Download Keys to Understanding Common Nerve Entrapments

Keys to Understanding Common Nerve
Entrapments
Course Description:
This course utilizes the text: Orthopedic Clinical Advisor by Derrick Sueki, PT, DPT, GCPT,
OCS and Jacklyn Brechter, PhD, PT. This course will help you access the information you
need to confidently handle multiple orthopedic conditions. Essential clinical reference
information provides up-to-date diagnostic and therapeutic information on common nerve
entrapments conditions in a bulleted, quick-reference format ideal for both students and
practitioners. Content is written entirely by orthopedic physical therapists and is logically
organized to promote accurate, efficient differential diagnosis and intervention.
Nerve Entrapments covered are:
Axillary Nerve Entrapment
Brachial Plexus Nerve Entrapment
Common Fibular Nerve Entrapment
Deep Fibular Nerve Entrapment
Femoral Nerve Entrapment
Interosseous Nerve Entrapment
Lateral Femoral Cutaneous Nerve Entrapment
Long Thoracic Nerve Pathology
Median Nerve Entrapment
Neurogenic Thoracic Outlet Syndrome
Obturator Nerve Entrapment
Plantar Nerve Entrapment
Radial Nerve Entrapment
Saphenous Nerve Entrapment
Sciatic Nerve Entrapment
Suprascapular Nerve Entrapment
Sural Nerve Entrapment
Tibial Nerve Entrapment
Vascular Thoracic Outlet Syndrome
Ulnar Nerve Entrapment
Each diagnosis covers:
Definition
Synonyms
Optimal Number of Visits/Maximal Number of Visits
Etiology
Epidemiology and Demographics
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Mechanism of Injury
Common Signs and Symptoms
Aggravating Activities
Easing Activities
24-Hour Symptom Pattern
Past History for the Region
Physical Examination
Important Objective Tests
Differential Diagnosis
Contributing Factors
Treatment
Surgical Options
Rehabilitation
Prognosis
Signs and Symptoms Indicating Referral to Physician
Methods of Instruction:
Online course available via internet
Target Audience:
Physical Therapists, Physical Therapist Assistants, Occupational Therapists, Occupational
Therapist Assistants and Athletic Trainers
Educational Level:
Intermediate
Prerequisites:
None
Course Goals and Objectives:
At the completion of this course, participants should be able to:
1. Identify areas of injury for Axillary Nerve Entrapment
2. Recognize the signs/symptoms of Brachial Nerve Entrapment
3. Identify the sensory distribution for Common Fibular Nerve Entrapment
4. Identify aggravating activities of Deep Fibular Nerve Entrapment
5. Recognize contributing factors of Femoral Nerve Entrapment
6. Recognize the differential diagnosis for Interosseous Nerve Entrapment
7. Identify the signs/symptoms of Lateral Femoral Cutaneous Nerve Entrapment
8. Recognize the most common complaint of Long Thoracic Nerve Pathology
9. Identify the demographics of Median Nerve Entrapment
10. Recognize the synonyms for Neurogenic Thoracic Outlet Syndrome
11. Recognize the signs/symptoms for physician referral of Obturator Nerve Entrapment
12. Identify the components of a physical examination for Plantar Nerve Entrapment
13. Differentiate between the classifications of nerve injury for Radial Nerve Entrapment
14. Identify the signs/symptoms of Saphenous Nerve Entrapment
15. Recognize the differential diagnosis for Suprascapular Nerve Entrapment
Criteria for Obtaining Continuing Education Credits:
A score of 70% or greater on the written post-test
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DIRECTIONS FOR COMPLETING
THE COURSE:
1.
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4.
5.
6.
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9.
This course is offered in conjunction with and with written permission
of Elsevier Science Publishing.
Review the goals and objectives for the module.
Review the course material.
We strongly suggest printing out a hard copy of the test. Mark your
answers as you go along and then transfer them to the actual test. A
printable test can be found when clicking on “View/Take Test” in your
“My Account”.
After reading the course material, when you are ready to take the
test, go back to your “My Account” and click on “View/Take Test”.
A grade of 70% or higher on the test is considered passing. If you
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please re-read the material and take the test again.
After passing the test, you will be required to fill out a short survey.
After the survey, your certificate of completion will immediately
appear. We suggest that you save a copy of your certificate to your
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CHAPTER 16
Axillary Nerve Entrapment
Nerve
BASIC INFORMATION
DEFINITION
• Axillary nerve entrapment pathologies
encompass any injury that interrupts
the function of the axillary nerve at any
point along its course.
• The axillary nerve is particularly vulnerable to injury at the following:
Surgical neck of the humerus
Inferior aspect of the glenohumeral
joint
Quadrilateral space
Deltoid muscle
• The loss of function results in muscle
weakness, pain, or sensory dysfunction.
SYNONYMS
Quadrilateral space syndrome
ICD-9CM CODES
354 Mononeuritis of upper limb and
mononeuritis multiplex
354.8 Other mononeuritis of upper
limb
354.9 Mononeuritis of upper limb
unspecified
6
MAXIMAL NUMBER OF VISITS
20
• The axillary nerve is the smaller of the
terminal branches of the posterior cord
and the shortest of the major terminal
branches of the brachial plexus. It is a
mixed motor and sensory nerve derived
from the C5 and 6 nerve roots that originates from the anterior aspect of the
subscapularis muscle, passes laterally
toward the inferior aspect of the shoulder joint, passes inferiorly to the head of
the humerus, above the tendons of latissimus dorsi and teres major, and passes
through the quadrilateral space, which
is bounded medially by the humerus,
laterally by the long head of the triceps muscle, superiorly by teres minor
(which it supplies), and inferiorly by
teres major.
• It then wraps horizontally around the
posterior aspect of the surgical neck
of the humerus and enters the deltoid muscle as three branches: an anterior branch to the middle and anterior
aspects of the deltoid, a posterior
branch to the posterior deltoid, and the
upper lateral brachial cutaneous nerve
branch to the skin in the area of the deltoid tuberosity
• The axillary nerve may be affected at
any point along its course by direct
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EPIDEMIOLOGY AND
DEMOGRAPHICS
• Axillary nerve injury is the most common nerve injury associated with the
shoulder, particularly in relation to
trauma such as fracture and dislocation.
• Quadrilateral space syndrome is an
uncommon pathology seen in throwing
athletes, as well as in sports with repetitive cocking action such as tennis or
volleyball. The cocking action involves
end-range shoulder abduction, extension, and external rotation followed by
rapid flexion and internal rotation.
MECHANISM OF INJURY
• Mechanisms of injury for the axillary
nerve are described in relation to their
location, as follows:
Direct trauma in the form of a humeral
neck fracture causing damage to the
nerve
Dislocation of the glenohumeral joint
in which the nerve is stretched across
the humeral neck by an anterior
dislocation
Operative procedures at the inferior
aspect of the shoulder such as capsular shift involving a deltoid-splitting incision that directly injures the
nerve
Blunt injury such as a heavy fall onto
the lateral aspect of the shoulder compressing the nerve within the deltoid
muscle
Overuse syndromes from repeated
scapular motions, leading to compression of the posterior humeral circumflex artery and the axillary nerve within
the quadrilateral space by fibrous
bands. The size of the quadrilateral
space is reduced in positions of abduction and external rotation. Overuse
syndrome occasionally occurs after
general anesthesia or sleeping prone
with the arms raised above the head.
COMMON SIGNS AND
SYMPTOMS
• Poorly localized posterior shoulder
pain
• Paraesthesia over the lateral aspect of
the shoulder and arm
• Weakness of deltoid and teres minor
resulting in difficulty abducting the
arm
• External rotation may be mildly weaker.
• Patient may describe shoulder weakness.
• Atrophy of the deltoid may be evident.
AGGRAVATING ACTIVITIES
• Activities that involve shoulder abduction
ORTHOPEDIC PATHOLOGY
ETIOLOGY
repair damage incurred but produce
adhesions to the nerve, limiting their
glide and increasing anoxia.
Section III
OPTIMAL NUMBER OF VISITS
trauma or compression entrapment,
causing nerve tissue hypoxia.The insult
to the nerve can be mechanical, thermal, chemical, or ischemic; however,
the axillary nerve is most commonly
injured by glenohumeral fractures and
dislocations.
• Axillary nerve entrapment is usually
related to trauma; nevertheless, pathology can occur in a number of ways, as
follows:
Direct trauma in the form of a humeral
neck fracture
Dislocation of the glenohumeral joint
in which the nerve is stretched across
the humeral neck by an anterior
dislocation
Operative procedures at the inferior
aspect of the shoulder such as capsular shift involving a deltoid-splitting
incision
Blunt injury such as a heavy fall onto
the lateral aspect of the shoulder
Overuse syndromes from repeated
scapular motions, leading to compression of the posterior humeral circumflex artery and the axillary nerve
within the quadrilateral space by
fibrous bands. The size of the quadrilateral space is reduced in positions of
abduction and external rotation.
• Nerve injury is classified according to
the severity of the injury and its potential for reversibility.
• Neurapraxia (first-degree injury) is a distortion of the myelin about the nodes of
Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance, which produces temporary loss
of nerve conduction.
• Axonotmesis (second-degree injury) is
an interruption of the axon with secondary wallerian degeneration.The supporting tissue surrounding the axon
is preserved, and the recovery period
depends on the distance between the
site of injury and the end organs.
• Neurotmesis is a complete disruption of
the nerve and its supporting structures.
Neurotmesis has been further divided
into the following three subcategories:
Third-degree
nerve injury: Endoneurium is disrupted with intact perineurium and epineurium.
Fourth-degree nerve injury: All neural
elements sparing the epineurium are
disrupted.
Fifth-degree nerve injury: Complete
transaction and discontinuity of
the nerve with no capacity for
regeneration
• Physiologically, there is disruption to
any part of the nerve responsible for
conduction.
In repetitive-type nerve entrapment,
it is proposed that repetitive work or
static postures produce an inflammatory process and fibroblasts appear to
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740
Axillary Nerve Entrapment
• Repetitive shoulder internal and/or
external rotation occurs particularly
when the shoulder is in an abducted
position.
EASING ACTIVITIES
Rest and/or modification of aggravating
activities
CHAPTER 16 • NERVE
tors, such as posture and patterning,
that will assist with rehabilitation and
activity modification. In the case of the
axillary nerve, the patient often demonstrates trick movements to accomplish
shoulder abduction through use of the
rotator cuff and proximal scapular and
cervical muscles.
24-HOUR SYMPTOM PATTERN
IMPORTANT OBJECTIVE TESTS
• Generally, the symptoms are related
to activity and do not follow a typical
24-hour pattern unless there is a strong
inflammatory component, which may
be seen in repetitive tasks.
• If there is an inflammatory component,
there may be worsening of symptoms
with use toward the end of the day, as
well as morning stiffness.
• Electromyography (EMG) may reveal
delayed conduction velocity and fibrillation potentials.
• Needle EMG should assist with determination of specific muscle involvement
and provide differential diagnosis from
the other shoulder neuropathies and
cervical radiculopathies.
• If quadrilateral space syndrome is suspected, there will be concomitant
posterior humeral circumflex artery
compression, and therefore a subclavian arteriogram can provide diagnostic
information.
PAST HISTORY FOR THE REGION
• History of trauma, fracture, or dislocation of the glenohumeral joint
• Repetitive overuse of the shoulder in
occupation or sports
• Generalized hypermobility
PHYSICAL EXAMINATION
• Examine the shoulder for signs of atrophy of the deltoid muscle.
• Manual muscle testing (MMT) may reveal
weakness in the following muscles:
Deltoid: Tested in shoulder flexion,
abduction, and extension for each of
the portions of the deltoid; however,
weakness is usually demonstrated in
pure abduction.
Teres minor: Tested in external rotation; however, the infraspinatus muscle is a stronger external rotator and
is likely to compensate for the loss of
the teres minor muscle.
• Sensation testing should be performed.
The cutaneous branch of the axillary
nerve supplies the lateral aspect of the
shoulder overlying the deltoid muscle
and tuberosity. Sensation testing should
include pinprick, two-point discrimination, and tuning fork tests and compared
for asymmetry with the unaffected side
(where available).
• Physical examination should also
exclude pathology in other areas, particularly performing active range of
motion (AROM) and passive ROM
(PROM) at the neck and shoulder, which
may reveal restrictions, other shoulder
pathology, and/or central involvement
of the nerve.
• Physical examination should also
include movement analysis to determine
the movement patterns that the patient
adopts when performing the aggravating activities. Movement analysis can
be done visually or with the assistance
of a video camera. The analysis should
give some clues as to predisposing fac-
TREATMENT
SURGICAL OPTIONS
• Surgery may be considered after a failure of conservative management.
• Surgery involves nerve grafting techniques and a rotational transfer of
deltoid removing the denervated
portion.
REHABILITATION
• Lesion to the posterior cord of
the brachial plexus
• C5 or C6 radiculopathy
• Suprascapular neuropathy produces a
similar pattern of weak arm abduction
and external rotation but no sensory
loss.
• Rotator cuff tears
• Rotator cuff tendinopathies
• Adhesive capsulitis
• Shoulder instability
• Degenerative joint disease at the glenohumeral or acromioclavicular (AC)
joints
• Underlying neuropathic disease
• Neuralgic amyotrophy
• Muscular dystrophy
• Tumors or space-occupying lesions
• Upper motor neuron lesion in the cerebrum
• The goal of rehabilitation should be
pain reduction to encourage pain-free
exercise and to provide task or sports
reeducation and interventions leading
to reacquisition of fine motor and sporting skills.
• Manual therapy
Pain
reduction can be achieved
through the use of ice and electrotherapeutic modalities.
Soft tissue release may assist with restoration of muscle balance around the
scapula, which is useful if compensations have occurred in other muscles
to make up for the loss of the deltoid
and teres minor muscles.
• Functional rehabilitation
Reeducation of movement patterns,
particularly proximal control of the
trunk and neck, to provide a stable
foundation for scapular stability
Scapular position education initially
with isometric hold and then the addition of controlled functional movement patterns
Prevention of aberrant movement patterns and contractures with ROM and
gentle stretch techniques
Specific muscle strengthening gradually increasing in intensity to restore
full power to the deltoid and teres
minor muscles
Integration of functional exercise and
strength work into sport- or task-specific skills
Graduated return to full strength,
speed, and power
CONTRIBUTING FACTORS
PROGNOSIS
• Trauma is the most common contributing factory for axillary nerve injuries;
however, for any nerve entrapments
that are nontraumatic, there is often an
element of repetitive activity involving
the affected limb.
• Typically in the case of the axillary
nerve, the repetitive action involves
shoulder abduction and external glenohumeral rotation.
• Postural factors may be involved, particularly with repetitive work or sporting
activities with reduction in proximal
stability and control, leading to an overuse of more distal muscle groups to perform a task.
• Prognosis depends entirely on the
extent of damage to the nerve.
• Neurapraxia should resolve rapidly and
lead to a complete restoration of function, usually within 2 to 3 months.
• If the injury is a more severe axonotmesis, the recovery time depends on the
distance from the site of injury to the
denervated tissue.
• Peripheral nerves have been reported
to recover at an approximate rate of
1 to 4 mm per day and may not result in
a complete restoration of function.
• If there has been a complete sectioning of the nerve (neurapraxia), then the
nerve will not fully recover.
DIFFERENTIAL
DIAGNOSIS
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Axillary Nerve Entrapment
CHAPTER 16 • NERVE
• The results of treating neurapraxia even
with surgical intervention are generally
not satisfactory.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
If axillary nerve entrapment is suspected,
all cases should be referred to a physician
for appropriate investigation.
SUGGESTED READINGS
Aldridge JW, Bruno RJ, Strauch RJ, Rosenwasser
MP. Nerve entrapment in athletes. Clin Sports
Med. 2001;20(1):95.
Goslin KL, Krivickas LS. Proximal neuropathies of the upper extremity. Neurol Clin.
1999;17(3).
Kibler WB, Murrell GAC. Shoulder pain. In:
Brukner P, Khan K, eds. Clinical Sports
Medicine. 3rd ed. Australia: McGraw-Hill
Book Company; 2006:243–288.
741
Leffert RD. Nerve lesions about the shoulder.
Orthop Clin North Am. 2000;31(2).
AUTHOR: JOSEPHINE LOUISE COULTER
Section III
ORTHOPEDIC PATHOLOGY
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Brachial Plexus Nerve Entrapment
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BASIC INFORMATION
DEFINITION
• The brachial plexus, composed of the
posterior cord (formed from the posterior divisions of the upper trunk from
C5 and C6 nerve roots, the middle trunk
from C7, and the lower trunk from C8
and T1), the lateral cord (formed from
the anterior divisions of the upper and
middle trunks), and the medial cord
(formed from the anterior division of
the lower trunk), communicates the
nerve supply between the cervical roots
and the upper limb, passing through the
scalene muscles and sternocleidomastoid, and under the clavicle.
• It may be subject to the following injuries:
Traction injury during birth if the
head is pulled away from the shoulder (Erb’s palsy in which the arm is
held in adduction and internal rotation with forearm pronation and wrist
and hand flexion, or Klumpke’s palsy
with Horner’s syndrome consisting of
meiosis, ptosis, and anhydrosis)
Traction injury from a traumatic event
Compression injury from trauma to
the cervical spine, clavicle, humerus,
or pectoral girdle; impact on Erb’s
point; or poor postures
Compression
injury from narrowing of the neural foramen with cervical hyperextension and ipsilateral
rotation
Compression injury from anatomical
variations in the cervical spine, clavicle, first rib, pectoral girdle, or posterior triangle
SYNONYMS
•
•
•
•
•
•
•
•
•
•
Brachial plexus injury
Cervical rib syndrome
Cervical pinch syndrome
Costoclavicular syndrome
Scalenus anticus syndrome
Hyperabduction syndrome
Thoracic outlet syndrome
Stinger
Burner syndrome
Chronic burner syndrome
ICD-9CM CODES
353.0 Brachial plexus lesions
953.4 Injury to brachial plexus
OPTIMAL NUMBER OF VISITS
Recovery normally occurs between 24
hours and 2 to 3 weeks.
MAXIMAL NUMBER OF VISITS
Symptoms persisting for more than 2 to
3 weeks, together with worsening neurological signs, warrant further clinical
investigation.
CHAPTER 16 • NERVE
ETIOLOGY
• Insult to the nerve may be mechanical, thermal, chemical, or ischemic. In
entrapment syndromes, compression
or direct trauma leads to nerve tissue
hypoxia.
• The brachial plexus may be compressed
from trauma to the cervical spine, shoulder, pectoral girdle, clavicle, or rib; from
postural issues, with direct pressure on
Erb’s point (punctum nervosum at the
union between C5 and C6 nerve roots
on the lateral cord 2 to 3 cm above the
clavicle); or from narrowing of the neural foramen with cervical hyperextension and ipsilateral rotation. Specific
anatomical features of entrapment in
the upper limb are described by Pratt.
• In entrapments, nerve trauma occurs
because the size of the neural structure
exceeds the anatomical space available
for it, resulting in increased pressure
that in turn leads to impaired blood
flow and subsequent hypoxia of the tissue and disruption to the axonal transport system. Nerve injury is classified
according to severity of the injury and
potential for reversibility.
• Original classifications described previously remain in current use, as follows:
First-degree neurapraxia involves distortion of myelin about the nodes of
Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance, resulting in temporary loss of
nerve conduction. Recovery is usually
rapid and complete.
Second-degree axonotmesis involves
interruption of the axon with secondary wallerian degeneration, but the
supporting tissue around the axon is
preserved. Recovery may be complete
but takes longer to occur and depends
on the distance between the site of
injury and the end structure (denervated muscle).
Third-degree
neurotmesis involves
extensive disruption of the nerve and
its supporting structures, but while
the endoneurium is disrupted, the
perineurium and epineurium remain
intact.
Fourth-degree neurotmesis involves
disruption of all neural components
except the epineurium.
Fifth-degree
neurotmesis involves
complete transaction and discontinuity of the nerve, with no capacity
for regeneration. Neurotmesis rarely
occurs from entrapment, but when
continuity has been disrupted, complete recovery is not possible, even
with surgical techniques, and the
eventual outcome depends on individual circumstances. A comprehensive overview of neurobiology, nerve
injury, and nerve repair is provided by
Dahlin.
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• Double-crush syndrome refers to the
fairly common phenomenon of nerve
entrapment and radiculopathy occurring in combination, although the syndrome is considered controversial.
Compression or irritation of the nerve
roots at the cervical level is thought to
increase sensitivity to compression or
movement restrictions more distally in
the structure.
• As noted, increasing pressure on the
nerve causes impaired blood flow, tissue hypoxia, and disruption to the
anterograde and retrograde intercellular transport of materials within axons,
eventually disturbing depolarization
within the nerve. In brachial plexus
compression, the pressure may result
directly from anatomical structures,
direct trauma, or from the associated
phenomena of edema, glenohumeral
dislocation, or clavicular fracture.
Mechanisms and patterns of injury are
discussed by Moran et al.
EPIDEMIOLOGY AND
DEMOGRAPHICS
• In adults, compression injury of the
brachial plexus tends to occur most
commonly from an accident or sportsrelated trauma to the cervical spine,
shoulder, pectoral girdle, and upper
quadrant, particularly sports involving
high impact such as contact sports and
gymnastics.
• It may also occur from the presence
of a cervical rib arising from C7 vertebra (cervical rib syndrome), narrowing
of the costoclavicular space between
the clavicle and the first rib as a result
of bony anomaly or combined depression and retraction of the shoulder as
occurs when carrying a rucksack (costoclavicular syndrome), compression at
the coracoid process when the upper
limb is held in hyperabduction (hyperabduction syndrome), or compression
between the anterior and medial scalenes (scalenus anticus syndrome).
• Pathology related to trauma tends to
occur in younger people predominantly
because of the type of activity usually
associated with the injury. Pathology
related to anatomical anomalies and
variation may occur across a broader
spectrum of the population.
MECHANISM OF INJURY
• Brachial plexus injury is discussed by
Mannan and Carlstedt and Bishop et al.
Impact trauma resulting in clavicular
fracture, glenohumeral dislocation, or
edema around the shoulder may result
in direct pressure on the brachial plexus
as it passes under the clavicle or at Erb’s
point (burner syndrome).
• The presence of a cervical rib reduces
the space between the scalenes, making
Brachial Plexus Nerve Entrapment
CHAPTER 16 • NERVE
compression more likely in the region
of the posterior triangle (cervical rib
syndrome).
• Bony anomaly or combined depression
and retraction of the shoulder reduces
the space between the clavicle and first
rib, making compression more likely at
this site (costoclavicular syndrome).
• Anatomical variations in the posterior
triangle and scalene muscles, particularly if combined with other associated
elements, may produce compression at
this site (scalenus anticus syndrome).
• Compression at the coracoid process
and pectoralis minor muscle may occur
with sustained overhead arm postures.
COMMON SIGNS AND
SYMPTOMS
• Activities and postures that involve
impact through the upper quadrant
• Cervical extension and ipsilateral rotation
• Poor posture with “drooping” shoulders
• Loading through the shoulder (particularly into depression and retraction)
such as carrying a rucksack or a heavy
object in the hand with the arm at the
side
• Activities involving sustained periods
with the arm overhead, such as painting
EASING ACTIVITIES
Adaptations in posture and reduction
in loading reduce the stress on the brachial plexus, as described in Aggravating
Activities.
24-HOUR SYMPTOM PATTERN
• In general, symptoms are more likely
to be associated with trauma, posture,
and activity rather than time. However,
when symptoms are aggravated by cervical spine or overhead arm positions,
there may be an increase in symptoms
• Presence of anatomical anomalies
• Impact trauma producing clavicular
fracture
• Glenohumeral dislocation
• Edema around the shoulder
• Hyperextension and ipsilateral rotation
of the cervical spine
PHYSICAL EXAMINATION
• Clinical assessment in brachial plexus
injuries is summarized by Mannan and
Carlstedt. Physical findings in brachial
plexus compression may include the
following:
Shoulder pain, radiating up into the
neck and down into the upper limb,
combined with weakness or paralysis
of the biceps brachii, deltoid, brachialis, brachioradialis, and coracobrachialis muscles and muscles supplied
by the axillary, musculocutaneous, and
radial nerves, together with associated
paraesthesia and numbness
Bony anomalies may be detected.
Erb’s point may be tender on palpation.
Grip strength may be reduced.
The upper limb may be held in adduction and medial rotation with forearm
pronation and wrist and hand flexion
(“waiter’s tip” position).
Individuals may describe sensation of
burning in the neck, weakness, cold,
“heaviness,” or “dead arm” and complain of clumsiness.
IMPORTANT OBJECTIVE TESTS
• Diagnostic accuracy of neurological
upper limb examination employing
a battery of standard test procedures
has been found to be reproducible and
reliable.
• For brachial plexus injuries, initial
assessment must focus on neurological function, cervical spine fracture, and
spinal cord injury before further testing
is performed.
• Radiography, ultrasound, and magnetic
resonance imaging (MRI) techniques
and neurophysiology and EMG testing
may be helpful in identifying underlying anatomical or traumatic issues and
clarifying clinical diagnosis.
• Spurling test: Brachial plexus symptoms
are reproduced with cervical extension,
ipsilateral rotation, and axial loading for
a positive result.
• Erb’s point palpation:Tenderness is elicited for a positive result.
• Costoclavicular maneuver: Brachial
plexus symptoms and a reduction in
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DIFFERENTIAL
DIAGNOSIS
• Cervical spine injuries, including spinal cord injury, bony trauma, soft
tissue injury, radiculopathy, and discogenic trauma
• Glenohumeral dislocation
• AC joint injury
• Shoulder impingement syndrome
• Thoracic outlet syndrome
• Peripheral neuropathies
• Vascular pathology
• Cardiac pathology
• Pulmonary pathology
• Pancoast’s syndrome
• Tobias or Ciuffini-Pancoast-Tobias syndrome
• Breast carcinoma
• Mesothelioma, plasmacytoma
• Lymphoma
• Metastatic carcinoma
CONTRIBUTING FACTORS
Traumatic injury is often a factor in brachial
plexus compression, but the presence of
anatomical anomalies in the cervical spine,
clavicle, and posterior triangle may predispose an individual to the pathology.
TREATMENT
SURGICAL OPTIONS
• An overview of basic neurosurgical
techniques is provided by Dahlin.When
compression is due to cervical or first
rib abnormalities, surgical resection of
the rib may be required if conservative
methods have failed to produce resolution. Division of fibrous bands, release
techniques for relevant soft tissues, and
correction, reduction, or fixation after
traumatic injury may also be appropriate, depending on the underlying cause
of the pathology. When severe and violent trauma has occurred, specialist
neurosurgery may be required, including nerve transfers, nerve grafts, and
neurolysis of scar tissue at the brachial
plexus.
ORTHOPEDIC PATHOLOGY
AGGRAVATING ACTIVITIES
PAST HISTORY FOR THE REGION
radial pulse are reproduced in the
upper limb with shoulder depression
and retraction in individuals with costoclavicular syndrome.
• Adson’s test (scalene test): Brachial
plexus symptoms and a reduction in
radial pulse are reproduced with cervical extension and ipsilateral rotation
while sustaining a deep inspiration for a
positive result.
• Wright’s test: Brachial plexus symptoms
and a reduction in radial pulse are reproduced with hyperabduction in sitting
and supine lying for a positive result.
Section III
• Shoulder pain, radiating up into the
neck and down into the upper limb
• Weakness or paralysis of the biceps
brachii, deltoid, brachialis, brachioradialis, and coracobrachialis muscles
and muscles supplied by the axillary,
musculocutaneous, and radial nerves,
together with associated paraesthesia
and numbness
• The upper limb may be held in adduction and medial rotation with forearm
pronation and wrist and hand flexion
(“waiter’s tip” position).
• Individuals may describe a sensation
of weakness, cold, “heaviness,” or “dead
arm” and complain of clumsiness.
• Pain may be referred up into the neck,
throughout the shoulder, and down into
the upper limb.
• Sensory and motor symptoms may
occur throughout the upper limb.
nocturnally as a consequence of sleeping postures.
• Increases in nocturnal pain are also
reported in which deafferentation pain
is present.
743
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Brachial Plexus Nerve Entrapment
• Very few presentations require surgical
intervention, but in common with other
neural entrapments affecting the upper
limb, surgery produces a good outcome
in approximately 90% of cases.
• Traumatic injuries requiring correction,
reduction, or fixation may need early
surgical intervention. Otherwise, surgery is indicated only in those cases in
which response to conservative management has been poor.
REHABILITATION
• In the acute stage, treatment is focused
on pain relief, antiinflammatory therapy,
and early mobilization.
• During the subacute stages, active exercise therapy aims to regain normal
movement, strength, posture, and functional control, with particular emphasis on support for the injured neural
structures.
• In the late recovery stages, further progression aims to return the individual to
preinjury fitness.
• Physiotherapy involves a comprehensive management program composed
of manual mobilization and soft tissue
techniques, electrotherapy modalities,
biomechanical analysis, postural reeducation and control, and functional
movement, strength, and stability work.
Appropriate aids to support the neck
and affected structures may be advisable to prevent further injury during
recovery.
PROGNOSIS
• Presence of anatomical anomalies in the
cervical spine, clavicle, pectoral girdle,
and posterior triangle, combined with a
past history of trauma in these regions
CHAPTER 16 • NERVE
and participation in high-impact contact
sports or high-loading activities with or
without sustained postures, predispose
an individual to brachial plexus trauma
and compression.
• Complications include chronic burner
syndrome, contractures, scoliosis, glenohumeral dislocation, and, rarely,
upper limb agnosia and deafferentation
pain, but the majority of cases show
complete resolution with conservative
management.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
Indications for further medical evaluation include evidence of underlying
trauma, worsening neurological function or symptoms, failure to respond to
conservative management, suspicion or
presence of underlying disease, and unexplained symptoms inconsistent with the
pathology.
SUGGESTED READINGS
Bishop AT, Spinner RJ, Shin AY. Brachial
plexus injuries in adults. Hand Clin. 2005;
21(1):ix–x.
Dahlin LB. Mini-symposium: hand trauma (ii)
nerve injuries. Curr Orthop. 2008;22(1):9–16.
Hall TM, Elvey RL. Nerve trunk pain: physical diagnosis and treatment. Man Ther.
1999;4(2):63–73.
Hassan S, Kay S. Brachial plexus injury. Surgery.
2003;21(10):262–264.
Jepsen JR, Laursen LH, Hagert C-G, Kreiner S,
Larsen AI. Diagnostic accuracy of the neurological upper limb examination I: interrelater reproducibility of selected findings
and patterns. BMC Neurol. 2006;6(8).
Jepsen JR, Laursen LH, Hagert C-G, Kreiner
S, Larsen AI. Diagnostic accuracy of the
9 of 57
neurological upper limb examination II:
relations to symptoms of patterns of findings. BMC Neurol. 2006;6(10).
Kinlaw D. Pre-/postoperative therapy for
adult plexus injury. Hand Clin. 2005;21(1):
103–108.
Levitz CL, Reilly PJ, Torg JS. The pathomechanics of chronic, recurrent cervical nerve root
neuropraxia. The chronic burner syndrome.
Am J Sports Med. 1997;25(1):73–76.
Mannan K, Carlstedt T. Injuries to the brachial
plexus. Surgery. 2006;24(12):415–420.
Markey KL, Di Benedetto M, Curl WW. Upper
trunk brachial plexopathy. The stinger
syndrome. Am J Sports Med. 1993;21(5):
650–655.
Moran SL, Steinmann SP, Shin AY. Adult brachial plexus injuries: mechanism, patterns
of injury, and physical diagnosis. Hand Clin.
2005;21(1):13–24.
Nithi K. Physiology of the peripheral nervous
system. Surgery. 2003;21(10):264a–264e.
Pratt N. Anatomy of nerve entrapment
sites in the upper quarter. J Hand Ther.
2005;18(2):216–219.
Reid S, Trent V. Brachial plexus injuries—report
of two cases presenting to a sports medicine practice. Phys Ther Sport. 2002;3(4):
175–182.
Seddon HJ. Surgical Disorders of the Peripheral Nerves. 2nd ed. Edinburgh: Churchill
Livingstone; 1975.
Shin AY, Spinner RJ, Steinmann SP, Bishop AT.
Adult traumatic brachial plexus injuries.
J Am Acad Orthop Surg. 2005;13:382–396.
Sunderland S. Nerve and Nerve Injuries. 2nd
ed. Edinburgh: Churchill Livingstone; 1978.
Weinberg J, Rokito S, Silber JS. Etiology, treatment, and prevention of athletic stingers.
Clin Sports Med. 2003;22(3):493–500.
Wilbourn AJ, Gilliat RW. Double crush syndrome: a critical analysis. Neurology. 1997;
49:21–29.
AUTHOR: SARAH GRAHAM
Common Fibular Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Common fibular nerve entrapment is a
mononeuropathy that results from compression or restricted movement of the
nerve usually found around the fibular
head or in the popliteal space behind the
knee.
