I. Peripheral Nerve Anatomy and Physiology
A. Connective tissue sheaths
1. Epineurium
a. The external epineurium is the outer layer of the peripheral nerve that provides supportive and protective framework.
b. The internal epineurium surrounds individual fascicles, cushions against external pressure, and allows longitudinal excursion. It has a well-developed vascular plexus with channels feeding endoneurial plexus. Along the nerve path, there are larger amounts of this layer at the level of joints.
2. Perineurium
a. Thin sheath with high tensile strength that surrounds each fascicle and acts as the blood-nerve barrier (ie, the extension of blood-brain barrier)
b. Composed of layers with flattened mesothelial cells, with tight junctions that act as a bidirectional barrier to diffusion
3. Endoneurium—Loose collagenous matrix that surrounds individual nerve fibers.
B. Fascicles
1. Groups of axons packed with endoneurial connective tissue
2. Smallest unit of the nerve that can be surgically manipulated
3. Form variable plexuses that are not simply parallel; structure changes rapidly and often along the length of a major nerve, with a maximal unaltered segment of 15 to 20 mm
C. Blood supply
1. Well-developed intraneural microvascular plexi
2. Both intrinsic and extrinsic segmental, longitudinal vessels run in the loose connective tissue surrounding the nerve.
D. Axoplasmic/axonal transport
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1. |
The neuron is a polarized cell with several intracellular transport systems that are adenosine triphosphate-dependent. |
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2. |
Transport of molecules from the cell body toward the terminus is known as anterograde transport; there are both slow and fast anterograde transport mechanisms, which are dependent on the carrier protein kinesin. |
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3. |
Retrograde transport allows the recycle of proteins (empty neurotransmitter vesicles) at one half to one third the rate of fast anterograde transport and relies on the carrier protein dynein. a. This transport mechanism picks up signals from the environment (eg, chromatolysis after axotomy). b. Herpes simplex virus, polio, rabies, and tetanus are transported by this mechanism. |
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5. |
Axonal transport mechanisms are altered with diabetes and acute myelogenous leukemia. |
E. Myelin—70% lipid and 30% protein.
F. Resting membrane potential and action potential
1. An electric potential difference exists between the two sides of the plasma membrane (PM), with the interior of the cell having a resting potential due to unequal distribution of monovalent ions that cannot cross the PM.
a. The resting potential is maintained with the Na+/K+ pump between 50 and 80 mV.
b. The inside of the neuronal cell is negative relative to outside the cell.
2. Action potential permits message transmission rapidly over long distances.
3. Depolarization occurs when the graded potentials summate beyond the threshold.
II. Basic Science of Nerve Compression
A. Schwann cell response—Dramatic Schwann cell response occurs early after chronic nerve compression injury. The response includes the following processes:
1. Schwann cell proliferation
2. Schwann cell apoptosis
3. Downregulation of promyelinogenic genes, including myelin-associated glycoprotein and myelin basic protein
4. Upregulation of proangiogenic molecules—vascular endothelial growth factor
5. Altered myelination with changes in internodal length and occurrence of Schmidt-Lanterman incisures
B. Macrophage recruitment
1. Occurs slowly and gradually
2. Increased upregulation of inducible nitric oxide synthase (iNOS)
3. Responsible for gradual change in the blood-nerve barrier
C. Axonal loss or degeneration—No axonal loss or degeneration early in disease course when there are dramatic cellular and molecular changes occurring.
D. Myelin stabilization—Myelin probably needs to be stabilized to prevent the ensuing pathologic changes with chronic nerve compression injury.
III. Electrophysiology
A. General information
1. Nerve conduction velocity (NCV) studies and electromyography (EMG) are used to evaluate the function of skeletal muscle and of motor and sensory nerves.
2. Differentiate between lower and upper motor neuron lesions and ventral horn motor neuron dysfunction versus peripheral lesion
3. Identify involved muscles to determine level and degree of dysfunction
4. Demonstrate muscle denervation, reinnervation, aberrant reinnervation, localized peripheral nerve lesions, and disturbances of neurotransmission at the motor end plate
5. There is growing evidence that standard NCV studies and EMG cannot detect pathology at early stages of disease because these tests evaluate only the large myelinated fibers, and the small- to medium-sized fibers are affected early.
B. NCV studies
1. Evaluate large myelinated fibers and can determine the presence and severity of peripheral nerve dysfunction, its localization, distribution, and pathophysiology (axonal degeneration versus axonal demyelination)
2. Stimulation and recording techniques—Electrical activity may be recorded extracellularly from muscle or nerve using surface electrodes.
3. Stimulus artifact—Deflection from baseline due to direct conduction of the stimulus.
4. Standard stimulus—A 0.1- to 0.2-ms square wave pulse at slow repetitive stimulation rate of 1 to 2 per second. The intensity is increased to maximal response and then increased further for maximal recruitment.
