneus, the talus, the lateral malleolus,
and the base of the fifth metatarsal can mimic the pain of injury to
the fibulocalcaneal ligament. Bursitis, tendinitis, and gout of the
midtarsal joints may coexist with ligament strain and may confuse the diagnosis. Tarsal tunnel syndrome may occur after ankle
trauma and may further confuse the clinical picture.
Treatment
Initial treatment of the pain and functional disability associated
with fibulocalcaneal pain syndrome should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy.
Local application of heat and cold may be beneficial. Avoidance
of repetitive activities that aggravate the patients symptoms and
short-term immobilization of the ankle joint may provide relief.
For patients who do not respond to these treatment modalities,
injection of the fibulocalcaneal ligament may be a reasonable
next step.
Clinical Pearls
It is estimated that approximately 25,000 individuals in
the United States sprain their ankle every day. Although
viewed as benign by the lay public, ankle sprains can result
in significant permanent pain and disability. The major
ligaments of the ankle joint include the deltoid, anterior
talofibular, calcaneofibular, and posterior talofibular ligaments, which provide most of the strength to the ankle
joint. Injection of the fibulocalcaneal ligament is extremely
effective in the treatment of pain secondary to fibulocalcaneal ligament strain. Coexistent arthritis, bursitis, and tendinitis also may contribute to medial ankle pain and may
require additional treatment with more localized injection
of a local anesthetic and depot steroid. The use of physical
modalities, including local heat and gentle range-of-motion
exercises, should be introduced several days after the patient
undergoes the injection technique for ankle pain. Vigorous
exercises should be avoided because they would exacerbate
the symptoms. Simple analgesics and NSAIDs may be used
concurrently with this injection technique.
Chapter 118
OS TRIGONUM PAIN SYNDROME
Testing
Plain radiographs are indicated in all patients with os trigonum
pain syndrome to rule out fractures and identify accessory ossicles
346
that may have become inflamed. Plain radiographs also often identify 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,
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
foot and ankle joint is indicated if joint instability, loose bodies,
occult mass, or tumor is suspected and to further clarify the diagnosis (Figure 118-2). Radionucleotide bone scanning may be useful in identifying stress fractures or tumors of the foot and ankle
and distal humerus that may be missed on plain radiographs.
Differential Diagnosis
Primary pathology of the foot and ankle, including gout and occult
fractures especially of the navicular tuberosity, may mimic the pain
and disability associated with an os trigonum bone. Entrapment
neuropathy of the posterior tibial nerve, bursitis, and tendinitis
also may confuse the diagnosisall of which may coexist with
os trigonum pain syndrome. Khlers bone disease and synovial
chondromatosis may mimic the pain associated with os trigonum
pain syndrome. Primary and metastatic tumors of the foot and
ankle also may manifest in a manner analogous to foot and ankle
pain secondary to os trigonum pain syndrome.
Treatment
Initial treatment of the pain and functional disability associated with os trigonum pain syndrome should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Local
application of heat and cold may be beneficial. Avoidance of
repetitive activities that aggravate the symptoms also may provide
relief. For patients who do not respond to these treatment modalities, injection of the os trigonum ossicle with a local anesthetic
and steroid may be a reasonable next step. For pain that persists,
or if the os trigonum pain syndrome is causing damage to the foot
and ankle joint, surgical removal is indicated.
Inflamed
accessory bone
Achilles
tendon
Navicular
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
Figure 118-2 A, Lateral radiograph of the ankle in a patient with posterior impingement. The os trigonum (arrow) is compressed between the posterior 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.)
Clinical Pearls
Pain emanating from the foot and ankle is a common problem encountered in clinical practice. Os trigonum pain
syndrome must be distinguished from fractures of the foot
and ankle, fractures of the os trigonum bone itself, entrapment neuropathies of the tibial nerves, bursitis, and tendinitis, and less common causes of posterior foot and ankle
pain, including Khlers bone disease, should be considered
when evaluating patients thought to have os trigonum pain
syndrome.
SUGGESTED READINGS
Chao W: Os trigonum, Foot Ankle Clin North Am 9:787796, 2004.
Soucanye de Landevoisin E, Jacopin S, Glard Y, etal: Surgical treatment of the
symptomatic os trigonum in children, Orthop Traumatol Surg Res 95:159163,
2009.
Waldman SD: Os trigonum. In Waldman SD, Campbell RSD, editors: Imaging of
pain, Philadelphia, 2010, Saunders, pp 449450.
Wansbrough GG, Eyres KS: Osteo-arthritis of the os trigonumcalcaneal joint,
Foot 17:159161, 2007.
Chapter 119
BUNIONETTE PAIN
deformity is the fact that bursitis and tendinitis of the foot and
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.
Treatment
The Clinical Syndrome
Occurring less commonly than the common bunion, bunionette is
a common cause of lateral foot pain. The term bunionette refers to
a constellation of symptoms, including soft tissue swelling over the
fifth metatarsophalangeal joint associated with abnormal angulation
of the joint resulting in a prominent fifth metatarsal head with associated medial angulation (Figure 119-1). Bunionette also is known
as tailors bunion. This deformity is analogous to the hallux valgus
deformity and occurs more commonly in women. The development 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
cause of bunionette formation is the wearing of tight, narrow-toed
shoes (Figure 119-2). High heels may exacerbate the problem.
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
resonance imaging (MRI) of the fifth metatarsophalangeal joint is
indicated if joint instability, occult mass, or tumor is suspected.
Differential Diagnosis
The diagnosis of bunionette is usually obvious on clinical grounds
alone. Complicating the care of a patient with a typical bunion
348
Figure 119-1 A, Tailors bunion deformity may be assessed radiographically with a lateral splaying in the distal fifth metatarsal. B, Clinically,
the patient generally presents with symptoms occurring laterally or
plantarlaterally, often with an adduction of the fifth toe. (From Clinical
Practice Guideline Forefoot Disorders Panel; Thomas JL, Blitch EL IV, Chaney
DM, etal: Diagnosis and treatment of forefoot disorders. IV. Tailors bunion.
J Foot Ankle Surg 2009;48:257263.)
Clinical Pearls
Pain from bunionette can be debilitating, and the deformity is cosmetically unacceptable for many patients. Injection 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 undergoes this injection technique for toe 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.
Fifth metatarsal
Phalanges:
Distal
Middle
Proximal
Figure 119-2 The most common cause of bunionette formation is the
wearing of tight, narrow-toed shoes.
SUGGESTED READINGS
Ajis A, Koti M, Maffulli N: Tailors bunion: a review, J Foot Ankle Surg 44:
236245, 2005.
Clinical Practice Guideline Forefoot Disorders Panel, Thomas JL, Blitch EL IV,
Chaney DM, etal: Diagnosis and treatment of forefoot disorders. II. Central
metatarsalgia, J Foot Ankle Surg 48:239250, 2009.
Clinical Practice Guideline Forefoot Disorders Panel, Thomas JL, Blitch EL IV,
Chaney DM, etal: Diagnosis and treatment of forefoot disorders. V. Trauma,
J Foot Ankle Surg 48:264272, 2009.
Roukis TS: The tailors bunionette deformity: a field guide to surgical correction,
Clin Podiatr Med Surg 22:223245, 2005.
Chapter 120
SESAMOIDITIS
Testing
Plain radiographs are indicated in all patients with sesamoiditis
to rule out fractures and identify sesamoid bones that may have
350
become inflamed (Figure 120-2). Based on the patients clinical presentation, 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 of the metatarsal bones or
sesamoid bones that may be missed on plain radiographs of the
foot (Figure 120-3).
Differential Diagnosis
Primary pathological processes of the foot, including gout and
occult fractures, may mimic the pain and disability associated
with sesamoiditis. Entrapment neuropathies such as tarsal tunnel
syndrome may confuse the diagnosis, as may bursitis and plantar
fasciitis of the foot, both of which may coexist with sesamoiditis. Metatarsalgia is another common cause of forefoot pain and
may be distinguished from sesamoiditis by the fact that the pain
of metatarsalgia is over the metatarsal heads and does not move
when the patient actively flexes his or her toes, as is the case with
sesamoiditis. Primary and metastatic tumors of the foot also
may manifest in a manner analogous to arthritis of the midtarsal
joints.
Treatment
Initial treatment of the pain and functional disability associated
with sesamoiditis should include a combination of nonsteroidal
anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2)
inhibitors and physical therapy. Local application of heat and
cold may be beneficial. Avoidance of repetitive activities that
aggravate the symptoms and short-term immobilization of the
midtarsal joint also may provide relief. For patients who do not
respond to these treatment modalities, injection of the affected
sesamoid bone with a local anesthetic and steroid may be a reasonable next step.