SYNONYMS
• Common peroneal nerve entrapment
• Strawberry picker’s knee
• Slimmer’s paralysis
ICD-9CM CODES
355.7 Other mononeuritis of lower
limb
OPTIMAL NUMBER OF VISITS
6 or fewer
MAXIMAL NUMBER OF VISITS
16
ETIOLOGY
EPIDEMIOLOGY AND
DEMOGRAPHICS
This condition is the most common
nerve entrapment syndrome in the
lower extremity after trauma. Certain
jobs or activities where repetitive or
prolonged knee flexion is required may
cause more fibular nerve compression
and develop into this pathology. No gender or age differences were noted in
the incidence of common fibular nerve
entrapment.
MECHANISM OF INJURY
COMMON SIGNS AND
SYMPTOMS
• The most identifiable symptom is weakness in the ankle dorsiflexors, which
tends to alter the normal gait pattern.
This symptom is usually the most concerning for the patient since it may lead
to tripping, loss of balance, and even
falls from inadequate foot clearance.
10 of 57
AGGRAVATING ACTIVITIES
•
•
•
•
Prolonged kneeling or squatting
Prolonged exercise
Wearing a tight knee brace or cast
Any activity that increases the local
pressure around the nerve, thus increasing the compression and therefore the
symptoms. Prolonged exercise, such as
running, in which the fibularis longus is
continually used may lead to more local
trauma and swelling.
EASING ACTIVITIES
• Rest
• Ice and local modalities
• Avoiding aggravating activities
24-HOUR SYMPTOM PATTERN
No specific pattern of symptoms is noted.
However, if there is a significant inflammatory component to the problem the
patient may experience night symptoms
or have increased symptoms in the morning that resolve slightly after about 30
minutes of light activity.
PAST HISTORY
Past history might include previous
bouts of the same condition, local trauma,
or previous lumbar spine or nerve disorder.
PHYSICAL EXAMINATION
• As mentioned, the most prominent
sign in this condition is ankle dorsiflexion weakness and gait difficulties.
They may manifest with a steppage gait
pattern where compensations, such as
increased knee flexion and hip flexion, occur during swing phase to clear
the foot. If considerable weakness is
present without compensations, the
patient may complain of tripping
caused by inadequate toe clearance. A
foot slap or absent heel strike may also
be present.
• Weakness of the tibialis anterior, extensor hallucis longus, and extensor digitorum longus should be noted on MMT.
• Sensation changes over the fibular head,
anterolateral leg, and dorsum of the foot
may be present. If the lesion or compression site is below the fibular neck,
the sensation on the lateral calf may be
spared, while still having changes on
the dorsum of the foot.
ORTHOPEDIC PATHOLOGY
The common fibular nerve entrapment
may occur after traumatic events such
as the following:
• Direct trauma
• Lacerations
• Femur or fibular fracture
• Gun shot wounds
• Local surgery
Open reduction and internal fixation
(ORIF)
Tibial osteotomy
Total knee replacement
• Knee dislocations
• Other factors that may lead to
entrapment:
Habitual leg crossing
Compression against bed railing or
hard mattress in debilitated patients
Prolonged immobilization
Improperly fitting cast or brace
Intraneural or extraneural ganglia
Schwannoma
Desmoid tumor
Angioma
Neuroma
Baker’s cyst
Chondromatosis
Exostosis
Well-developed muscles in the athletic population
• Sensory loss and paresthesias are noted
in the distribution of the common fibular nerve, which includes the lateral
leg over the fibular head, anterolateral
lower leg/calf region, and the dorsum of
the foot.
• Although pain is less likely in this condition, it may be present if significant
soft tissue swelling and inflammation
accompany the entrapment.
Section III
• Originating from the sciatic nerve in
the middle distal third of the thigh, the
common fibular nerve descends to the
popliteal fossa along the lateral aspect
of the distal thigh under the long and
short head of the biceps femoris to the
fibular head. The nerve then courses
around the fibular neck through an
opening near the superficial head of the
fibularis longus. Here, the common fibular nerve divides into the superficial and
deep fibular nerves.
• Motor innervation of the common fibular nerve is as follows:
Short head of the biceps femoris
Fibularis longus and brevis (via superficial fibular nerve)
Tibialis anterior, extensor hallucis longus, extensor digitorum longus, and fibularis tertius (via deep fibular nerve)
• Sensory distribution of the common fibular nerve is as follows:
The common fibular nerve innervates
the anterolateral leg and the dorsum
of the foot through the superficial and
deep branches.
The common fibular nerve itself innervates a portion of the lateral leg, over
the head of the fibula.
• Typical entrapment sites of the common fibular nerve are as follows:
In the fibroosseous opening below
the fibular head and near the superficial head of the fibularis longus the
nerve passes through at a very acute
angle. Here, the connective tissue may
be tough since it helps secure the
nerve to the proximal portion of the
fibula. These factors make this a common area for entrapment.
Repeated stress or injury to the lateral
aspect of the knee may lead to entrapment of either the superficial or deep
branch of the common fibular nerve.
The superficial branch passes through
the deep fascia and junction between
the middle and distal third of the
leg. Here, the fascia may be tough or
restricted, limiting mobility of the
nerve.
745
746
Common Fibular Nerve Entrapment
IMPORTANT OBJECTIVE TESTS
• Gait analysis: Gait changes as noted are
more obvious when there is significant
or long-standing compression of the
common fibular nerve.
• Tinel’s sign: Tapping around the fibular
head and head of the fibularis longus
may reproduce symptoms into the distribution of the nerve.
• MMT and myotomal testing should
reveal weakness of the extensor hallucis longus, tibialis anterior, and possibly
fibularis brevis.
• Sensory testing is important to confirm that changes are occurring in only
a peripheral nerve distribution related
to the common fibular nerve. If symptoms are in a more dermatomal distribution, other proximal causes should
be considered, such as lumbar spine
radiculopathy.
• Neurodynamic testing may implicate a
neurogenic source of symptoms.
• Lumbar ROM testing, accessory mobility testing, and palpation
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
Lumbar spine radiculopathy (L4)
Local fracture
Local tumor or space-occupying lesion
Compartment syndrome
Infection
CONTRIBUTING FACTORS
• Excessive weight loss may contribute
to this condition since it can lead to a
decrease in the fat pad over the fibular
head. This lack of protection may leave
the nerve more vulnerable to local
compression.
• Bulky lower extremity muscles, may also
increase the pressure on the common
fibular nerve, especially if combined
with repetitive lower extremity activities such as running.
• Jobs or activities with repetitive knee
flexion or kneeling may lead to more
compression on the nerve.
• Hyperthyroidism, diabetes mellitus, vascular disorders, and leprosy have all
been shown to have some effect on
lower extremity nerve entrapment.
CHAPTER 16 • NERVE
TREATMENT
PROGNOSIS
MEDICAL/SURGICAL
OPTIONS
• Spontaneous recovery is noted in many
cases of this condition, so nonoperative management is recommended for 3
to 4 months. However, if anterior compartment syndrome (ACS) is suspected,
an immediate referral to physician,
urgent care, or emergency department
is needed because this is an emergency
situation in which a fasciotomy needs
to be performed as soon as possible to
relieve pressure on the nerve and surrounding structures.
• For common fibular nerve entrapment,
a surgical decompression may be performed, especially in the case of spaceoccupying lesions.
• Nonsteroidal antiinflammatory drugs
(NSAIDs), oral corticosteroids, or local
injections may help alleviate symptoms
if there is significant pain or inflammation.
REHABILITATION
• The first goal of rehabilitation is to identify and remove the cause of the nerve
compression if possible.
• If significant weakness and gait deviations occur, bracing such as an
ankle-foot orthotic (AFO), splint, or
orthopedic shoes may help to normalize gait patterns. A lightweight rigid
AFO or a hinged AFO with dorsiflexion
assist may be appropriate.
• If the patient has significant pain or if an
inflammatory component is suspected,
local modalities, such as ice, ultrasound,
interferential current, phonophoresis, or
massage, may help manage symptoms.
• In the presence of positive neurodynamic findings and suspected restricted
nerve mobility without significant compression, soft tissue mobilization along
with neurodynamic mobilizations may
be warranted. Butler suggests techniques that attempt to glide, slide, or put
tension on the nervous system to free
up local adhesions that may be restricting movement and preventing normal
signal transmission.
11 of 57
• In a number of cases, spontaneous
recovery has been noted in patients
with this condition. This also depends
on the cause of the lesion because a
transient compression will have much
better results with therapy compared
to a space-occupying lesion, such as a
tumor, or internal factors such as a hardware used to fixate a fibular fracture.
• Wheeless noted that for partial fibular
nerve palsy, >80% of patients recover
completely and for complete nerve
palsy <40% of patients have complete
recovery.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Constant, unrelenting pain may indicate tumor or infection needing further
medical management or workup.
• Symptoms not following the normal
common fibular nerve distribution may
indicate a different pathology that may
require further physical therapy or medical evaluation.
• Increased pain or pressure in the anterior shin with tibialis anterior weakness
may indicate ACS; immediate treatment
by fasciotomy is needed to relieve the
buildup of internal fluid and pressure.
SUGGESTED READINGS
Butler DS. The Sensitive Nervous System.
Adelaide, Australia: Noigroup Publications;
2000.
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingston; 1991.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia, PA: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics.
Philadelphia: Elsevier; 2005.
http://www.wheelessonline.com/ortho/
peroneal_nerve
AUTHOR: CHRIS IZU
Deep Fibular Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Deep fibular nerve entrapment is a
mononeuropathy caused by compression
or restriction of movement of the nerve
in the anterior compartment of the lower
leg or in the lateral ankle.
SYNONYMS
• Deep peroneal nerve entrapment
• Anterior tarsal tunnel syndrome (ATTS)
• Ski-boot syndrome
ICD-9CM CODES
355.7 Other mononeuritis of lower
limb
laterally, the interosseous membrane
posteriorly, and the anterior fascia
anteriorly.
The deep fibular nerve may also be
entrapped at the anterior tarsal tunnel, which is formed by the talotibial
joint, the talonavicular joint, and the
extensor retinaculum. Here, the nerve
and the dorsalis pedis artery pass
beneath the retinaculum. Repeated
mechanical irritation beneath the retinaculum is the most common form of
tarsal tunnel syndrome.
The deep fibular nerve may also be
compressed in the tunnel by osteophytes, exostosis, bony prominences,
or space-occupying lesions such as
ganglia.
decreased dorsiflexion in swing may be
noted.
• Loss of sensation in the web space of
the first and second digits is common,
as this is main sensory distribution of
the nerve.
AGGRAVATING ACTIVITIES
•
•
•
•
•
•
•
•
EPIDEMIOLOGY AND
DEMOGRAPHICS
OPTIMAL NUMBER OF VISITS
Wearing tight shoes
Wearing boots or athletic wear
Walking
Prolonged standing
Ascending or descending stairs
Sitting with foot in plantar flexion
Sleeping with feet under the covers
Some of the previous activities and external pressure on the foot may compress
the nerve. Other activities with increased
plantar flexion may place a stretch on
the nerve, shortening its diameter.
EASING ACTIVITIES
16
No reports on the incidence of this
pathology were found. Clinically, it is
commonly seen along with other injuries
such as ACS or localized trauma to the
anterior shin.
ETIOLOGY
MECHANISM OF INJURY
24-HOUR SYMPTOM PATTERN
• Branching off the common fibular nerve
just distal to the fibular head, the deep
fibular nerve enters the anterior compartment in the front of the leg near the
interosseus membrane. It then courses
distally lateral to the tibialis anterior
muscle near the extensor digitorum longus, where it eventually goes under the
extensor hallucis just above the ankle
mortise. Passing in front of the ankle,
the deep fibular nerve goes under the
extensor retinaculum, where it divides
into the lateral and medial branches.
• Sensory distribution of the deep fibular
nerve: The nerve supplies sensation to
the web space of the first and second
toes, the adjacent metatarso phalangeal
joint, and the nearby interphalangeal
joints.
• Motor distribution of the deep fibular
nerve:The lateral branch of the deep fibular nerve supplies the tibialis anterior,
extensor digitorum brevis, extensor hallucis brevis, the adjacent tarsal and tarsometatarsal joints, and sometimes the
second and third dorsal interossei. The
medial branch innervates the extensor
hallucis longus tendon and the extensor
hallucis brevis muscle.
• Typical areas for deep fibular nerve
entrapment are as follows:
With repeated stress or injury to
surrounding musculature or fascia,
fibrotic scarring may occur and entrap
the deep fibular nerve.
The
nerve is commonly trapped
within either the anterior compartment or the anterior tarsal tunnel.
The anterior compartment is formed by the tibia medially, the fibula
• Direct trauma, such as snake bites or
a blunt force, may cause injury to this
area.
• Other common injuries leading to possible nerve entrapment include muscle
inflammation secondary to prolonged
exercise and local arterial bleeding.
• Forced or uncontrolled plantar flexion
and inversion of the ankle can place
this region under lots of stress.
• It is thought that repeated ankle sprains
may be a contributing factor to fibular
nerve entrapment in this area.
• Postural changes in the lower extremity
that alter biomechanics may place more
stress on the deep fibular nerve.
• Footwear that has a tight strap over the
anterior part of the ankle can add external compression.
• Prolonged sitting with the foot in plantarflexion may also place strain on the
deep fibular nerve.
Since activities such as prolonged walking
or standing are aggravating activities, more
pain might be noted later in the day. Pain
also could occur at night with plantar flexion of the foot under the covers or in the
case of a strong inflammatory component
to the condition. Associated pain in the
morning might also be present.
6 or fewer
MAXIMAL NUMBER OF VISITS
12 of 57
Properly fitting footwear
Sitting
Rest
Modalities
PAST HISTORY
No specific past history is noted in the literature, but it seems feasible that repetitive trauma or past injury to the front of
the shin or ankle may predispose an individual to this problem. Repetitive injury
or poor healing from another injury may
lead to fibrotic scarring around surrounding nerve fascia.
PHYSICAL EXAMINATION
• Sensory changes within the web space
of the first and second digit are commonly present with deep fibular nerve
entrapment.
• Antalgic gait or gait with limited dorsiflexion or toe extension may also be
present.
IMPORTANT OBJECTIVE TESTS
• Lower quarter neurological examination
Sensory examination may find sensory changes as noted previously.
Motor examination should be normal
with myotomal testing, but pain may
be present with dorsiflexion or slight
weakness with toe extension
Reflexes should be normal since this
neuropathy is below the level of the
patellar tendon reflex and a different
ORTHOPEDIC PATHOLOGY
• The most common complaint is a vague
pain, burning, or cramping over the dorsum of the foot, usually with pain within
the web space of the first and second
digit.
• Weakness in the toe extension may be
present as the deep fibular nerve provides motor input to both the extensor
digitorum brevis and the extensor hallucis brevis.
• Because of weakness and pain in the
foot, the patient may complain of gait
difficulties. If the proximal component
of the nerve (common fibular nerve)
is involved, footdrop or foot slap with
•
•
•
•
Section III
COMMON SIGNS AND
SYMPTOMS
747
748
Deep Fibular Nerve Entrapment
branch of the sciatic nerve that does
not innervate the Achilles tendon.
• The following tests may also help to
rule out possible proximal causes such
as lumbar radiculopathy:
Tinel’s test:Tapping at the anterior tarsal tunnel may reproduce more distal
symptoms.
Palpation: Palpation of surrounding musculature in the anterior compartment
or anterior surface of the ankle may also
reproduce symptomatic complaints.
Neurodynamic examination: Using the
straight leg raise (SLR) with plantar
flexion and inversion, the clinician may
be able to differentiate between neurogenic (deep fibular nerve) and nonneurogenic (local muscles or tendons).
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
•
•
Bony impingement
Cystic masses
Lumbar spine radiculopathy
Common fibular nerve entrapment
Sciatic nerve entrapment
ACS
Shin splints
CONTRIBUTING FACTORS
• Improper footwear
• Abnormal foot positioning: Pes planus
or cavus
• Thyroid dysfunction
• Diabetes
TREATMENT
SURGICAL OPTIONS
• If there is significant increase in pressure within the anterior compartment
(ACS), a fasciotomy, in which a small
incision is made in the anterior fascia,
is necessary to reduce building pressure. This situation can be a medical
CHAPTER 16 • NERVE
emergency, and failure to do such a procedure may result in permanent damage to the local and distal structure of
the lower extremity.
• Surgical release of the deep fibular
nerves may also be performed. This has
been reported to produce immediate
relief of symptoms and requires an excision of the nerve from the perceived
entrapment site.
• Removal of osteophytes or space-occupying lesions are an important part of
surgical management.
REHABILITATION
• The first goal of rehabilitation is to
reduce symptoms and associated inflammation sensitizing the nerve.
• Modalities, such as ultrasound, phonophoresis, iontophoresis, interferential
current therapy, ice, and compression,
are theorized to help during more acute
or inflammatory stages.
• Addressing postural faults and foot positioning may help to take stress off the
deep fibular nerve. Taping and orthotic
prescription may assist in this task.
• Once symptoms are alleviated, other
techniques, such as soft tissue mobilization, may help free the nerve from surrounding fibrotic tissue.
• Neurodynamic techniques to help slide,
glide, or place the nerve under tension
may be warranted at this time to help
restore the normal mobility of the nervous system.
• Other biomechanical faults or impairments that are hypothesized to place
more stress on the deep fibular nerve
must also be addressed before the rehabilitation program can be considered
complete.
PROGNOSIS
No data were found at this time for the
long-term outcomes of deep fibular nerve
entrapment. Wheeless noted that for partial fibular nerve palsy >80% of patients
13 of 57
recover completely and for complete
nerve palsy <40% of patients have complete recovery.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Severe unrelenting pain occurring
through the anterior shin may indicate ACS and worsening compression
on the nerve. A fasciotomy must be
done as soon as possible to release this
pressure.
• Unrelenting symptoms, especially combined with worse pain at night, may
indicate a local tumor.
• Lack of improvement within the
expected time frame or symptoms that
are not affected by physical therapy in
a few visits should be referred back to
the physician because a space-occupying lesion may be present.
• A recent history of trauma with suspected
fracture may warrant further imaging
before continuing physical therapy.
• Impaired circulation or vascular compromise may also warrant more medical management.
SUGGESTED READINGS
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingston; 1991.
Butler DS. The Sensitive Nervous System. Adelaide,
Australia: Noigroup Publications; 2000.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005.
http://www.wheelessonline.com/ortho/
peroneal_nerve
AUTHOR: CHRIS IZU
Femoral Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Femoral nerve entrapment is a mononeuropathy that results from compression or
restriction of movement of the nerve, usually in the anterior abdominal wall as it
passes through the femoral triangle under
the inguinal ligament.
ICD-9CM CODES
355.2 Other lesion of femoral nerve
OPTIMAL NUMBER OF VISITS
6 or fewer
MAXIMAL NUMBER OF VISITS
16
ETIOLOGY
• The femoral nerve may become injured
or entrapped from local trauma to the
anterior hip or thigh such as a contusion or repetitive strain.
• It may also be injured or compressed
during stressful abduction or external
rotation activities such as during birth
(vaginal deliveries).
• Intrapelvic injury and injury to the
inguinal region have also been documented to lead to nerve entrapment.
• Common traumatic events include the
following:
Gunshot wounds
Knife wounds
Puncture wounds
Pelvic surgeries
Total hip replacement (anterior approach)
Pelvic fractures
• Other noted factors that can lead to
compression include the following:
Pelvic radiation therapy
Appendical or renal abscess
Tumors
Compartment-like compression
COMMON SIGNS AND
SYMPTOMS
AGGRAVATING ACTIVITIES
• Walking or standing may aggravate
symptoms secondary to a stretch on
the femoral nerve with hip extension,
especially during trailing limb posture
in gait.
• Walking may also be difficult if significant quadriceps weakness is present.
EASING ACTIVITIES
EPIDEMIOLOGY AND
DEMOGRAPHICS
One reference stated that this entrapment
syndrome is thought to be a rare occurrence and that earlier reported cases may
have been mislabeled as femoral nerve
neuropathies instead of other proximal
causes.
•
•
•
•
Sitting
Hip flexion or external rotation
Rest
Local modalities
24-HOUR SYMPTOM PATTERN
No specific pattern of symptoms is noted.
However, if there is a significant inflam-
14 of 57
PAST HISTORY
• Prior history of surgery in the pelvic
region (i.e., hernia, cesarean section, or
hysterectomy)
• Past history of a patient with this condition may include previous trauma to the
area, repetitive stress injuries, or other
lumbopelvic problems.
• Prior history of prostate or uterine
pathology
PHYSICAL EXAMINATION
• Weakness with hip flexion and knee
extension are the most common symptoms associated with femoral nerve
entrapment. Gait deviations may be
noted to compensate for quadriceps
weakness, and a quadriceps avoidance
pattern of limited knee flex during loading response may be present.
• A diminished patellar tendon reflex
is most likely present secondary to
impaired nerve conduction.
• Sensory deficits are likely present in the
anteromedial aspect of the thigh and
may be in the medial aspect of the leg
because of the saphenous branch of the
femoral nerve.
• Pain may be noted with resisted hip
flexion from the possible involvement
of the psoas muscle and with stretching
into combined hip extension and knee
flexion.
• Palpation around the lateral portion of
the femoral triangle, psoas, or iliacus
muscle may be painful compared to
the unaffected side and may reproduce
symptoms down into the anteromedial
aspect of the thigh or knee.
IMPORTANT OBJECTIVE TESTS
• Strength testing
Motor deficits in hip flexion and knee
extension might be the most obvious
signs of femoral nerve compression.
However, weakness in the area alone
should not be considered diagnostic
because an L3 radiculopathy may produce the same result.
• Lower quarter neurological examination
To make sure symptoms are only
the result of an isolated peripheral
nerve problem, a full lower quadrant neurological examination is
warranted. Symptoms that follow
along a more dermatomal or myotomal pattern indicate a more proximal problem.
Symptoms that cross one or more
dermatomes or peripheral nerve
regions may be the result of a
polyneuropathy.
ORTHOPEDIC PATHOLOGY
• Weakness in knee extension is common because of the motor input of the
femoral nerve to the large quadriceps
muscles. Hip flexion may also be difficult from the contribution of the rectus
femoris.
• Gait difficulties or functional activities
like squatting may become more difficult because of the weakness in knee
extension.
• Sensation loss in the anterior aspect of
the thigh may be present if the anterior cutaneous branch of the femoral
nerve is affected.An individual with this
condition may also have sensation loss
to the medial aspect of the knee from
involvement of the saphenous branch.
• Pain may be present in the inguinal region
from the cause of the compression.
matory component to the problem, one
may experience night symptoms or may
have increased symptoms in the morning
that resolve slightly after about 30 minutes of light activity.
Section III
• The femoral nerve originates from the
ventral rami of L2, L3, and L4 near the
psoas major and travels inferiorly in
the intermuscular groove between the
psoas and the iliacus muscle. From there,
it passes under the inguinal ligament in
the femoral triangle lateral to the femoral artery and vein. It then divides into
both sensory and motor branches.
• The cutaneous sensory branches of the
nerve innervate the proximal upper
and anterior thigh.
• The femoral nerve sends branches to
the large quadriceps muscles.
• Because of the location of the femoral
nerve, there is a multitude of factors that
can cause femoral nerve entrapment.The
most common entrapment area occurs
underneath the inguinal ligament.
• It also may be entrapped or compressed
more inferiorly where the nerve is close
to the humeral head and attachments
of the vastus intermedius and psoas
tendons. Problems with those tendons
or muscles may cause femoral nerve
restrictions or irritation.
• Local tumors, psoas abscesses, lymph
node enlargement, hematomas, and penetrating trauma are some of the most
commonly documented causes of internal compression of the femoral nerve.
• Tissue healing after trauma or surgery
has also been hypothesized to lay down
scar tissue that may restrict the mobility
of the femoral nerve within its neural
container.
MECHANISM OF INJURY
749
750
Femoral Nerve Entrapment
• Slump knee bend test
Performing
this test in sidelying,
according to Butler, with cervical
flexion and extension as a sensitizing maneuver may help determine
if neurogenic symptoms are present, as in the case of femoral nerve
entrapment.
• Lumbar ROM testing, accessory mobility testing, and palpation may help differentiate a lumbar spine problem from
an isolated femoral nerve entrapment.
DIFFERENTIAL
DIAGNOSIS
• Lumbar radiculopathy (L3 most
likely)
• Local muscular strain
• Pelvic fracture
• Hip fracture
• Hip joint pathology
• Appendical or renal abscess
• Tumors
CONTRIBUTING FACTORS
•
•
•
•
Diabetes mellitus
Thyroid problems
Poor posture
Impaired trunk and motor control
TREATMENT
SURGICAL OPTIONS
Microsurgical nerve decompression
CHAPTER 16 • NERVE
REHABILITATION
• The initial goals of rehabilitation are to
reduce the pain and inflammation in
the present state of the condition.
• Modalities, such as ultrasound, phonophoresis, iontophoresis, interferential
current therapy, light massage, and cold,
may help to accomplish this.
• If there are any external compression
factors such as tight clothes, modification of attire is necessary.
• After symptoms have calmed, rehabilitation may focus on improving the health
and mobility of the nerve.
• Soft tissue mobilization directed at
fibrotic scarring around the nerve may
be beneficial.
• Neurodynamic mobilizations aimed at
sliding, gliding, or placing tension on
the nerve may also be warranted to
restore normal mobility to the nervous
system.
• A complete rehabilitation program will
also work to address any other biomechanical faults or impairments that
might be leading to stress or strain on
the femoral nerve.
PROGNOSIS
One study reported up to 70% improvement of symptoms in this population,
although improvement may take up
to a year. If there is severe axonal loss,
it is thought that there will be some
recovery of function, although not
complete.
15 of 57
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Unrelenting pain not related to biomechanical factors
• Weight loss
• Bowel or bladder dysfunction
• Saddle paresthesias
• Gait disturbances: Clumsiness or ataxic
gait
• Bilateral glove or sock numbness
• Symptoms that do not initially improve
with symptoms
SUGGESTED READINGS
Butler DS. The Sensitive Nervous System.
Adelaide, Australia: Noigroup Publications;
2000.
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingston; 1991.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics.
Philadelphia: Elsevier; 2005.
http://www.emedicine.com/Or thoped/
topic422.htm
AUTHOR: CHRIS IZU
Interosseous Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Compression of the posterior interosseous nerve (which arises from the
radial nerve) at the tendinous margin of
the extensor carpi radialis brevis, fibrous
bands anterior to the head of the radius,
radial recurrent blood vessels, or between
the two supinator heads in the arcade of
Frohse, which is a fibrous arch occurring
in 30% of the population.
SYNONYMS
• Radial tunnel syndrome
• Posterior interosseous nerve syndrome
ICD-9CM CODES
955.3 Injury to radial nerve
OPTIMAL NUMBER OF VISITS
Conservative management should produce some reduction in symptoms within
3 to 6 weeks.
MAXIMAL NUMBER OF VISITS
ETIOLOGY
EPIDEMIOLOGY AND
DEMOGRAPHICS
• Posterior interosseous nerve entrapment is an uncommon cause of lateral
elbow and forearm symptoms.
• Since the causes for this pathology are
so diverse, it occurs across a broad spectrum of the population.
MECHANISM OF INJURY
• The nerve entrapment may be caused
by local edema from irritation of the
neighboring tissues or volume changes
16 of 57
COMMON SIGNS AND
SYMPTOMS
• Posterior interosseous nerve entrapment commonly manifests with pain in
the extensor region of the lateral forearm. The pain is most intense over the
supinator, sometimes extending to the
wrist and proximal humerus. It can be
combined with pain on resisted supination when the elbow is flexed and
resisted extension of the middle finger when the elbow is extended, weakness in wrist and finger extension, and
paraesthesias in the hand and lateral
forearm, although this is disputed by
some authors.
• Clinical signs and symptoms for radial tunnel syndrome and posterior interosseous
compression, with indications and
options for surgical treatment, are presented by Markiewitz and Merryman.
• The typical referral pattern for posterior interosseous nerve entrapment is
local pain at the elbow and lateral forearm, extending to the wrist and upper
regions of the humerus.
AGGRAVATING ACTIVITIES
• Repetitive forearm rotation
• Resisted supination from pronation
with wrist flexion
• Full-range pronation
• Elbow extension
• These movement patterns occur with a
range of activities but are prevalent in
office workers, manual workers, musicians, and athletes.
EASING ACTIVITIES
• Reducing load
• Avoiding the aggravating movement
patterns
• Positioning
• Rest (absolute or relative with the aid of
splinting or taping)
24-HOUR SYMPTOM PATTERN
Symptoms worsen with aggravating activities, but pain may also increase nocturnally, which is similar to many entrapment
neuropathies.
ORTHOPEDIC PATHOLOGY
• The insult to the nerve may be mechanical, thermal, chemical, or ischemic.
• In entrapment syndromes, compression
or direct trauma leads to nerve tissue
hypoxia.
• Posterior interosseous nerve entrapment pathology may occur with repetitive or overuse movement patterns
involving supination and pronation of
the forearm, trauma, surgery, underlying rheumatoid disease, ganglions, and
tumors.
• In entrapments, nerve trauma occurs
because the size of the neural structure
exceeds the anatomical space available
for it, resulting in increased pressure,
which in turn leads to impaired blood
flow and subsequent hypoxia of the tissue and disruption of the axonal transport system.
• Nerve injury is classified according
to severity of the injury and potential
for reversibility. Original classifications
described previously remain in current
use.
First-degree neuropraxia involves distortion of myelin about the nodes of
Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance, resulting in temporary loss of
nerve conduction. Recovery is rapid
and complete in most cases.
Second-degree axonotmesis involves
interruption of the axon with second-
in surrounding tissues generated by
mechanical overload via repetitive
activity or impact trauma, specifically
in supinator and extensor carpi radialis
brevis.
• Posterior interosseous nerve entrapment may be compounded by the presence of certain anatomical features:
Fibrous bands anterior to the radial head
or within the supinator arch (the arcade
of Frohse) and the specific location of
the radial recurrent blood vessels.
• Other causes include fractures, inappropriately positioned surgical fixings and
plates, surgical trauma, rheumatoid synovitis, ganglions, and tumors.
Section III
If there is little or no response to conservative management after 12 weeks, a surgical opinion should be obtained.
ary wallerian degeneration, but the
supporting tissue around the axon is
preserved. Recovery may be complete
but takes longer to occur and depends
on the distance between the site of
injury and the end structure (denervated muscle).
Third-degree
neurotmesis involves
extensive disruption of the nerve and
its supporting structures, but while
the endoneurium is disrupted, the
perineurium and epineurium remain
intact.
Fourth-degree neurotmesis involves
disruption of all neural components
except the epineurium.
Fifth-degree
neurotmesis involves
complete transaction and discontinuity of the nerve with no capacity for
regeneration.
• Neurotmesis rarely occurs from entrapment, but where continuity has been
disrupted, complete recovery is not
possible, even with surgical techniques,
and the eventual outcome depends on
individual circumstances.
• Double-crush syndrome refers to the
fairly common phenomenon of nerve
entrapment and radiculopathy occurring in combination, although the syndrome is considered controversial.
Compression or irritation of the nerve
roots at the cervical level is thought to
increase sensitivity to compression or
movement restrictions more distally in
the structure.
• As noted earlier, increasing pressure on
the nerve causes impaired blood flow,
tissue hypoxia, and disruption to the
anterograde and retrograde intercellular transport of materials within axons,
eventually disturbing depolarization
within the nerve. In overuse-type entrapments, it is proposed that repetitive work
or static postures produce an inflammatory response. Fibroblasts appear to
repair the damage incurred but generate
adhesions that limit neural glide and subsequently increase anoxia. Other studies
have found that cortical dedifferentiation
may occur from repetitive motion activities and nerve injuries. This may result
in reinforced poor posturing and use of
aberrant motor pathways.
751
752
Interosseous Nerve Entrapment
PAST HISTORY FOR THE REGION
• Previous history of trauma, surgery, or
overuse-type injury at the elbow, forearm, or wrist
• History of rheumatoid disease
PHYSICAL EXAMINATION
• Pain over the anterolateral forearm with
referral as described previously.
• Maximum tenderness is approximately
6 to 8 cm distal to the lateral epicondyle,
over the supinator.
• Pain is provoked or worsened with
resisted supination, elbow extension
with pronation, and extension of the
middle finger.
• Depending on the site of compression, weakness may also be present in
wrist extension (extensor carpi ulnaris
and extensor digitorum communis are
affected), finger extension (extensor
digiti quinti, extensor digitorum communis, and extensor indicis proprius are
affected), and thumb movement (abductor pollicis longus, extensor pollicis longus, and brevis are affected).
IMPORTANT OBJECTIVE TESTS
• Radiography and MRI facilitate detection of underlying factors such as fractures, ganglions, tumors, or other tissue
abnormality.
• Local injection at the lateral epicondyle
may distinguish between lateral epicondylitis (when it is usually much more
effective) and radial tunnel syndrome
(when it has little or no effect).
• EMG and nerve conduction studies may
be inconclusive, so clinical findings previously described, in conjunction with
neural tension techniques, may provide
the most reliable aid to diagnosis.
• Diagnostic accuracy of neurological
upper limb examination employing a battery of standard test procedures has been
found to be reproducible and reliable.
DIFFERENTIAL
DIAGNOSIS
• Cervical radiculopathy (C7 pathology affects triceps brachii and wrist flexors)
• Lateral epicondylitis (maximal tenderness is at the lateral epicondyle rather
than distal to it)
• Trigger finger (passive, as well as active,
movement is affected)
• Extensor tendon rupture (fingers fail to
extend on passive wrist flexion)
• Adverse neural tension
CONTRIBUTING FACTORS
•
•
•
•
Anatomical arrangement
Presence of other underlying disease
Past history of trauma or surgery
Lifestyle activities involving elbow or
forearm movement patterns
CHAPTER 16 • NERVE
TREATMENT
PROGNOSIS
SURGICAL OPTIONS
• An overview of basic neurosurgical techniques is provided by Dahlin.
Individuals who fail to respond to conservative management may require
decompression surgery.
• Two main techniques, anterolateral and
posterior, may be employed. The anterolateral technique is preferred because
it allows greater access to more of the
entrapment sites, facilitating release at
the supinator, arcade of Frohse, fibrous
margin of extensor carpi radialis brevis,
distal fascia, and dissection of the nerve
from scar tissue posttrauma.
• If symptoms are arising from fixation
devices, corrective surgery will be
required.
• If compression is due to ganglion or
tumor, surgical technique will obviously
depend on precise location.
• In addition to the standard risks associated with any surgery, there is a risk
of further damage to the nerve during
the procedure. However, success rates
of 90% have been reported for neurapraxic injuries, with fast recovery to full
normal function.
• Individuals who have failed to respond
to conservative management after a
period of 8 to 12 weeks should be considered for surgical opinion. In addition,
any worsening of neurological function
despite intervention should be evaluated (Cravens and Kline).
REHABILITATION
• Cleary provided an overview of concepts and evidence for conservative
management in radial tunnel syndrome
but notes that definitive clinical evidence is scarce.
• Conservative treatment consists of manual techniques consisting of soft tissue
release work, myofascial release work,
and neural stretching or mobilizing
techniques.
• Depending on the underlying cause of
the pathology, antiinflammatory modalities may also be useful, combined with
offloading the stressed structures.
• The effectiveness of antiinflammatory
medication is disputed, although many
authors recommend including these in
the management regimen since they
produce benefit in some cases.
• It may be appropriate to teach individuals stretching or mobilizing techniques
to be applied between treatment
sessions.
• If abhorrent movement patterns are
the result of other muscle imbalance or
recruitment issues, it may be appropriate to address these issues as part of the
rehabilitative process.
17 of 57
• As previously noted, factors that contribute or predispose an individual
to the pathology include anatomical
arrangement, presence of other underlying disease, past history of trauma or
surgery, or lifestyle activities involving
elbow and forearm movement patterns.
• Prognosis for full recovery is good, with
almost all cases responding to either
conservative or surgical management.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Worsening neurological function or symptoms
• Failure to respond to conservative management
• Suspicion or presence of underlying
disease
• Unexplained symptoms inconsistent
with the pathology
SUGGESTED READINGS
Brukner P, Khan K. Clinical Sports Medicine.
3rd ed. New York: McGraw-Hill; 2006.
Cleary CK. Management of radial tunnel syndrome: a therapist’s clinical perspective. J
Hand Ther. 2006;9(2):166–191.
Cravens G,Kline DG.Posterior interosseous nerve
palsies. Neurosurgery. 1990;27(3):397–402.
Dahlin LB. Mini-symposium: hand trauma
(ii) nerve injuries. Curr Orthop. 2008;
22(1):9–16.
Hall TM, Elvey RL. Nerve trunk pain: physical
diagnosis and treatment. Man Ther. 1999;
4(2):63–73.
Jepsen JR, Laursen LH, Hagert C-G, Kreiner S,
Larsen AI. Diagnostic accuracy of the neurological upper limb examination I: interrelater reproducibility of selected findings
and patterns. BMC Neurol. 2006;6(8).
Jepsen JR, Laursen LH, Hagert C-G, Kreiner S,
Larsen AI. Diagnostic accuracy of the neurological upper limb examination II: relations
to symptoms of patterns of findings. BMC
Neurol. 2006;6(10).
Magee DJ. Orthopaedic Physical Assessment.
5th ed. Philadelphia: Saunders; 2008.
Markiewitz AD, Merryman J. Radial nerve compression in the upper extremity. J Am Soc
Surg Hand. 2005;5(2):87–99.
Pratt N. Anatomy of nerve entrapment sites
in the upper quarter. J Hand Ther. 2005;
18(2):216–219.
Seddon HJ. Surgical Disorders of the Peripheral
Nerves. 2nd ed. Edinburgh: Churchill
Livingstone; 1975.
Sunderland S. Nerve and Nerve Injuries. 2nd
ed. Edinburgh: Churchill Livingstone; 1978.
Wilbourn AJ, Gilliat RW. Double crush syndrome: a critical analysis. Neurology.
1997;49:21–29.
AUTHOR: SARAH GRAHAM
Lateral Femoral Cutaneous Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Lateral femoral cutaneous nerve (LFCN)
entrapment is a mononeuropathy that
results from either compression or restriction of movement of the nerve, most likely
as it passes under the inguinal ligament
near the anterior superior iliac spine.
SYNONYMS
Meralgia paresthetica
ICD-9CM CODES
355.1 Meralgia paresthetica
OPTIMAL NUMBER OF VISITS
6 or fewer
MAXIMAL NUMBER OF VISITS
12
ETIOLOGY
• As the incidence of rapid weight gain
increases in those who are middle-aged,
so does the incidence of entrapment of
the LFCN.
• Construction workers, mechanics, or
other professionals, whose jobs require
Direct trauma, stretch injuries, and is chemi a are the most likely culprits, which
would lead to compromise of the LFCN.
Some documented traumatic events that
have led to this condition include seatbelt injuries in motor vehicle accidents
(MVAs), pelvic fractures, and surgical procedures. It has also been noted that LFCN
entrapment may occur after lying in the
fetal position for a long period of time.
COMMON SIGNS AND
SYMPTOMS
• Most important to note is that there is
likely no motor deficit with this condition since the LFCN is purely sensory.
Some local muscle guarding may appear
as a result of pain and muscle inhibition
in both hip flexion and extension as the
nerve is either further compressed or
stretched.
• The hallmark of LFCN entrapment is
altered sensation over the lateral aspect
of the mid-thigh. This may include
numbness, tingling, or even a burning
pain, a dull ache, or itching.
• Symptoms are usually unilateral, although
they may be bilateral in cases of rapid
weight gain that affect the body
symmetrically.
AGGRAVATING ACTIVITIES
• Walking or prolonged standing
• Wearing tight clothes or accessories
• Activities that include sustained or
repetitive hip extension or flexion
• Tight clothing and garments add external compression to the superficial
region of the nerve, whereas hip extension activities may place stretch on surrounding structures that would in turn
increase the local pressure around the
nerve. Hip extension may also place the
LFCN under more tensile stress.
EASING ACTIVITIES
•
•
•
•
Sitting or rest
Removal of tight clothing
Avoiding excessive hip extension
Once the external compression is
removed, improved axonal flow and
neuronal blood flow should help alleviate some of the symptoms.
24-HOUR SYMPTOM PATTERN
Current research has not addressed a
24-hour pattern of symptoms of this
disorder. However, if there is a significant inflammatory component of the
disorder, symptoms may be worse in the
18 of 57
PAST HISTORY
Previous trauma to the area or incidence
of the same condition may predispose a
person to LFCN entrapment.
PHYSICAL EXAMINATION
• Altered sensation is the hallmark of the
condition and should manifest as numbness, paresthesias, or pain in the anterolateral thigh.
• Motor examination or MMT of lower
extremity myotomes should be normal
since the LFCN is purely sensory. The
patient may have pain with hip flexion
or knee extension secondary to local
attachment near the dysfunctional area,
but strength should be symmetrical.
IMPORTANT OBJECTIVE TESTS
• Sensation testing
It is important to map out the specific area or distribution of symptoms to differentiate the cause from a
potential more proximal lumbar spine
cause. Symptoms that occur more distally than the anterolateral thigh, such
as down to the lateral leg or foot, suggest further lumbar spine testing. One
suggestion has been to use a marker
or pen to accurately draw the area on
the patient’s leg.
• Tinel’s test
With tapping over the superficial
region over the nerve (over the lateral and upper part of the inguinal ligament), symptoms should be
reproduced.
• LFCN test
This test is performed as a variation
of the slump knee bend test. Butler
(2000) added adduction and internal
rotation of the hip to stress the LFCN
and to help determine if the symptoms are neurogenic by using cervical
extension and flexion as a sensitizing
maneuver.
• Lumbar ROM testing, accessory mobility testing, and palpation
Because of the chance that a more
upper lumbar spine problem may refer
symptoms distally into this region, it
is important to rule out that area as a
potential source of symptoms.
DIFFERENTIAL
DIAGNOSIS
• Lumbar spine referral
Disc dysfunction
Somatic referred pain
Nerve root irritation
• Muscle strain
• Pelvic fracture
• Pelvic neoplasm
ORTHOPEDIC PATHOLOGY
EPIDEMIOLOGY AND
DEMOGRAPHICS
MECHANISM OF INJURY
morning or may even cause wakening in
the night.
Section III
• The nerve originates from the lumbar
plexus and travels distally through the
pelvis near the psoas major muscle and
eventually through a tunnel formed by
the lateral attachment on the inguinal
ligament and the anterior superior iliac
spine (ASIS). The nerve travels superficially to supply the skin about 10 cm
distal to the inguinal ligament. Here, the
nerve has less protection than it does
more proximally in the pelvis.
• Both internal and external factors can
compromise the LFCN. Research and case
studies have pointed toward tight clothing, such as jeans, underwear, or a belt, as
possible external factors that could lead to
nerve compression. Internal factors could
include a pendulous abdomen, rapid
increase in weight, or space-occupying
lesions as potential causes of LFCN entrapment. Examples may include contained
iliopsoas hemorrhage or neoplasm.
• Another hypothesis of the cause of
nerve entrapment is that the surrounding tissues that form the neural container may restrict or limit its ability to
slide or glide as a result of dysfunction
of nearby fascial layers. These tissues
may leave the nerve bound to adjacent
structures after trauma and healing
have taken place such as in abdominal
surgery or recent pelvic fracture.
them to wear tight or heavy attire
around their waists, have a higher incidence of this condition.
• There is no difference in incidence between
right and left sides of the body, and symptoms may also appear intermittently.
753
754
Lateral Femoral Cutaneous Nerve Entrapment
• Polyneuropathy
• Retroperitoneal hemorrhage
CONTRIBUTING FACTORS
• Diabetes can affect the health of the
nervous system and predispose a person to nerve entrapment syndromes.
• Obesity and especially rapid weight
gain can increase the pressure or compression on the superficial region of the
LFCN.
• Pregnancy is a common contributing factor for the same reason as rapid
weight gain.
• Occupational requirements that include
tight attire around the waste such as
tight pants or work belts
TREATMENT
SURGICAL OPTIONS
• If conservative measures fail, surgical decompression may be considered.
Successful predictors of good outcomes
after surgery include a positive Tinel’s
test, abnormal electrodiagnostic findings (that do not suggest other potential
causes), and immediate relief of symptoms after local nerve block.
• In very rare instances, the nerve can be
surgically transected.The long-term outcomes are suspect, and since the nerve
has no motor function, which may lead
to more serious disability, this option is
not recommended.
• A physician may be able to do a focal
nerve block near the inguinal ligament
using a combination of lidocaine and
corticosteroids.This is a good treatment
option if the pain is severe and may provide relief for several days to weeks.
REHABILITATION
• The most important factor in treatment
is to remove the cause of the problem.
Patient education on avoidance of tight
clothing or accessories usually helps
resolve the symptoms. If obesity or
rapid gain is thought to be at fault, those
factors also need to be addressed.
• Concurrent rehabilitation may include
modalities, such as ultrasound, interferential current therapy, and phonophoresis, to reduce swelling and
inflammation.
• It is also important to address other contributing factors such as the following:
Ergonomics
Postural changes and adaptations
General fitness level, including stretching
• If positive neurodynamic testing suggests nerve entrapment from restricted
nerve mobility, other methods of treatment may include local soft tissue mobilization followed by nerve gliding with
respect to irritability of symptoms.
• Neurogenic pain medications, such as
carbamazepine or gabapentin, have
been shown to have some effect on
symptoms in select patients, but the
effects are usually minimal.
PROGNOSIS
Because of the pure sensory function of
the LFCN, it is not typical for this condition to lead to severe functional loss or
disability. Research shows that it is not
associated with mortality or significant
morbidity. Typically, the paresthesias
resolve slowly over time, but numbness
in the peripheral nerve distribution may
persist. Removal of the cause of the nerve
compression usually results in good
outcomes.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Constant or unrelenting deep, boring
pain may be a sign of a space-occupying
lesion causing the nerve entrapment.
These symptoms are even more of a
19 of 57
CHAPTER 16 • NERVE
•
•
•
•
concern if not in the distribution of the
LFCN such as the back, pelvis, or anterior
hip.
Pain or symptoms that do not change
with treatment or removal of the
hypothesized cause of the nerve compression may also point toward infection or tumor.
Symptoms associated with trauma that
has not been screened with radiographs
or other imaging studies may be caused
by concurrent pelvic fracture.
Any other neurological signs, such as
myotomal weakness or dermatomal
sensory changes, may require further
work-up or diagnostics, to rule out more
proximal causes of symptoms.
Severe pain preventing the patient from
participating in therapy may require
nerve block or other management
before continuing.
SUGGESTED READINGS
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingston; 1991.
Butler DS. The Sensitive Nervous System.
Adelaide, Australia: Noigroup Publications;
2000.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005.
http://www.emedicine.com/Or thoped/
topic422.htm
AUTHOR: CHRIS IZU
Long Thoracic Nerve Pathology
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Long thoracic nerve pathologies encompass any injury that interrupts the function of the long thoracic nerve at any
point along its course. The loss of function results in serratus anterior muscle
dysfunction and often pain.
SYNONYMS
• Long thoracic nerve palsy
• Serratus anterior muscle palsy
• Rucksack palsy
ICD-9CM CODES
354 Mononeuritis of upper limb and
mononeuritis complex
354.8 Other mononeuritis of upper
limb
354.9 Mononeuritis of upper limb
unspecified
OPTIMAL NUMBER OF VISITS
6
MAXIMAL NUMBER OF VISITS
ETIOLOGY
EPIDEMIOLOGY AND
DEMOGRAPHICS
The prevalence of long thoracic nerve
injury has not been reported in the literature, but it is generally believed to be
uncommon; no age groups have been
reported as more prone to damage to the
nerve and no gender specificity has been
reported in the literature.
MECHANISM OF INJURY
• The long thoracic nerve is most susceptible to acute or recurrent trauma
caused by traction or pressure.
• Nontraumatic pressure on the nerve
can result at a number of sites along its
path, by the following:
Within musculature (seen commonly
in the scalene medius muscle) and
inflamed bursa in the shoulder region
Between the first two ribs and the
clavicle or between the coracoid process and the first or second ribs
In the axillary region from the presence of an axillary mass, excessive
or poor use of old-style crutches,
and overly tight bandage or plaster
applications.
• Traction trauma to the long thoracic
nerve can occur in the following ways:
Repetitive isolated stretch with cervical flexion, lateral flexion, and rotation away, combined with ipsilateral
20 of 57
COMMON SIGNS AND
SYMPTOMS
• The most common complaint is an
insidious onset of shoulder girdle weakness with or without pain.
• Pain can often be present in the first
few days to weeks followed by weakness with overhead activities.
• The patient may report decreased active
shoulder ROM, particularly into forward
flexion. This is accompanied by scapular winging, especially when pushing
forward against resistance.
• The pain is often described as a burning, aching, or sharp pain in the shoulder, which may radiate to the scapula,
arm, or scalene muscle region.
AGGRAVATING ACTIVITIES
• Aggravating activities involve repetitive
positions that place stress on the nerve
(cervical flexion, lateral flexion, and
rotation away, combined with ipsilateral
arm flexion) such as throwing (baseball, javelin, or football), serving in tennis, spiking or serving in volleyball, and
driving a golf ball.
• Patients may also report symptom
aggravation and reduced ability to pull
and/or carry heavy objects, overhead
lifting, tackling, and wrestling.
ORTHOPEDIC PATHOLOGY
• The anatomy of the nerve is as follows:
Motor nerve that is 22 to 24 cm long
with a superficial course
Comprises the ventral rami of the
C5 to C7 nerve roots (also the C8
nerve roots and intercostal nerves in
some)
C5 and C6 roots merge and pierce the
scalene medius muscle, while the C7
root travels between the anterior and
middle scalene muscles.
The C5, C6, and C7 roots join to form
the long thoracic nerve sitting anteriorly to the posterior scalene muscle.
The nerve travels between the clavicle and first rib, laterally toward the
midaxillary line, and here it sends out
branches and innervates the serratus
anterior muscle.
• Physiologically there is disruption to
any part of the nerve responsible for
conduction.
• In repetitive nerve injury, it is proposed
that repetitive work or static postures
produce an inflammatory process,
fibroblasts appear to repair the damage
incurred but produce adhesions to the
nerve, limiting their glide and increasing anoxia.
• Lacerations generally result in neurotmesis injury.The pathology is essentially an
injury to the long thoracic nerve. Nerve
injury can be classified according to the
severity of the injury and its potential
for reversibility.
arm flexion. The cervical movement
places an anterior, medial, and superior pull on the proximal portion of
the nerve with the scalenus medius
muscle, while the distal nerve segment is tensioned with the overhead
arm position in a posterior, lateral, and
inferior direction with the serratus
anterior muscle. The scalenus medius
and serratus anterior muscles act as
points of fixation, resulting in excessive elongation of the nerve.This position of stretch is commonly seen with
throwing in baseball, javelin, and football; serving in tennis; spiking or serving in volleyball; and driving a golf
ball. Additionally, tackling, wrestling,
and lifting heavy weights overhead
may also traction the nerve.
Repetitive bow-stringing of the nerve
over a fascial band in shoulder abduction and external rotation.
Repetitive carrying of heavy loads
or an injury involving sudden forced
scapular depression
• Direct trauma to the nerve as it sits
superficially in the supraclavicular fossa
or chest may also occur with MVAs, falls,
and strong massage.
• Iatrogenic injury to the nerve is also
common during first rib resection and
heart or breast surgery.
• Neuralgic amyotrophy, vaccinations, or
infections may also affect the long thoracic nerve, either selectively or with
other nerve involvement.
Section III
20
• The following is a basic overview of the
Sunderland classification of nerve injury,
which describes five degrees of nerve
pathology (an expansion of Seddon’s
three-tier classification of neurapraxia,
axonotmesis, and neurotmesis).
Neurapraxia
(first-degree injury):
Distortion of the myelin around the
nodes of Ranvier caused by ischemia,
mechanical compression, or electrolyte imbalance produces temporary
loss of nerve conduction.
Axonotmesis (second-degree injury):
Interruption of the axon with secondary wallerian degeneration; the supporting tissue surrounding the axon
is preserved and the recovery period
depends on the distance between the
site of injury and the end-organs.
Neurotmesis: Complete disruption of
the nerve and its supporting structures.
• Neurotmesis has been further divided
into the following three subcategories:
Third-degree nerve injury: Endoneurium is disrupted with intact perineurium and epineurium.
Fourth-degree nerve injury: All neural
elements sparing the epineurium are
disrupted.
Fifth-degree nerve injury: Complete
transaction and discontinuity of the
nerve with no capacity for regeneration
755
756
Long Thoracic Nerve Pathology
• Positions that cause overstretching of
the serratus anterior muscle will also
aggravate the pathology. These include
forward flexion movements and arm
weight-bearing positions that create
excessive scapular winging.
EASING ACTIVITIES
• Rest and/or modification of aggravating
activities
• Placing the neck, arm, and scapula in a
neutral, supported position that does
not tension the nerve.
24-HOUR SYMPTOM PATTERN
Generally, the symptoms are related to
activity and do not follow a typical 24-hour
pattern unless there is a strong inflammatory component such as may be seen in
repetitive strain. If there is an inflammatory component, there may be worsening
of symptoms with use toward the end of
the day, pain at night, and morning stiffness with ache.
PAST HISTORY FOR THE REGION
• The patient commonly reports a history
of the following:
Vigorous and/or repetitive overhead
activity, including throwing in baseball,
javelin, or football; serving in tennis;
spiking or serving in volleyball; driving a golf ball, tackling, or wrestling.
Repetitive carrying of heavy loads
Injury involving sudden forced scapular depression
Excessive or poor use of old-style
crutches and overly tight bandage or
plaster applications into the axilla
Direct trauma to the supraclavicular
region or chest, including MVAs, falls,
and strong massage
First rib resection and heart or breast
surgery
Vaccinations or infections
PHYSICAL EXAMINATION
• Inferior scapular winging at rest
• Reduced active shoulder flexion range
and/or strength
• Scapular winging inferiorly and medially
with active shoulder flexion and/or pressing against a wall or doing push-ups (as
the forward arm movement places a posteriorly directed force on the medial border of the scapula, which is unopposed
with a weak serratus anterior muscle)
• Weakened active shoulder abduction
(with minimal loss of range as the lower
trapezius can compensate for the lack
of serratus anterior to upwardly rotate
the scapula)
• MMT reveals weakness in the serratus
anterior muscle.
• Poor scapulohumeral rhythm with
active shoulder movements caused by
CHAPTER 16 • NERVE
impaired scapular rotation (with possible resultant positive impingement
signs)
• Visible atrophy of the serratus anterior
muscle
• Possible reduction of range and/or
reproduction of pain on cervical lateral
flexion away
• Upper limb neurodynamic testing may
reveal adverse neurodynamics and elicit
symptoms.
IMPORTANT OBJECTIVE TESTS
• It is important to confirm the diagnosis
of long thoracic nerve neuropathy with
electrodiagnostic evaluation. Needle
examination testing is the most reliable
test to evaluate the severity of long thoracic nerve damage and can be used
to monitor progress of the condition.
Nerve conduction studies, however,
have been deemed unreliable to test for
long thoracic nerve trauma, although
they can be used for differential diagnosis of other brachial plexus lesions.
• A plain radiograph is also useful to
assess for the presence of a cervical rib
and for calcifications, although most
often results are normal.
• MRI of the cervical spine and brachial
plexus can also be used to exclude cervical or brachial pathologies.
DIFFERENTIAL
DIAGNOSIS
• Cervical
Cervical spondylosis
Cervical disc disease
Cervical nerve root syndrome
• Shoulder
Shoulder impingement
Malunion of scapular fracture
Rotator cuff tear or tendinopathy
Adhesive capsulitis
Instability of the glenohumeral or
acromioclavicular joints
Degenerative
arthritis of the glenohumeral or acromioclavicular joints
Scapulothoracic or scapulohumeral
bursitis syndromes
• Nerve
Spinal accessory nerve or trapezius palsy
Dorsal scapular nerve or rhomboid
palsy
Suprascapular nerve palsy
Thoracic outlet syndrome
Brachial plexus neuropathy (ParsonageTurner syndrome)
Quadrilateral space syndrome
• Other
Polymyositis
Diffuse peripheral neuropathy
Osteochondroma
Muscular dystrophy
21 of 57
CONTRIBUTING FACTORS
• For any nerve pathology that is nontraumatic, there is often an element of repetitive activity involving the affected limb.
Typically, in the case of the long thoracic
nerve, the repetitive action that may create a traction or compressive neuropathy
involves cervical flexion, lateral flexion,
and rotation away, combined with ipsilateral arm flexion. Individuals involved in
overhead sporting or occupational activity are therefore more at risk.
• Other repetitive tasks or activities, such
as carrying loads in heavy manual work,
weight lifting, tackling, and wrestling,
may also predispose to long thoracic
nerve injury.
• Postural factors may be involved, particularly with repetitive work or sporting
activities, with reduction in proximal
stability and scapular control leading to
increased strain on the nerve.
TREATMENT
SURGICAL OPTIONS
• Safran reviewed literature pertaining
to surgical options and found the most
favorable results from the surgical transfer of the sternal head of the pectoralis
major to replace serratus anterior function. The author felt that this particular
transfer allowed the most similar muscle
activity to that of the serratus anterior as
a result of the orientation of the fibers
and similar excursion levels. The semitendinosus-gracilis graft was also favored
for its strength, low morbidity, and harvest efficiency. The pectoralis minor,
rhomboid, and teres minor muscles have
also been used for muscle transfers.
• Supraclavicular neurolysis of the long
thoracic nerve and nerve transfers
using the thoracodorsal or medial pectoral nerves have also been reported.
• Nath et al advocate the use of microneurolysis with supraclavicular decompression with patients who have a history
pertaining to injury of the long thoracic
nerve in the scalene musculature.
• Scapulothoracic fusion has also been used
to stabilize the scapula in more extreme
cases and if previous surgery has failed.
• Safran reported very good results with
outcome measures such as function,
pain, and scapular winging for pectoralis major transfer surgery.
• A significant loss of range of elevation is
expected with scapulothoracic fusion,
and this outcome should be considered
for determining if this type of surgery is
appropriate.
• Nath et al also reported very good
outcomes after microneurolysis with
supraclavicular
decompression
in
Long Thoracic Nerve Pathology
CHAPTER 16 • NERVE
patients with a history of long thoracic
nerve injury occurring in the scalene
musculature.
• Surgery may be indicated if the patient
has not responded to conservative management after 1 to 2 years and if no
improvement has been seen on EMG
testing.
REHABILITATION
PROGNOSIS
22 of 57
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
All patients with suspected long thoracic
nerve pathology should be referred to a
physician for appropriate investigation.
SUGGESTED READINGS
Cleary CK. Management of radial tunnel syndrome: a therapist’s clinical perspective. J
Hand Ther. 2006;9(2):166–191.
Dumestre G. Long thoracic nerve palsy. J Man
Manipulative Ther. 1995;3(2):44–49.
Goslin KL, Krivickas LS. Proximal neuropathies of the upper extremity. Neurol Clin.
1999;17(3):525–548.
Hermann DN, Logigian EL. Electrodiagnostic
approach to the patient with suspected
mononeuropathy of the upper extremity.
Neurol Clin. 2002;20(2):451–478.
Kendall FP, McCreary EK, Provance PG, Rodgers
MM,RomaniWA.Muscles Testing and Function
with Posture and Pain. 5th ed. Philadelphia:
Lippincott Williams & Wilkins; 2005.
Nath RK, Lyons AB, Bietz G. Microneurolysis
and decompression of long thoracic nerve
injury are effective in reversing scapular
winging: Long term results in 50 cases. BMC
Musculoskelet Disord. 2007;8:25.
Pecina MM, Krmpotic-Nemanic J, Markiewitz
AP. Tunnel Syndromes: Peripheral Nerve
Compression Syndromes. 3rd ed. CRC Press;
2001.
Safran MR. Nerve injuries about the shoulder
in athletes, Part 2: long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med.
2007;32(4).
Seddon HJ. Surgical Disorders of the Peripheral
Nerves. Edinburgh: Churchill; 1975.
Sunderland S. Nerve and Nerve Injuries. 2nd
ed. Edinburgh: Churchill Livingstone; 1978.
Sunderland S. Nerve Injuries and Their. Repair.
A Critical Appraisal. Edinburgh: Churchill
Livingstone; 1991.
AUTHOR: KATINA DIMOPOULOS
ORTHOPEDIC PATHOLOGY
• Most cases of nontraumatic long thoracic nerve pathology resolve within a
year, with improvements seen for up to
2 years. However, as with all peripheral
nerve pathologies, the prognosis depends
on the extent of damage to the nerve.
• Neurapraxia should resolve rapidly and
lead to a complete restoration of function, usually within several months. If
the injury is a more severe axonotmesis,
the recovery time depends on the distance from the site of injury to the denervated tissue. Peripheral nerves have
been reported to recover at an approximate rate of between 1 and 4 mm per
day but recovery may not result in a
complete restoration of function. The
extensive length of the long thoracic
nerve results in a longer reinnervation
distance, thus a longer recovery time
(up to 2 years).
• If there has been a complete sectioning of the nerve (neurotmesis), then a
full recovery will not occur. The results
of treating neurotmesis will depend on
surgical outcome.
Section III
• The aim of rehabilitation is to promote
healing of the nerve and denervated
muscles.This can be achieved by reducing symptoms, encouraging pain-free
exercise, and providing task or sports
reeducation and interventions leading
to reacquisition of function.
• Manual therapy
Symptom reduction can be achieved
through use of ice, electrotherapeutic modalities, and relative rest (forward elevation of the arm should be
avoided). Scapular taping and bracing
have been described in the literature
to reduce overstretch of the serratus
anterior muscle and to add proprioception to the area.
Stretching, soft tissue release, and trigger point therapy of the periscapular
muscles may also help alleviate the
associated hypertonicity and/or pain
caused by muscle compensations for
the loss of the serratus anterior muscle and help restore muscle balance
around the scapula.
Joint mobilization to the cervical and
thoracic spine, as well as to the ribs,
scapula, and acromioclavicular and
glenohumeral joints, may also be useful to increase mobility and alleviate
pain.
Muscle energy techniques may also
be necessary to increase mobility and
alleviate pain in the upper and middle
rib cage (because of serratus anterior
muscle attachments).
• Gentle active-assisted shoulder ROM
exercises should be started early to prevent joint contracture.
• Scapular position education initially
with active-assisted exercise and isometric hold and then the addition of controlled functional movement patterns
• Periscapular muscle strengthening as
required may help optimize scapular
position and stability, starting in neutral,
unloaded positions.
• Neuromuscular electrical stimulation
(NMES) can be used if the patient demonstrates some activity in the serratus anterior muscle. It can be used to
reduce atrophy by applying the electrodes to motor points and stimulating
the muscle at rest or during an active
exercise.
• Nerve gliding exercises have been purported to disperse intraneural edema,
increase blood flow, optimize axonal
transport, and lengthen nerve adhesions.
Neural mobilization can be achieved
using scapular mobilization both actively
and passively into elevation, depression,
protraction, and retraction.
• Functional rehabilitation should include
the following:
Reeducation of movement patterns,
particularly proximal control of the
trunk and neck, to provide a stable
foundation for scapular stability
Specific muscle strengthening by gradually increasing intensity to restore
full power to the serratus anterior
Integration of functional exercise and
strength work into sport- or task-specific skills
Graduated return to full strength,
speed, and power
757
Median Nerve Entrapment
758
BASIC INFORMATION
DEFINITION
The median nerve may be compressed or
entrapped at several places in the arm. It
can be entrapped proximal (pronator syndrome) or distal (anterior interosseous
nerve syndrome, or Kiloh-Nevin syndrome) to the anterior interosseous
branch as it passes between the two
heads of the pronator teres. It can also be
entrapped as it passes under the ligament
of Struthers (found in 1% of the population) that runs between an abnormal process on the shaft of the humerus to its
medial epicondyle (humerus supracondylar process syndrome). Entrapment can
occur as the lacertus fibrosis is tensioned
on pronation at the bicipital tuberosity of
the radius. The median nerve can also be
entrapped at the carpal tunnel between
the flexor tendons, the carpal bones, and
the transverse carpal ligament (carpal tunnel syndrome).
SYNONYMS
•
•
•
•
•
Anterior interosseous syndrome
Kiloh-Nevin syndrome
Pronator teres compression syndrome
Pronator syndrome
Humerus supracondylar process syndrome
• Carpal tunnel syndrome
ICD-9CM CODES
955.1 Injury to median nerve
354.0 Carpal tunnel syndrome
OPTIMAL AND MAXIMAL
NUMBER OF VISITS
For anterior interosseous syndrome, surgical intervention should be considered
after 8 to 12 weeks if response to conservative management is poor. For other
pathologies, the number of visits depends
on progression. Mild-to-moderate presentations may be successfully treated or
managed with conservative intervention.
If the underlying cause involves biomechanical issues associated with lifestyle,
such interventions may need to continue
for protracted time periods. More severe
presentations and unrelenting, unresponsive, or worsening symptoms may warrant
earlier medical or surgical intervention.
ETIOLOGY
• Insult to the nerve may be mechanical,
thermal, chemical or ischemic.
• In entrapment syndromes, compression
or direct trauma leads to nerve tissue
hypoxia.
• Median nerve entrapment pathology
may occur with repetitive or overuse
CHAPTER 16 • NERVE
movement patterns involving the
elbow, wrist and hand, vibration injuries, trauma, pregnancy, menopause,
obesity, underlying disease and medical issues (diabetes mellitus, thyroid
myxedema, osteoarthritis, acromegaly,
amyloidosis, renal dialysis, or alcoholism), space-occupying entities (neurofibroma, lipoma, aneurysm, hemangioma,
ganglion, or xanthoma), presence of anatomical anomalies, and psychological
stress. Some authors have also reported
possible inherited predisposition. While
all of these factors have been linked to
median nerve entrapments, many cases
are described as idiopathic, and it is
likely that most are multifactorial.
• In entrapments, nerve trauma occurs
because the size of the neural structure
exceeds the anatomical space available
for it, resulting in increased pressure,
which in turn leads to impaired blood
flow and subsequent hypoxia of the tissue and disruption to the axonal transport system.
• Nerve injury is classified according
to severity of the injury and potential
for reversibility. Original classifications
described previously remain in current
use, as follows:
First-degree neurapraxia involves distortion of myelin around the nodes of
Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance, resulting in temporary loss of
nerve conduction. Recovery is rapid
and complete in most cases.