Distal phalanx
3
4
5
Proximal phalanx
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.)
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.)
Clinical Pearls
Pain emanating from the forefoot is a common problem
encountered in clinical practice. Sesamoiditis must be distinguished from stress fractures of the metatarsal bones,
metatarsalgia, Mortons neuroma, and fractures of the sesamoid bones. Although the previously mentioned injection
technique provides palliation of the pain of sesamoiditis,
the patient often also requires shoe orthoses that include
padded insoles to help remove pressure from the affected
sesamoid bones. Coexistent bursitis and tendinitis also may
contribute to metatarsal pain and may require additional
treatment with more localized injection of an anesthetic
and depot steroid. 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 sesamoiditis 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.
SUGGESTED READINGS
Anwar R, Anjum SN, Nicholl JE: Sesamoids of the foot, Curr Orthop 19:4048,
2005.
Cohen BE: Hallux sesamoid disorders, Foot Ankle Clin North Am 14:91104,
2009.
Kennedy JG, Hodgkins CW, Columbier J-A, Hamilton WG: Baxters the foot and
ankle in sport, ed 2, Philadelphia, 2008, Mosby, pp 469483.
Sanders TG, Rathur SK: Imaging of painful conditions of the hallucal sesamoid
complex and plantar capsular structures of the first metatarsophalangeal joint,
Radiol Clin North Am 46:10791092, 2008.
Umans HR: Imaging sports medicine injuries of the foot and toes, Clin Sports Med
25:763780, 2006.
Waldman SD: Sesamoiditis. In Waldman SD, Campbell RSD, editors: Imaging of
pain, Philadelphia, 2010, Saunders, pp 455456.
Chapter 121
METATARSALGIA
Differential Diagnosis
Primary pathology of the foot, including gout and occult fractures, may mimic the pain and disability associated with metatarsalgia (Figure 121-2). Entrapment neuropathies such as tarsal
tunnel syndrome, bursitis, and plantar fasciitis of the foot also
may confuse the diagnosis; bursitis and plantar fasciitis may coexist with sesamoiditis. Sesamoid bones beneath the heads of the
metatarsal bones are present in some individuals and are subject to the development of inflammation termed sesamoiditis.
Sesamoiditis is another common cause of forefoot pain and may
be distinguished from metatarsalgia by the fact that the pain of
metatarsalgia is centered over the patients metatarsal heads and
does not move when the patient actively flexes his or her toes,
as is the case with sesamoiditis. The muscles of the metatarsal
joints and their attaching tendons are susceptible to trauma and
wear and tear from overuse and misuse and may contribute to
Callus
5
Metatarsal
heads
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 presentation, 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
radiographs of the foot.
353
Clinical Pearls
Treatment
Initial treatment of the pain and functional disability associated
with metatarsalgia should include a combination of nonsteroidal
anti-inflammatory drugs (NSAIDs) or cyclooxygenase-2 (COX-2)
inhibitors and physical therapy. Local application of heat and cold
may be beneficial. Avoidance of repetitive activities that aggravate
Chapter 122
SUBMETATARSAL ADVENTITIAL
BURSITIS
Testing
Plain radiographs are indicated in all patients with forefoot 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
resonance imaging (MRI) of the foot is indicated to confirm the
diagnosis and identify commonly occurring concomitant forefoot
pathological conditions, such as metatarsalgia, metatarsal stress
fractures, and Mortons neuroma (Figure 122-1). Radionucleotide
bone scanning is useful to identify stress fractures of the metatarsals not seen on plain radiographs. Ultrasound imaging and color
Doppler evaluation are also useful in helping identify submetatarsal
adventitial bursitis (Figure 122-2).
Differential Diagnosis
Submetatarsal adventitial bursitis generally is identified easily on
clinical grounds. Because other forefoot pathological conditions,
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
*
C
*
*
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.)
Treatment
Initial treatment of the pain and functional disability associated
with submetatarsal adventitial bursitis should include a combination of nonsteroidal anti-inflammatory drugs (NSAIDs) or
cyclooxygenase-2 (COX-2) inhibitors and physical therapy. Avoidance of painful shoes or shoes with a narrow toe box should be
considered, as should the use of thick-soled shoes with an orthotic
device to relieve pressure on the inflamed bursa. Local application
of heat and cold may be beneficial. The patient should be encouraged to avoid repetitive activities responsible for the evolution of
the bursitis, such as jogging. For patients who do not respond to
these treatment modalities, injection with a local anesthetic and
steroid may be a reasonable next step. Sometimes, surgical excision
of the bursa and shaving of the offending metatarsal head may be
the only option to provide long-lasting relief of the forefoot pain.
Clinical Pearls
Submetatarsal adventitial bursitis occurs in the areas of
excessive friction between the metatarsal heads and overlying supporting soft tissues and skin. It frequently coexists with other forefoot pathological conditions, which may
require additional treatment with a more localized injection
of a local anesthetic and depot steroid.
The injection of submetatarsal adventitial bursitis is a
safe procedure if careful attention is paid to the clinically
relevant anatomy in the areas to be injected. The key to
the successful treatment of submetatarsal adventitial bursitis
is to identify the underlying pathology responsible for the
formation of this adventitial bursa and treat it aggressively.
SUGGESTED READINGS
Bardelli M, Turelli L, Scoccianti G: Definition and classification of metatarsalgia,
Foot Ankle Surg 9:7985, 2003.
Hochman MG, Ramappa AJ, Newman JS, Farraher SW: Imaging of tendons and
bursae. In Weissman BN, editor: Imaging of arthritis and metabolic bone disease,
Philadelphia, 2009, Saunders, pp 196238.
Sanders TG, Rathur SK: Imaging of painful conditions of the hallucal sesamoid
complex and plantar capsular structures of the first metatarsophalangeal joint,
Radiol Clin North Am 46:10791092, 2008.
Studler U, Mengiardi B, Bode B, etal: Fibrosis and adventitious bursae in plantar
fat pad of forefoot: MR imaging findings in asymptomatic volunteers and MR
imaginghistologic comparison, Radiology 246:863870, 2008.
Waldman SD: Metatarsalgia. In Waldman SD, editor: Pain review, Philadelphia,
2009, Saunders, p 326.
Atlas of
Uncommon Pain
Syndromes
THIRD EDITION
Steven D. Waldman, MD, JD
Clinical Professor of Anesthesiology
Professor of Medical Humanities and Bioethics
University of MissouriKansas City School of Medicine
Kansas City, Missouri
iii
ISBN: 978-1-4557-0999-1
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Library of Congress Cataloging-in-Publication Data
Waldman, Steven D.
Atlas of uncommon pain syndromes / Steven D. Waldman. 3rd ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4557-0999-1 (hardcover : alk. Paper)
I.Title.
[DNLM: 1. Paindiagnosis. 2. Pain Management. WB 176]
616.0472dc23
2012046149
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1
PREFACE
It has been said that the three most dangerous things in medicine are (1) a medical student with a sharp object, (2) a resident
with a recently published study from the New England Journal of
Medicine, and (3) an attending physician with an anecdote. One
must suspect that point 2 was at play when in the 1940s while
on rounds at the University of Maryland Hospital in Baltimore,
Maryland, Theodore Woodward, MD, stated, If you hear hoof
beats out on Green Street, dont look for zebras! How this admonition to aspiring physicians morphed into when you hear hoof beats,
look for horses, not zebras is anybodys guess. (My son, an ophthalmology resident in Baltimore, suggests that it was also just as likely
that this sage piece of advice was accompanied by a long-winded
and confusing anecdotesee point 3.)
On the surface, most of us would agree with Dr. Woodwards
logic that the most common things are the most common. Occam
agreed, when in the fourteenth century he put forth the philosophical tenant of parsimony, which proposes that simpler explanations are, all things being equal, almost always better than more
complex ones. He used a razor to shave away unnecessary or
extraneous data to get to the simplest solution. The razor was all
the rage as a medical instrument in the fourteenth century, so it is
not surprising that Occam chose it as his preferred medical device.
Occams razor certainly has a nice ring to itbetter than Occams
MRI, which would no doubt be the name of his maxim if he had
lived in the twenty-first century, given that currently the MRI
is certainly our most popular medical device for shaving away
extraneous data.