Second-degree axonotmesis involves
interruption of the axon with secondary wallerian degeneration, but the
supporting tissue around the axon
is preserved. Recovery may be complete but takes longer to occur and
depends on the distance between the
site of injury and the end-structure
(denervated muscle).
Third-degree
neurotmesis involves
extensive disruption of the nerve and
its supporting structures, but while
the endoneurium is disrupted, the
perineurium and epineurium remain
intact.
Fourth-degree neurotmesis involves
disruption of all neural components
except the epineurium.
Fifth-degree
neurotmesis involves
complete transaction and discontinuity of the nerve with no capacity
for regeneration. Neurotmesis rarely
occurs from entrapment, but where
continuity has been disrupted, complete recovery is not possible, even
with surgical techniques, and the
eventual outcome depends on individual circumstances. A comprehensive overview of neurobiology, nerve
injury, and nerve repair is provided by
Dahlin.
23 of 57
• Double-crush syndrome refers to the
fairly common phenomenon of nerve
entrapment and radiculopathy occurring in combination, although the syndrome is considered controversial.
Compression or irritation of the nerve
roots at the cervical level is thought to
increase sensitivity to compression or
movement restrictions more distally in
the structure.
• In overuse-type entrapments, it is proposed that repetitive work or static
postures produce an inflammatory
response. Fibroblasts appear to repair
the damage incurred but generate adhesions that limit neural glide and subsequently increase anoxia. Other studies
found that cortical dedifferentiation
may occur from repetitive motion activities and nerve injuries. This may result
in reinforced poor posturing and use of
aberrant motor pathways.
EPIDEMIOLOGY AND
DEMOGRAPHICS
• Carpal tunnel syndrome is among the
most commonly reported nerve entrapments, anterior interosseous syndrome
and pronator syndrome occur much
less frequently, and humerus supracondylar process syndrome is rare.
• Anterior interosseous syndrome, pronator syndrome, and humerus supracondylar process syndrome tend to be linked
to specific activity, trauma, disease, or
anatomical makeup rather than associated with a particular age group.
• Carpal tunnel syndrome presentations
tend to be more than twice as common in females compared to males, and
most commonly occur between 45 and
54 years of age, although the syndrome
also occurs quite frequently during
pregnancy.
• Median nerve entrapments occur
more frequently among office workers,
manual workers, and individuals who
engage in repetitive movement pattern
activities such as musicians, artists, and
sports participants.
MECHANISM OF INJURY
• Specific anatomical sites for entrapment in the upper limbs are described
by Pratt. Anterior interosseous nerve
syndrome may occur when the nerve is
compressed at the tendinous origin of
the deep head of pronator teres (most
common presentation) or as it passes
between the two heads of pronator teres,
by impingement from a bicipital tendon
bursa or radial and ulnar artery abnormalities in the forearm, by fascial bands
at the origin of flexor digitorum superficialis, or by anatomical anomalies within
the deep palmar compartment involving flexor pollicis longus or palmaris
profundus. A review of compression
Median Nerve Entrapment
CHAPTER 16 • NERVE
•
•
•
•
COMMON SIGNS AND
SYMPTOMS
•
•
•
AGGRAVATING ACTIVITIES
• Repetitive movement patterns at the
elbow, wrist, and hand, particularly
repetitive pronation and supination,
tend to exacerbate the symptoms.
• The pathology may be worsened with
sustained postures, especially those
involving the wrist, head, and neck and
activities that increase the volume of
structures, which may be implicated in
entrapment such as those that may lead
to pronator hypertrophy.
EASING ACTIVITIES
• Relative or absolute rest may assist in
alleviating symptoms in cases where
the pathology has been caused by overuse or repetitive movement patterns.
24 of 57
• Adapting movement strategies and altering or correcting posture may reduce
loading on irritated structures where
absolute rest is not possible.
• Use of splints to maintain more neutral
positions and thus reduce neural tension, either during activity or overnight,
may also be helpful.
24-HOUR SYMPTOM PATTERN
• Symptoms are worsened with aggravating activities but also tend to increase
nocturnally, particularly paraesthesia
and numbness.
• In females, symptoms may show hormonal variation; in individuals in whom
the presentation is related to another
medical condition, symptoms may vary
according to physiological balance associated with the underlying condition.
PAST HISTORY FOR THE REGION
• Median nerve entrapment can occur
from a broad spectrum of associated
causative factors; consequently, past history for the pathology may vary widely
between individuals.
• Anatomical anomalies involving bony
structures (supracondylar process
on humerus and the presence of the
ligament of Struthers and form and
alignment of carpal bones), vascular
structures (radial, ulnar, and median
arteries), and connective tissue (fascia) may predispose individuals to the
pathology, together with the presence
of underlying disease and medical
issues (diabetes mellitus, thyroid myxedema, osteoarthritis, obesity, pregnancy,
menopause, space-occupying entities
such as neurofibroma or lipoma, aneurysm, hemangioma, ganglion, xanthoma,
acromegaly, amyloidosis, renal dialysis,
or alcoholism).
• Trauma history may include work or leisure activities involving repetitive movement patterns or vibration exposure (all
median nerve entrapment pathologies),
partial rupture at the musculotendinous
junction of biceps brachii (lacertus
fibrosis tension), fractures of the upper
limb, particularly Colles’ fracture, or
fracture or subluxation and dislocation
injuries, particularly those involving the
carpal bones (carpal tunnel syndrome).
PHYSICAL EXAMINATION
• Anterior interosseous syndrome commonly presents with weakness and difficulty moving the index and middle
fingers (flexor digitorum profundus),
combined with weakness in the thumb
(flexor pollicis longus), making pinch
grip difficult from loss of flexion in the
fingers and thumb as the distal phalanges remain extended or hyperextended.
• Variations in innervation for the
hand mean that the presentation for
ORTHOPEDIC PATHOLOGY
• Anterior interosseous syndrome commonly presents with weakness and difficulty moving the index and middle
fingers (flexor digitorum profundus,
combined with weakness in the thumb
(flexor pollicis longus), making pinch
grip difficult.
• However, variations in innervation for
the hand, particularly the Martin Gruber
anastomosis (in which the motor nerve
crosses over from the median nerve
to the ulnar nerve, present in 10% to
15% of the population), mean that the
presentation for entrapment may vary
significantly and could involve flexor
pollicis brevis, adductor pollicis, abductor pollicis brevis, lumbrical, and abductor digiti minimi muscles, or even the
entire hand.
• Pronator syndrome commonly manifests with pain in the forearm and wrist,
combined with weakness and atrophy
of the thenar muscles. Flexor carpi radialis, palmaris longus, and flexor digitorum
muscles are affected, with or without
the addition of those muscles usually
supplied by the anterior interosseous
nerve—flexor pollicis longus, flexor digitorum profundus, and pronator quadratus muscles. However, the tendency for
variation in muscle innervation patterns
in the hand should be remembered.
• Paraesthesia in median nerve distribution may occur with repetitive pronation
•
and supination, and individuals may
experience early fatigue in muscles of
the forearm, particularly with excessive
pronation.
Lacertus fibrosis tension produces pain
radiating from the elbow to the forearm
with pronation or resisted supination
with the forearm in flexion, combined
with localized symptoms around the
fibrous arcade at the origin of flexor
digitorum superficialis with resisted
middle-finger flexion.
Humerus supracondylar process syndrome may manifest with pain and
paraesthesia in median nerve distribution, combined with weakness in the
muscles as described for pronator syndrome but with the addition of pronator teres. Individuals may report weak
grip and pronation and may exhibit
forearm atrophy.
Carpal tunnel syndrome commonly
manifests with progressively worsening pain (classically described as aching
and burning in nature) and paraesthesia
in the thumb, forefinger, middle finger,
hand, and wrist, which may extend to
the forearm, elbow, shoulder, and neck.
Symptoms are often worse nocturnally.
Individuals may complain of problems
with grip and weakness in the wrist and
hand.
Anterior interosseous syndrome produces weakness in the thumb, forefinger, and middle finger, although other
regions of the hand may be affected.
Pronator syndrome produces pain in
the forearm and wrist, combined with
paraesthesia and weakness in the thumb,
fingers, and wrist. Lacertus fibrosis tension produces pain radiating from the
elbow to the forearm. Humerus supracondylar process syndrome produces
pain, paraesthesia, and weakness in
the elbow, wrist, and hand. Carpal tunnel syndrome produces pain and significant paraesthesia in the hand and
wrist, which may extend to the forearm,
elbow, shoulder, and neck.
Section III
syndromes in the median nerve is given
by Koo and Szabo.
Pronator syndrome refers to median
nerve compression between the two
pronator teres heads before it branches
to form the anterior interosseous
nerve.
Lacertus fibrosis (bicipital aponeurosis)
tension may cause median nerve compression as it is pulled across the nerve
with pronation as the bicipital tuberosity of radius passes posteriorly or when
the forearm is maintained in resisted
supination and flexion.
Humerus supracondylar process syndrome may occur when the median
nerve is compressed above the elbow as
it passes under the ligament of Struthers
in individuals in whom the structure is
present.
Carpal tunnel syndrome refers to compression of the median nerve as it
passes, together with the tendons of
flexor digitorum profundus, flexor digitorum superficialis, flexor pollicis longus, and flexor carpi radialis, through
the enclosure created by trapezoid, capitate, the flexor retinaculum (transverse
carpal ligament) and its attachments to
the scaphoid tubercle, trapezium, hook
of hamate, and pisiform.
759
760
Median Nerve Entrapment
•
•
•
•
•
entrapment may vary significantly and
could involve the flexor pollicis brevis,
adductor pollicis, abductor pollicis brevis, lumbrical, and abductor digiti minimi muscles or even the entire hand.
Individuals with pronator syndrome
may exhibit weakness and atrophy of
the thenar muscles. Flexor carpi radialis,
palmaris longus, and flexor digitorum
muscles are affected with or without the
addition of the muscles usually supplied
by the anterior interosseous nerve—
flexor pollicis longus, flexor digitorum
profundus, and pronator quadratus.
Paraesthesia in median nerve distribution may occur with repetitive pronation and supination, and individuals may
experience early fatigue in muscles of
the forearm, particularly with excessive
pronation. Tinel’s sign may be positive
in the mid to proximal forearm rather
than at the wrist.
Lacertus fibrosis tension produces
pain radiating from the elbow to the
forearm with pronation or resisted
supination with the forearm in flexion, combined with localized symptoms around the fibrous arcade at the
origin of flexor digitorum superficialis with resisted middle-finger flexion.
Past trauma history may also indicate
this syndrome.
Individuals with humerus supracondylar process syndrome may report pain
and paraesthesia in median nerve distribution. In addition to the weakness and
atrophy patterns observed in the hand
with more distal compression, there
may also be evidence of forearm atrophy with weakness noted in both grip
and pronation.
Individuals with carpal tunnel syndrome present with significant paraesthesia and numbness in the hand and
wrist. Additionally, atrophy of abductor
pollicis brevis may be noted and Tinel’s
sign (at the wrist), Phalen’s test, and
wrist flexion provocation tests may be
positive.
IMPORTANT OBJECTIVE TESTS
• Diagnostic accuracy of neurological
upper limb examination employing
a battery of standard test procedures
has been found to be reproducible and
reliable.
• Neurophysiology and EMGs may produce positive findings, particularly
for carpal tunnel syndrome. Results
are often inconclusive for anterior
interosseous syndrome because of
the deep location of the structures. If
pronator syndrome is suspected, an
initial negative test accompanied by
a strong suggestive history should be
repeated after approximately 6 weeks.
Radiographic, ultrasound, and MRI may
identify anatomical anomalies, and vas-
CHAPTER 16 • NERVE
•
•
•
•
•
•
cular tests may be helpful in differential
diagnosis.
Pinch test (precision grip): Individuals
with anterior interosseous syndrome
are unable to flex the distal phalanges
of the thumb, forefinger, and middle finger so that contact can only be made
through the pads rather than the tips of
the digits.
Tinel’s sign: Tapping over the median
nerve distribution reproduces sensory
symptoms distal to the test site.This test
is positive at the proximal to mid-forearm rather than at the wrist in pronator syndrome and positive at the wrist
over the carpal tunnel in carpal tunnel
syndrome.
Phalen’s test: Maximal wrist flexion
either with gravity or pressure applied
by the examiner reproduces sensory
symptoms in the thumb, forefinger,
and middle finger. (Normal subjects
may experience similar symptoms after
1 minute.) A variation of this is the
reverse Phalen’s test where the subject
grips the examiner’s hand as the wrist is
extended and direct pressure is applied
over the carpal tunnel for 1 minute.
A positive test reproduces the same
symptoms.
Wrist flexion provocative test: Constant
digital pressure over the median nerve at
the carpal tunnel with elbow extended
and forearm supinated reproduces
paraesthesia and numbness within 30
seconds for a positive test.
Durkan compression test (carpal compression test): With the wrist in neutral
and forearm supinated, carpal compression is applied either manually or with
a pressure-sensitive instrument. A positive test is recorded if sensory symptoms occur within 30 seconds.
Sensory discrimination tests may also
be helpful in defining the affected area.
DIFFERENTIAL
DIAGNOSIS
• Anterior interosseous syndrome:
Cervical radiculopathy (C8), pronator
syndrome, carpal tunnel syndrome, lacertus fibrosis tension, humerus supracondylar process syndrome, lateral cord
lesion, ulnar neuropathy, flexor digitorum profundus tendon rupture or avulsion, or flexor pollicis longus rupture
• Pronator syndrome: Cervical radiculopathy (C6 to C7), lacertus fibrosis tension,
flexor superficialis syndrome, humerus
supracondylar process syndrome, anterior interosseous syndrome, carpal
tunnel syndrome, soft tissue overuse
syndromes, vascular pathologies, or cardiac pathologies
• Lacertus fibrosis tension: Cervical radiculopathy (C6 to C7), pronator syndrome,
25 of 57
humerus supracondylar process syndrome, anterior interosseous syndrome,
carpal tunnel syndrome, soft tissue overuse pathologies, or cardiac pathologies
• Humerus supracondylar process syndrome: Cervical radiculopathy (C6/
C7), anterior interosseous syndrome,
pronator syndrome, lacertus fibrosis
tension, carpal tunnel syndrome, soft
tissue overuse syndromes, or vascular
pathologies
• Carpal tunnel syndrome: Cervical radiculopathy (C6/C7, T1), thoracic outlet
syndrome, anterior interosseous syndrome, pronator syndrome, lacertus
fibrosis tension, humerus supracondylar process syndrome, ulnar neuropathy,
vascular pathologies, soft tissue overuse syndromes, carpometacarpal arthritis, shoulder bursitis, transient ischemic
attack, or myocardial ischemia
CONTRIBUTING FACTORS
• Presence of anatomical anomalies
• Underlying disease or medical condition
• Repetitive work or leisure activities
• Past trauma history
• Psychological stress
• Genetic predisposition
TREATMENT
SURGICAL OPTIONS
• An overview of basic neurosurgical
techniques is provided by Dahlin.
Anterior
interosseous syndrome:
Decompression at pronator heads,
fascial release at flexor digitorum
superficialis or the deep palmar compartment, exploration techniques to
release pressure generated by bursa
or vascular abnormalities
Pronator syndrome: Release of the
humeral head of pronator teres combined with fascial release at flexor
digitorum superficialis
Lacertus fibrosis tension: Release of
lacertus fibrosis, possibly with associated repair for biceps brachii
Humerus supracondylar process syndrome: Release at the bony process
and ligament of Struthers
Carpal tunnel syndrome: Open or
endoscopic release techniques to
divide the transverse carpal ligament,
restore neural glide, relieve adhesions,
and where the condition results from
compression caused by some form
of space-occupying lesion, appropriate techniques to address the specific
lesion.
• When accurate diagnosis has been made,
surgical intervention produces good
results for all the pathologies described,
with success rates around 90% and low
recurrence rate. Recovery depends on
Median Nerve Entrapment
CHAPTER 16 • NERVE
level of nerve injury, with neurapraxias
showing the fastest and most complete
return to function.
• Surgery may be indicated for individuals with severe, worsening, or unrelenting symptoms that are nonresponsive
to conservative management involving
antiinflammatory medication, splinting, and manual and electrotherapy
physiotherapy modalities and addressing of ergonomic issues. Early surgical
intervention (within 8 to 12 weeks) is
generally recommended for anterior
interosseous syndrome to achieve the
best outcome.
REHABILITATION
• Factors that contribute to median nerve
entrapment pathology include the presence of anatomical anomalies, an underlying disease or medical condition,
repetitive work or leisure activities, past
trauma history, psychological stress, and
genetic predisposition.
• Systematic review found inconclusive
evidence for conservative management
of carpal tunnel syndrome, but as noted
• Severe or worsening neurological function or symptoms
• Failure to respond to conservative management
• Suspicion or presence of underlying
disease
• Unexplained symptoms inconsistent
with the pathology
SUGGESTED READINGS
Akalin E, El O, Peker O, et al. Treatment of carpal tunnel syndrome with nerve and tendon
gliding exercises. Am J Phys Med Rehabil.
2002;81(2):108–113.
Chin DHCL, Meals R. Anterior interosseous
nerve syndrome. J Am Soc Surg Hand.
2001;1(4):249–257.
Cleary CK. Management of radial tunnel syndrome: a therapist’s clinical perspective. J
Hand Therapy. 2006;9(2):166–191.
Dahlin LB. Mini-symposium: hand trauma
(ii)
nerve
injuries.
Curr
Orthop.
2008;22(1):9–16.
Freedman J. Acupuncture for carpal tunnel syndrome. Acupunct Med. 2002;20(1):39–40.
Gomes I, Becker J, Ehlers JA, Nora DB. Prediction
of the neurophysiological diagnosis of carpal tunnel syndrome from the demographic
and clinical data. Clin Neurophysiol.
2006;117(5):964–971.
Hall TM, Elvey RL. Nerve trunk pain: physical diagnosis and treatment. Man Ther.
1999;4(2):63–73.
Jepsen JR, Laursen LH, Hagert C-G, Kreiner S,
Larsen AI. Diagnostic accuracy of the neurological upper limb examination I: inter-
26 of 57
AUTHOR: SARAH GRAHAM
ORTHOPEDIC PATHOLOGY
PROGNOSIS
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
relater reproducibility of selected findings
and patterns. BMC Neurol. 2006;6(8).
Jepsen JR, Laursen LH, Hagert C-G, Kreiner S,
Larsen AI. Diagnostic accuracy of the neurological upper limb examination II: relations
to symptoms of patterns of findings. BMC
Neurol. 2006;6(10).
Koo JT, Szabo RM. Compression neuropathies
of the median nerve. J Am Soc Surg Hand.
2004;4(3):156–175.
Latinovic R, Gulliford MC, Hughes RA. Incidence
of common compressive neuropathies in primary care. J Neurol Neurosurg Psychiatry.
2006;77(2):263–265.
Magee DJ. Orthopaedic Physical Assessment.
5th ed. Philadelphia: Saunders; 2008.
Naeser MA, Hahn KA, Lieberman BE, Branco
KF. Carpal tunnel syndrome treated with
low level laser and microamperes transcutaneous electric nerve stimulation: a
controlled study. Arch Phys Med Rehabil.
2002;83(7):978–988.
Nithi K. Physiology of the peripheral nervous
system. Surgery. 2003;21(10):264a–264e.
Piazzini DB, Aprile I, Ferrara PE, et al. A systematic review of conservative treatment
of carpal tunnel syndrome. Clin Rehabil.
2007;21(4):299–314.
Pratt N. Anatomy of nerve entrapment
sites in the upper quarter. J Hand Ther.
2005;18(2):216–219.
Premoselli S, Sioli P, Grossi A, Cerri C. Neutral
wrist splinting in carpal tunnel syndrome:
a 3 and 6 months clinical and neurophysiologic follow up evaluation of nightonly splinting therapy. Eura Medicophys.
2006;42(2):121–126.
Seddon HJ. Surgical Disorders of the Peripheral
Nerves. Edinburgh: Churchill Livingstone;
1975.
Seitz WH, Matsuoka H, McAdoo J, Sherman G,
Stickney DP.Acute compression of the median
nerve at the elbow by the lacertus fibrosis. J
Shoulder Elbow Surg. 2007;16(1):91–94.
Sunderland S. Nerve and Nerve Injuries. 2nd
ed. Edinburgh: Churchill Livingstone; 1978.
Tetro AM, Bradley EA, Hollstien SB, Gelberman
RH. A new provocative test for carpal tunnel syndrome. Assessment of the wrist
and nerve compression. J Bone Joint Surg.
1998;80(3):493–498.
Wilbourn AJ, Gilliat RW. Double crush syndrome: a critical analysis. Neurology.
1997;49:21–29.
Section III
• Rehabilitation may focus on two goals:
Addressing the underlying causative
factors and reducing the symptoms. In
cases where repetitive movement patterns or exposure to vibration trauma
feature in the development of the
pathology, a detailed ergonomic assessment may be helpful in identifying areas
in which loading stress may be reduced
by changes in behavior, activity, or posture or through use of appropriate
braces.
• Therapeutic techniques to alleviate symptoms may include soft tissue
manual techniques, neural mobilizing
techniques, massage, acupuncture, and
electrotherapy techniques to address
pain, inflammation, and loss of movement and function. When psychological
stress is considered a significant factor,
individuals may benefit from more general therapeutic exercise programs.
by other researchers, definitive statements regarding prognosis are difficult
because differential diagnosis is not
always achieved. Mild-to-moderate presentations of median nerve entrapments
may be effectively treated or well-controlled with conservative intervention.
In individuals with more severe presentations or who have failed to respond to
conservative measures, surgical procedures generally have a good outcome in
terms of symptom relief and functional
outcome.
761
Neurogenic Thoracic Outlet Syndrome
762
BASIC INFORMATION
CHAPTER 16 • NERVE
OPTIMAL NUMBER OF VISITS
10
DEFINITION
MAXIMAL NUMBER OF VISITS
• Thoracic outlet syndrome (TOS) encompasses numerous scenarios of compression (neurological and vascular) in the
thoracic outlet region of the shoulder
girdle. Although vascular and neurological classifications exist, it must be
noted that these conditions can also be
observed together.
• Neurogenic TOS involves compression of various portions of the brachial
plexus and is the most common form
of TOS (over 90% of cases).The brachial
plexus is formed by the C5 to T1 nerve
roots, although the most caudal root or
“lower plexus” (C8 and T1) is most commonly affected. The “upper plexus” may
also be involved, and this affects the C5,
C6, or C7 nerves, or in rare cases may be
involved in combination with the lower
plexus.
• Defining the syndrome has been fraught
with difficulty in the literature because
of its variable etiology and presentation
and often minimal clinical findings.
• Two main neurogenic TOS classifications exist as a result of the following
variable clinical presentations:
True neurogenic TOS, where patients
present with a typical clinical presentation with positive neurological findings on examination
Nonspecific neurogenic or “classic”
TOS, in which pain is a predominant
feature with minimal neurological findings on examination.This subcategory
comprises most TOS presentations.
30
SYNONYMS
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Cervical rib syndrome
First rib syndrome
Scalenus anticus syndrome
Costoclavicular syndrome
First thoracic rib syndrome
Hyperabduction syndrome
Scalenus medius syndrome
Pectoralis minor syndrome
Subcoracoid-pectoralis minor syndrome
Brachiocephalic syndrome
Nocturnal paresthetic brachialgia
Rucksack palsy
Droopy shoulder syndrome
Fractured clavicle-rib syndrome
Motor type neurogenic TOS
ICD-9CM CODES
353 Nerve root and plexus disorders
354 Mononeuritis of upper limb and
mononeuritis complex
354.8 Other mononeuritis of upper
limb
354.9 Mononeuritis of upper limb
unspecified
ETIOLOGY
• The current belief of the cause of TOS
is the underlying existence of bony or
fibromuscular anomalies with overlying
injury and/or spasm in the thoracic outlet region causing compromise.The anatomical anomalies are generally seen as
predisposing factors.
• The pathology involves compression
of portions of the brachial plexus in
the thoracic outlet region as a result
of underlying bony or fibromuscular
anomalies with overlying muscle injury
and/or spasm.
• Local spasm in the thoracic outlet region
can result in muscle swelling and place
the local neural structures under strain
or traction, resulting in nerve edema. As
the condition becomes more chronic,
scarring and fibrosis of the nerve can
take place.
• Bony anomalies can be congenital, traumatic, or posttraumatic and
include the presence of a cervical rib,
elongated C7 transverse process, first
rib deformity, displaced first rib fracture, excessive callus formation after
first rib fracture, rib hemangioma, fractured or subluxed clavicle, and pseudarthroses. Cervical ribs are known to
exist in approximately 0.5% of the
population, with 10% to 20% resulting
in symptoms, although this depends
on their size.
• Soft tissue anomalies can also be congenital, traumatic, or posttraumatic and
include altered scalene muscle insertions and origins, presence of scalenus
minimus or scalenus pleuralis muscle,
hypertrophy or injury of scalene muscles, presence of congenital fibromuscular bands (classified into types 1 to 10)
or dense fibrous sheaths, cervical ligaments and bands, and pectoralis minor
shortening.
• Anatomical variations of the passage
of the brachial plexus through the thoracic outlet, the adherence of the nerves
to the scalene muscles, can also predispose to TOS.
• The superimposed injury involved in
causing TOS symptoms may include
whiplash, direct or indirect blow to the
shoulder, repetitive strain through prolonged upper limb activity, accessory
breathing, and/or poor posture.
• The following three spaces in the thoracic outlet region have been identified as potential areas of brachial plexus
compression (Atasoy):
Interscalene space or triangle is bordered anteriorly by the anterior sca-
27 of 57
lene muscle, posteriorly by the middle
scalene muscle, and inferiorly by the
first rib. The brachial plexus passes
posteriorly to the anterior scalene
muscle here, in close relation and
directly superior to the subclavian
artery.
Costoclavicular
space is bordered
anteriorly by the medial aspect of the
clavicle, subclavian muscle and tendon, and costocoracoid ligament. The
posterolateral border is formed by the
upper border of the scapula and the
posteromedial border by the first rib
anterior and middle scalene muscle
insertions. Here, the brachial plexus
travels with the subclavian vein and
artery under the clavicle and subclavius muscle toward the subpectoralis minor space.
Subpectoralis minor space is located
inferior to the coracoid process and
posterior to the pectoralis minor muscle insertion. Here, the brachial plexus
continues to travel with the subclavian vein and artery beneath the pectoralis muscle toward the axilla.
The interscalene and costoclavicular spaces are equally common sites
of compression in neurogenic TOS,
while compression in the subpectoralis minor space is much less common.
• Hypertrophy, degeneration, and fibrosis
of the anterior scalene muscle caused
from a previous single traumatic incident or repeated trauma is believed to
be the current overlying cause of compressive symptoms. Various studies
have demonstrated histological abnormalities in the anterior scalene muscles,
including type 1 muscle fiber proliferation, reduction of type 2 muscle fibers,
and increased connective tissue content and muscle scarring.
• Physiologically, there is disruption to the
underlying nerve of the brachial plexus,
which is responsible for conduction.
• Neurogenic TOS involves a continuum
of damage from periodic nerve ischemia to chronic ischemia resulting in
segmental demyelination (neurapraxic
injury). This may progress to axonotmesis injury (in more severe cases of continued nerve compression) in which
interruption of the axon with secondary wallerian degeneration will occur.
EPIDEMIOLOGY AND
DEMOGRAPHICS
• Nonspecific neurogenic TOS is fairly
common, although its prevalence is
difficult to estimate because diagnosis is difficult. It can be missed or
overdiagnosed.
• True neurogenic TOS is uncommon.
• Young and middle-aged adults are the
most susceptible to nonspecific neurogenic TOS.
Neurogenic Thoracic Outlet Syndrome
CHAPTER 16 • NERVE
• True neurogenic TOS symptom onset is
most common in teenagers and young
adults.
• Females are at least three times as likely
to develop nonspecific neurogenic TOS
as males.
• True neurogenic TOS mainly affects
females.
MECHANISM OF INJURY
• The superimposed injury involved in
causing TOS symptoms may include
whiplash, direct or indirect blow to the
shoulder, repetitive strain through prolonged upper limb activity, and/or poor
posture.
• Positions and postures that place
increased strain on the thoracic outlet
include the following:
Prolonged writing or use of keyboard
or telephone
Assembly line works
Poor posture (i.e., droopy shoulders)
Prolonged overhead or reaching activity such as styling hair, painting, playing musical instruments (e.g., violin or
flute), and swimming
Excessive carrying of heavy objects
such as suitcases and shopping bags
Prolonged carrying of a heavy backpack
AGGRAVATING ACTIVITIES
• Overhead arm or hand positions or
arm elevated repetitive activities. These
commonly include styling hair, painting, working overhead, playing musical
instruments (e.g., violin or flute), and
swimming.
• Carrying heavy objects such as suitcases
and shopping bags
• Prolonged use of arm as in writing and
typing
• Cervical contralateral rotation and/
or lateral flexion can often aggravate
symptoms resulting from upper plexus
involvement.
• Symptoms may be delayed until after
arm activity in some cases.
EASING ACTIVITIES
• Rest from aggravating activities
• Arm adduction and flexion across
body
• Shoulder girdle support by using an arm
rest, placing hand in pocket, or using a
sling
24-HOUR SYMPTOM PATTERN
• Morning
Stiffness and ache depends on inflammatory component
• Daytime
Depends on arm activity
• Nighttime
Entire arm may feel numb or weak
during the night, especially if patient
sleeps on the ipsilateral side with the
arm overhead and elbow flexed
May often wake from pain, especially
if patient has engaged in repetitive
arm activity during the day.
PAST HISTORY FOR THE REGION
• The patient may report a previous history of whiplash injury or a direct or
indirect blow to the shoulder resulting in first rib, muscular, or clavicular
trauma. Symptoms generally develop
from 1 month up to several months
after whiplash injury.
28 of 57
PHYSICAL EXAMINATION
• Nonspecific neurogenic TOS
Poor posture (including downwardly
rotated and protracted scapula, large
breasts and/or obesity, forward head
posture)
Exaggerated upper chest or accessory
breathing
Neurological tests negative
Altered neurodynamics on upper limb
neurodynamic tests and/or brachial
plexus tension tests
Reproduction of arm symptoms and/
or local discomfort on palpation over
the brachial plexus (also known as
pressure provocation test or Spurling
maneuver)
Positive Tinel’s sign for reproduction
of arm pain and/or paraesthesias or
symptoms over brachial plexus
Muscle
spasm, tenderness, and/or
shortening of anterior scalene muscle
on palpation and length testing
Muscle
spasm, tenderness, and/or
shortening of pectoralis minor muscle
on palpation and length testing
Ipsilateral elevated first rib
Positive
Roos, Adson’s, Halsted’s,
and Wright’s hyperabduction tests:
Increased arm pain and paraesthesias
Hypomobility of the lower cervical
and upper thoracic spinal levels
• Lower and upper plexus involvement:
The following objective findings are
more specific to which part of the
plexus is involved. Although rare, mixed
plexus TOS also exists. As implied, it
manifests with a combination of upper
and lower plexus TOS symptoms.
Lower
plexus involvement (most
common)
Weakened
interossei, flexor carpi
ulnaris, thenar, and hypothenar muscles (patients may present with weakness of various C8/T1 innervated
muscles).
Slightly reduced triceps muscle strength
(triceps partially supplied by C8)
Reduced sensation on light touch and
pinprick testing in the medial arm and
medial one-and-a-half fingers (ulnar
nerve distribution).
Tinel’s test performed over the lower
brachial plexus is positive for local discomfort and reproduction of referred
pain.
Pressure provocation test positive
over the lower brachial plexus
Lower brachial plexus tension test is
positive for reproduction of medial
arm symptoms, with the arm at 90
degrees, and the elbow and wrist
extended and supinated.
ORTHOPEDIC PATHOLOGY
• Nonspecific neurogenic TOS.
• Pain generally involves the neck, head,
chest, scapula, shoulder, arm, and hand
(area of pain depends on which part of
the brachial plexus is involved).
• Numbness or paresthesias of the arm
and hand (area depends on which part
of the brachial plexus is involved).
• Coldness of the hand and increased sensitivity to cold exposure
• Whole arm numbness and heaviness
with arm elevation
• Clumsiness with fine hand activities
and weakness on gripping
• True neurogenic TOS
Pain absent
Clumsiness with fine hand activities
and weakness on gripping
If the lower plexus (C8 or T1 nerves)
is involved, the patient may present
with the following:
Ipsilateral anterior or posterior shoulder pain extending to the medial arm,
forearm, and hand
Ipsilateral paresthesias into the ring
and small fingers (in the sensory distribution of the ulnar nerve)
Ipsilateral pain in the clavicular region
extending to the occipital region
and mastoid (headaches can be quite
severe)
Ipsilateral anterior chest pain
• If the upper plexus (C5, C6, or C7
nerves) is involved, the patient may
present with the following:
• The onset of symptoms may also be
insidious but may reveal increased or
unaccustomed prolonged or repetitive
upper limb activity.
Section III
COMMON SIGNS AND
SYMPTOMS
Ipsilateral cervical pain with radiation to the ear, face, and head (mandibular, temporal, and occipital
regions)
Ipsilateral “stuffy” ear
Ipsilateral pain in the medial scapular, anterior clavicular, upper chest,
and lateral shoulder and arm pain (in
the sensory distribution of C5 or C6
nerve roots)
Ipsilateral sympathetic-mediated swelling of the face, night vision difficulties,
and rarely, an eyelid droop
Dizziness, vertigo, blurred vision
763
764
Neurogenic Thoracic Outlet Syndrome
• Upper plexus involvement
Weakness of the deltoid, biceps, and
triceps (C5-C7)
Reduced sensation on light touch and
pinprick testing in the lateral shoulder and arm extending to the thumb,
index, and middle finger
Tinel’s test performed over the upper
brachial plexus is positive for local discomfort and reproduction of referred
pain.
Pressure provocation test positive
over the upper brachial plexus
Upper brachial plexus tension test
positive for reproduction of lateral
arm symptoms with arm in exaggerated waiter’s tip posture.
• True neurogenic TOS
The distinguishing feature of this TOS
category is that neurological tests are
always positive (reduced strength and
sensation: The muscles and areas of
skin affected depend on which part
of the brachial plexus is involved).
In more severe cases, atrophy of the
hand is evident. Reflexes, however, are
normal.
•
•
IMPORTANT OBJECTIVE TESTS
• Four tests (Adson’s, Halsted’s, Wright’s
hyperabduction, and Roos) have traditionally been used to diagnose TOS.
These tests have been extensively discussed, criticized, and “modified” in the
literature as a result of poor sensitivity
and specificity.
• First, since the Adson’s, Halsted’s,
and Wright’s tests monitor the radial
pulse, they should be considered tests
for arterial TOS rather than neurogenic TOS. More recently, these tests
are generally considered provocative
tests for pain or paraesthesias in neurogenic TOS, although they remain
invalidated.
• Furthermore, if these tests are used to
provoke pain from brachial plexus compression, then only one site of nerve
compression should be provoked.
None of these tests is specific enough
to exclude other pathology. Thus various authors have postulated new or
modified tests to diagnose neurogenic
TOS.
• The Roos test (or elevated arm stress
test) is generally described as the most
reliable test for all types of TOS. As
described, the reproduction of cervical,
shoulder, and arm pain and paresthesias
is seen as a positive test. If a patient is
unable to complete the test because of
symptoms, it can also reflect the severity of their condition. Because of its
lack of specificity, Novak et al, as cited
by Mackinnon and Novak, have suggested the use of a modified test, which
was shown to be positive in 95% of a
patient group with TOS in their study.
•
•
•
•
•
CHAPTER 16 • NERVE
The patient places both arms into elevation with elbows extended and forearms in neutral (pronation/supination).
With the wrists in neutral, they maintain
this position for 1 minute. The test is
positive for neurogenic TOS if there is a
reproduction of cervical, shoulder, and
arm pain and paresthesias. Furthermore,
when using this modified Roos test, the
authors found that when they applied
sustained direct pressure over the brachial plexus, they reproduced symptoms
in their TOS patients. Thus a combination of a provocative test with compression of the entrapment site may also be
used to help diagnose TOS and other
nerve entrapment neuropathies.
Vibration or pressure threshold testing was also shown to be abnormal
in a study of patients with neurogenic
TOS, with arm elevation and sustained
pressure over the brachial plexus. Twopoint discrimination was found to be
normal, however, except in cases of
coexisting carpal and cubital tunnel
syndrome.
Tinel’s sign has more recently been
found to be quite useful in assessing
nerves that are subject to irritation
rather than just assessing for nerve
regeneration. The median, ulnar, and
radial nerves should be tested because
double-crush syndromes exist in up to
50% of cases.
An extensive neurological examination
should also be performed to differentiate true and nonspecific neurogenic
TOS and to rule out a cervical nerve
root disorder.
Cervical spine, shoulder, and chest x-rays
are necessary to identify bony abnormalities and/or degenerative changes in
the thoracic outlet region.
MRI and/or MRI neurograms may also be
necessary to identify soft tissue abnormalities in the thoracic outlet region. It
is, however, more useful in excluding
the presence of cervical nerve root or
thoracic pathology.
Computed tomography (CT) is indicated for suspected bony abnormalities
(rib or pulmonary) especially in true
neurogenic TOS.
Nerve conduction studies (motor and
sensory) and EMG tests may be useful to
diagnose true neurogenic TOS (may find
evidence of demyelination and axonal
loss) but have difficulties in application
and interpretation. These tests, however, are very useful to rule out other
nerve pathologies (such as the median
and ulnar nerve) that commonly coexist
with this condition.They are of little use
for the diagnosis of nonspecific neurogenic TOS (low specificity and sensitivity) because a negative result does not
exclude the possibility of the presence
of this condition.
29 of 57
• Anterior scalene blocks can be used to
test if symptoms are being caused by
scalene spasm but do not provide information about other underlying anatomical causes.
DIFFERENTIAL
DIAGNOSIS
• Shoulder pathologies
Glenohumeral instabilities
Subacromial or subcoracoid impingement
Subacromial bursitis
Glenohumeral labral tears
Rotator cuff tendinopathies
Biceps tendinopathy
Adhesive capsulitis
Degenerative arthritis of the glenohumeral or AC joints
Myofascial pain from scapulohumeral
musculature
• Cervical or thoracic pathologies
Cervical spondylosis
Cervical degenerative disc disease
Cervical nerve root syndrome
Cervical spine stenosis
Thoracic facet syndrome
T4 syndrome
Rib dysfunction
• Peripheral nerve entrapments
Ulnar nerve entrapment (cubital tunnel/Guyon’s canal)
Median nerve entrapment (carpal tunnel/pronator teres)
Radial nerve entrapment (forearm)
Multiple crush syndrome
• Other
Muscular dystrophy
Polymyositis
Complex
regional pain syndrome
(CRPS)
Diffuse peripheral neuropathy
Angina and other cardiac conditions
Rheumatoid arthritis (RA)
Lupus
Pancoast’s tumor
Multiple sclerosis
Spinal cord lesion
Hypothyroidism
Pleuritis and other pulmonary conditions
Raynaud’s phenomenon
Head, neck, or upper quadrant tumors
Lymphedema
CONTRIBUTING FACTORS
• Underlying existence of bony or fibromuscular anomalies in the thoracic
outlet region (always found in true neurogenic TOS)
• Previous history of whiplash injury or a
direct or indirect blow to the shoulder
resulting in first rib, muscular, or clavicular trauma.
• Exposure to increased or unaccustomed
prolonged or repetitive upper limb
Neurogenic Thoracic Outlet Syndrome
CHAPTER 16 • NERVE
•
•
•
•
•
•
activity (e.g., overhead sport, occupation, or playing a musical instrument)
Large breasts, breast implants, radical
mastectomy surgery, pregnancy, and/or
obesity
Poor posture (e.g., downwardly rotated
scapula, forward head posture)
Accessory or upper chest breathing patterns
Generalized low muscle tone
Anterior shoulder instabilities
Overdeveloped neck, trapezius, or pectoralis musculature as seen in weight
lifters, swimmers, tennis players, and
baseball pitchers.
TREATMENT
SURGICAL OPTIONS
REHABILITATION
30 of 57
PROGNOSIS
• Patients generally respond very well to
conservative treatment, with most studies reporting positive outcomes in 60%
to 90% of cases.
• Prognosis strongly depends on the
extent of damage to the brachial plexus
and compliance to conservative treatment. Favorable outcomes are seen in
those who comply with exercise programs and modify their behavior at work
and home. Obesity, double-crush syndrome, psychosocial issues, and more
severe and long-standing symptoms are
seen as negative prognostic factors.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• The following presentations should be
referred to a physician for appropriate
investigation:
• No response to conservative treatment
after several weeks
ORTHOPEDIC PATHOLOGY
• The main goal of treatment is to reduce
the compression on the brachial plexus
to alleviate symptoms. Additionally,
restoration of ideal neurodynamics,
posture, breathing, and movement
patterns is necessary for successful
rehabilitation.
• Initially, pain and symptom relief is
paramount. In latter stages, improving functional stability and preventing
recurrence becomes the priority.
• Pain therapy or behavior modification
Pain medication, including NSAIDs
and muscle relaxants
Electrotherapeutic modalities, including TENS, interferential current therapy, or ultrasound
Ice or heat packs
• Education
Rest from aggravating activities, including heavy lifting
Postural or ergonomic advice: Arms
should remain supported in sustained
activities, and correct lumbopelvic posture allows and assists maintenance of cervicoscapular neutral
positioning.
Standing: Hands may be placed in
pockets initially to reduce the drag on
shoulders.
Sleeping position: Patient should lie
supine or on the unaffected side with
an extra pillow to support the affected
arm in front of the body. Patients who
sleep in a supine position may need
to place a wedge under the shoulder
and flex the elbow to unload neural
structures.
• Manual or soft tissue therapy
Mobilization of the cervical and thoracic spine (including ribs); sternoclavicular, AC, and glenohumeral
joints; and scapula may help unload
the region. Cervical traction may also
help reduce symptoms.
Anterior accessory mobilizations of
the lower cervical spine and first and
second ribs are also very useful techniques, although low grades should
initially be employed.
Caudal
mobilizations and muscle
energy techniques (MET)for the first
rib may also be effective, especially if
the patient presents with an elevated
first rib.
Soft tissue therapy may include a combination of trigger point therapy, soft
tissue release, or myofascial or positional release techniques to reduce
tension associated with the production of symptoms and poor posture.
The main muscles requiring treatment
include the scalenes, levator scapulae, sternocleidomastoid, suboccipital,
upper trapezius, rhomboids, and pectoralis major and minor.
Additionally, the outer abdominal muscle
unit (external and internal oblique and
rectus abdominis muscles) may need
releasing to allow more optimal breathing patterns into the lower rib cage.
• Exercise therapy
Lateral
costal with diaphragmatic
breathing in supine followed by a variety of functional positions
Cervical ROM exercises maintaining
good alignment
Neurodynamic
gliding exercises
emphasizing upper or lower brachial
plexus or involved nerves
Motor control and stability functional
rehabilitation exercises for proximal muscles of the trunk, neck, and
shoulder include deep cervical flexor
strengthening in supine, ensuring that
the superficial cervical musculature
remains relaxed.
Stretching of tight muscles, particularly pectoralis minor and major, levator scapulae, and scalenes, to reduce
fibrous bands and adhesions in muscles compressing the brachial plexus.
Care should be taken not to reproduce symptoms.
Gradual introduction of strengthening
exercises for any muscles that have been
subjected to motor loss, including fine
motor and dexterity skills reacquisition.
Progressive cardiovascular training program, especially for those in poor aerobic condition.Weight loss programs will
also be necessary for obese patients.
Section III
• The following is a simplified summary
of current surgical approaches for neurogenic TOS:
Transaxillary first rib resection (approach used for lower plexus neurogenic TOS)
Supraclavicular first rib resection (approach used for upper or lower plexus
neurogenic TOS)
Anterior and middle scalenectomy
(used for obese patients in whom rib
resection is difficult and for upper
plexus neurogenic TOS)
Combined rib resection and scalenectomy (combined approach most commonly used now, especially because
of the lower rate of success of a secondary operation)
Comprehensive supraclavicular decompression with scalenectomy
Epineurectomy with anterior scalenectomy
• Success rates for most of the current
surgical techniques range from 70%
to over 90%. Poor outcomes, however,
are seen on reoperation (15% rate of
success). Failure is often attributed
to poor patient compliance to postoperative therapy or recurrent injury.
Transaxillary first rib resection surgery
has been found to have lower success
rates for upper plexus neurogenic TOS.
Lower rates of success with surgery
have also been seen with patients who
suffer from work-related TOS than from
MVAs.
• Surgical indicators include the following:
Failure
of conservative treatment
after 3 to 6 months (ongoing pain and
dysfunction)
Worsening neurological status
Presence of significant muscle atrophy with cervical rib (true neurogenic
TOS)
All differential diagnoses have been
treated or excluded. Since TOS patients
often suffer from coexisting nerve
entrapments (especially at the carpal tunnel and cubital tunnel), it is
important to consider surgery on these
areas, possibly before consideration of
TOS surgery because alleviation of
pressure distally can affect and relieve
TOS symptoms.
765
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Neurogenic Thoracic Outlet Syndrome
• Worsening neurological status
• Atypical symptoms
• Vascular symptoms (see the section on
Vascular TOS)
• Presence of significant muscle atrophy
with cervical rib (true neurogenic TOS)
• Red flags (e.g., unexplained weight loss).
SUGGESTED READINGS
Atasoy E. Thoracic outlet syndrome: anatomy.
Hand Clin. 2004;20(1):7–14.
Ault J, Suutala K. Thoracic outlet syndrome.
J Man Manipulative Ther. 1998;6(3):
118–129.
Brantigan CO, Roos DB, David B. Etiology of
neurogenic thoracic outlet syndrome. Hand
Clin. 2004a;20(1):17–22.
Brantigan CO, Roos DB. Diagnosing thoracic
outlet syndrome. Hand Clin. 2004b;20(1):
27–36.
Crosby CA, Wehbe MA. Conservative treatment
for thoracic outlet syndrome. 2004;20(1):
43–49.
Dawson DM, Hallett M, Milender LH.
Entrapment Neuropathies. 2nd ed. Boston:
Little, Brown; 1990.
CHAPTER 16 • NERVE
Demondian X, Herbinet P, Van Sint Jan S,
Boutry N, Chantelot C, Cotton A. Imaging
assessment of thoracic outlet syndrome. Radiographics. 2006;26:1735–1750.
Edgelow PL. 2003:Neurovascular consequences
of cumulative trauma disorders affecting the
thoracic outlet: A patient-centred treatment
approach. In: Donatelli RA, ed. Physical
Therapy of the Shoulder. Philadelphia:
Churchill Livingstone;.
Mackinnon SE, Novak CB. Thoracic outlet
syndrome.
Curr
Probl
Surg.
2002;39(11):1070–1145.
Novak CB, Mackinnon SE, Patterson GA.
Evaluation of patients with thoracic outlet
syndrome. J Hand Surg. 1993;18A:292–299.
Pecina MM, Krmpotic-Nemanic J, Markiewitz
AP. Tunnel Syndromes: Peripheral Nerve
Compression Syndromes. 3rd ed. Boca Raton,
FL: CRC Press; 2001.
Safran MR. Nerve injuries about the shoulder
in athletes, Part 2: Long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med.
2007;32(4):1063–1076.
Sanders RJ, Hammond MD. Etiology and pathology. Hand Clin. 2004;20(1):23–26.
31 of 57
Sanders RJ, Hammond SL. Supraclavicular first
rib resection and total scalenectomy: technique and results. Hand Clin. 2004;20(1):
61–70.
Urschel Jr HC, Kourlis Jr H. Thoracic outlet
syndrome: A 50-year experience at Baylor
University Medical Center. Baylor Univ Med
Cent Proc. 2007;20(2):125–135.
Urschel Jr HC, Razzuk MA. Neurovascular compression in the thoracic outlet. Changing
management over 50 years. Ann Surg.
1998;228(4):609–617.
Vanti C, et al. Conservative treatment of thoracic outlet syndrome: A review of the literature. Eura Medicophys. 2007;43(1):55–70.
Wehbe MA. Thoracic outlet syndrome. Guest
editor. Hand Clin. 2004;20(1).
Whitenack SH, Hunter JM, Read RL. Thoracic
outlet syndrome: a brachial plexopathy. In:
Mackin EJ, Schneider LH, Callahan AD, et al.,
eds. Rehabilitation of the Hand and Upper
Extremity. 5th ed. St Louis: Mosby; 2002.
AUTHOR: KATINA DIMOPOULOS
Obturator Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
COMMON SIGNS AND
SYMPTOMS
DEFINITION
• Pain in the groin region, near the inguinal ligament, is common.
• Gait changes or problems may occur
because of the instability or weakness
of the hip adductors.
• Sensory changes or numbness might be
noted in the medial portion of the thigh.
• Exercise-induced symptoms may be
present in athletes with a decreased
performance in jumping or running.
• If the condition becomes more severe, the
patient might have more severe loss of
internal rotation, adduction, or abduction.
Obturator nerve entrapment is a rare
mononeuropathy that results from compression or restriction of movement of
the obturator nerve through the obturator foramen as it passes by the obturator
externus.
SYNONYMS
None currently used
ICD-9CM CODES
355.7 Other mononeuritis of lower
limb
OPTIMAL NUMBER OF VISITS
6 or fewer
MAXIMAL NUMBER OF VISITS
AGGRAVATING ACTIVITIES
•
•
•
•
•
Walking
Prolonged standing
Running
Jumping
Stretching of the hip into adduction or
abduction
16
EASING ACTIVITIES
ETIOLOGY
• Rest
• Sitting
• Modalities
No specific data were found on the incidence of this condition; however, some
authors have stated that this condition is
not very common.
MECHANISM OF INJURY
• Most injuries are associated with acute
trauma such as the following:
Childbirth: The head of the fetus may
compress the nerve against the bony
structures of the pelvis
Pelvic fracture
Postsurgical, after total hip replacement
Malpositioning of the lower limb for
prolonged periods
Contusion or strain of the adductor
muscles
No studies on a particular pattern of
symptoms were found for obturator nerve
entrapment. Increased symptoms at night
or lasting symptoms in the morning may
point to a strong inflammatory component to the symptoms. This may also suggest a space-occupying lesion, such as a
tumor, so careful attention should be paid
to other factors and the progression of
symptoms.
PAST HISTORY
Previous similar injuries or repetitive injuries in a similar area might be found in
a patient’s history that may predispose
them to such a nerve entrapment.
PHYSICAL EXAMINATION
• Antalgic or unsteady gait is probably
one of the most common features of
this condition because of the innervation of the adductor muscles and their
importance during gait.
• If the condition has been prolonged,
the patient may present with atrophy
or wasting of the adductor muscles.
• Sensation changes may be present in
the middle portion of the medial thigh.
Pain or paresthesias may also be found
in the same distribution.
• Passive movements of the hip are likely
to be guarded, and full internal rotation
or adduction may increase the compression and be symptomatic. Abduction
may also be uncomfortable because the
tissues around the nerve or the nerve
itself is put on tension.
32 of 57
• Sensation testing in the medial lower
extremity may help confirm obturator nerve involvement and differentiate between more proximal lumbar or
sacral pathology.
• MMT of the adductors may also help
to confirm weakness or pain in those
muscles.
• Palpation of the adductor muscles and
surrounding structures may reproduce
symptoms into the nerve distribution.
• Neurodynamic testing (Butler, 2000)
may also help differentiate between a
neurogenic and nonneurogenic source
of symptoms. A variation of the slump
knee bend test with cervical extension
and flexion as a sensitizing maneuver
may be performed.
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
•
•
Adductor muscle strain
Osteitis pubis
Stress fracture
Inguinal ligament enthesopathy
Femoral nerve entrapment
Inguinal hernia
Lumbar plexopathy or sacral plexopathy
CONTRIBUTING FACTORS
•
•
•
•
Diabetes mellitus
Thyroid problems
Poor posture
Impaired trunk and motor control
TREATMENT
SURGICAL OPTIONS
In athletes, surgery may be the preferred
treatment for neuropathy. The surgery
may involve dividing the fascia over the
pectineus and adductor longus muscle.
To reveal the anterior branch of the
nerve from the fascia, it may require dissecting the space between these two
muscles.
REHABILITATION
• Addressing irritable symptoms with
modalities, such as ultrasound, interferential current therapy, phonophoresis,
or ice and to address pain and inflammation may be the first step of treatment.
• In the case of antalgic gait or poor gait
mechanics, an assistive device, such as a
single-point cane, may be warranted to
decrease the mechanical stress on the
nerve and adductors during walking.
• Soft tissue mobilization can be a beneficial technique to help address both pain
and fibrotic scarring of surrounding fascia that may be restricting the nerve.
• If it is hypothesized that abnormal
neurodynamic movement exists, then
ORTHOPEDIC PATHOLOGY
EPIDEMIOLOGY AND
DEMOGRAPHICS
24-HOUR SYMPTOM PATTERN
IMPORTANT OBJECTIVE TESTS
Section III
• Arising from the anterior branches of
L2, L3, and L4, the obturator nerve follows the medial border of the psoas
distally to the lateral wall of the lesser
pelvis through the obturator foramen.
It then divides into the anterior branch,
which descends between the adductor longus and brevis, and the posterior
branch, which descends between the
adductor magnus and brevis.
• The obturator nerve innervates the
adductor, the obturator externus, the
gracilis, and the pectineus muscles.
• The obturator nerve supplies the middle portion of the medial thigh.
• Entrapment of the obturator nerve usually
happens within the obturator foramen or
nearby the proximal portion of the adductor muscles.The nerve may be compressed
by external factors or also entrapped by
fibrosis of surrounding fascia.
767
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Obturator Nerve Entrapment
neurodynamic techniques described
by Butler (1991) that attempt to slide,
glide, and put tension on the nervous
system can be beneficial.
• Any other biomechanical faults or
impairments that may lead to putting
more stress on the adductors or hip
should also be assessed.
PROGNOSIS
Because of the rarity of this condition, no
literature has been found on long-term
prognosis. However, it most likely follows
patterns of other nerve entrapment syndromes that have good outcomes if discovered early and proper management is
implemented.
CHAPTER 16 • NERVE
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Unrelenting pain not related to biomechanical factors
• Weight loss
• Bowel or bladder dysfunction
• Saddle paresthesias
• Gait disturbances: Clumsiness or ataxic
gait
• Bilateral glove or sock numbness
• Symptoms that do not initially improve
with symptoms
SUGGESTED READINGS
Butler DS. The Sensitive Nervous System. Adelaide,Australia: Noigroup Publications; 2000.
33 of 57
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingstone; 1991.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics.
Philadelphia: Elsevier; 2005.
AUTHOR: CHRIS IZU
Plantar Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
EPIDEMIOLOGY AND
DEMOGRAPHICS
DEFINITION
• The incidence of true plantar nerve
pathology is difficult to distinguish
since it is often grouped with distal tibial nerve entrapment (proximal tarsal
tunnel syndrome) because the clinical
picture and management may be very
similar.
• It is thought that there may be a slight
female predominance, and the age range
has been stated from 14 to 80 years of
age.
• Medial plantar nerve entrapment has
been noted to occur commonly in athletes or runners, thus the term “jogger’s
foot.”
Plantar nerve entrapment is a neuropathy
from compression or restriction of movement of the medial or lateral plantar nerve
most commonly under the deep fascia of
the plantar surface of the foot.
SYNONYMS
• Distal tarsal tunnel syndrome
• Jogger’s foot
ICD-9CM CODES
355.5 Tarsal tunnel syndrome
OPTIMAL NUMBER OF VISITS
8 or fewer
MAXIMAL NUMBER OF VISITS
16
ETIOLOGY
• Traction injuries from repetitive motions
of the foot and ankle
• Direct blow or trauma to foot
• Space-occupying lesions
• Constant pressure (e.g., improper fitting orthotic)
• More often the onset is insidious or
gradually builds up over time.
COMMON SIGNS AND
SYMPTOMS
AGGRAVATING ACTIVITIES
•
•
•
•
Prolonged standing
Walking
Running
Wearing high heels or walking without
shoes
• Any activity with increased weight bearing usually aggravates the symptoms
of plantar nerve entrapment because
of local pressure or stretching of the
nerve. If the symptoms are less irritable,
it may take prolonged running or even
jumping to bring on symptoms.
EASING ACTIVITIES
•
•
•
•
Rest
Sitting
Wearing proper fitting shoes
Modalities for pain or inflammation
24-HOUR SYMPTOM PATTERN
• One author suggested that there may
be more pain at night that is eased with
standing and walking.
• Intuitively, it would seem that the pain
may be worse later in the day if the
34 of 57
PAST HISTORY
No specific history of symptoms has been
documented in this population. However,
a history of previous trauma to the foot
and ankle would make sense as they may
develop fibrosis of the surrounding muscle fascia. A previous history of similar
nerve entrapment syndromes may also be
noted in their history.
PHYSICAL EXAMINATION
• Pain and dysesthesias in the plantar surface of the foot are the most common
findings in this population.
• Antalgic gait and pain with increased
weight bearing may also be noted. A
rapid pronation may be noted during
the initial stance phase of gait or a lack
of supination may be noted during the
terminal stance phase.
• Balance activities may be slightly more
difficult or painful on the affected side,
caused by the activation of the abductor hallucis and quadratus during these
activities.
• Pain on palpation may also be a key
finding.
IMPORTANT OBJECTIVE TESTS
• Lower quarter neurological testing
Sensory testing should reveal altered
symptoms within the plantar surface
of the foot. Using Semmes-Weinstein
monofilaments may help with increasing sensitivity of the examination.
Motor
testing should be normal,
except for possible pain-inhibited
weakness with repetitive plantarflexion in standing.
Reflexes: The Achilles and the patellar
tendon should be normal secondary
to the lesion below the level of tested
reflexes.
• Palpating the surrounding fascia and
muscles may reproduce pain into the
distribution of the medial or lateral
plantar nerve.
• Neurodynamic testing: Using the slump
or SLR test with sensitizing maneuvers
may help to distinguish neurogenic
(plantar nerves) from nonneurogenic
(surrounding musculature) as a source
of symptoms. The addition of forefoot
inversion to the SLR test may add more
tension to the medial plantar nerve,
while forefoot eversion may add more
tension to the lateral plantar nerve.
DIFFERENTIAL
DIAGNOSIS
• Heel spur
• Plantar fasciitis
• Polyneuropathy
ORTHOPEDIC PATHOLOGY
• Patients typically complain of vague, diffuse pain in the plantar surface of the
foot.They may also note chronic, intractable heel pain if more of the calcaneal
branches are involved.
• Gait or balance problems may be noted
as difficulties with the foot’s intrinsic
muscles may occur.
• It may be difficult to run, jog, or perform
repetitive lower extremity exercises or
activities.
patient is required or chooses to do a
lot of standing or walking.
Section III
• The medial plantar nerve is the larger
branch of the tibial nerve that passes
distally between the abductor hallucis
and the flexor digitorum brevis. It then
divides into both cutaneous and muscular branches.
• The lateral plantar nerve is the smaller
branch of the tibial nerve that passes
laterally underneath the foot between
the quadratus plantae and flexor digitorum brevis. From there it divides into
superficial and deep branches.
• The medial plantar nerve supplies the
medial side of the sole of the foot and
sides of the first three digits.
• The lateral plantar nerve supplies the
skin on the sole of the lateral side of the
foot, which can be delineated by a line
that splits the fourth digit.
• The medial plantar nerve innervates the
abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and the first
lumbrical.
• The lateral plantar nerve innervates
the quadratus plantae, abductor digiti
minimi brevis, plantar interossei, dorsal
interossei, lateral three lumbricals, and
abductor hallucis.
• The medial plantar nerve is commonly
entrapped in the area of the master
knot of Henry, which is a fibrous slip
between the flexor hallucis longus and
the flexor digitorum longus that binds
the medial plantar surface.
• The lateral plantar nerve is usually
entrapped beneath the deep fascia of the
abductor hallucis or the quadratus plantae. It is theorized that this entrapment
may result from repeated stretching and
tethering of the nerve caused by abnormal forces at the foot such as excessive
valgus, external rotation, or pronation.
MECHANISM OF INJURY
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Plantar Nerve Entrapment
• Systemic disorders
• Lumbar spine radiculopathy
CONTRIBUTING FACTORS
•
•
•
•
•
•
•
•
•
•
•
Tenosynovitis of adjacent tendons
Partial or complete rupture of tendons
Obesity
Ankylosing spondylitis
Acromegaly
Talocalcaneal coalition
Diabetes mellitus
RA
Abnormal foot positioning
Alcoholism
Thyroid disease
TREATMENT
SURGICAL OPTIONS
• Surgical release of the surrounding tissue may help with relief of compression
on the nerve. In most cases, a full release
of both the posterior tibial nerve and the
lateral plantar nerve is recommended.
• If a space-occupying lesion is noted to
have a significant effect on the nerve,then
removal by surgery is recommended.
REHABILITATION
• Initially rehabilitation should focus on
reduction of symptoms, finding easing
activities, and managing inflammation.
• Modalities, such as ultrasound, phonophoresis, iontophoresis, ice massage,
and interferential current therapy, may
help to manage initial symptoms.
• Taping or orthotic prescription to control abnormal foot motions or support
CHAPTER 16 • NERVE
the medial longitudinal arch may also
help reduce symptoms by decreasing
abnormal strain.
• During less irritable conditions, more
vigorous treatment, such as soft tissue
mobilization, may help free fibrotic
scarring or fascial thickening around
the nerve sheath.
• Neurodynamic mobilization, using techniques to slide, glide, or place tension
on the nerve, may help restore more
normal mobility to neural structures.
Alterations of the slump test or SLR test
may be good places to start when dealing with plantar nerve mobility.
• Exercises should address lower extremity impairments or biomechanical
faults that may place further stress on
the plantar nerve. Common activities
include improving forefoot, rearfoot,
or entire lower extremity control with
attempts to decrease abnormal or rapid
pronation.
PROGNOSIS
• After surgical release procedures, one
study reported good-to-excellent results
in about 84% of patients.
• Although no data were found, clinical
observations of plantar nerve entrapment have shown good response to
conservative rehabilitation when few
contributing factors are present.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• If suspected worsening compression on
the nerve is suspected from a compartment syndrome, immediate referral to
35 of 57
•
•
•
•
a physician is warranted. A fasciotomy
may be done to release this pressure.
Unrelenting symptoms, especially combined with worse pain at night, may
indicate a local tumor.
Lack of improvement within the
expected time frame or symptoms that
are not affected by physical therapy in
a few visits should be referred back to
the physician because a space-occupying lesion may be present.
A recent history of trauma with suspected fracture may warrant further
imaging done before continuing physical therapy.
Impaired circulation or vascular compromise may also warrant more medical management.
SUGGESTED READINGS
Butler DS. The Sensitive Nervous System.
Adelaide, Australia: Noigroup Publications;
2000.
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingstone; 1991.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005.
AUTHOR: CHRIS IZU
Radial Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Radial nerve entrapment pathologies
encompass any injury that interrupts the
function of the radial nerve at any point
along its course. The loss of function
results in muscle weakness, pain, or sensory dysfunction.
SYNONYMS
• Saturday night palsy or syndrome
• Radial tunnel syndrome (RTS)
• Posterior interosseous nerve (PIN)
syndrome
ICD-9CM CODES
354 Mononeuritis of upper limb and
mononeuritis multiplex
354.3 Lesion of radial nerve
OPTIMAL NUMBER OF VISITS
6
MAXIMAL NUMBER OF VISITS
20
36 of 57
EPIDEMIOLOGY AND
DEMOGRAPHICS
• Of the three major nerves in the upper
limb, entrapment of the radial nerve is
least common.
• The most common site for entrapment
and injury is the spiral groove of the
humerus related to humeral fracture.
ORTHOPEDIC PATHOLOGY
• The radial nerve is derived from C5-C8
nerve roots with an additional sensory
component from T1.
• The radial nerve is the larger terminal
branch of the posterior cord of the brachial plexus.
• It arises proximal to the lower border
of subscapularis, then runs posterolaterally inferior to latissimus dorsi and
teres major at their attachment to the
humerus.
• It descends obliquely across the posterior portion of the midshaft of the
humerus in the spiral/radial groove
between the medial and lateral heads of
the triceps brachii muscle.
• While in the groove, it is accompanied
by the deep brachial vessels, the groove
ends just distal to the deltoid tuberosity, and at that point the nerve enters
the anterior compartment of the arm
through the fibrous intermuscular septum in a deep position between the brachialis and brachioradialis muscles.
• It continues to descend to supply extensor carpi radialis longus and brevis
superficially and deeply to the lateral
elbow capsule and the radial tunnel.
• The superficial branch continues
through the forearm deep to the brachioradialis and provides cutaneous innervation to the dorsolateral hand.
• The deep branch (posterior interosseous
nerve) curves around the neck of the
radius between the two layers of the
supinator muscle, emerging as multiple
tive pronation and supination tasks in
sport or occupation
Compression between the tendons of
the brachioradialis and extensor carpi
radialis longus muscles and through
the antebrachial fascia again seen
in repetitive pronation, supination,
pinching, grasping, or heavy pushing
and pulling tasks
Compression of the superficial branch
over the lateral aspect of the forearm
by direct trauma or by straps, watches,
and wrist bands
• Nerve injury is classified according to
the severity of the injury and its potential for reversibility as follows:
Neurapraxia (first-degree injury): Distortion of the myelin around the
nodes of Ranvier caused by ischemia,
mechanical compression, or electrolyte imbalance produces temporary
loss of nerve conduction.
Axonotmesis (second-degree injury):
Interruption of the axon with secondary wallerian degeneration. The supporting tissue surrounding the axon
is preserved, and the recovery period
depends on the distance between the
site of injury and the end-organs.
Neurotmesis: Complete disruption
of the nerve and its supporting
structures
• Neurotmesis has been further divided
into the following three subcategories:
Third-degree nerve injury: Endoneurium is disrupted with intact perineurium and epineurium
Fourth-degree nerve injury: All neural
elements sparing the epineurium are
disrupted.
Fifth-degree nerve injury: Complete transaction and discontinuity of the nerve
with no capacity for regeneration
• Physiologically, there is disruption to
any part of the nerve responsible for
conduction.