Which brings us to KISSnot the Gene Simmons rock band
KISS, but the admonition Keep it simple, stupid. KISS was set
forth by Lockheed aeronautical engineer, Kelly Johnson, when he
handed his design team a few simple tools and challenged them to
design combat jets that could be easily fixed with the simple tools
that were available in combat situations. It is still not exactly clear
to me who was stupid, but I certainly hope it is not the guys
who fix the jets I fly on. KISS makes sense when designing jet
engines, but what does this have to do with the individual patient?
The sick one? The scared one? The one you worry about in the
middle of the night? Unfortunately, very little. Because for the
individual patient with a difficult diagnosis, Hickam was probably
more correct than Occam.
Harry Hickam, MD, while on teaching rounds at Duke University, admonished his students and residents that Patients can
have as many diseases as they damn well please! (also see point 3).
He correctly posited that when diagnosing the individual patient,
using Occams razor often provides the correct diagnosis. More
vii
INDEX
A
Angina
abdominal, 212214, 212f213f
vs. anterior cutaneous nerve entrapment, 202
Angiography, celiac, for abdominal angina,
212213
Angioplasty, for abdominal angina, 213
Ankle and foot pain syndromes
accessory navicular pain syndrome as, 340342,
340t, 341f
Achilles bursitis as, 335337, 336f
anterior talofibular pain syndrome as, 338339,
338f
bunionette pain as, 348349, 348f349f
fibulocalcaneal pain syndrome as, 343345,
343f344f
metatarsalgia as, 353354, 353f354f
midtarsal joint pain as, 327330
os trigonum pain syndrome as, 346347, 347f
posterior tibial tendinitis as, 331334, 331f333f
sesamoiditis as, 350352, 351f352f
submetatarsal adventitial bursitis as, 355357,
355f356f
subtalar joint pain as, 324326, 325f326f
Ankylosing spondylitis, 230232, 231f232f, 232t
vs. cervicothoracic interspinous bursitis, 57
Anterior chest wall tumors, vs. pectoralis major tear
syndrome, 9394
Anterior cutaneous nerve entrapment, 202204,
203f
Anterior interosseous nerve compression, vs. pronator syndrome, 104
Anterior interosseous syndrome, 130132,
131f132f
Anterior talofibular pain syndrome, 338339, 338f
Antibiotics
for epidural abscess, 216
for prostatodynia, 241243
for vulvodynia, 254255
Anticholinergics
for abdominal angina, 213
for radiation enteritis, 207
Anticonvulsants
for Charlins syndrome, 9
for Ramsay Hunt syndrome, 34
for red ear syndrome, 47
for spasmodic torticollis, 5556
for SUNCT headache, 17
Antidepressants
for gluteus medius syndrome, 249
for Ramsay Hunt syndrome, 34
tricyclic. See Tricyclic antidepressants.
Antipersitaltics, for radiation enteritis, 207
Antiviral agents, for Ramsay Hunt syndrome, 34
Appendicitis, vs. devils grip, 179
Arnold-Chiari malformations, cough headache
associated with, 1314, 14f
Arteriovenous malformations, vs. lumbar myofascial
pain syndrome, 236
Arteritis, temporal. See Temporal arteritis.
Arthritis. See Osteoarthritis.
carpometacarpal joint, vs. ulnar tunnel syndrome,
134
degenerative, of knee
359
360 Index
Arthritis (Continued)
vs. coronary ligament strain, 302
vs. iliotibial band bursitis, 313
vs. pes anserine bursitis, 320
vs. runners knee, 308
elbow, vs. cubital bursitis, 106
hip, with snapping hip syndrome, 286
infectious, acute
midtarsal joint pain in, 327
subtalar joint pain from, 324
vs. scapulocostal syndrome, 60
inflammatory
vs. ankylosing spondylitis, 230
vs. gluteus maximus pain syndrome, 245
vs. levator ani pain syndrome, 264
vs. lumbar myofascial pain syndrome, 236
vs. spondylolisthesis, 228
knee
vs. jumpers knee, 293
vs. quadriceps expansion syndrome, 307
manubriosternal joint pain secondary to, 190
posttraumatic
midtarsal joint pain from, 327
in scapulocostal syndrome, 60
rheumatoid
midtarsal joint pain from, 327
subtalar joint pain from, 324
in tibiofibular pain syndrome, 291
vs. scapulocostal syndrome, 60
shoulder
vs. quadrilateral space syndrome, 99
vs. subacromial impingement syndrome, 82
vs. suprascapular nerve entrapment, 97
subtalar joint pain from, 324
in tibiofibular pain syndrome, 291, 291f
vs. scapulocostal syndrome, 60
Arthrocentesis, in fabella syndrome, 315
Arthrography
in accessory navicular pain syndrome, 341f
in subtalar joint pain, 324, 326f
Arthropathy, rotator cuff tear, vs. scapulocostal
syndrome, 60
Arthroscopy, in glomus tumor of knee, 311312,
312f
Athletic supporter, for orchialgia, 251253
Atypical facial pain, vs. nervus intermedius
neuralgia, 44
Atypical odontalgia, 3739, 37f38f, 38t39t
Avascular necrosis
of hip, 265267, 265f267f, 265t
vs. adductor tendinitis, 281
of scaphoid, 165168
clinical pearls on, 168b
clinical syndrome of, 165, 165f
complications and pitfalls of, 166168
differential diagnosis of, 165166
signs and symptoms of, 165, 166f
testing for, 165, 166f167f
treatment of, 166
vs. flexor carpi radialis tendinitis, 172
vs. scapholunate ligament tear syndrome,
155
Avulsion fractures
vs. anterior talofibular pain syndrome, 339
vs. fibulocalcaneal pain syndrome, 344
Axillary nerve anatomy, through quadrilateral space,
100f
Baclofen
for glossopharyngeal neuralgia, 4950
for nervus intermedius neuralgia, 4445
for Parsonage-Turner syndrome, 6364
for spasmodic torticollis, 5556
Bakers cyst
ruptured
vs. fabella syndrome, 315316
vs. semimembranosus insertion syndrome, 297
vs. hamstring tendinitis, 318
Bence Jones protein, in multiple myeloma,
219220
Biopsy, temporal artery, for temporal arteritis, 28
Bone
growth of, abnormal, in and about axial skeleton,
causes of, 225t
Pagets disease of, 222224, 223f
tumors of, vs. Pagets disease, 222223
Bornholm disease, 178. See also Devils grip.
vs. liver pain, 210
Botulinum toxin injections, for spasmodic
torticollis, 56
Botulinum toxin type A injection, for gluteus
medius syndrome, 249
Bowel obstruction, intermittent, vs. anterior
cutaneous nerve entrapment, 202
Boxers knuckle, 146148, 146f147f
Brachial plexopathy
causes of, 6263
vs. os acromial pain syndrome, 86
vs. scapulocostal syndrome, 60
vs. subacromial impingement syndrome, 82
Brachial plexus block, for Parsonage-Turner syndrome, 64
Brachial plexus pain syndromes
cervicothoracic interspinous bursitis as, 5759,
58f59f
Parsonage-Turner syndrome as, 6265, 62f, 63t,
64f
scapulocostal syndrome as, 6061, 61f
Brain tumor, vs. headache associated with temporal
arteritis, 28
Breaststrokers knee, 303305, 303f305f
Bupivacaine/methylprednisolone injection. See also
Anesthetic/steroid injection.
for Achilles bursitis, 335, 336f
for breaststrokers knee, 305
for cervicothoracic interspinous bursitis, 57
for fabella syndrome, 316, 317f
for iliotibial band bursitis, 313314, 314f
for infraspinatus tendinitis, 7778, 80f
for lumbar myofascial pain syndrome, 236237,
236f
for quadriceps expansion syndrome, 307, 307f
for runners knee, 309, 309f
for slipping rib syndrome, 199
for snapping hip syndrome, 286287, 290f
for supraspinatus tendinitis, 75f, 75, 76f
Burning mouth syndrome, 4042, 40f, 41t
Bursitis
Achilles, 335337, 336f
ankle, vs. midtarsal joint pain, 327
cervicothoracic interspinous, 5759, 58f59f
cubital, 106107, 106f107f
elbow, vs. os supratrochlearerelated elbow pain,
111
gluteal, 260261, 260f261f
iliopectinate, 283285, 283f284f
iliotibial, with runners knee, 308
iliotibial band, 313314, 314f
knee, vs. fabella syndrome, 315316
patellar, vs. jumpers knee, 293
pes anserine, 320323, 321f322f. See also
Pes anserine bursitis.