• In repetitive-type nerve entrapment,
it is proposed that repetitive work or
static postures produce an inflammatory response, and fibroblasts appear
to repair damage incurred but produce
adhesions to the nerve, limiting their
glide and increasing anoxia.
• Other studies found that cortical dedifferentiation can result from repetitive
motion activities and nerve injuries.This
may result in reinforced poor posturing
and use of aberrant motor pathways.
Section III
ETIOLOGY
branches that supply the deep posterior
muscles of the forearm and wrist joint.
• The radial nerve is vulnerable to injury
at several points along its course, as
follows:
Proximally at the axilla
Along the shaft of the humerus while
in the spiral groove
By the lateral heads of triceps and as it
passes through the fibrous intermuscular septum
While in the radial tunnel by a fibrous
band at the level of the radial head, by
the radial recurrent artery, or by the
tendinous edge of extensor carpi radialis brevis
Within the arcade of Frohse
Within the supinator or by the distal
edge of the supinator
Between the tendons of the brachioradialis and extensor carpi radialis
longus muscles and through the antebrachial fascia
Superficially over the lateral aspect of
the forearm
• The radial nerve may be affected at any
point along its course by direct trauma
or compression entrapment causing nerve tissue hypoxia. The insult to
the nerve can be mechanical, thermal,
chemical, and ischemic.
• This pathology can occur in of the following ways:
Through compression at the axilla
such as occurs when falling asleep
with the arm over the back of a chair
(Saturday night palsy) or with the use
of shoulder crutches
By direct damage to the nerve during a humeral shaft fracture or from
compression against callus formation
along the spiral groove after a traumatic humeral injury
Compression by the lateral head of
the triceps and as the nerve passes
through the fibrous intermuscular
septum sometimes seen in weight
lifting or other activity that involves
heavy repetitive triceps activation
Compression in the radial tunnel by a
fibrous band at the level of the radial
head or by the radial recurrent artery
(leash of Henry) in which the tunnel
does not provide adequate space for
the course of the nerve
Compression by the tendinous edge
of extensor carpi radialis brevis when
subjected to repetitive wrist and finger extension activity such as in some
factory and office-based tasks
Compression within the arcade of
Frohse by a space-occupying lesion
or simply by anatomical restriction of
the arcade space
Compression within the supinator
muscle or by the distal edge of the
supinator that may occur with repeti-
771
772
Radial Nerve Entrapment
• Work-related entrapments are becoming more common, in particular with
computer use and seated postures.
• RTS has a very small incidence (1% to
2%) of upper extremity entrapments.
RTS most commonly involves patients
in the fourth to sixth decade of life
without significant gender predilection.
MECHANISM OF INJURY
• There are a number of mechanisms of
injury for the radial nerve that will be
described in relation to their location:
Through compression at axilla such as
falling asleep with the arm over the
back of a chair (Saturday night palsy)
or with the use of shoulder crutches
By direct damage to the nerve during a humeral shaft fracture or from
compression against callus formation
along the spiral groove after a traumatic humeral injury
Compression by the lateral head of
the triceps and as the nerve passes
through the fibrous intermuscular
septum as sometimes seen in weight
lifting or other activity that involves
heavy repetitive triceps activation
Compression in the radial tunnel by a
fibrous band at the level of the radial
head or by the radial recurrent artery
(leash of Henry) where the tunnel
does not provide adequate space for
the course of the nerve.
Compression by the tendinous edge
of extensor carpi radialis brevis when
subjected to repetitive wrist and finger extension activity such as found in
some factory and office-based tasks.
Compression within the arcade of
Frohse by a space-occupying lesion
or simply by anatomical restriction of
the arcade space.
Compression within the supinator
muscle or by the distal edge of the
supinator that may occur with repetitive pronation and supination tasks in
sport or occupation
Compression between the tendons of
the brachioradialis and extensor carpi
radialis longus muscles and through
the antebrachial fascia again seen
in repetitive pronation, supination,
pinching, grasping, or heavy pushing
and pulling tasks
Compression of the superficial branch
over the lateral aspect of the forearm
by direct trauma or by straps, watches,
and wrist bands.
COMMON SIGNS AND
SYMPTOMS
• High radial nerve palsies
Weakness of the elbow extension
(triceps)
Mild
weakness of elbow flexion
(brachioradialis)
CHAPTER 16 • NERVE
Mild weakness of wrist and finger
extension
There may be variable loss of sensation over the posterior arm forearm
and hand.
Triceps and brachioradialis reflexes
are lost or reduced.
Often result in a characteristic posture of wrist drop with slight flaccid
flexion, the hand pronated and thumb
adducted (waiter’s tip position).
Generally, this is an injury to the entire
lower brachial plexus not just the
radial nerve so the medial and ulnar
branches may also be involved and
must be assessed.
Spiral groove lesions are similar to
high radial nerve palsies, but the triceps power and reflexes are spared.
Posterior interosseous neuropathies
are generally motor; pain may be present but is not the major symptom.
There is a resultant finger drop with
variable weakness of wrist extension.
When wrist extension is attempted,
there may be weak dorsoradial deviation caused by the preservation of the
radial wrist extensors.
• RTS
Deep, dull lateral elbow pain
Pain over the extensor mass
Wrist aching
Middle or upper third humeral pain
Increased pain on resisted supination
of the forearm
Increased
pain with middle-finger
extension (also evident in extensor
tendinopathies)
Paraesthesias
(tingling and numbness) over the dorsal hand and lateral
forearm
Neural tension tests may reproduce
the symptoms.
To
distinguish between RTS and
extensor tendinopathies the location
of the pain is less localized to the lateral epicondyle and more likely to be
over the extensor mass and supinator.
The pain of RTS is more achy and produces more muscle fatigue.
RTS appears to be more related to
repetitive pronation and supination
rather than repeated wrist extension
for extensor tendinopathy.
RTS and extensor tendinopathy occur
together in 5% of cases.
• Superficial branch of the radial nerve
results in sensory loss over the dorsum
of the hand, most commonly of the dorsal thumb, index, and middle fingers;
occasionally the dorsolateral half of the
ring finger is also involved. This type of
nerve compression can cause poorly
localized pain in this distribution and
above.
• For all levels of radial nerve injury,
there may have been loss of nerve
37 of 57
representation of the nerve injured area
on the somatosensory cortex.
AGGRAVATING ACTIVITIES
• Any repeated actions of the forearm
extensors, supination, or pronation.
• Repetitive, forceful pushing and pulling, bending the wrist, gripping and
pinching
• Screwdriver motion
• Work tasks involving repetitive finger
work such as typing or mouse work
• Higher radial nerve injuries may be provoked by repetitive elbow extension
activating the triceps such as weight
lifting.
• Sports involving gripping, pronation, supination, or wrist and finger
extension.
EASING ACTIVITIES
Rest and/or modification of aggravating
activities
24-HOUR SYMPTOM PATTERN
• Generally the symptoms are related
to activity and do not follow a typical
24-hour pattern unless there is a strong
inflammatory component such as may
be seen in occupational repetitive
tasks.
• If there is an inflammatory component,
there may be worsening of symptoms
with use toward the end of the day and
morning stiffness.
PAST HISTORY FOR THE REGION
• History of trauma, fracture, dislocation,
or blow to the radial nerve distribution.
• Repeated activity involving pushing, pulling, gripping, supination, or
pronation
• Work tasks involving exertions of
greater than 1 kg of force more than 10
times an hour, static pinching or squeezing objects or tools, working with the
elbow extended, and maintaining positioning of the forearm in pronation or
supination.
• Racquet sports: Repetitive pronation
and supination, gripping and wrist
extension
• When the superficial branch is involved
the patient should be questioned about
any straps, watches, or wristbands
worn.
• Working with hand tools or power tools
(vibration)
PHYSICAL EXAMINATION
• Examine the limb for signs of autonomic
dysfunction trophic changes such as
edema, inflammation, and alteration in
skin texture
• Reflex testing, paying particular attention to limb asymmetries of the triceps
and brachioradialis reflexes
Radial Nerve Entrapment
CHAPTER 16 • NERVE
• Needle EMG is valuable for evaluating
the extent of motor fiber loss within a
nerve territory. EMG assists with determining the location of the injury and to
monitor progression over time.
• X-ray of the humerus may reveal an
undiagnosed fracture of the humeral
shaft or callus formation from a previous injury.
• MRI is increasingly being used in the
assessment of peripheral nerve injuries
to rule out cervical nerve root involvement and determine the presence of
edema, space restriction, or space-occupying lesion along the course of the
radial nerve.
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
•
•
•
•
Forearm extensor tendinopathy
Underlying neuropathic disease
Idiopathic brachial neuritis
Myopathies
Muscular dystrophy
Isolated neuropathy in the diabetic
Tumors or space-occupying lesions
C6 or C7 cervical radiculopathy
Upper motor neuron lesion in the
cerebrum
• De Quervain’s tenosynovitis
CONTRIBUTING FACTORS
TREATMENT
IMPORTANT OBJECTIVE TESTS
• The earliest electrodiagnostic sign of
entrapment is a loss of the nerve action
potential seen during a nerve conduction study. To isolate the specific location of the conduction block, serial
stimulations are delivered to the nerve
above and below the suspected lesion.
SURGICAL OPTIONS
• Surgery is generally considered a last
resort if conservative management fails.
• Nerve palsy after a closed fracture of
the humerus is generally observed over
6 to 12 weeks to determine the effect of
the swelling subsiding. However, if the
38 of 57
REHABILITATION
• Current best evidence for the conservative management of RTS consists primarily of expert opinion and inferences
taken from studies on other nerve
compressions.
• The goal of rehabilitation should be to
reduce pain, to encourage pain-free exercise, to provide ergonomic education
and interventions, and if the neuropathy
has been prolonged, to introduce cortical reorganization activities.
• Splinting should be used to provide
immobilization to allow the reduction in
swelling and inflammation. Functional
splinting can also be employed to prevent contracture and facilitate normal
movement patterns (e.g., for a high
radial nerve palsy the use of a static
wrist extension splint with dynamic
extension apparatus for the proximal
phalanges).
• Elimination of aggravating tasks by
avoiding or modifying those tasks to
prevent further damage
• Use of ice to reduce inflammation and
prevent secondary cell damage
• Theoretically, ultrasound may be helpful to promote nerve regeneration,
improve profusion to the healing nerve,
and decrease inflammation.
• Direct low-intensity electrical stimulation has been found to increase the
number of vasa nervorum and nerve
fiber density in rats.
• Steroid injection is often advocated to
reduce inflammation particularly in
RTS.
• Iontophoresis with dexamethasone and
lidocaine
• Nerve gliding exercise, have been purported to disperse intraneural edema,
increase blood flow, optimize axonal
transport, and lengthen nerve adhesions. Neural mobilization can be
assessed using the brachial plexus provocation test positions to identify symptom reproduction and these positions
and movements can also be used both
actively and passively for a treatment
technique.
• Use of soft tissue mobilization and muscle stretching techniques to reduce
fibrous bands and adhesions in muscles surrounding the radial nerve.
Stretches must not produce tingling or
discomfort because this may indicate
ORTHOPEDIC PATHOLOGY
• For any nerve entrapments that are nontraumatic, there is often an element of
repetitive activity involving the affected
limb. Typically, in the case of the radial
nerve, the repetitive action involves,
elbow extension, forearm pronation, supination, gripping, forceful pushing and
pulling, and/or wrist and finger extension.
• Postural factors may be involved, particularly with repetitive work or sporting
activities with reduction in proximal
stability and control leading to an overuse of more distal muscle groups to perform a task.
• Excessive loads, such as in heavy manual
work or sports, involving weight lifting
can overload the capacity of the muscles to adapt, thus creating inflammation
and subsequent nerve compression.
• The use of tight wristbands, cuffs, or
other strapping across the wrist may
contribute to superficial radial nerve
compression.
palsy continues, then surgical intervention is indicated.
• The goal of surgical intervention would
be to relieve pressure or entrapment
along the course of the nerve, (e.g., surgical release of the superficial head of
supinator and division of the ligament
of Frohse to expand the available space
in the radial tunnel).
Section III
• MMT may reveal weakness in any of the
following muscles:
Triceps (C7, C8): Extend elbow against
resistance
Brachioradialis (C5, C6): Flex elbow
with forearm half way between pronation and supination
Extensor carpi radialis longus (C6,
C7): Extend wrist to the radial side
with fingers extended
Supinator (C5, C6): Arm by side resist
hand pronation.
Extensor digitorum (C7, C8): Maintain
finger extension at the MCP joints
Extensor carpi ulnaris(C7, C8): Extend
wrist to ulnar side
Abductor pollicis longus (C7, C8):
Abduct thumb to 90degrees to palm
Extensor pollicis brevis (C7, C8):
Extend thumb at MCP
Extensor pollicis longus (C7, C8):
Resist thumb flexion at IP joint
• Sensation: The cutaneous branches
of the radial nerve supply the dorsal aspect of the forearm from below
the elbow down over the lateral part
of the hand to include the thumb to
the interphalangeal joint and the fingers distal to the interphalangeal joint,
including index and middle fingers
but not the little finger. Sensation testing should include pinprick, two-point
discrimination, tuning fork, and joint
position sense and compared for asymmetry with the unaffected side (where
available).
• Tinel’s sign may be positive over the
anatomical snuff box.
• Physical examination should also
exclude pathology in other areas, particularly performing AROM and PROM
at the neck and shoulder, which may
reveal restrictions and central involvement of the nerve.
• Upper limb neural tissue provocation
testing may reveal changes in nerve
mobility and elicit symptoms.
• Physical examination should also
include movement analysis to determine the movement patterns that the
patient adopts when performing the
aggravating activities. Movement analysis can be done visually or with the
assistance of a video camera. The analysis should give some clues as to predisposing factors, such as posture and
patterning, that will assist with rehabilitation and activity modification.
773
774
Radial Nerve Entrapment
•
•
•
•
•
decreased blood flow to the already
stressed nerve.
Motor control and stability functional
rehabilitation exercise for proximal muscles of the trunk, neck, and shoulder.
Gradual introduction of strengthening exercises for any muscles that have
been subjected to motor loss
Ergonomic interventions, workplace
assessment, provision of ergonomic aides
such as tilted keyboards or altered mouse
shape
Cortical reorganization techniques such
as use of mirror box
Reacquisition of fine motor and dexterity skills
PROGNOSIS
• Prognosis depends entirely on the
extent of damage to the nerve.
• Neurapraxia should resolve rapidly and
lead to a complete restoration of function, usually within 2 to 3 months.
CHAPTER 16 • NERVE
• If the injury is a more severe axonotmesis, the recovery time depend on the
distance from the site of injury to the
denervated tissue.
• Peripheral nerves have been reported
to recover at an approximate rate of
between 1 and 4 mm per day, but complete function might not be restored.
• If there has been a complete sectioning
of the nerve (neurapraxia), then a full
recovery will not occur.
• The results of treating neurapraxia even
with surgical intervention are generally
not satisfactory.
SUGGESTED READINGS
Bencardino JT, Rosenberg ZS. Entrapment neuropathies of the shoulder and elbow in the
athlete. Clin Sports Med. 2006;25:465–487.
Cleary CK. Management of radial tunnel syndrome: A therapist’s clinical perspective. J
Hand Ther. 2006;19(2):186–191.
Pratt N. Anatomy of nerve entrapment
sites in the upper quarter. J Hand Ther.
2005;18(2):216–229.
Roquelaure Y, Raimbeau G, Dano X. Occupational risk factors for radial tunnel syndrome
in industrial workers. Scand J Work Environ
Health. 2000;26:507–513.
AUTHOR: JOSEPHINE LOUISE COULTER
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
If radial nerve entrapment is suspected, all
cases should be referred to a physician for
appropriate investigation.
39 of 57
Saphenous Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Saphenous nerve entrapment is a mononeuropathy that results from compression
or restriction of movement of the saphenous nerve in the distal thigh as it passes
through the adductor canal.
SYNONYMS
None currently used
ICD-9CM CODES
355.7 Other mononeuritis of lower
limb
OPTIMAL NUMBER OF VISITS
6 or fewer
MAXIMAL NUMBER OF VISITS
•
•
•
•
•
Pes anserine bursitis
Postsurgical vein operations
Medial knee arthrotomies
Postsurgical meniscal repairs
Improperly protected leg during surgery
COMMON SIGNS AND
SYMPTOMS
• The most common complaint of
saphenous nerve entrapment is medial
knee pain. Usually, it is described as a
dull, aching sensation in the knee, but
the patient may also have discomfort in
the medial thigh.
• Paresthesias may be found in the cutaneous distribution of the saphenous
nerve, which includes the medial knee
and medial region of the lower leg
down into the medial ankle and foot.
• It is important to note that since the
nerve is purely sensory, no motor deficits or gait abnormalities should be part
of the symptoms.
20
ETIOLOGY
EASING ACTIVITIES
• Rest and avoiding aggravating activities
• Antiinflammatories
24-HOUR SYMPTOM PATTERN
If there is a significant inflammatory component to the symptoms or a space-occupying lesion, more night symptoms may
be expected. Following this, symptoms
may also be worse in the morning. One
study has noted that two thirds of the
patients with saphenous nerve entrapment in their study had increased symptoms at night.
PAST HISTORY
It is believed that this condition, as well
as peroneal nerve entrapment, is the most
common form of lower extremity nerve
entrapment syndrome.
As a result of the traumatic or repetitive
stress injury causes of saphenous nerve
entrapment, there may be no significant
items noted on their history. Since fibrosis of the surrounding tissues may be a
contributing factor to this nerve entrapment, a previous history of trauma may be
found.
MECHANISM OF INJURY
PHYSICAL EXAMINATION
• Direct trauma
• Entrapment by femoral vessels
• Usually, sensory deficits and pain are
the only presentation of this condition.
EPIDEMIOLOGY AND
DEMOGRAPHICS
40 of 57
IMPORTANT OBJECTIVE TESTS
• Sensation testing: Light touch, pinprick,
or sharp/dull testing should reveal
altered sensation in the saphenous
nerve distribution.
• Lower quarter neurological examination should be performed to help
rule out more proximal causes of
the symptoms such as lumbar spine
radiculopathy. Again, no motor or
reflex deficits should be found on
examination.
• Palpation should be done along the
path of the nerve, especially at the superior to the medial epicondyle where the
nerve passes through the dense connective tissue.
• Tinel’s test: Tapping along the path of
the nerve, especially where it is more
superficial because it is above or below
the medial epicondyle, may reproduce
symptoms.
• Slump knee bend test, as described by
Butler, may help to determine a neurogenic cause of symptoms. Similar to
testing the femoral nerve in sidelying,
using the sensitizing maneuver of cervical extension and flexion may help
to differentiate between neurogenic
(saphenous nerve) and nonneurogenic
(local muscle or other knee pathology)
source of symptoms.
• Lumbar ROM, accessory mobility testing, and palpation
All three of these examinations may
help to differentiate a lumbar spine
problem from an isolated saphenous
nerve entrapment.
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
•
•
•
•
Lumbar spine radiculopathy
Lumbar spine stenosis
Lumbar spine somatic referral
Femoral or tibial fracture
Medial collateral ligament injury
Meniscal pathology
Osteoarthritis
Patellofemoral pain
Pes anserine bursitis
CONTRIBUTING FACTORS
• Increased age (over 40 years of age)
• Increased thigh obesity
• Genu varum, with or without tibial
torsion
ORTHOPEDIC PATHOLOGY
• Repetitive knee motions that place
stress on the surrounding fascia or muscles may cause increased symptoms
such as running or biking.
• Prolonged standing or walking
• Stair climbing
• It is believed that active knee extension
may place more stress or tension on the
involved nerve. Therefore any activities,
such as standing, walking, or stair climbing, that require knee extension may be
symptomatic.
• Gait and functional testing may be painful, but no motor deficits should be
noted with MMT.
• Avoidance with knee extension might
be noted but should not be thought of
as diagnostic since many other competing conditions will also have pain with
or limited knee extension.
Section III
• The saphenous nerve (from L3 and L4)
arises off the femoral nerve slightly distal to the inguinal ligament and courses
down the medial thigh. Between the
sartorius and gracilis muscles, about
10 cm proximal to the medial epicondyle, the nerve pierces the connective tissue toward the medial knee and
continues down the medial side of the
lower leg.
• The saphenous nerve is purely sensory
and does not innervate the muscle in
the lower leg.
• Its cutaneous branches supply the skin
of the anteromedial knee, the medial
side of the lower leg, and the medial
side of the foot distally (sometimes as
far as the first metatarso phalangeal
joint).
• Most commonly, the nerve is entrapped
where it pierces the connective tissue
(referred to as Hunter’s canal) and may
be irritated by repetitive contraction and
relaxation of the surrounding musculature; this may be caused by the angulation of the saphenous nerve as it enters
the canal traction to the nerve.The nerve
may also undergo compression around
the top of the calf region from external
pressure such as tight garments.
AGGRAVATING ACTIVITIES
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776
Saphenous Nerve Entrapment
TREATMENT
SURGICAL OPTIONS
After conservative measures of treatment
have failed, a surgical decompression may
be considered. Other possible methods
may be surgical removal of the nerve or
neurolysis.
REHABILITATION
• Initially, the goals of physical therapy
are management of the symptoms
and patient education regarding the
dysfunction.
• Modalities, such as interferential current therapy, ultrasound, phonophoresis, iontophoresis, ice, or compression,
may help address any symptoms more
related to an inflammatory component.
• Soft tissue massage dealing with the
location of hypothesized nerve entrapment may help the fibrosis or scarring
of surrounding fascia.
• After soft tissue treatments, neural mobilization techniques that help slide, glide,
or place tension on the nervous system
CHAPTER 16 • NERVE
could be used to help restore more normal movement the saphenous nerve.
• Addressing other biomechanical factors, such as foot or lower extremity
alignment, is also necessary for a comprehensive rehabilitation program.
PROGNOSIS
In general, the prognosis for this condition is good. It is not associated with
mortality or high rates of morbidity.
Conservative treatment methods have
been shown to be successful, and surgical options have few postoperative complications because of the pure sensory
function of the nerve.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Night pain and unrelenting symptoms
may indicate a local tumor.
• Symptoms that do not improve within
the expected time or that are not
affected by physical therapy in a few
visits should be referred back to the
41 of 57
physician since a space-occupying
lesion may be present.
• A recent history of trauma with suspected fracture may need imaging studies done before starting treatment.
• Impaired circulation or vascular compromise may also warrant more medical management.
SUGGESTED READINGS
Butler DS. The Sensitive Nervous System. Adelaide,Australia: Noigroup Publications; 2000.
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingstone; 1991.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics.
Philadelphia: Elsevier; 2005.
http://www.emedicine.com/Orthoped/topic422.
htm
AUTHOR: CHRIS IZU
Sciatic Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Sciatic nerve entrapment is a neuropathy
that results from compression or restriction of movement of the sciatic nerve,
usually found in the posterior gluteal
region near the piriformis muscle.
SYNONYMS
Piriformis syndrome
ICD-9CM CODES
355.0 Lesion of sciatic nerve
OPTIMAL NUMBER OF VISITS
8 or fewer
MAXIMAL NUMBER OF VISITS
20
ETIOLOGY
• The prevalence of this condition is difficult to assess secondary to the lack of
agreement of its diagnosis and its close
• Blunt injury may cause scarring of the
surrounding structures.
• Prolonged pressure, such as sitting, may
cause compression.
• Postsurgical complications (e.g., total
hip replacement)
• After vigorous activity, causing strain on
the piriformis muscle or surrounding
structures
• The onset of symptoms from sciatic
nerve entrapment can be sudden after
trauma as noted or gradual overtime. In
overuse injuries or gradual buildup of
stress over time on the affected areas,
symptoms may take time to come on
or become problematic enough to seek
medical attention.
COMMON SIGNS AND
SYMPTOMS
• Pain originating in the gluteal region
that progresses down into the posterior
thigh and lower leg is the most common complaint in patients with this
condition. In certain cases, pain is felt
more distally in the lower extremity and
less in the gluteal region.
• Weakness may be present in the lower
extremity muscles that control the foot
and ankle along with knee flex.
• Gait is almost always affected, and
patients usually complain of pain with
bearing weight on the affected leg.
AGGRAVATING ACTIVITIES
• Walking
• Prolonged standing
• Sitting, with pressure on the affected
area
• Sitting cross-legged
• Sleeping or lying with the hip in a flexed
or adducted position
• Driving, especially when the right lower
extremity is affected
• Walking or standing may cause an overuse of the piriformis, especially as it may
attempt to assist with pelvic and hip stability during gait. Other activities that
add local compression or place the piriformis on stretch may also irritate the
symptoms.
EASING ACTIVITIES
• Rest
• Ice or modalities to reduce inflammation
42 of 57
24-HOUR SYMPTOM PATTERN
No specific pattern has been reported in
the literature. A presence of more nighttime symptoms or increased pain the
morning or after resting may be more
related to an inflammatory component of
the disorder. It may also suggest another
underlying pathology, such as a tumor,
compressing the sciatic nerve.
PAST HISTORY
Previous similar symptoms, low back injuries, or other lower extremity injuries that
may predispose someone to sciatic nerve
entrapment may be found in the patient’s
history.
PHYSICAL EXAMINATION
• This condition is often very painful and
usually leads to an antalgic gait pattern,
in which less time is spent in single-leg
stance on the affected leg and with an
ipsilateral trunk lean. It is also common
to see external rotation of the affected
extremity.
• Sciatic nerve entrapment may have
few distinguishing factors from that of
a lumbar spine radiculopathy, stenosis,
or discogenic dysfunction. Patients may
also present with pain in the lumbar
spine.
• Patients may assume a posture in sitting or standing in which less pressure
is placed through the affected lower
extremity.
• Weakness is most likely noted with
resisted hamstring testing, either to
the result of pain or decreased nerve
conduction from sciatic nerve compression. Other lower extremity muscles below the knee may also be weak
because of the sciatic nerve’s contribution to the tibial and common fibular nerve.
• Assessing neurodynamics is also important if sciatic nerve entrapment is
suspected because it may help to differentiate between a neurogenic source
of pain (the sciatic nerve itself) and an
nonneurogenic source (hamstrings).
IMPORTANT OBJECTIVE TESTS
• Palpation is often helpful in differentiating between symptoms of the lumbar spine, sacroiliac, and local muscles.
Deep palpation of the piriformis muscle proximally in the posterior gluteal
ORTHOPEDIC PATHOLOGY
EPIDEMIOLOGY AND
DEMOGRAPHICS
MECHANISM OF INJURY
• Heat to relax local musculature
• Frequently changing positions, either
from sitting or from sitting to standing
• Sitting with legs apart
• Sleeping or lying with a pillow between
legs
• Either decreasing the abnormal pressure
on the piriformis by removing compressive forces or placing it in a resting position should help to alleviate symptoms.
Section III
• The large sciatic nerve originates from
the sacral plexus (L4 to S3) and enters
the gluteal region through the greater
sciatic foramen near the piriformis muscle. It then descends along the posterior
aspect of the thigh, dividing into the tibial and common peroneal nerve.
• The sciatic nerve innervates all of the
hamstring with the exception of the
short head of the biceps. Because it
branches into the tibial and common
peroneal nerves, it sends motor input to
the entire lower part of the leg.
• The sciatic nerve branches off into the
tibial and common peroneal nerves,
which supply the superficial area of the
entire lower leg except for the medial
side of the leg and ankle (saphenous
nerve).
• The most common cause of sciatic nerve
entrapment is irritation of the piriformis
muscle. It is reported that 10% to 20% of
individuals actually have a sciatic nerve
that courses through the piriformis muscle instead of anterior to it.
• Two different theories in which the sciatic nerve could become entrapped by
the piriformis muscle are as follows:
By a spasm of the muscle that becomes
tight around the nerve
By irritation of the muscle if the muscle is long and weak
• Other causes of nerve entrapment
include the following:
Muscle anomalies
Fibrosis caused by trauma
Myositis ossificans
relationship to lumbar spine pathology
when the lumbar plexus is involved.
Some report that the condition may be
very rare (6% of sciatica cases), whereas
others note that when looking at the
incidence of low back pain with the
inclusion of lower extremity symptoms,
it may be more common than reported.
• There seems to be a higher female prevalence with sciatic nerve entrapment
and some estimates are as high as 6:1.
777
778
Sciatic Nerve Entrapment
•
•
•
•
region and along the length of the
sciatic nerve down in the posterior
thigh should reproduce symptoms.
Freiberg’s test: Forced internal rotation
of the hip with the hip in extension may
reproduce the symptoms by placing the
piriformis and other deep hip external rotators on stretch. Combining this
motion with abduction and external
rotation of the hip while in hip flexion
(Beatty maneuver) may help increase
the sensitivity of testing.
FAIR test: The patient is positioned in
the sidelying position, with the patient’s
affected leg placed in flexion, adduction, and internal rotation. A positive
test will reproduce the patient’s symptoms in the buttock and leg.
A full lower quarter neurological examination is also necessary to help differentiate a possible sciatic nerve entrapment
from a lumbar spine radiculopathy or
disc problem.
Slump or SLR tests to assess neurodynamic mobility also help differentiate
or implicate neural structures.
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
•
Lumbar spine radiculopathy
Lumbar spine stenosis
Lumbar spine discogenic dysfunction
Hamstring strain or tear
Ischial tuberosity bursitis
Sciatica
CONTRIBUTING FACTORS
• Diabetes mellitus
• Leg length discrepancy
• Morton’s foot: Prominent second metatarsal head and changing gait pattern
TREATMENT
SURGICAL OPTIONS
Surgical treatment of this condition is considered a last resort.The piriformis muscle
could be resected or could be released
CHAPTER 16 • NERVE
near its insertion at the superior aspect
of the greater trochanter. Although these
surgical procedures have been noted with
some success and, one author stated, are
not associated with postoperative disability, one should be skeptical. There should
be certainty that symptoms are not arising
from the lumbar spine or other structure
and postoperative management of appropriate tissue healing should be worked
out before surgery is attempted.
REHABILITATION
• With the lack of clinical trials supporting treatment efficacy, most evidence
comes from clinical practice.
• Modalities that help reduce pain and
inflammation, such as ultrasound, interferential current therapy, or cold pack,
should be considered acutely and during highly irritable states, suggesting an
inflammatory response.
• In the case of extremely irritable symptoms and antalgic gait, assistive devices,
such as a single-point cane, can be used
to decrease weight bearing on the
affected leg and the strain on muscles,
such as the piriformis, to help stabilize
the pelvis during walking.
• Activity modification to avoid situations where prolonged sitting or standing, especially in known aggravating
conditions like a very firm chair, is an
important part of the patient education
process.
• Soft tissue mobilization and hip joint
mobilization should also be considered to help improve the mobility of
surrounding structures. Care should
be taken to match the appropriate soft
tissue technique and vigor to the area
secondary to the possible irritability or
altered pain processing damage to neural structures.
• Other manual techniques, such as contract-relax, positional release, or straincounterstrain, have been suggested to
treat the piriformis.
• Treating the functional biomechanical deficits is also important to have
successful outcomes. Stretching tight
43 of 57
muscles that may alter normal movement is important. Strengthening the
hip abductors and external rotators is
a common beneficial addition to a treatment program to decrease strain on the
piriformis.
PROGNOSIS
This condition is not life-threatening but
can be associated with significant morbidity caused by pain and weakness. It is
generally believed that if it is recognized
early, the treatment outcomes are relatively good.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Unrelenting pain not related to biomechanical factors
• Weight loss
• Bowel or bladder dysfunction
• Saddle paresthesias
• Gait disturbances: Clumsiness or ataxic
gait
• Bilateral glove or sock numbness
• Symptoms that do not initially improve
SUGGESTED READINGS
Butler DS. The Sensitive Nervous System.
Adelaide, Australia: Noigroup Publications;
2000.
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingstone; 1991.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics.
Philadelphia: Elsevier; 2005.
http://www.emedicine.com/Orthoped/topic422.
htm
AUTHOR: CHRIS IZU
Suprascapular Nerve Entrapment
CHAPTER 16 • NERVE
BASIC INFORMATION
DEFINITION
Suprascapular nerve entrapment pathologies encompass any injury that interrupts the function of the suprascapular
nerve at any point along its course. The
loss of function results in muscle weakness, pain, or sensory dysfunction.
SYNONYMS
Bra strap palsy
ICD-9CM CODES
354 Mononeuritis of upper limb and
mononeuritis multiplex
354.8 Other mononeuritis of upper
limb
354.9 Mononeuritis of upper limb
unspecified
OPTIMAL NUMBER OF VISITS
6
MAXIMAL NUMBER OF VISITS
20
44 of 57
EPIDEMIOLOGY AND
DEMOGRAPHICS
• Relatively rare entrapment is seen in
sports with repetitive cocking action
such as tennis or volleyball.
• The cocking action involves end-range
shoulder abduction, extension, and
external rotation followed by rapid flexion and internal rotation.
• Suprascapular nerve injuries are often
related to degenerative changes in the
glenohumeral joint, and the incidence
of entrapment increases with increasing age of the patient and with capsular laxity.
• Also seen in occupations involving carrying heavy objects on the shoulder
such as a camera operator and furniture
mover.
MECHANISM OF INJURY
• There are a number of mechanisms of
injury for the suprascapular nerve that
will be described in relation to their
location:
Direct trauma in the form of a blow
to the base of the neck or posterior
shoulder
Shoulder dislocation leading to tractioning of the nerve, particularly if
the shoulder is forced into end-range
external rotation
Scapular fracture that distorts the
bony confines of the suprascapular or
spinoglenoid notches
The nerve may be stretched or kinked
by extremes of scapular motion associated with the throwing action.
Kinking of the nerve can be exaggerated by a resting position of depression or forward rotation of the
shoulder girdle.
Compression entrapment within the
suprascapular notch through hypertrophy of the transverse scapular
ligament, an anatomically narrow
suprascapular notch, or presence of a
ganglion cyst.
Compression at either notch from a
tumor or varicosities
Compression of the nerve in the
spinoglenoid notch by a ganglion cyst
arising from the glenohumeral joint.
Ganglion cysts may be formed as a
result of degenerative shoulder conditions and also after acute glenoid
labral lesions such as SLAP lesions.
Overuse syndromes from repeated
scapular motions leading to compression of the nerve may occur in sports
with repetitive overhead throwing
action such as volleyball, serving in
tennis, or baseball.
ORTHOPEDIC PATHOLOGY
• The suprascapular nerve is derived
from the upper trunk of the brachial
plexus formed by the C5 and 6 nerve
roots; however, up to 50% receive contributions from the C4 nerve root.
• The suprascapular nerve is a mixed sensory and motor nerve that descends
along the posterior neck triangle,
beneath the anterior border of trapezius,
to the superior border of the scapula.
• The nerve passes into the supraspinous
fossa through the suprascapular notch,
and the roof is formed by the transverse
scapular ligament.
• It supplies the supraspinatus, as well
as receiving sensory articular branches
from the glenohumeral and AC joints.
• The nerve then curves around the lateral edge of the base of the spine of the
scapula by the spinoglenoid notch (in
close proximity to the glenohumeral
joint) to innervate the infraspinatus in
the infraspinatus fossa.
• The nerve has no cutaneous component.
• The suprascapular nerve is particularly
vulnerable to injury at the following
two points along its course:
The suprascapular notch
The spinoglenoid notch
• The suprascapular nerve may be
affected at any point along its course by
direct trauma or compression entrapment, leading to nerve tissue hypoxia.
• The insult to the nerve can be mechanical, thermal, chemical, or ischemic.
process, fibroblasts appear to repair
damage incurred but produce adhesions to the nerve limiting their glide
and increasing anoxia.
Section III
ETIOLOGY
• The suprascapular nerve is most commonly entrapped at the suprascapular
and spinoglenoid notches.
• The pathophysiology of suprascapular
nerve entrapment is usually related to a
compressive lesion of the nerve; nevertheless, pathology can occur in a number of ways as follows:
Direct trauma in the form of a blow
to the base of the neck or posterior
shoulder
Shoulder dislocation leading to tractioning of the nerve
Scapular fracture
Compression entrapment within the
suprascapular notch through hypertrophy of the transverse scapular ligament, a narrow suprascapular notch,
or presence of a ganglion cyst
Compression of the nerve in the
spinoglenoid notch by a ganglion cyst
arising from the glenohumeral joint.
Ganglion cysts may be formed as a
result of degenerative shoulder conditions and also after acute glenoid
labral lesions such as superior labrum
from anterior to posterior (SLAP)
lesions.
Overuse syndromes from repeated
scapular motions leading to compression of the nerve
• Nerve injury is classified according to
the severity of the injury and its potential for reversibility, as follows:
Neurapraxia
(first-degree injury):
Distortion of the myelin about the
nodes of Ranvier caused by ischemia,
mechanical compression, or electrolyte imbalance produces temporary
loss of nerve conduction.
Axonotmesis (second-degree injury):
Interruption of the axon with secondary wallerian degeneration. The supporting tissue surrounding the axon
is preserved, and the recovery period
depends on the distance between the
site of injury and the end-organs.
Neurotmesis: Complete disruption of
the nerve and its supporting structures.
• Neurotmesis has been further divided
into the following three subcategories:
Third-degree
nerve injury: Endoneurium is disrupted with intact
perineurium and epineurium.
Fourth-degree nerve injury: All neural
elements sparing the epineurium are
disrupted.
Fifth-degree nerve injury: Complete
transection and discontinuity of
the nerve with no capacity for
regeneration.
• Physiologically, there is disruption to
any part of the nerve responsible for
conduction.
• In repetitive-type nerve entrapment, it is
proposed that repetitive work or static
posture produces an inflammatory
779
780
Suprascapular Nerve Entrapment
Compression of the nerve by weighted
objects being carried repeatedly on
the shoulder such as may occur with a
barbell in weight lifting, camera work,
backpacking, furniture removals, or
other load-carrying occupations.
COMMON SIGNS AND
SYMPTOMS
• Pain that is deep and poorly localized,
often felt posterior and lateral in the
shoulder or referred to the arm, neck, or
anterior chest wall.
• Patients may describe shoulder weakness.
• Wasting of the supraspinatus and/or
infraspinatus
• Weakness of abduction and external
rotation
• May have tenderness over the suprascapular notch
• If there is combined supraspinatus and
infraspinatus weakness, the entrapment
is most likely to be at the suprascapular
notch.
• Isolated infraspinatus weakness may
occur when the nerve is compressed in
the spinoglenoid notch and the motor
branch to the supraspinatus is spared.
• Occasionally, deltoid muscle atrophy
accompanies the injury because of
disuse.
AGGRAVATING ACTIVITIES
• Activities that involve repetitive shoulder internal and/or external rotation,
particularly when the shoulder is in an
abducted position
• Activities that involve horizontal adduction of the arm, such as reaching across
the chest, can exacerbate the pain
• Carrying loads on the top of the
shoulder
EASING ACTIVITIES
Rest and/or modification of aggravating
activities
24-HOUR SYMPTOM PATTERN
• Generally, the symptoms are related
to activity and do not follow a typical
24-hour pattern unless there is a strong
inflammatory component such as may
be seen in repetitive tasks.
• If there is an inflammatory component,
there may be worsening of symptoms
with use toward the end of the day and
morning stiffness.
PAST HISTORY FOR THE REGION
• History of trauma, fracture, or dislocation of the glenohumeral joint
• History of forceful scapular depression such as a fall onto the point of the
shoulder
• Repetitive overuse of the shoulder in
occupation or sports
• Generalized hypermobility
CHAPTER 16 • NERVE
PHYSICAL EXAMINATION
• Examine the shoulder for signs of atrophy around the shoulder blade, particularly in the supraspinatus and
infraspinatus fossae.
• MMT may reveal weakness in the following muscles:
Supraspinatus: Weakness
of glenohumeral abduction can be assessed
using the scaption position in which
the shoulder arm is resisted in 90
degrees of flexion in the plane of the
scapular.
Infraspinatus: Weakness of external
rotation at the glenohumeral joint,
particularly biased toward infraspinatus when external rotation is resisted
in 90 degrees of shoulder abduction.
• There may be loss of fine proprioceptive control of the glenohumeral and AC
joints due to the loss of afferent conduction. Therefore the therapist may notice
an alteration in the control of those
joints during functional movement
patterns.
• Physical examination should also
exclude pathology in other areas, particularly when performing AROM and
PROM at the neck and shoulder, which
may reveal restrictions, other shoulder
pathology, and/or central involvement
of the nerve.
• Physical examination should also
include movement analysis to determine the movement patterns that the
patient adopts when performing the
aggravating activities. Movement analysis can be done visually or with the assistance of a video camera. The analysis
should give some clues to predisposing
factors, such as posture and patterning,
that assist with rehabilitation and activity modification.
IMPORTANT OBJECTIVE TESTS
• EMG may reveal delayed conduction
velocity and fibrillation potentials; however, EMGs are often reported as normal, and therefore a negative EMG does
not rule out the diagnosis of suprascapular nerve entrapment.
• MRI is considered to be the most effective study for suprascapular nerve
entrapment since it can reveal lesions
to the glenoid labrum and the presence
of a ganglion cyst in the region of the
nerve.
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
Rotator cuff tears
Rotator cuff tendinopathies
Subacromial bursitis
Adhesive capsulitis
Shoulder instability
45 of 57
• Degenerative joint disease at the glenohumeral or AC joints
• Underlying neuropathic disease
• Neuralgic amyotrophy
• Muscular dystrophy
• Isolated neuropathy in the diabetic
• Tumors or space-occupying lesions
• C4, C5, or C6 cervical radiculopathy
• Upper motor neuron lesion in the
cerebrum
CONTRIBUTING FACTORS
• For any nerve entrapments that are nontraumatic, there is often an element of
repetitive activity involving the affected
limb.
• Typically, in the case of the suprascapular
nerve, the repetitive action will involve
shoulder abduction and repetitive internal and external glenohumeral rotation.
• Other repetitive tasks involving crossbody adduction, such as polishing or
reaching repeatedly across the body,
may create a traction neuropathy.
• Postural factors may be involved, particularly in repetitive work or sporting
activities with reduction in proximal
stability and control leading to an overuse of more distal muscle groups to perform a task.
• Excessive loads, such as in heavy manual work or sports involving weight
lifting, can create compression of the
nerve, particularly when the load is carried over the trapezius muscle.
TREATMENT
SURGICAL OPTIONS
• Surgery will be considered after a failure of conservative management.
• There are a number of surgical approaches
to achieve decompression of the suprascapular nerve, involving enlargement of
the suprascapular notch, as follows:
Anterior approach
Posterior trapezius splitting approach
Posterior trapezius elevating approach
Superior cranial approach
• When there is entrapment at the
spinoglenoid notch,a different approach
is required because generally there is an
underlying shoulder pathology leading
to the formation of a ganglionic cyst
that compresses the nerve.
• Therefore, shoulder arthroscopy initially is performed to examine for a
SLAP lesion, followed by debridement
and repair if required. At the time of
arthroscopy, the cyst can be evacuated
and decompressed.
REHABILITATION
• The goal of rehabilitation should be
pain reduction to encourage pain-free
exercise and to provide task or sports
Suprascapular Nerve Entrapment
CHAPTER 16 • NERVE
reeducation and interventions leading
to reacquisition of fine motor and sporting skills.
• Manual therapy
Pain
reduction can be achieved
through the use of ice and electrotherapeutic modalities.
Soft tissue release may assist with restoration of muscle balance around the
scapula, which will be useful if compensations have occurred in other
muscles to make up for the loss of
rotator cuff control.
Nerve gliding exercises have been purported to disperse intraneural edema,
increase blood flow, optimize axonal
transport, and lengthen nerve adhesions.
Neural mobilization can be achieved
using scapular mobilization, both
actively and passively into elevation,
depression, protraction, and retraction
• Functional rehabilitation
Reeducation of movement patterns,
particularly proximal control of the
trunk and neck to provide a stable
foundation for scapular stability
Scapular position education initially,
with isometric hold and then the addi-
tion of controlled functional movement patterns
Specific muscle strengthening gradually increasing intensity to restore full
power to the rotator cuff
Integration of functional exercise
and strength work into sport- or taskspecific skills
Graduated return to full strength,
speed, and power.
781
• The results of treating neurapraxia even
with surgical intervention are generally
not satisfactory.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
If suprascapular nerve entrapment is suspected, all cases should be referred to a
physician for appropriate investigation.
PROGNOSIS
SUGGESTED READINGS
• Prognosis depends entirely on the
extent of damage to the nerve.
• Neurapraxia should resolve rapidly and
lead to a complete restoration of function usually within 2 to 3 months.
• If the injury is a more severe axonotmesis, the recovery time will depend
on the distance from the site of injury
to the denervated tissue. Peripheral
nerves have been reported to recover
at an approximate rate of between 1 and
4 mm per day, but complete function
might not be restored.
• If there has been a complete sectioning
of the nerve (neurapraxia), a full recovery will not occur.
Aldridge JW, Bruno RJ, Strauch RJ, Rosenwasser
MP. Nerve entrapment in athletes. Clin Sports
Med. 2001;20(1):95.
Goslin KL, Krivickas LS. Proximal neuropathies of the upper extremity. Neurol Clin.
1999;17(3).
Kibler WB, Murrell GAC. Shoulder pain. In:
Brukner P, Khan K, eds. Clinical Sports
Medicine. 3rd ed. Australia: McGraw-Hill;
2006:243–288.
Leffert RD. Nerve lesions about the shoulder.
Orthop Clin North Am. 2000;31(2).
Moore TP, Hunter RE. Suprascapular nerve
entrapment. Oper Tech Sports Med.
1996;4(1):8–14.
AUTHOR: JOSEPHINE LOUISE COULTER
Section III
ORTHOPEDIC PATHOLOGY
46 of 57
782
Sural Nerve Entrapment
BASIC INFORMATION
DEFINITION
Sural nerve entrapment is a mononeuropathy that results from compression
or restriction of movement of the sural
nerve, usually at the deep fascia of the leg
in the calf and lateral lower leg region.
SYNONYMS
None currently used
CHAPTER 16 • NERVE
MECHANISM OF INJURY
• Fractures: Fifth metatarsal, cuboid, calcaneus, fibula
• Lateral ankle sprains
• Peroneal tendon rupture
• Engorged lesser saphenous veins: Chronic
venous insufficiency
• Ganglions
• Hematomas
• Postsurgical scarring
• Improper fitting boots
COMMON SIGNS AND
SYMPTOMS
ICD-9CM CODES
355.7 Other mononeuritis of lower
limb
OPTIMAL NUMBER OF VISITS
6 or fewer
• Pain and dysesthesias in the sural nerve
distribution, especially around the lateral ankle, are the most common sensory complaint.
• Gait deviations from pain with ankle or
foot motions might also be noted in the
present history.
MAXIMAL NUMBER OF VISITS
AGGRAVATING ACTIVITIES
20
•
•
•
•
•
•
•
•
ETIOLOGY
• Arising from branches off the tibial
nerve, the sural nerve descends between
the two heads of the gastrocnemius and
becomes superficial at the middle of the
leg. It descends along side the saphenous vein and passes inferior to the lateral malleolus to the lateral side of the
foot.
• The sural nerve supplies the skin on
the posterior and lateral aspects of the
lower leg and lateral side of the foot up
to the base of the fifth metatarsal.
• The sural nerve is believed to be purely
sensory and has very little if any motor
involvement. A few recent cadaver and
clinical studies have found some motor
fibers within the sural nerve. Still, the
nerve is viewed primarily as a sensory
nerve.
• Since the sural nerve becomes more
superficial in the lower leg, it is believed
to be more at risk of compression.
Internal compression, such as a ganglion cyst or tumor, has been noted to
compress the nerve. Stretch injuries
may also create strain on the nerve and
repetitive injuries or trauma may be the
catalyst for more fibrotic scarring of the
surrounding fascia that may entrap the
nerve.
EPIDEMIOLOGY AND
DEMOGRAPHICS
• This condition is thought to be relatively rare; although a small number of
studies stated that it is a common syndrome in athletes.
• A gender difference has not been strictly
reported, but one study of 13 patients
with sural nerve entrapment noted that
11 were male and 2 were female.
Physical exertion with lower extremities
Heel raises or going up on toes
Prolonged standing
Walking
Running
Cycling
Wearing tight boots or hockey skates
Calf stretches
EASING ACTIVITIES
• Rest
• Ice or modalities for inflammation
• Massage
24-HOUR SYMPTOM PATTERN
No writings on a particular pattern of
symptoms were found for sural nerve
entrapment. Increased symptoms at night
or lasting symptoms in the morning may
point to a strong inflammatory component to the symptoms. This may also suggest space-occupying lesion, such as a
tumor, so careful attention should be paid
to other factors and the progression of
symptoms.
PAST HISTORY
No typical past history has been noted
for sural nerve entrapment. One study’s
review of their participants noted that
the leg of one subject, before onset of this
problem, had been run over by a truck,
possibly contributing to fibrotic scarring
around the nerve sheath. Following this
theory, one might find a previous incident,
trauma, or overuse that may have led to
neurodynamic restrictions and internal
changes in the nerve connective tissue or
nerve itself.
PHYSICAL EXAMINATION
• The most common physical finding is
altered sensation in the sural nerve’s
47 of 57
sensory distribution in the lateral lower
part of the leg, calf, and lateral ankle.
• Gait deviations might be noted and associated with changed mechanics caused
by pain.
• It is important to note that normal muscle strength should be tested since this
nerve is purely sensory. If weakness
is found, another peripheral nerve or
more proximal lesions, such as on the
lumbar spine, must be examined.
IMPORTANT OBJECTIVE TESTS
• Lower quarter neurological examination is as follows:
Sensory examination: Light touch, pinprick, or sharp/dull may be used to
determine altered sensation in a specific distribution.
Motor
examination: No myotomal
weakness should be noted with examination. However, pain may be noted
with contracting muscle surrounding
the nerve such as the gastrocnemius.
No reflexive changes should be noted.
Tinel’s test: Tapping on the superficial
regions of the nerve may reproduce
symptoms into the specific nerve
distribution.
Palpation: Muscles around the nerve,
especially gastrocnemius, may reproduce symptoms or may have noted
soft tissue restrictions that possibly
indicate fibrotic scarring around the
nerve.
SLR test (or slump test)
• A neurodynamic examination helps
differentiate neurogenic (sural nerve)
from nonneurogenic (gastrocnemius or
peroneals) sources of symptoms.
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
•
•
•
Local muscle strain
Knee ligamentous strain
Meniscal pathology
Osteoarthritis
Deep vein thrombosis
Lumbar spine radiculopathy
Lumbar spine stenosis
Polyneuropathy
CONTRIBUTING FACTORS
• Running and overuse of the lower
extremity muscles
• Poor lower quarter alignment
• Poor trunk or lower extremity
• Diabetes mellitus
• Alcoholism
TREATMENT
SURGICAL OPTIONS
• Surgical decompression may be recommended to release the nerve from surrounding fibrotic connective tissues.
Sural Nerve Entrapment
CHAPTER 16 • NERVE
• Surgical neurolysis is not recommended
but may be done when the condition is
unresponsive to other measures.
REHABILITATION
• The first goal of rehabilitation should be
to decrease any inflammation or irritation around the nerve, thereby decreasing symptoms.
• Modalities, such as ultrasound, phonophoresis, iontophoresis, ice, interferential current therapy, or light massage
techniques, may assist in decreasing
symptoms.
• Taping, bracing, or footwear modification have also been suggested, which
may help decrease strain on the affected
region.
• If fibrotic scarring is one of the hypothesized mechanisms for sural nerve
entrapment, then more vigorous massage techniques to free up the nerve
may be beneficial. This could be followed up with neurodynamic techniques that attempt to glide, slide, or
place tension on the nerve to restore
normal mobility.
• It is also important to address any biomechanical faults that may be contributing to stress or strain on the sural nerve.
PROGNOSIS
No specific data on long-term outcomes
were found after sural nerve entrapment.
Because of the pure sensory function of
the sural nerve, it is most likely not associated with high rates of morbidity. One
author did suggest that return of sensation may take up to a year after surgery.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
• Unrelenting pain not related to biomechanical factors
• Weight loss
• Bowel or bladder dysfunction
• Saddle paresthesias
• Gait disturbances: Clumsiness or ataxic
gait
783
• Bilateral glove or sock numbness
• Symptoms that do not initially improve
with symptoms
SUGGESTED READINGS
Butler DS. Mobilisation of the Nervous System.
New York: Churchill Livingston; 1991.
Butler DS. The Sensitive Nervous System.
Adelaide, Australia: Noigroup Publications;
2000.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics.
Philadelphia: Elsevier; 2005.
http://www.emedicine.com/Orthoped/topic422.
htm
AUTHOR: CHRIS IZU
Section III
ORTHOPEDIC PATHOLOGY
48 of 57
784
Tibial Nerve Entrapment
BASIC INFORMATION
DEFINITION
Tibial nerve entrapment syndrome is a
mononeuropathy that results from compression or restriction of movement of
the tibial nerve, usually through the tarsal
tunnel in the ankle.
SYNONYMS
Tarsal tunnel syndrome: Sometimes
referred to as proximal tarsal tunnel syndrome since the distal tarsal tunnel may
be used to describe the region in which
the distal plantar branches of the tibial
nerve may become entrapped.
ICD-9CM CODES
355.5 Tarsal tunnel syndrome
OPTIMAL NUMBER OF VISITS
6 or fewer
MAXIMAL NUMBER OF VISITS
20
ETIOLOGY
• The tibial nerve is a branch of the
large sciatic nerve in the posterior leg
that runs distally between the heads of
the gastrocnemius muscle deep to the
soleus muscle. It usually lies between
the flexor digitorum longus and the tibialis posterior muscle. Traveling distally
and posterior to the medial malleolus,
it continues through the tarsal tunnel,
where it eventually divides into the
medial and lateral plantar nerves.
• The tibial nerve may become entrapped
anywhere along its pathway, such as
the popliteal fossa, but is most likely
affected in the tarsal tunnel. The tunnel is formed by the medial surface of
the talus, the inferomedial navicular,
the sustentaculum tali, and the medial
surface of calcaneus and the flexor
retinaculum. The deep and superficial
aponeuroses of the leg help form the
flexor retinaculum, which is closely
attached to the surrounding muscle
sheaths.
• Compression of the tibial nerve can
be from space-occupying lesions such
as neuromas, ganglion cysts, lipomas,
osteochondromas, tumors, or abnormal
varicosities.
• Limited space within the tarsal tunnel
may also be caused by tenosynovitis or
rupture of adjacent tendons.
• Biomechanical factors have also been
proposed as a cause of tibial nerve
entrapment since it has been noted
that pressure within the tarsal tunnel
increases with full dorsiflexion/eversion of the foot and ankle and also full
CHAPTER 16 • NERVE
inversion. Abnormal standing postures
or gait may continually put stress on the
tarsal tunnel.
• Because of the network of fibrous connective tissue around the tarsal tunnel
and surrounding musculature, it has also
been suggested that limited mobility of
the nerve may come from tethering of
the nerve sheath to adjacent structures.
EPIDEMIOLOGY AND
DEMOGRAPHICS
Of the nerves in the foot and ankle, the tibial nerve is the most likely to be entrapped.
Some studies point to a slight female predominance, and in general the age ranges
from about 14 to 80 years of age with a
peak in the 50 to 60 years age range. It is
common in nonathletes but also has been
noted in distance runners.
MECHANISM OF INJURY
• A gradual or insidious onset is most
commonly seen in this condition as
space-occupying lesions continue to
add compression to the area or biomechanical factors continue to strain local
tissues.
• Types of injuries that may lead to tibial
nerve entrapment include the following:
Direct blunt trauma
Traction injury
Repeated ankle sprains
Fractures of the surrounding bones
COMMON SIGNS AND
SYMPTOMS
• Common symptoms of this condition
are pain, burning, and paresthesias in
the distribution of the tibial nerve on
the plantar surface of the foot.
• Symptoms are generally unilateral but
may be on both sides.
• Symptoms occasionally radiate more
proximally into the medial leg.
AGGRAVATING ACTIVITIES
•
•
•
•
Prolonged standing or walking
Extreme dorsiflexion
Increased weight-bearing activities
Wearing nonsupportive shoes or sandals
EASING ACTIVITIES
•
•
•
•
Rest and relief of weight-bearing activities
Sitting
Massage
Ice or antiinflammatories
24-HOUR SYMPTOM PATTERN
• If there is a significant inflammatory
component to the symptoms or a
space-occupying lesion, more nighttime
symptoms may be expected. Following
this, symptoms may also be worse in the
morning.
• Often, there is less pain in the morning
after rest, but there may be pain on the
first step when getting out of bed.
49 of 57
PAST HISTORY
Patients may note previous bouts with
the same condition. They may also report
previous lower extremity or lumbar
spine injuries, which in turn might have
affected lower quarter biomechanics.
Patients may have a previous history of
other space-occupying lesions, such as a
Baker’s cyst.
PHYSICAL EXAMINATION
• Abnormal foot or lower extremity
alignment, such as a pes planus or pes
cavus, may be noted. Looking from the
more proximal view, it may be associated with tibial or femoral internal or
external rotation. From the posterior
view, the calcaneal position may also be
altered.
• An examination of gait may also reveal
a corresponding deviation with abnormal pronation or supination of the foot
during the loading response to terminal
stance phases.
• Palpation of the local areas most likely
reproduce the patient’s symptoms into
the heel or foot.
• A sensory examination usually reveals
abnormal sensation in the distribution
of the tibial nerve.
• Neurodynamic testing most likely helps
differentiate a neurogenic source of
symptoms from other local or referred
sources.
IMPORTANT OBJECTIVE TESTS
• Tinel’s test: Tapping on the tarsal
tunnel most likely reproduces the
patient’s symptoms in a tibial nerve
distribution.
• Sensory examination: Using SemmesWeinstein monofilaments, an area of
altered or diminished sensation should
be noted in the same distribution distal
to the side of the lesion.
• Manual compression: Sustained pressure at the tarsal tunnel may also reproduce symptoms and help confirm
diagnosis.
• Motor examination: Weakness might be
found in plantar flexion of the ankle or
in knee flexion.
• Gait examination: Contributing biomechanical factors during walking, jogging, or running need to be assessed
since these may be impairments that
could be addressed in rehabilitation.
Neurodynamic
Lower quarter neurological exam
Lumbar spine ROM
Lumbar spine palpation
Lumbar
spine accessory motion:
These tests are important to help
determine contribution of proximal
sources to the symptoms in the case
of lumbar spine radiculopathy or
double-crush.
Tibial Nerve Entrapment
CHAPTER 16 • NERVE
DIFFERENTIAL
DIAGNOSIS
•
•
•
•
•
•
•
•
Lumbar spine radiculopathy
Exostosis
Malunions
Osteochondromas
Fractures
Tibialis posterior tendinitis
Plantar fasciitis
Heel spur
CONTRIBUTING FACTORS
•
•
•
•
•
•
•
•
•
•
Obesity
Ankylosing spondylitis
Acromegaly
Talocalcaneal coalition
Diabetes
RA: Proliferative synovitis
Foot deformities
Varicose veins
Alcoholism
Thyroid disease
•
•
•
•
•
TREATMENT
•
SURGICAL OPTIONS
• Rehabilitation of this condition should
focus not only on alleviating the
50 of 57
• If suspected worsening compression on
the nerve is suspected from a compartment syndrome, immediate referral to
a physician is warranted. A fasciotomy
may be done to release this pressure.
• Night pain and unrelenting symptoms
may indicate a local tumor.
• Symptoms that do not improve within
the expected time or that are not
affected by physical therapy in a few
visits should be referred to the physician because a space-occupying lesion
may be present.
• A recent history of trauma with suspected fracture may need imaging studies done before starting treatment.
• Impaired circulation or vascular compromise may also warrant more medical management.
SUGGESTED READINGS
Butler DS. Mobilisation of the Nervous System.
New York, NY: Churchill Livingston; 1991.
Butler DS. The Sensitive Nervous System.
Adelaide, Australia: Noigroup Publications;
2000.
Dawson DM, Hallett M, Wilbourn AJ, eds.
Entrapment Neuropathies. Philadelphia:
Lippincott-Raven; 1999.
Moore KL, Dalley AF. Clinical Oriented
Anatomy. 4th ed. Philadelphia: Lippincott
Williams & Wilkins; 1999.
Placzek JD, Boyce DA, eds. Orthopedic Physical
Therapy Secrets. 2nd ed. Philadelphia:
Elsevier; 2006.
Shacklock M. Clinical Neurodynamics.
Philadelphia: Elsevier; 2005.
AUTHOR: CHRIS IZU
ORTHOPEDIC PATHOLOGY
REHABILITATION
PROGNOSIS
Another study following postoperative patients after tarsal tunnel release
showed good-to-excellent results in
84% of cases. No statistics were found
regarding improvement with conservative measures; however, clinically it is
thought that with proper management
of contributing factors, in the absence
of a space-occupying lesion or marked
fixed-foot deformity, outcomes are
relatively good.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
Section III
• Tarsal tunnel decompression has been
shown to be fairly successful for shortterm relief of symptoms. Some authors
noted that 1 month after surgery, 24 out
of 26 patients had good outcomes.
• In the case of cystic lesions, aspiration
might also provide relief of pressure
within the tarsal tunnel and reduce
symptoms.
• A surgical release of the flexor retinaculum or removal of the space-occupying lesion are common procedures to
address tarsal tunnel syndrome.
• From a clinician’s perspective, it is important to follow surgery by addressing any
biomechanical contributing factors that
may have led to the condition.
symptoms but also on the underlying
cause of compression.
NSAIDs and relative rest, ice, compression, and elevation (RRICE) should
initially be implemented in acute or
inflammatory stages to help relieve
symptoms.
In more severe cases, individuals with
tibial nerve entrapment may benefit
from immobilization, such as using a
walking boot or cast or splint, and limiting weight bearing with use of assistive
devices.
Other modalities, such as ultrasound,
interferential current therapy, or phonophoresis, may be administered to help
with local symptoms.
Taping and use of orthoses have clinically shown to be effective when
addressing abnormal foot mechanics
and positioning.
If neurodynamic restriction is suspected,
soft tissue mobilization and techniques
to slide, glide, and place tension on the
nerve as described by Butler may be
warranted.
More complete rehabilitation should
also address other lower extremity or
trunk impairments or motor control
problems that may lead to increased
pressure at the tarsal tunnel. For example, inadequate timing or force production of the gluteus medius during gait
may influence the pronation component of the foot, leading to increased
strain of the medial ankle structures.
785
Vascular Thoracic Outlet Syndrome
786
BASIC INFORMATION
DEFINITION
• TOS encompasses numerous scenarios
of compression (neurological and vascular) in the thoracic outlet region of the
shoulder girdle. Although vascular and
neurological classifications exist, it must
be noted that these conditions can also
be observed together. It is also believed
that in 98% of TOS cases, the resultant
symptoms are neurogenic. Defining the
syndrome has been difficult in the literature because of its variable etiology
and presentation and often minimal
clinical findings.
• The following vascular TOS classifications exist:
Arterial TOS is caused by compression of the subclavian and/or axillary
artery and is very uncommon, occurring in only 3% to 4% of cases.
Venous TOS is caused by compression
of the subclavian and/or axillary vein
and occurs in only 6% to 7% of cases.
• The subclavian vein and artery receive
new nomenclature as the axillary vein
and artery, once they pass the first rib).
SYNONYMS
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Cervical rib syndrome
First rib syndrome
Scalenus anticus syndrome
Costoclavicular syndrome
First thoracic rib syndrome
Hyperabduction syndrome
Scalenus medius syndrome
Pectoralis minor syndrome
Subcoracoid-pectoralis minor syndrome
Brachiocephalic syndrome
Paget-Schroetter syndrome (effort vein
thrombosis of subclavian vein)
Nocturnal paresthetic brachialgia
Rucksack palsy
Droopy shoulder syndrome
Fractured clavicle-rib syndrome
ICD-9CM CODES
353 Nerve root and plexus disorders
442.82 Aneurysm of subclavian artery
OPTIMAL NUMBER OF VISITS
Not applicable
MAXIMAL NUMBER OF VISITS
Not applicable
ETIOLOGY
• Current belief of the cause of TOS is the
underlying existence of bony or fibromuscular anomalies with overlying
injury and/or spasm in the thoracic outlet region causing compromise.The anatomical anomalies are generally seen as
predisposing factors.
CHAPTER 16 • NERVE
• Bony anomalies can be congenital, traumatic, or posttraumatic and include the
presence of: a cervical rib, elongated C7
transverse process, first rib deformity,
displaced first rib fracture, excessive
callus formation after first rib fracture,
rib hemangioma, fractured or subluxed
clavicle, and pseudarthroses.
• Cervical ribs are known to exist in
approximately 0.5% of the population,
with 10% to 20% resulting in symptoms,
although this depends on their size.
• Soft tissue anomalies can also be congenital, traumatic, or posttraumatic and
include altered scalene muscle insertions and origins, presence of scalenus
minimus or scalenus pleuralis muscle,
hypertrophy or injury of scalene muscles, presence of congenital fibromuscular bands (classified as type 1 to 10)
or dense fibrous sheaths, cervical ligaments and band, and pectoralis minor
shortening.
• The following three spaces in the thoracic outlet region have been identified as potential areas of vascular
compression:
Interscalene space or triangle is bordered anteriorly by the anterior scalene muscle, posteriorly by the middle
scalene muscle, and inferiorly by the
first rib. Here the subclavian artery
passes posterior to the anterior scalene muscle (in close relation with the
brachial plexus), then superior to the
first rib. The subclavian vein bypasses
this space by traveling anteromedial
to the anterior scalene muscle.
Costoclavicular
space is bordered
anteriorly by the medial aspect of
the clavicle, subclavian muscle and
tendon, and costocoracoid ligament.
The posterolateral border is formed
by the upper scapula, and the first rib
and the anterior and middle scalene
muscle insertions create the posteromedial border. Here the subclavian
vein and artery travel with the brachial plexus under the clavicle and
subclavius muscle toward the subpectoralis minor space.
Subpectoralis minor space is located
inferior to the coracoid process and
posterior to the pectoralis minor muscle insertion. Here the subclavian vein
and artery continue to travel with the
brachial plexus beneath the pectoralis
muscle toward the axilla.