prepatellar, vs. quadriceps expansion syndrome,
307
psoas, 268270, 268f269f
shoulder
vs. infraspinatus tendinitis, 77
vs. quadrilateral space syndrome, 99
Bursitis (Continued)
vs. suprascapular nerve entrapment, 97
vs. supraspinatus tendinitis, 74
submetatarsal adventitial, 355357, 355f356f
suprapatellar
vs. jumpers knee, 293
vs. quadriceps expansion syndrome, 307
trochanteric, with snapping hip syndrome, 286
vs. extensor carpi ulnaris tendinitis, 169
vs. posterior tibial tendinitis, 332
Calcifications
in calcific tendinitis of quadriceps tendon, 306
in gluteal bursitis, 260
in triceps tendinitis, 116, 116f
Calcitonin, for Pagets disease, 223
Carbamazepine
for Charlins syndrome, 9
for glossopharyngeal neuralgia, 49
for nervus intermedius neuralgia, 44
for Parsonage-Turner syndrome, 63
for quadrilateral space syndrome, 99
for Ramsay Hunt syndrome, 34
Cardiac pain. See also Heart attack.
vs. liver pain, 210
Carnetts test, for anterior cutaneous nerve
entrapment, 202, 203f
Carpometacarpal joint arthritis, vs. ulnar tunnel
syndrome, 134
Cash brace
for multiple myeloma, 221
for Pagets disease, 223
Catching tendon sign, in trigger wrist, 175, 176f
Celiac artery stenosis, in abdominal angina, 213f,
212
Cephalgias, trigeminal autonomic, 16f, 16t. See also
Trigeminal autonomic cephalgias.
Cerebellopontine angle tumors, vs. neck-tongue
syndrome, 72
Cervical disc, herniated, lateral, vs. ParsonageTurner syndrome, 63
Cervical nerve root tumors, vs. Parsonage-Turner
syndrome, 63
Cervical radiculopathy
vs. anconeus epitrochlearis, 109
vs. anterior interosseous syndrome, 130
vs. cheiralgia paresthetica, 136137
vs. cubital tunnel syndrome, 122
vs. infraspinatus tendinitis, 77
vs. Parsonage-Turner syndrome, 6263, 63t
vs. pronator syndrome, 104
vs. quadrilateral space syndrome, 99
vs. radial tunnel syndrome, 120
vs. scapulocostal syndrome, 60
vs. suprascapular nerve entrapment, 97
vs. supraspinatus tendinitis, 74
vs. ulnar tunnel syndrome, 134
Cervical spine
immobilization of, for neck-tongue syndrome, 72
tumors of, vs. Parsonage-Turner syndrome, 63
Cervical spondylosis, vs. Parsonage-Turner
syndrome, 63
Cervicothoracic interspinous bursitis, 5759,
58f59f
Charlins syndrome, 910, 10f, 10t
Cheiralgia paresthetica, 136138, 136f137f, 138t
Chemotherapy, for multiple myeloma, 221
Chest wall, anterior, tumors of, vs. pectoralis major
tear syndrome, 9394
Chest wall pain syndromes. See Thoracic pain
syndromes.
Cholecystitis, vs. anterior cutaneous nerve entrapment, 202
Index 361
Chordoma, clival, 5254, 52t, 53f
Chronic paroxysmal hemicrania, 78, 7f, 8f, 7t. See
also Hemicrania, chronic paroxysmal.
Chvosteks sign, in multiple myeloma, 219
Cimetidine, for acute intermittent porphyria, 206
Claudication, jaw. See Jaw claudication.
Clavicular fractures, vs. os acromial pain syndrome,
86
Clitoral priapism, 258259, 258f259f, 258t259t
Clitoromegaly, causes of, 259t
Clival chordoma syndrome, 5254, 52t, 53f
Cluster headache
pain location in, 18f
vs. Charlins syndrome, 9, 10t
vs. chronic paroxysmal hemicrania, 78, 7t
vs. cough headache, 14
vs. headache associated with temporal arteritis, 28
vs. ice pick headache, 1
vs. red ear syndrome, 47
vs. sexual headache, 12
vs. SUNCT headache, 1617, 17t
Coin-shaped headache, 25
Colitis, ischemic, 213, 213f
Collagen-vascular diseases
vs. ankylosing spondylitis, 230
vs. anterior cutaneous nerve entrapment, 202
vs. midtarsal joint pain, 327
vs. scapulocostal syndrome, 60
vs. subtalar joint pain, 324
vs. tibiofibular pain syndrome, 292
Colonoscopy
for proctalgia fugax, 238
for radiation enteritis, 207
Computed tomography (CT)
of accessory navicular pain syndrome, 341f
of ankylosing spondylitis, 230
of anterior cutaneous nerve entrapment, 202
of atypical odontalgia, 38f
of avascular necrosis of scaphoid, 165
of Charlins syndrome, 9
of chronic paroxysmal hemicrania, 7
of clitoral priapism, 258259
of clival chordoma syndrome, 52
of cough headache, 1314
of devils grip, 178, 179f
of diffuse idiopathic skeletal hyperostosis, 225
of Eagles syndrome, 35, 36f
of epidural abscess, 215
of glossopharyngeal neuralgia, 48
of hypnic headache, 2324
of levator ani pain syndrome, 263264, 263f
of liver pain, 209210, 210f
of manubriosternal joint pain, 190, 191f
of neck-tongue syndrome, 72
of nummular headache, 25
of os acromial pain syndrome, 86, 88f
in os trigonum pain syndrome, 346
of osteonecrosis of elbow joint, 113114, 115f
of Parsonage-Turner syndrome, 63
of pectoralis major tear syndrome, 92
of postmastectomy pain, 185186
of proctalgia fugax, 238
of prostatodynia, 241
of radiation enteritis, 207
of red ear syndrome, 4647
of sexual headache, 12
of spasmodic torticollis, 55
of spondylolisthesis, 227
of sternalis syndrome, 188, 189f
of sternoclavicular syndrome, 182183, 183f
of subacromial impingement syndrome, 8182
of subtalar joint pain, 326f
of SUNCT headache, 16
of supraorbital neuralgia, 3
of temporal arteritis, 28
362 Index
Diabetic neuropathy, femoral, vs. psoas bursitis, 269
Diabetic polyneuropathy. See also Neuropathic pain.
vs. anterior cutaneous nerve entrapment, 202,
204t
Diffuse idiopathic skeletal hyperostosis (DISH),
225226, 225t, 226f
DISH (diffuse idiopathic skeletal hyperostosis),
225226, 225t, 226f
Double crush syndrome
anconeus epitrochlearis in, 109
anterior interosseous syndrome in, 130
cheiralgia paresthetica in, 136137
cubital tunnel syndrome in, 122
drivers elbow in, 126
gluteal bursitis in, 260261
iliopectinate bursitis in, 284
pronator syndrome in, 104
psoas bursitis in, 269
Drainage, of epidural abscess, 215216
Drivers elbow, 126129
clinical pearls on, 129b
clinical syndrome of, 126
complications and pitfalls of, 127129
differential diagnosis of, 126
signs and symptoms of, 126, 126f, 127t
testing for, 126, 128f
treatment of, 126127
Drugs, implicated in priapism, 258t, 259
Dry pleurisy, 178. See also Devils grip.
Duchennes sign, 127t
Dull type sexual headache, 11
Dural puncture, headache after, 3031, 31f
Dystonia, in spasmodic torticollis, 55
Electromyography (Continued)
in femoral neuropathy, 271
in foreign body synovitis, 141
in glomus tumor of hand, 144
in glomus tumor of knee, 311312
in gluteal bursitis, 260
in iliotibial band bursitis, 313
in Kienbcks disease, 162
in lunotriquetral instability pain syndrome, 159
in obturator neuralgia, 277
in orchialgia, 251
in osteonecrosis of elbow joint, 113114
in Parsonage-Turner syndrome, 63
in postmastectomy pain, 185186
in pronator syndrome, 104
in prostatodynia, 241
in quadrilateral space syndrome, 99
in radial tunnel syndrome, 120
in runners knee, 308
in saphenous neuralgia, 273
in scapholunate ligament tear syndrome, 155
in Secretans syndrome, 139
in serratus anterior muscle syndrome, 195
in spondylolisthesis, 227228
in sternalis syndrome, 188
in superior cluneal nerve entrapment syndrome,
233
in suprascapular nerve entrapment, 9697
in triangular fibrocartilage tear syndrome, 150
in ulnar tunnel syndrome, 134
in vulvodynia, 254
in winged scapula syndrome, 200
Empyema, vs. devils grip, 179
Enemas, steroid and sucralfate, for radiation
enteritis, 207
Enteritis
infectious
vs. abdominal angina, 213
vs. radiation enteritis, 207
radiation, 207t, 207208, 208f
Entrapment neuropathies
vs. accessory navicular pain syndrome, 340
vs. adductor tendinitis, 281
vs. coronary ligament strain, 302
vs. iliotibial band bursitis, 313
vs. metatarsalgia, 353354
vs. midtarsal joint pain, 327
vs. os supratrochlearerelated elbow pain, 111
vs. os trigonum pain syndrome, 346
vs. pes anserine bursitis, 320
vs. runners knee, 308
vs. semimembranosus insertion syndrome, 297
vs. sesamoiditis, 350
vs. subtalar joint pain, 324
vs. tibiofibular pain syndrome, 292
Epicondylitis
elbow, vs. os supratrochlearerelated elbow pain,
111
lateral. See Tennis elbow.