A further region involved in vascular
TOS has also been described at the
head of humerus, where the axillary
artery gives off posterior humeral circumflex branches. This area is often
not involved in vascular TOS but is
commonly seen.
• Arterial TOS
Compression of the subclavian artery
in TOS can be acute or chronic and
51 of 57
can occur in the interscalene triangle,
costoclavicular space, or subpectoralis minor space.This occurs as a result
of underlying bony or fibromuscular anomalies with overlying muscle
injury and/or spasm.
In most cases of arterial TOS, compression is caused by the tip of the
cervical rib or an elongated C7 transverse process. Compression in the
subpectoralis space is less common
and is referred to as hyperabduction
syndrome. This is in reference to the
arm position during which the neurovascular structures are compromised.
Additionally, vascular compression has
been reported to occur at the humeral
head. Here the axillary artery may be
tethered via its circumflex branches,
as a result of excessive movement of
the head of humerus.
Although rare, chronic compression
can lead to occlusive and aneurysmal
disease.
The subclavian artery sustains chronic
intimal damage, which can result
in either thrombosis or occlusion.
Poststenotic dilations may also develop.
If the rate of occlusion is slow, the
body is able to develop sufficient
collateral circulation, so the patient
may only feel symptoms with excessive arm use. Rapid occlusion creates
more obvious claudication symptoms,
as well as symptoms with minimal
arm activity or at rest.
Damage to the full thickness of the
subclavian artery wall (aneurysmal
disease) can also produce debris,
which may dislodge and create distal
emboli in the arm, hand, or fingers.
• Venous TOS
Compression of the subclavian vein
in the thoracic outlet region can have
an acute onset (generally known as
effort thrombosis or Paget-Schroetter
syndrome) or an insidious one. The
most common pathological cause of
this syndrome is a congenital anomaly
of the costoclavicular ligament combined with anterior scalene muscle
hypertrophy, resulting in venous compression and occlusion.
Thromboses may also occur from subclavian venous catheters (intravenous
[IV] therapy), dialysis treatment, and
the presence of abnormalities in blood
factors, antibodies, and proteins.
Chronic compression of the subclavian vein produces an inflammatory
reaction, endothelial damage, and
venous stasis.
EPIDEMIOLOGY AND
DEMOGRAPHICS
• Arterial TOS is very rare.
• Arterial TOS occurs more often in the
younger, active population.
Vascular Thoracic Outlet Syndrome
CHAPTER 16 • NERVE
• Carrying heavy objects such as suitcases
and shopping bags
• Arterial TOS occurs equally among
males and females.
• Venous TOS is quite rare.
• Venous TOS occurs more often in the
younger population.
• Venous TOS occurs most often in young
males.
EASING ACTIVITIES
MECHANISM OF INJURY
Unknown, not applicable, and not related
to activity.
• Note that despite the following classifications, some patients also demonstrate
neurogenic TOS symptoms.
• Arterial TOS
Arm coldness, heaviness, pulselessness, pallor, loss of strength or fatigue
with exercise (i.e., true arm claudication during activity, particularly overhead activity)
Weakened grip and reduced finger
function (difficulty gripping and carrying bags)
• Venous TOS
Swelling, edema, cyanosis, and arm
discomfort with activity
If the subclavian vein has thrombosed,
the patient presents with a sudden
onset of edema in the arm with associated discomfort and cyanosis.
Symptoms usually develop in the
dominant arm
AGGRAVATING ACTIVITIES
• Overhead arm and hand positions or
arm elevated repetitive activities. These
commonly include styling hair, painting,
working overhead, pitching or throwing a ball, playing musical instruments
(e.g., violin or flute), and swimming.
24-HOUR SYMPTOM PATTERN
PAST HISTORY FOR THE REGION
• Arterial
The onset of symptoms usually reveals
increased or unaccustomed prolonged
or repetitive upper limb activity (i.e.,
pitching in baseball but may also be
insidious in nature).
The patient may report a previous history of whiplash injury or a direct or
indirect blow to the shoulder resulting in first rib, muscular, or clavicular
trauma.
• Venous
The onset of symptoms usually reveals
increased or unaccustomed prolonged
or repetitive upper limb activity but
may also be insidious in nature.
Recent use of a subclavian venous
catheter (intravenous therapy) and
dialysis treatment.
The patient may report a previous history of whiplash injury or a direct or
indirect blow to the shoulder resulting in
first rib, muscular, or clavicular trauma.
PHYSICAL EXAMINATION
• Arterial TOS
Loss or reduction of radial pulse with
arm activity
Difference of blood pressure between
the arms of >20 mm Hg
Positive Roos, Adson’s, Halsted’s, and
Wright’s hyperabduction tests
Loss of radial pulse and arm discomfort and/or development of arm pallor
during the Roos test with subsequent
hyperemia after lowering the arm
Coldness of hand and fingers
Trophic changes in fingernails or skin
Gangrene of finger tips (in extreme
cases of peripheral embolization)
Pulsatile mass palpable in the supraclavicular fossa (not common but
indicative of a subclavian aneurysm)
• Venous TOS
Superficial vein distention in upper
limb and chest
Edema of the upper limb (measurement of limb girth)
Discoloration of the limb
Arm discomfort with activity
Positive Roos test: Development of
cyanosis and arm swelling during test
• Any of the following physical findings
of neurogenic TOS may also be present:
Poor posture (including downwardly
rotated and protracted scapula, large
52 of 57
IMPORTANT OBJECTIVE TESTS
• Observation of the affected arm is
important in the diagnosis of vascular
TOS. Arm size, color, temperature, and
pulses must be compared to the normal side at rest, during overhead activity, and after activity.
• Palpation of the supraclavicular fossa is
important for detection of aneurysms.
• Three tests (Adson’s, Halsted’s, and
Wright’s hyperabduction tests) have
traditionally been used to diagnose
TOS because they monitor the radial
pulse. These tests have been extensively discussed, criticized, and “modified” in the literature because of the
high level of false positives and false
negatives (many asymptomatic people demonstrate pulse changes during
these tests).
• Roos test (elevated arm stress test),
however, is described as the most reliable test for all types of TOS. If a patient
is unable to complete the test because
of their symptoms, it can also reflect
the severity of their arterial or venous
compromise.
• Patients may also demonstrate a bruit
in the subclavian artery on auscultation
during these tests indicating arterial
TOS.
• Arterial TOS
Doppler studies
Arteriography in provocative positions and followed to digits to pick-up
embolus
Magnetic resonance angiograms (MRAs)
• Venous TOS
Doppler studies
Positional venography
Coagulation studies
DIFFERENTIAL
DIAGNOSIS
• Shoulder pathologies
Glenohumeral instabilities
ORTHOPEDIC PATHOLOGY
COMMON SIGNS AND
SYMPTOMS
Rest from aggravating activities
breasts and/or obesity, or forward
head posture)
Exaggerated upper chest or accessory
breathing
Neurological tests negative
Altered neurodynamics on upper limb
neurodynamic tests
Reproduction of arm pain or symptoms
on palpation over brachial plexus
Positive Tinel’s sign for reproduction
of arm pain or symptoms over brachial plexus
Muscle spasm and/or shortening of
anterior scalene muscle on palpation
and length testing
Muscle spasm and/or shortening of
pectoralis minor muscle on palpation
and length testing
Ipsilateral elevated first rib
Section III
• The most common cause of vascular
TOS is repetitive strain through prolonged or vigorous upper limb activity.
Other causes may include a history of
whiplash and direct or indirect blows
to the shoulder.
• The superimposed injury involved in
causing TOS symptoms may include
whiplash, direct or indirect blow to the
shoulder, repetitive strain through prolonged upper limb activity, accessory
breathing, and/or poor posture.
• Positions or postures that place
increased strain on the vascular structures of the thoracic outlet include the
following:
Prolonged writing or use of keyboard
or telephone
Assembly line workers
Poor posture (i.e., droopy shoulders)
Prolonged overhead or reaching activity such as styling hair, painting, playing
musical instruments (e.g., violin or flute),
swimming, playing tennis, and pitching.
Excessive carrying of heavy objects
such as suitcases and shopping bags
Prolonged carrying of a heavy backpack
787
788
Vascular Thoracic Outlet Syndrome
Subacromial or subcoracoid impingement
Subacromial bursitis
Glenohumeral labral tears
Rotator cuff tendinopathies
• Cervical or thoracic pathologies
Cervical spondylosis
Cervical degenerative disc disease
Cervical nerve root syndrome
Cervical spine stenosis
Thoracic facet syndrome
T4 syndrome
Rib dysfunction
• Peripheral nerve entrapments
Ulnar nerve entrapment (cubital tunnel/Guyon’s canal)
Median nerve entrapment (carpal tunnel/pronator teres)
Radial nerve entrapment (forearm)
• Other
Muscular dystrophy
Polymyositis
CRPS
Diffuse peripheral neuropathy
Angina and other cardiac conditions
RA
Lupus
Pancoast’s tumor
Multiple sclerosis
Spinal cord lesion
Hypothyroidism
Pleuritis and other pulmonary conditions
Raynaud’s phenomenon
Head, neck, or upper quadrant tumors
Lymphedema
CONTRIBUTING FACTORS
• Underlying existence of bony or fibromuscular anomalies in the thoracic outlet region
• Previous history of whiplash injury or a
direct or indirect blow to the shoulder
resulting in first rib, muscular, or clavicular trauma.
• Exposure to increased or unaccustomed prolonged or repetitive upper
limb activity (e.g., overhead sport, occupation, playing a musical instrument)
• Presence of glenohumeral instability
or hypertrophy of the humeral head or
local muscular hypertrophy (arterial)
• Exposure to cold temperatures combined with trauma (venous)
• Presence of blood clotting factors
(venous)
• The use of a subclavian venous catheter (IV
therapy) and dialysis treatment (venous)
TREATMENT
SURGICAL OPTIONS
• The following is a list of current surgical techniques that are used alone or in
combination to treat vascular TOS. The
surgical techniques chosen depend on
the degree of damage to the vessel, his-
CHAPTER 16 • NERVE
tory of symptoms, and degree of compression in the thoracic outlet region.
• Arterial TOS
Rib resection (transaxillary approach)
Aneurysm resection with graft
Thrombectomy
Embolectomy
Artery reconstruction or replacement
Dorsal sympathectomy
• Venous TOS
Rib resection (transaxillary approach)
Scalenectomy
Fibrous band or adhesion resection
Thrombectomy (limited use)
Claviculectomy
SURGICAL OUTCOMES
• Arterial TOS
Good results are generally seen with
surgery, although outcomes are less
favorable with delayed diagnosis and
surgery, and the presence of distal
embolism (Durham et al 1995).
• Venous TOS
The combination of a prompt diagnosis, contrast venography with catheter-directed thrombolytic therapy,
and consequent TOS decompressive
surgery has shown very good results.
Delayed thrombolytic therapy with
surgery (>3 months from onset of
condition) also had a less positive
outcome.
SURGICAL INDICATORS
• Arterial TOS
Presence of arterial aneurysm, occlusion,
or thrombosis
Persistence of symptoms
• Venous TOS
Presence of thrombosis
Persistence of symptoms
Positive venogram exhibiting compression at rest or during provocative
testing.
REHABILITATION
• Surgical intervention is the mainstay of
treatment of vascular TOS, although its
use is more controversial in less serious cases. A patient is therefore more
likely to present for postsurgical rehabilitation on the request of the vascular
surgeon.
• The following rehabilitation guidelines
are based on the principles of reducing
ongoing trauma to the subclavian vessels in the thoracic outlet region, relieving symptoms, restoring upper limb
function, and improving cardiovascular
health. The guidelines are not meant to
be used as a definitive postsurgical rehabilitation program.
• Refer to the neurogenic TOS section
for additional rehabilitation techniques
for patients who present with combined neurogenic and vascular TOS
symptoms.
53 of 57
• Arterial TOS
Rest from aggravating activities
Postural or ergonomic advice
Lateral costal combined with diaphragmatic breathing techniques
Motor control and stability functional
rehabilitation exercises for trunk,
scapula, neck, and shoulder (especially in cases of axillary artery injury
that present with an unstable head of
humerus)
Gradual
return to overhead arm
activity
Progressive
cardiovascular training
program, especially for those in poor
aerobic condition
• Venous TOS
Edema
control (e.g., compression
sleeves, bandages, and gloves and supported elevation)
Massage of upper limb to promote
drainage of edema
Gentle exercises of upper limb to promote drainage of edema
Rest from aggravating activities
Postural or ergonomic advice
Lateral costal combined with diaphragmatic breathing techniques
Motor control and stability functional
rehabilitation exercises for trunk,
scapula, neck, and shoulder
Gradual
return to overhead arm
activity
Progressive
cardiovascular training
program, especially for those in poor
aerobic condition
PROGNOSIS
• Arterial TOS
Since most cases of arterial TOS require
surgery, the prognosis depends on
surgical outcomes. Good results are
generally seen with surgery, although
outcomes are less favorable with
delayed diagnosis and surgery and the
presence of distal embolism.
• Venous TOS
Since most cases of venous TOS require
surgery, the prognosis depends on
surgical outcomes. The combination
of a prompt diagnosis, contrast venography with catheter-directed thrombolytic therapy, and consequent TOS
decompressive surgery has shown
very good results. Delayed thrombolytic therapy with surgery (>3
months from onset of condition) had
a less positive outcome. Conservative
treatment tends to demonstrate the
poorest outcomes.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
If vascular TOS is suspected, all cases
should immediately be referred to a physician for prompt investigation and medical
intervention.
Vascular Thoracic Outlet Syndrome
CHAPTER 16 • NERVE
SUGGESTED READINGS
Atasoy E. Thoracic outlet syndrome: anatomy.
Hand Clin. 2004;20(1):7–14.
Ault J, Suutala K. Thoracic outlet syndrome.
J Man Manipulative Ther. 1998;6(3):
118–129.
Brantigan CO, Roos DB, David B. Etiology of
neurogenic thoracic outlet syndrome. Hand
Clin. 2004a;20(1):17–22.
Brantigan CO, Roos DB. Diagnosing thoracic
outlet syndrome. Hand Clin. 2004b;20(1):
27–36.
Crosby CA, Wehbé MA. Conservative treatment
for thoracic outlet syndrome. Hand Clin.
2004 Feb;20(1):43–49, vi.
Dawson DM, Hallett M, Milender LH.
Entrapment Neuropathies. 2nd ed. Boston:
Little, Brown; 1990.
Demondian X, Herbinet P, Van Sint Jan S, Boutry
N, Chantelot C, Cotton A. Imaging assessment
of thoracic outlet syndrome. Radiographics.
2006;26:1735–1750.
Durham JR, Yao JST, Pearce WH, Nuber G, Mc
Carthy WJ.Arterial injuries in the thoracic outlet syndrome. J Vasc Surg. 1995;21:57–70.
Edgelow PL. Chapter 7 Neurovascular consequences of cumulative trauma disorders
affecting the thoracic outlet: a patient-centred treatment approach. In: Donatelli
RA. Physical Therapy of the Shoulder.
Philadelphia: Churchill Livingstone; 2003.
Mackinnon SE, Novak CB. Thoracic outlet
syndrome. Curr Probl Surg. 2002;39(11):
1070–1145.
Pecina MM, Krmpotic-Nemanic J, Markiewitz
AP. Tunnel Syndromes: Peripheral Nerve
Compression Syndromes. 3rd ed. Boca Raton,
FL: CRC Press; 2001.
Safran MR. Nerve injuries about the shoulder
in athletes, Part 2: long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med.
2007;32(4):1063–1076.
Sanders RJ, Hammond MD. Etiology and pathology. Hand Clin. 2004;20(1):23–26.
Sanders RJ, Hammond SL. Supraclavicular first rib
resection and total scalenectomy: technique
and results. Hand Clin. 2004;20(1):61–70.
Shebel ND, Marin A. Effort thrombosis (PagetSchroetter Syndrome) in active young adults:
789
Current concepts in diagnosis and treatment.
J Vasc Nurs. 2006;24:116–126.
Urschel Jr HC, Kourlis Jr H. Thoracic outlet
syndrome: A 50-year experience at Baylor
University Medical Center. Baylor Univ Med
Cen Proc. 2007;20(2):125–135.
Urschel Jr HC, Razzuk MA. Neurovascular
compression in the thoracic outlet. changing management over 50 years. Ann Surg.
1998;228(4):609–617.
Vanti C, Natalini L, Romeo A, Tosarelli D,
Pillastrini P. Conservative treatment of thoracic outlet syndrome: A review of the literature. Eura Medicophys. 2007;43(1):55–70.
Wehbe MA. Thoracic outlet syndrome. Hand
Clin. 2004;20(1). Guest Editor.
Whitenack SH, Hunter JM, Read RL. Thoracic
outlet syndrome: a brachial plexopathy. In:
Mackin EJ, Callahan AD, Skirven TM, Schneider
LH, Osterman AL, eds. Rehabilitation of the
Hand and Upper Extremity. 5th ed. St Louis:
Mosby; 2002.
AUTHOR: KATINA DIMOPOULOS
Section III
ORTHOPEDIC PATHOLOGY
54 of 57
Ulnar Nerve Entrapment
790
BASIC INFORMATION
DEFINITION
Ulnar nerve entrapment pathologies
encompass any injury that interrupts the
function of the ulnar nerve at any point
along its course. The loss of function
results in muscle weakness, pain, or sensory dysfunction.
SYNONYMS
• Cubital tunnel syndrome
• Ulnar nerve palsy
ICD-9CM CODES
354 Mononeuritis of upper limb and
mononeuritis multiplex
354.2 Lesion of ulnar nerve
OPTIMAL NUMBER OF VISITS
6
MAXIMAL NUMBER OF VISITS
20
ETIOLOGY
• The ulnar nerve is a mixed sensory and
motor nerve derived from C8 and T1
nerve roots.
• It comes from the terminal branch of
the medial cord of the brachial plexus.
• It travels within the axillary sheath posterior to pectoralis minor and continues medially to the axillary artery and
the brachial artery to the middle of the
arm.
• It becomes the ulnar nerve after piercing the intermuscular septum and follows the medial head of the triceps to
the groove between the medial epicondyle and the olecranon.
• It then crosses the elbow, giving off
articular branches to the elbow and
motor branches to the flexor carpi
ulnaris and the medial half of flexor digitorum profundus.
• It gives off a large dorsal sensory branch
proximal to the wrist that supplies the
skin of the dorsal wrist and ulnar side of
the hand and continues into the hand
via Guyon’s canal, then splits into superficial and deep branches. Guyon’s canal
is bounded proximally and distally
by the pisiform bone and the hook of
hamate; it is covered by the volar carpal ligament and the palmaris brevis
muscle.
• Superficial branch supplies the palmaris
brevis, the skin of the hypothenar eminence, and digital nerves to the fifth and
ulnar side of the fourth fingers.
• Deep branch passes between the abductor digiti minimi and flexor digiti minimi brevis with the deep branch of the
ulnar artery.
CHAPTER 16 • NERVE
• It perforates the opponens digiti quinti
and follows the deep volar arch across
the interossei and supplies the three
small muscles of the fifth finger, third
and fourth lumbricales, the volar and
dorsal interossei, the adductor pollicis,
and the deep head of flexor pollicis
brevis
• The ulnar nerve is vulnerable to injury
at several points along its course:
Proximally at the axilla
At the myofascial band, called the
arcade of Struthers, proximal to the
medial epicondyle
The medial head of triceps muscle
In the area of the medial epicondyle
Within the ulnar groove of the medial
epicondyle
Within the cubital tunnel formed distal to the medial epicondyle as the
nerve passes between the two heads
of the flexor carpi ulnaris
At the flexor-pronator aponeurosis
Within Guyon’s canal
• The ulnar nerve may be affected at any
point along its course by direct trauma
or compression entrapment leading to
tissue hypoxia. The insult to the nerve
can be mechanical, thermal, chemical,
and ischemic.
• Nerve injury is classified according to
the severity of the injury and its potential for reversibility:
Neurapraxia
(first-degree injury):
Distortion of the myelin about the
nodes of Ranvier, caused by ischemia,
mechanical compression, or electrolyte imbalance, produces temporary
loss of nerve conduction.
Axonotmesis (second-degree injury):
Interruption of the axon with secondary wallerian degeneration. The
supporting tissue surrounding the
axon is preserved, and the recovery period depends on the distance
between the site of injury and the
end-organs.
Neurotmesis: Complete disruption of
the nerve and its supporting structures.
• Neurotmesis has been further divided
into the following three subcategories:
Third-degree
nerve injury: Endoneurium is disrupted with intact perineurium and epineurium.
Fourth-degree nerve injury: All neural
elements sparing the epineurium are
disrupted.
Fifth-degree nerve injury: Complete
transaction and discontinuity of
the nerve with no capacity for
regeneration
• Physiologically, there is disruption to
any part of the nerve responsible for
conduction.
• In repetitive-type nerve entrapment, it is
proposed that repetitive work or static
postures produce an inflammatory process, fibroblasts appear to repair damage
55 of 57
incurred but produce adhesions to the
nerve, limiting their glide and increasing anoxia.
EPIDEMIOLOGY AND
DEMOGRAPHICS
• The ulnar nerve is the most commonly
compressed nerve in the elbow region
and is the second most common compressive neuropathy of the upper
extremity.
• Males develop perioperative neuropathies of the ulnar nerve at the elbow
more frequently than females possibly
because females have more fat content in the medial elbow overlying the
tubercle of the ulnar coronoid process
(Berman).
• Most commonly seen in the throwing
athlete but also seen in skiing, weight
lifting, and racquet sports.
MECHANISM OF INJURY
• A number of mechanisms of injury for
the ulnar nerve are described in relation
to their location.
• Direct trauma at any point along the
course of the nerve
• Proximally at the axilla through direct
trauma or compression often sustained
when the arm lies across a firm object
such as a chair back for a sustained
period of time or through the use of
axillary crutches
• Compression beneath the arcade of
Struthers, proximal to the medial epicondyle
• Compression from the medial head of
triceps muscle, which, when hypertrophied, can snap over the medial epicondyle, causing friction neuritis.
• In the area of the medial epicondyle, a
fracture callus or valgus deformity can
chronically stretch the ulnar nerve.
• Frictional neuritis within the ulnar
groove of the medial epicondyle if the
groove is congenitally shallow or has a
torn fibrous roof, allowing the nerve to
sublux.
• Superficial compression at the elbow
from repeated leaning on elbows or a
direct blow.
• Compression within the ulnar groove by
fracture fragments, spurs, soft tissue ganglia, or other space-occupying lesions.
• Compression within the cubital tunnel during elbow flexion as the tunnel
flattens, causing pressure to increase
around the nerve. For example, in the
throwing athlete, the position of elbow
flexion with wrist extension creates a
threefold increase in pressure in the
cubital tunnel; this increases to six times
the resting pressure during the cocking
position of a throw. Therefore repetitive pressure and stress on the nerve
at this point can create cubital tunnel
syndrome.
Ulnar Nerve Entrapment
CHAPTER 16 • NERVE
• Compression at the flexor-pronator
aponeurosis as the nerve exits the flexor
carpi ulnaris to perforate the fascial
layer between flexor digitorum superficialis and flexor digitorum profundus.
• Compression within Guyon’s canal by a
fractured hook of hamate or ganglion
COMMON SIGNS AND
SYMPTOMS
• Tasks involving repetitive fine hand
motions may reveal fatigue and
weakness.
• Sports involving repetitive throwing
actions with forceful elbow flexion and
rapid extension
• Occupational tasks involving sustained
elbow flexion such as computer work
or assembly line tasks
• Leaning on elbows, particularly on hard
surfaces
EASING ACTIVITIES
Rest and/or modification of aggravating
activities
PAST HISTORY FOR THE REGION
• History of trauma, fracture, dislocation,
or blow to the ulnar nerve distribution.
• Repeated activity repetitive elbow flexion and extension such as may occur
in forceful throwing activities such as
pitching in baseball
• Occupations involving sustained elbow
flexion
PHYSICAL EXAMINATION
• Examine the limb for signs of autonomic
dysfunction trophic changes such as
edema, inflammation, and alteration in
skin texture
• Examine the limb for any characteristic posturing of the hand; with chronic
ulnar neuropathy the hand may develop
a claw appearance, with the fourth and
fifth digits flexed.
• The clinician may note wasting of the
hand intrinsics.
• Froment sign: The patient is unable to
tightly grasp a piece of paper between
the index finger and thumb because of
weakness of the adductor pollicis and
first dorsal interosseous muscles. The
thumb also may flex at the interphalangeal joint because the flexor pollicis
longus activates in an attempt to compensate for the weakness.
• MMT may reveal weakness in any of the
following muscles:
Dorsal interossei
Volar interossei
Abductor digiti minimi
Flexor digitorum profundus
Flexor carpi ulnaris
• To measure flexor carpi ulnaris and
flexor digitorum profundus strength,
ask the patient to cross the third finger
over the fourth finger
• If the neuropathy occurs at the wrist,
there will be weakness of hand intrinsics with the forearm flexors spared,
which generally implies that the compression has occurred at Guyon’s canal.
• Intrinsic weakness with no sensory loss
would imply that the deep branch has
been compressed after the bifurcation
from the superficial sensory branch.
• Sensation: The cutaneous branch of the
ulnar nerve supplies the fifth finger
and the ulnar side of the fourth digit.
Sensation testing should include pinprick, two-point discrimination, tuning
56 of 57
•
•
•
•
fork, and joint position sense and should
be compared for asymmetry with the
unaffected side (where available).
Tinel’s sign may be positive at the elbow
in the ulnar groove or over the cubital
tunnel.
Physical examination should also
exclude pathology in other areas, particularly performing AROM and PROM
at the neck and shoulder, which may
reveal restrictions and central involvement of the nerve.
Upper limb neural tissue provocation
testing may reveal changes in nerve
mobility and elicit symptoms.
Physical examination should also
include movement analysis to determine the movement patterns that the
patient adopts when performing the
aggravating activities. Movement analysis can be done visually or with the
assistance of a video camera. The analysis should give some clues to predisposing factors, such as posture and
patterning, that will assist with rehabilitation and activity modification.
IMPORTANT OBJECTIVE TESTS
• The earliest electrodiagnostic sign of
entrapment is a loss of the nerve action
potential seen during a nerve conduction study.
• To isolate the specific location of the
conduction block, serial stimulations
are delivered to the nerve above and
below the suspected lesion.
• Needle EMG is valuable for evaluating
the extent of motor fiber loss within a
nerve territory. EMG assists with determining the location of the injury and
monitoring progression over time.
• MRI is increasingly being used in the
assessment of peripheral nerve injuries
to rule out cervical nerve root involvement and to determine the presence
of edema, space restriction, or a spaceoccupying lesion along the course of
the ulnar nerve.
• Ultrasonography can detect cysts in
Guyon’s canal.
DIFFERENTIAL
DIAGNOSIS
• Medial epicondylitis
• Thoracic outlet syndrome
• Ulnar artery aneurysms or thrombosis
at the wrist
• Underlying neuropathic disease
• Idiopathic brachial neuritis
• Myopathies
• Muscular dystrophy
• Isolated neuropathy in the diabetic
• Tumors or space-occupying lesions
• Cervical radiculopathy
• Upper motor neuron lesion in the
cerebrum
ORTHOPEDIC PATHOLOGY
AGGRAVATING ACTIVITIES
• Generally, the symptoms are related
to activity and do not follow a typical
24-hour pattern unless there is a strong
inflammatory component such as may
be seen in an occupational repetitive
task.
• If there is an inflammatory component,
there may be worsening of symptoms
with use toward the end of the day and
morning stiffness.
Section III
• Ulnar neuropathies often result in the
following:
Sensory changes in the fourth and
fifth digits: Feelings of tingling, numbness, or burning
Pain rarely occurs in the hand.
Pain tends to be felt farther up the
arm toward the elbow.
Patients rarely notice the specific muscular atrophy, but it may be noticed by
the clinician.
Wartenberg sign: Patient complains
that the little finger gets caught on
the edge of trouser pockets when
attempting to put hands in pockets
(patient cannot pull the fifth finger
tightly against the fourth).
Patient may complain that their grip is
weak.
Pincer grip may also be weak.
Difficulty opening jars or doors
Early fatigue or weakness if work
requires repetitive hand motions.
Numbness and paraesthesias when
resting on elbows
• Cubital tunnel syndrome generallymanifests as follows:
Medial elbow pain
Paraesthesia of the fifth digit and ulnar
side of the fourth digit
Reduced fine motor control and weak
grip
• Neural tension tests may reproduce the
symptoms.
• The severity of complaints can vary
from mild transient paresthesias in
the fourth and fifth fingers to clawing
of these digits, severe intrinsic muscle
atrophy, and severe pain at the elbow
and wrist with radiation into the hand
or up into the shoulder and neck.
24-HOUR SYMPTOM PATTERN
791
792
Ulnar Nerve Entrapment
CHAPTER 16 • NERVE
CONTRIBUTING FACTORS
• Fracture or dislocation of the elbow,
particularly if it results in increasing valgus deformity of the forearm away from
the midline.
• Repetitive throwing action
• Occupations
requiring
significant
elbow flexion throughout the day such
as typing, computer work, or assembly
line work
• Repeatedly leaning heavily on the
elbows, particularly on hard surfaces
• Nerve compressions are more common
in people with arthritis, diabetes, thyroid problems, and alcoholism.
TREATMENT
•
•
•
•
•
•
SURGICAL OPTIONS
• Indications for surgery include the
following:
No improvement in the presenting
symptoms after 6 to 12 weeks of conservative treatment
Progressive palsy or paralysis
Clinical evidence of long-standing
lesion: Clawing of fourth and fifth digits and muscle wasting
• Several surgical options have been
reported to relieve ulnar nerve compression, including the following:
In situ decompression
Medial epicondylectomy with or without decompression
Anterior transposition
Intramuscular transposition
REHABILITATION
• The goals of rehabilitation should be
pain reduction to encourage pain-free
exercise, to provide ergonomic education and interventions, and if the neuropathy has been prolonged, to introduce
cortical reorganization activities.
• Splinting should be used to provide
immobilization to allow the reduction
in swelling and inflammation. Night
splinting in 45 degrees of elbow flexion
•
•
•
•
•
•
with a neutrally rotated forearm can be
used.
Avoid leaning on the elbows.
Eliminate aggravating tasks by avoiding
or modifying those tasks to prevent further damage.
Use ice to reduce inflammation and prevent secondary cell damage.
Theoretically, ultrasound may help
promote nerve regeneration, improve
profusion to the healing nerve, and
decrease inflammation.
Direct low-intensity electrical stimulation has been found to increase the
number of vasa nervorum and nerve
fiber density in rats.
Nerve-gliding exercises have been purported to disperse intraneural edema,
increase blood flow, optimize axonal
transport, and lengthen nerve adhesions. Neural mobilization can be
assessed using the brachial plexus provocation test positions to identify symptom reproduction, and these positions
and movements can also be used both
actively and passively for a treatment
technique.
Use of soft tissue mobilization and muscle stretching techniques to reduce
fibrous bands and adhesions in muscles surrounding the ulnar nerve.
Stretches must not produce tingling or
discomfort because this may indicate
decreased blood flow to the already
stressed nerve.
Motor control and stability functional
rehabilitation exercise for proximal muscles of the trunk, neck, and shoulder
Gradual introduction of strengthening exercises for any muscles that have
been subjected to motor loss
Ergonomic interventions, work place
assessment, or provision of ergonomic
aids, such as tilted keyboards or altered
mouse shape
Cortical reorganization techniques such
as use of mirror box
Reacquisition of fine motor and dexterity skills
57 of 57
PROGNOSIS
• Prognosis depends entirely on the
extent of damage to the nerve.
• Neurapraxia should resolve rapidly and
lead to a complete restoration of function, usually within 2 to 3 months.
• If the injury is a more severe axonotmesis, the recovery time depends on the
distance from the site of injury to the
denervated tissue.
• Peripheral nerves have been reported
to recover at an approximate rate of
between 1 and 4 mm per day, and recovery may not result in a complete restoration of function.
• If there has been a complete sectioning
of the nerve (neurapraxia), a full recovery will not occur.The results of treating
neurapraxia, even with surgical intervention, are generally not satisfactory.
• In chronic palsy, surgical outcome is
less certain and improvement may be
limited.
SIGNS AND SYMPTOMS
INDICATING REFERRAL
TO PHYSICIAN
If ulnar nerve entrapment is suspected,
then all cases should be referred to a physician for appropriate investigation.
SUGGESTED READINGS
Bencardino JT, Rosenberg ZS. Entrapment neuropathies of the shoulder and elbow in the
athlete. Clin Sports Med. 2006;25:465–487.
Berman SA. Ulnar neuropathy. Emedicine.
www.emedicine.com/neuro/topic387.html;
2007.
Izzi J, Dennison D, Noerdlinger M, Dasilva M,
Akelman E. Nerve injuries of the elbow,
wrist, and hand in athletes. Clin Sports Med.
2001;20(1).
Pratt N. Anatomy of nerve entrapment
sites in the upper quarter. J Hand Ther.
2005;18(2):216–229.
Stern M. Ulnar nerve entrapment. Emedicine.
www.emedicine.com/Orthoped/topic574.
html; 2004.
AUTHOR: JOSEPHINE LOUISE COULTER