Epidural abscess, 215218, 216f217f, 217t
Epidural blood patch, for postdural puncture
headache, 3031
Epidural nerve blocks
for ankylosing spondylitis, 231232
for diffuse idiopathic skeletal hyperostosis, 226
for prostatodynia, 241243
for spondylolisthesis, 228
Erythrocyte sedimentation rate, for temporal
arteritis, 28
Erythromelelgia of ear, vs. red ear syndrome, 47
Etidronate, for Pagets disease, 223
Exertional headache, benign
vs. cough headache, 14
vs. hypnic headache, 24
Expansions, in quadriceps tendon, 306
Gabapentin
for burning mouth syndrome, 41
for Charlins syndrome, 9
for Eagles syndrome, 36
for glossopharyngeal neuralgia, 49
for nervus intermedius neuralgia, 44
for obturator neuralgia, 277279
Index 363
Gabapentin (Continued)
for Parsonage-Turner syndrome, 63
for postmastectomy pain, 186
for proctalgia fugax, 238239
for quadrilateral space syndrome, 99
for Ramsay Hunt syndrome, 34
for red ear syndrome, 47
for saphenous neuralgia, 273
for SUNCT headache, 17
for thunderclap headache, 21
Gallbladder attack
vs. devils grip, 179
vs. liver pain, 210
Gasserian ganglion, balloon decompression of, for
SUNCT headache, 17
Geniculate ganglion, herpes zoster involvement of,
in Ramsay Hunt syndrome, 32, 32f
Geniculate neuralgia, 43
Genitofemoral neuralgia
vs. iliopectinate bursitis, 284
vs. orchialgia, 251
Giant cell arteritis, 27. See also Temporal arteritis.
Glaucoma
vs. Ramsay Hunt syndrome, 33
vs. supraorbital neuralgia, 3, 6f
Glenohumeral joint, tumors of, vs. glomus tumor of
shoulder, 9091
Glomus tumor
of hand, 144145, 144f145f
of knee, 311312, 311f312f
of shoulder, 9091, 90f
Glossopharyngeal nerve, radiofrequency destruction
of, for glossopharyngeal neuralgia, 50
Glossopharyngeal nerve block, for glossopharyngeal
neuralgia, 50, 50f
Glossopharyngeal neuralgia, 4851, 48f50f
vs. Eagles syndrome, 35
vs. hyoid syndrome, 66
vs. neck-tongue syndrome, 72
Glossopharyngeal root, microvascular decompression of, for glossopharyngeal neuralgia, 50, 50f
Glucose, for acute intermittent porphyria, 206
Gluteal bursitis, 260261, 260f261f
vs. gluteus medius syndrome, 249
vs. superior cluneal nerve entrapment syndrome,
233
Gluteal nerve entrapment, vs. gluteus medius
syndrome, 249
Gluteus maximus muscle, function of, 244, 244f
Gluteus maximus pain syndrome, 244247,
244f246f
Gluteus medius pain syndrome, 248250,
248f249f
vs. levator ani pain syndrome, 264
Golfers elbow
vs. anconeus epitrochlearis, 109
vs. cubital bursitis, 106
vs. cubital tunnel syndrome, 122
vs. drivers elbow, 126
Gout
elbow
vs. cubital bursitis, 106
vs. os supratrochlearerelated elbow pain, 111
vs. radial tunnel syndrome, 120
vs. accessory navicular pain syndrome, 340
Grip of the phantom, 178. See also Devils grip.
Groin pain syndromes. See Abdominal/groin pain
syndromes.
364 Index
Infraspinatus tendinitis (Continued)
differential diagnosis of, 77
signs and symptoms of, 77, 78f
testing for, 77, 79f
treatment of, 7778, 80f
Inguinal hernia
vs. adductor tendinitis, 281
vs. psoas bursitis, 269
Injection technique and needle placement. See also
specific injection.
for Achilles bursitis, 335, 336f
for cervicothoracic interspinous bursitis, 57, 59f
for cubital bursitis, 107, 107f
for Eagles syndrome, 3536, 36f
for gluteal bursitis, 261, 261f
for gluteus maximus pain syndrome, 245246,
245f
for hyoid syndrome, 66, 67f
for iliopectinate bursitis, 284, 284f
for infraspinatus tendinitis, 7778, 80f
for lumbar myofascial pain syndrome, 236237,
236f
for omohyoid syndrome, 70, 70f
for osteonecrosis of elbow joint, 114
for quadriceps expansion syndrome, 307, 307f
for runners knee, 309, 309f
for slipping rib syndrome, 199
for snapping hip syndrome, 286287, 290f
for subacromial impingement syndrome, 82
for superior cluneal nerve entrapment syndrome,
233234
for supraorbital nerve block, 4, 6f
for supraspinatus tendinitis, 75, 76f
for trigger wrist, 176
Insect stings, clitoral priapism treatment and, 259
Intercostaobrachial nerve damage, in postmastectomy pain, 185, 185f
Intermittent porphyria, acute, 205206, 205f
Intracranial pathology, vs. Ramsay Hunt syndrome,
33
Intrapelvic tumors, vs. gluteus maximus pain
syndrome, 245
Knee (Continued)
degenerative arthritis of, vs. coronary ligament
strain, 302
glomus tumor of, 311312, 311f312f
hemarthrosis of, vs. semimembranosus insertion
syndrome, 297
jumpers, 293295, 294f295f
runners, 308310, 308f309f
surfers, 273
Knee pain syndromes
breaststrokers knee, 303305, 303f305f
coronary ligament strain as, 301302, 301f
fabella syndrome as, 315317, 315f317f
glomus tumor of knee as, 311312, 311f312f
hamstring tendinitis as, 318319, 318f
iliotibial band bursitis as, 313314, 314f
jumpers knee as, 293295, 294f295f
pes anserine bursitis as, 320323, 321f322f. See
also Pes anserine bursitis.
quadriceps expansion syndrome as, 306307,
306f307f
runners knee as, 308310, 308f309f
semimembranosus insertion syndrome as,
296300, 296f299f. See also Semimembranosus insertion syndrome.
tibiofibular pain syndrome as, 291f, 291292,
291f
Khlers bone disease
vs. accessory navicular pain syndrome, 340
vs. os trigonum pain syndrome, 346
Lamotrigine
for red ear syndrome, 47
for SUNCT headache, 17
Larynx, tumors of, vs. Eagles syndrome, 35
Lateral antebrachial cutaneous nerve syndrome, vs.
cheiralgia paresthetica, 136137
Lateral epicondylitis. See Tennis elbow.
Levator ani muscle
function of, 262
origin of, 262, 262f
Levator ani pain syndrome, 262264, 262f263f
Levodopa, for spasmodic torticollis, 5556
Lidocaine/methylprednisolone injection, for
superior cluneal nerve entrapment syndrome,
233234
Ligament
coronary, strain of, 301302, 301f
of Struthers, median nerve entrapment by, vs.
pronator syndrome, 104
Lithium carbonate, for hypnic headache, 24
Liver pain, 209211, 209f210f
Loves test
for glomus tumor of hand, 144
for glomus tumor of knee, 311
Low back strain
vs. ankylosing spondylitis, 230
vs. spondylolisthesis, 228
Lower extremity pain. See Ankle and foot pain
syndromes; Hip and lower extremity pain
syndromes; Knee pain syndromes.
Lumbar bursitis
vs. ankylosing spondylitis, 230
vs. spondylolisthesis, 228
Lumbar fibromyositis
vs. ankylosing spondylitis, 230
vs. spondylolisthesis, 228
Lumbar myofascial pain syndrome, 235237,
235f236f
Lumbar plexopathy
vs. obturator neuralgia, 277
vs. superior cluneal nerve entrapment syndrome,
233
Lumbar radiculopathy
vs. coronary ligament strain, 302
vs. femoral neuropathy, 271
vs. gluteal bursitis, 260261
vs. iliopectinate bursitis, 284
vs. iliotibial band bursitis, 313
vs. midtarsal joint pain, 327
vs. obturator neuralgia, 277
vs. pes anserine bursitis, 320
vs. psoas bursitis, 269
vs. runners knee, 308
vs. saphenous neuralgia, 273
vs. spondylolisthesis, 228
vs. subtalar joint pain, 324
vs. superior cluneal nerve entrapment syndrome,
233
vs. tibiofibular pain syndrome, 292
Lumbar spine and sacroiliac joint pain syndromes
ankylosing spondylitis as, 230232, 231f232f, 232t
diffuse idiopathic skeletal hyperostosis as,
225226, 225t, 226f
epidural abscess as, 215218, 216f217f, 217t
lumbar myofascial pain syndrome as, 235237,
235f236f
multiple myeloma as, 219221, 219f220f
Pagets disease as, 222224, 223f
spondylolisthesis as, 227229, 227f229f
superior cluneal nerve entrapment syndrome as,
233234, 234f
Lumbar strain, vs. lumbar myofascial pain syndrome, 236
Lumbosacral plexopathy, vs. gluteus maximus pain
syndrome, 245
Lumbosacral radiculopathy
vs. gluteus maximus pain syndrome, 245
vs. levator ani pain syndrome, 264
Lunate cysts, vs. Kienbcks disease, 162
Lunate fractures
vs. extensor carpi ulnaris tendinitis, 169
vs. lunotriquetral instability pain syndrome, 159
Lunotriquetral instability pain syndrome, 159161,
159f161f
Lunotriquetral ligament complex, anatomy of, 159f
Lyme disease
vs. midtarsal joint pain, 327
vs. scapulocostal syndrome, 60
Index 365
Magnetic resonance imaging (MRI) (Continued)
of anconeus epitrochlearis, 109, 109f
of ankylosing spondylitis, 230, 232f
of anterior interosseous syndrome, 130, 132f
of anterior talofibular pain syndrome, 338
of atypical odontalgia, 3738, 38f
of avascular necrosis of hip, 266, 266f267f
of avascular necrosis of scaphoid, 165, 167f
of boxers knuckle, 146
of breaststrokers knee, 304, 304f
of bunionette pain, 348
of cervicothoracic interspinous bursitis, 57, 59f
of Charlins syndrome, 9, 10f
of cheiralgia paresthetica, 136
of chronic paroxysmal hemicrania, 7, 8f
of clitoral priapism, 258259
of clival chordoma syndrome, 53f, 52
of coronary ligament strain, 302
of cough headache, 1314
of cubital bursitis, 106
of cubital tunnel syndrome, 122, 124f
of diffuse idiopathic skeletal hyperostosis, 225,
226f
of drivers elbow, 126, 128f
of epidural abscess, 215, 217f
of extensor carpi ulnaris tendinitis, 169, 170f
of fabella syndrome, 315, 316f
of femoral neuropathy, 271, 272f
of fibulocalcaneal pain syndrome, 343, 344f
of flexor carpi radialis tendinitis, 172, 173f
of foreign body synovitis, 141, 142f
of glomus tumor of hand, 144, 145f
of glomus tumor of knee, 311312, 311f312f
of glomus tumor of shoulder, 90, 90f
of glossopharyngeal neuralgia, 48, 49f
of gluteal bursitis, 260
of gluteus maximus pain syndrome, 245, 246f
of hamstring tendinitis, 318
of hyoid syndrome, 66
of hypnic headache, 2324
of ice pick headache, 1, 2f
of iliopectinate bursitis, 284
of iliotibial band bursitis, 313
of infraspinatus tendinitis, 77
of jumpers knee, 293, 295f
of Kienbcks disease, 162, 163f164f
of levator ani pain syndrome, 263264, 263f
of liver pain, 209210, 210f
of lumbar myofascial pain syndrome, 236
of lunotriquetral instability pain syndrome, 159
of manubriosternal joint pain, 190
of metatarsalgia, 353
of midtarsal joint pain, 327, 329f
of multiple myeloma, 219220, 220f
of neck-tongue syndrome, 72
of nervus intermedius neuralgia, 4344, 44f
of nummular headache, 25, 26f
of obturator neuralgia, 277
of omohyoid syndrome, 69
of orchialgia, 251
of os acromiale pain syndrome, 86, 88f
of os supratrochlearerelated elbow pain, 111
of os trigonum pain syndrome, 346, 347f
of osteonecrosis of elbow joint, 113114, 114f
of Pagets disease, 222
of Parsonage-Turner syndrome, 63, 64f
of pectoralis major tear syndrome, 92, 95f
of pes anserine bursitis, 320, 321f322f
of postdural puncture headache, 30
of posterior tibial tendinitis, 331, 333f
of postmastectomy pain, 185186
of proctalgia fugax, 238, 239f
of pronator syndrome, 104
of prostatodynia, 241
of psoas bursitis, 269
366 Index
Neers test
for os acromial pain syndrome, 86
for subacromial impingement syndrome, 81, 85f
Nerve(s)
of Bell, trauma to, in winged scapula syndrome, 200
glossopharyngeal, radiofrequency destruction of,
for glossopharyngeal neuralgia, 50
Nerve block(s)
differential, in atypical odontalgia diagnosis,
3738, 39t
glossopharyngeal, for glossopharyngeal neuralgia,
50, 50f
for Ramsay Hunt syndrome, 33
for supraorbital neuralgia, 4, 6f
trigeminal, for atypical odontalgia, 39
Nerve conduction velocity testing
for diffuse idiopathic skeletal hyperostosis, 225
for spondylolisthesis, 227228
Nerve entrapment, suprascapular, 96, 96f97f
Nervus intermedius, section of, for nervus intermedius neuralgia, 45
Nervus intermedius neuralgia, 4345, 43f44f
Neuralgia
genitofemoral
vs. iliopectinate bursitis, 284
vs. orchialgia, 251
glossopharyngeal, 4851, 48f50f
vs. Eagles syndrome, 35
ilioinguinal
vs. iliopectinate bursitis, 284
vs. orchialgia, 251
nasociliary, 910, 10f, 10t
nervus intermedius, 4345, 43f44f
obturator, 277279, 277f278f
postherpetic, 33
saphenous, 273276, 274f275f. See also Saphenous neuralgia.
supraorbital, 36, 3f, 4f, 5f, 6f, 6f
trigeminal. See Trigeminal neuralgia.
Neurofibromatosis, vs. epidural abscess, 215216
Neuroma, Mortons, vs. submetatarsal adventitial
bursitis, 355357
Neuropathic pain
chest wall
vs. sternalis syndrome, 189
vs. sternoclavicular syndrome, 183
vs. liver pain, 210
vs. manubriosternal joint pain, 190
vs. postmastectomy pain, 186
vs. serratus anterior muscle syndrome, 195
vs. slipping rib syndrome, 199
Neuropathy, handcuff, 136
Neurovascular orofacial pain (NVOP), pain
location in, 18f
Nimodipine, for thunderclap headache, 21
Nonsteroidal antiinflammatory drugs (NSAIDs)
for accessory navicular pain syndrome, 341
for Achilles bursitis, 335
for adductor tendinitis, 281
for anconeus epitrochlearis, 109
for ankylosing spondylitis, 231232
for anterior cutaneous nerve entrapment, 203
for anterior interosseous syndrome, 130
for anterior talofibular pain syndrome, 339
for avascular necrosis of hip, 267
for avascular necrosis of scaphoid, 166
for boxers knuckle, 146
for breaststrokers knee, 304305
for bunionette pain, 348
for cervicothoracic interspinous bursitis, 57
for cheiralgia paresthetica, 137
for coronary ligament strain, 302
for cubital bursitis, 107
for cubital tunnel syndrome, 122
for devils grip, 180
Nortriptyline
for anterior interosseous syndrome, 130
for atypical odontalgia, 39
for hyoid syndrome, 66
for obturator neuralgia, 277279
for omohyoid syndrome, 6970
for postmastectomy pain, 186
for proctalgia fugax, 238, 238239
for pronator syndrome, 104
for saphenous neuralgia, 273
for suprascapular nerve entrapment, 97
for vulvodynia, 254255
Nummular headache, 2526, 25f26f
Index 367
Parsonage-Turner syndrome, 6265, 62f, 63t, 64f
vs. os acromial pain syndrome, 86
vs. quadrilateral space syndrome, 99
vs. subacromial impingement syndrome, 82
vs. suprascapular nerve entrapment, 97
Patellar bursitis, vs. jumpers knee, 293
Pectoralis major tear syndrome, 9295
clinical pearls on, 95b
clinical syndrome of, 92, 93f95f
complications and pitfalls of, 9495
differential diagnosis of, 9394
signs and symptoms of, 92, 95f
testing for, 92
treatment of, 94
Pelvic examination, for vulvodynia, 254
Pelvic floor muscle strain, vs. levator ani pain
syndrome, 264
Pelvic pain syndrome(s)
chronic, 241
clitoral priapism as, 258259, 258f259f,
258t259t
distinguishing features, 242f
gluteal bursitis as, 260261, 260f261f
gluteus maximus pain syndrome as, 244247,
244f246f
gluteus medius syndrome as, 248250, 248f249f
levator ani pain syndrome as, 262264, 262f263f
orchialgia as, 251253, 252f, 252t253t
proctalgia fugax as, 238240, 239f
prostatodynia as, 241243, 242f, 243t
vulvodynia, 254257, 255f256f, 256t257t. See
also Vulvodynia.
Pelvis
fractures of
stress, vs. gluteus maximus pain syndrome, 245
vs. adductor tendinitis, 281
tumors in, vs. gluteus maximus pain syndrome, 245
Peptic ulcer disease, vs. anterior cutaneous nerve
entrapment, 202
Peripheral neuropathy, vs. obturator neuralgia, 277
Persistent orodental pain syndrome, 3739,
37f38f, 38t39t
Pes anserine bursitis, 320323
clinical pearls on, 323b
clinical syndrome of, 320, 321f
complications and pitfalls of, 320323
differential diagnosis of, 320
signs and symptoms of, 320
testing for, 320, 321f322f
treatment of, 320
Physical therapy
for ankylosing spondylitis, 231232
for cubital bursitis, 107
for cubital tunnel syndrome, 122
for diffuse idiopathic skeletal hyperostosis, 226
for flexor carpi radialis tendinitis, 173
for foreign body synovitis, 141
for gluteal bursitis, 261
for gluteus maximus pain syndrome, 245
for gluteus medius syndrome, 249
for infraspinatus tendinitis, 77
for levator ani pain syndrome, 264
for lumbar myofascial pain syndrome, 236
for orchialgia, 251253
for os acromial pain syndrome, 8687
for Parsonage-Turner syndrome, 64
for radial tunnel syndrome, 120
for Secretans syndrome, 139
for spondylolisthesis, 228
for subacromial impingement syndrome, 82
for supraspinatus tendinitis, 7475
Piriform sinus tumors
vs. clival chordoma syndrome, 5253
vs. glossopharyngeal neuralgia, 49
vs. neck-tongue syndrome, 72
Radiculopathy
cervical. See Cervical radiculopathy.
lumbar. See Lumbar radiculopathy.
Radiofrequency destruction, of glossopharyngeal
nerve, for glossopharyngeal neuralgia, 50
Radiography
in abdominal angina, 212213, 213f
in accessory navicular pain syndrome, 340, 341f
in Achilles bursitis, 335
in adductor tendinitis, 280
in anconeus epitrochlearis, 109
in ankylosing spondylitis, 230, 231f
in anterior cutaneous nerve entrapment, 202
in anterior interosseous syndrome, 130
in anterior talofibular pain syndrome, 338
in atypical odontalgia, 3738
in avascular necrosis of hip, 266
in avascular necrosis of scaphoid, 165, 166f
in boxers knuckle, 146, 147f
in breaststrokers knee, 304
in bunionette pain, 348, 348f
in cheiralgia paresthetica, 136
in coronary ligament strain, 302
in cubital bursitis, 106
in cubital tunnel syndrome, 122
in devils grip, 178, 179f
in diffuse idiopathic skeletal hyperostosis, 225
in Eagles syndrome, 35
in extensor carpi ulnaris tendinitis, 169
in fabella syndrome, 315
in femoral neuropathy, 271
in fibulocalcaneal pain syndrome, 343
in flexor carpi radialis tendinitis, 172, 174f
in gluteal bursitis, 260
in gluteus maximus pain syndrome, 245
in hamstring tendinitis, 318
in iliopectinate bursitis, 284, 284f
in iliotibial band bursitis, 313
in infraspinatus tendinitis, 77, 79f
in jumpers knee, 293
in Kienbcks disease, 162, 164f
in levator ani pain syndrome, 263264
in liver pain, 209210
in lumbar myofascial pain syndrome, 236
in lunotriquetral instability pain syndrome, 159,
161f
in manubriosternal joint pain, 190, 190f
in metatarsalgia, 353, 354f
in midtarsal joint pain, 327
in multiple myeloma, 219220, 220f
in obturator neuralgia, 277
in os supratrochlearerelated elbow pain, 111
in os trigonum pain syndrome, 346, 347f
in osteonecrosis of elbow joint, 113114
in Pagets disease, 222
in pes anserine bursitis, 320, 322f
in posterior tibial tendinitis, 331, 332f
in postmastectomy pain, 185186
in pronator syndrome, 104
in psoas bursitis, 269, 269f
in quadriceps expansion syndrome, 307
in runners knee, 308
in saphenous neuralgia, 273
in scapholunate ligament tear syndrome, 155,
157f
in scapulocostal syndrome, 60
in Secretans syndrome, 139
in semimembranosus insertion syndrome, 297
in serratus anterior muscle syndrome, 195
in sesamoiditis, 350, 351f
in slipping rib syndrome, 198
in snapping hip syndrome, 286
in spondylolisthesis, 227, 228f
in sternalis syndrome, 188
in sternoclavicular syndrome, 182183
368 Index
Radiography (Continued)
in submetatarsal adventitial bursitis, 355
in subtalar joint pain, 324
in superior cluneal nerve entrapment syndrome,
233
in supraspinatus tendinitis, 74
in tibiofibular pain syndrome, 291292
in triangular fibrocartilage tear syndrome, 150
in triceps tendinitis, 116117, 116f
in trigger wrist, 175
in xiphodynia, 193
Radionuclide bone scans
in accessory navicular pain syndrome, 340
in Achilles bursitis, 335
in adductor tendinitis, 280
in fabella syndrome, 315
in glomus tumor of knee, 311312
in metatarsalgia, 353
in os trigonum pain syndrome, 346
in Pagets disease, 222, 223f
in posterior tibial tendinitis, 332
in postmastectomy pain, 185186
in scapulocostal syndrome, 60
in semimembranosus insertion syndrome, 297
in sesamoiditis, 350
in submetatarsal adventitial bursitis, 355
Radius, distal, fractures of
vs. avascular necrosis of scaphoid, 165166
vs. flexor carpi radialis tendinitis, 172
Ramsay Hunt syndrome, 3234, 32f33f
Raynauds syndrome, vs. glomus tumor of hand, 144
Rectal examination, for proctalgia fugax, 238
Rectal malignancy, vs. proctalgia fugax, 238
Red ear syndrome, 4647, 46f
Reflex sympathetic dystrophy
of face, vs. atypical odontalgia, 3839
vs. clitoral priapism, 259
vs. glomus tumor of hand, 144
vs. glomus tumor of knee, 312
vs. glomus tumor of shoulder, 9091
vs. prostatodynia, 241
vs. Secretans syndrome, 139
vs. vulvodynia, 254
Reiters syndrome, vs. ankylosing spondylitis, 230
Renal calculi, vs. anterior cutaneous nerve entrapment, 202
Resisted abduction release test, for snapping hip
syndrome, 286, 289f
Retroorbital tumors, vs. Ramsay Hunt syndrome, 33
Retropharyngeal tumors, vs. atypical odontalgia,
3839
Rheumatoid arthritis. See Arthritis, rheumatoid.
Rib-tip syndrome, 198
Rotator cuff
tears of
vs. infraspinatus tendinitis, 77
vs. supraspinatus tendinitis, 74
tendinopathy/tendinitis of
vs. os acromial pain syndrome, 86
vs. subacromial impingement syndrome, 82
Rotator cuff tear arthropathy, vs. scapulocostal
syndrome, 60
Runners knee, 308310, 308f309f
Index 369
Splint
nighttime, for trigger wrist, 175176
for sternoclavicular syndrome, 183
Spondylitis, ankylosing, 230232, 231f232f,
232t
vs. cervicothoracic interspinous bursitis, 57
Spondylolisthesis, 227229, 227f229f
vs. lumbar myofascial pain syndrome, 236
Spondylosis, cervical, vs. Parsonage-Turner
syndrome, 63
Stabbing headache
primary, vs. red ear syndrome, 47
vs. SUNCT headache, 17
Stellate ganglion block, for burning mouth syndrome, 41
Sternalis syndrome, 188189, 188f189f
Sternoclavicular syndrome, 182184,
182f183f
Steroid enemas, for radiation enteritis, 207
Steroids. See also Corticosteroids.
high-dose
for Charlins syndrome, 9
for multiple myeloma, 221
for Pagets disease, 223
for red ear syndrome, 47
for SUNCT headache, 17
Strain, coronary ligament, 301302, 301f
Stress fractures
acromial, vs. os acromial pain syndrome, 86
ankle
vs. Achilles bursitis, 335
vs. posterior tibial tendinitis, 332
metatarsal, vs. submetatarsal adventitial bursitis,
355357
olecranon, vs. triceps tendinitis, 117
pelvic, vs. gluteus maximus pain syndrome,
245
vs. bunionette pain, 348
vs. levator ani pain syndrome, 264
Stylohyoid syndrome, 3536, 35f36f
Styloid syndrome, vs. hyoid syndrome, 66
Subacromial bursitis
vs. os acromial pain syndrome, 86
vs. subacromial impingement syndrome, 82
Subacromial impingement syndrome, 8185,
81f85f, 84t
causes of, 84t
clinical pearls on, 85b
clinical syndrome of, 81, 81f84f, 84t
complications and pitfalls of, 8285
differential diagnosis of, 82
signs and symptoms of, 81, 85f
testing for, 8182, 83f84f
treatment of, 82
vs. os acromial pain syndrome, 86
Subacromial space, 81, 81f
Subarachnoid hemorrhage
thunderclap headache and, 19, 19t20t
vs. postdural puncture headache, 30
Submetatarsal adventitial bursitis, 355357,
355f356f
Subtalar joint pain, 324326, 325f326f
Subungual melanoma, vs. glomus tumor of hand,
144
Sucralfate enemas, for radiation enteritis, 207
Sudden unilateral neuralgiform conjunctival injection tearing (SUNCT) headache, 1618,
16f18f, 16t18t
vs. red ear syndrome, 4647
Sulfasalazine, for ankylosing spondylitis,
231232
SUNCT headache, 1618, 16f18f, 16t18t
Superior cluneal nerve entrapment syndrome,
233234, 234f
vs. gluteus medius syndrome, 249
Tendinitis (Continued)
vs. triangular fibrocartilage tear syndrome, 150
flexor carpi radialis, 172174, 172f174f
hamstring, 318319, 318f
infraspinatus, 7780, 78f80f. See also
Infraspinatus tendinitis.
knee, vs. fabella syndrome, 315316
posterior tibial, 331334, 331f333f
shoulder
vs. quadrilateral space syndrome, 99
vs. suprascapular nerve entrapment, 97
supraspinatus, 7476, 75f76f
triceps, 116118, 116f117f
vs. Achilles bursitis, 335
Tennis elbow
vs. cubital bursitis, 106
vs. radial tunnel syndrome, 119t, 120
Tenosynovitis, vs. glomus tumor of shoulder,
9091
Tension headache, vs. headache associated with
temporal arteritis, 28
Testicular pain, 251
chronic, treatment options for, 253t
Thoracic outlet syndrome, vs. pronator syndrome,
104
Thoracic pain syndromes
devils grip as, 178181. See also Devils grip.
manubriosternal joint pain as, 190192,
190f191f
postmastectomy pain as, 185187, 185f186f
serratus anterior muscle syndrome as, 195197,
196f
slipping rib syndrome as, 198199, 198f
sternalis syndrome as, 188189, 188f189f
sternoclavicular syndrome as, 182184,
182f183f
winged scapula syndrome as, 200201, 201f
xiphodynia as, 193194, 193f194f
Thunderclap headache, primary, 1922, 19t20t,
20f21f
Thyroglossal duct cyst, vs. hyoid syndrome, 66
Tibial plateau fracture, vs. semimembranosus
insertion syndrome, 297
Tibiofibular pain syndrome, 291f, 291292,
291f
Tics, vs. spasmodic torticollis, 55
Tietzes syndrome
vs. devils grip, 179
vs. serratus anterior muscle syndrome,
195
vs. slipping rib syndrome, 198199
vs. sternalis syndrome, 188189
vs. sternoclavicular syndrome, 183
Tinels sign
in cheiralgia paresthetica, 136, 137f
in cubital tunnel syndrome, 122
in drivers elbow, 126, 126f
in orchialgia, 251
in pronator syndrome, 103
in superior cluneal nerve entrapment syndrome,
233
in ulnar tunnel syndrome, 133
Tolosa-Hunt syndrome, vs. Ramsay Hunt
syndrome, 33
Tonsillar fossa tumors
vs. clival chordoma syndrome, 5253
vs. glossopharyngeal neuralgia, 4849
vs. neck-tongue syndrome, 72
Torticollis, spasmodic, 5556, 56f
Total joint arthroplasty
for avascular necrosis of hip, 266267
for osteonecrosis of elbow joint, 113114
Transcutaneous electrical nerve stimulation
for gluteus medius syndrome, 249
for Ramsay Hunt syndrome, 34
370 Index
Trauma
manubriosternal joint pain secondary to, 190,
190f191f
serratus anterior muscle syndrome secondary to,
195
slipping rib syndrome secondary to, 198
Traumatic tumor, vs. epidural abscess, 215216
Traveling salesman shoulder, 60
Trefoil spinal canal, vs. lumbar myofascial pain
syndrome, 236
Trendelenburg gait, in avascular necrosis of hip,
265266
Triangular fibrocartilage complex
anatomy of, 149f
function of, 149, 150t
tears of
vs. avascular necrosis of scaphoid, 165166
vs. extensor carpi ulnaris tendinitis, 169
vs. flexor carpi radialis tendinitis, 172
vs. Kienbcks disease, 162
vs. lunotriquetral instability pain syndrome,
159
Triangular fibrocartilage tear syndrome, 149154
causes of, 149, 150t
clinical pearls on, 154b
clinical syndrome of, 149, 149f, 151f
complications and pitfalls of, 150154
differential diagnosis of, 150
signs and symptoms of, 149150, 151f
testing for, 150, 152f154f
treatment of, 150
Triceps tendinitis, 116118, 116f117f
Tricyclic antidepressants
for ankylosing spondylitis, 231232
for anterior interosseous syndrome, 130
for atypical odontalgia, 39
for hyoid syndrome, 66
for manubriosternal joint pain, 191192
for obturator neuralgia, 277279
for omohyoid syndrome, 6970
for postmastectomy pain, 186
for proctalgia fugax, 238
for pronator syndrome, 104
for quadrilateral space syndrome, 99
for saphenous neuralgia, 273
for suprascapular nerve entrapment, 97
for vulvodynia, 254255
Trigeminal autonomic cephalgias (TACs),
16f, 16t
chronic paroxysmal hemicrania as, 7f. See also
Hemicrania, chronic paroxysmal.
cluster headache as. See Cluster headache.
pain location in, 18f
red ear syndrome as, 46
sudden unilateral neuralgiaform conjunctival
injection tearing headache as, 1618,
16f18f, 16t18t
Trigeminal nerve block, for atypical odontalgia,
39
Trigeminal neuralgia
vs. atypical odontalgia, 3739, 38t
vs. Charlins syndrome, 9
vs. chronic paroxysmal hemicrania, 8
vs. clival chordoma syndrome, 5253
vs. cough headache, 14
vs. headache associated with temporal arteritis,
28
vs. hypnic headache, 24
vs. ice pick headache, 2
vs. nummular headache, 25
vs. Ramsay Hunt syndrome, 33
vs. red ear syndrome, 47
vs. sexual headache, 12
vs. SUNCT headache, 17
vs. supraorbital neuralgia, 34
Index 371
Wrist and hand pain syndromes (Continued)
Kienbcks disease as, 162164, 162f164f
lunotriquetral instability pain syndrome as,
159161, 159f161f
scapholunate ligament tear syndrome as,
155158, 156f157f. See also Scapholunate ligament tear syndrome.
Secretans syndrome as, 139140, 139f
triangular fibrocartilage tear syndrome as,
149154, 149f, 151f154f. See also Triangular fibrocartilage tear syndrome.