5. Motor nerve conduction—Nerve supramaximally stimulated at superficial location with distal response from a muscle.
a. Compound muscle action potential (CMAP)/evoked motor response is the sum of the action potentials of the individual muscle fibers.
b. Latency—Time (in ms) from the application of the stimulus to the initial deflection from the baseline.
i. Onset latency includes time from site of stimulation, plus time to activate postsynaptic terminal (neuromuscular transmission time), plus time for the action potential to propagate along the muscle membrane to recording potential.
ii. Conduction velocity (CV) = distance (mm) between proximal and distal stimulating sites/[proximal latency (ms) - distal latency].
c. CV for myelinated axons is influenced by myelin thickness, internode distance, age, and temperature.
d. CVs in newborns are 50% of adult values; they increase to 75% by 12 months of age, and 100% by 4 to 5 years of age.
e. Amplitude of CMAP—Measured from baseline to the negative peak (unit: mV). With supramaximal stimulation, the area under the negative peak is directly proportional to the number of muscle fibers depolarized. Both provide an estimate of amount of functioning axons and muscles.
f. Duration—Reflection of the range of CVs and the synchrony of contraction of the muscle fibers. If there are axons with different CVs, duration will be greater (as occurs in acute demyelinating diseases).
6. Sensory nerve conduction—Sensory potentials are unaffected by lesions proximal to the dorsal root ganglion (DRG) even if there is a sensory loss.
a. Useful to detect pathology proximal (root or spinal cord) or distal (plexus or nerve) to DRG
b. Smaller amplitude than CMAP
c. Larger distances increase dispersion and decrease amplitude.
d. CV same for orthodromic and antidromic stimulation.
C. EMG—Used to study the electrical activity of individual muscle fibers and motor units.
1. Can help determine whether the origin of the lesion is neural, muscular, or junctional
2. Can determine whether there is insertional or spontaneous activity
a. Insertional activity
i. >300 to 500 ms reflects early denervation, as with polymyositis, myotonic disorders, or myopathies.
ii. Reduction in insertional activity may occur after prolonged denervation has replaced the muscle fibers with connective tissue and fibrosis.
3. Spontaneous activity
a. The only normal spontaneous activities are the end plate potentials and the end plate spikes.
b. Pathologic spontaneous activity includes fibrillation potentials, positive sharp waves, fasciculation potentials, myokimic discharges, and complex repetitive discharges.
4. Fibrillations
a. Action potentials that arise spontaneously from single muscle fibers caused by oscillations in the resting membrane potential of denervated fibers
b. Positive sharp waves and fibrillations do not appear for 3 to 5 weeks after the nerve lesion and stay until the lesion is resolved or the muscle becomes fibrotic.
c. May also appear with first-degree muscle disorders (disorders where the muscle tissue itself and not its neural supply is abnormal), such as muscular dystrophy
5. Fasciculation potentials—Caused by spontaneous discharge of group of muscle fibers within the muscle.
a. Common with amyotrophic lateral sclerosis, progressive spinal muscle atrophy, and degenerative diseases of the anterior horn such as polio and syringomyelia
b. Seen on physical examination as "undulating bag of worms"-type involuntary muscle discharges
IV. Common Compression Neuropathies
A. History and epidemiology
1. Documented intrinsic risk factors include female sex, pregnancy, diabetes, hypothyroidism, and rheumatoid arthritis.
2. Other factors include advanced age and mucopolysaccharidosis or mucolipidosis.
B. Physical examination—Conducted to evaluate the motor and sensory distribution of the affected areas.
1. Motor
a. Muscle strength graded on a scale from 1 to 5.
b. Mild compression yields no motor dysfunction.
c. Moderate compression produces muscle weakness.
d. Severe compression results in denervation and muscle wasting.
2. Sensory
a. Threshold testing for compression injury includes Semmes-Weinstein monofilament testing and vibrometer or a 256-Hz tuning fork.
b. Most sensitive physical examination test for carpal tunnel syndrome is carpal compression test (altered sensation/pain in the area distal to the site of compression).
c. Other tests include Tinel sign (percussion directly over the nerve) and the Phalen maneuver (wrist flexion).
C. Carpal tunnel syndrome (median nerve compression at the wrist)
1. Overview
a. Canal is defined by the scaphoid tubercle and trapezium radially, the hook of the hamate and the pisiform ulnarly, and the transverse carpal ligament palmarly (the roof). It contains nine flexor tendons: the flexor pollicis longus (FPL), the flexor digitorum sublimis (FDS) tendons, and the flexor digitorum profundus (FDP) tendons.
b. Normal carpal pressure is 2.5 mm Hg at rest (wrist in neutral and fingers in full extension) to 30 mm Hg with wrist flexion; with carpal tunnel syndrome, resting pressure is 30 mm Hg with 90 to 110 mm Hg at flexion/extension.
2. Potential etiologies—Congenital anomalies (persistent median artery, proximal lumbrical muscles, etc), fluid abnormalities (pregnancy and obstructive cholestasis during pregnancy), flexortenosynovitis, malunion of distal radius, and certain occupational activities.
3. Pathoanatomy—Synovial biopsy from the carpal canal from idiopathic carpal tunnel syndrome shows fibrous tissue and variable edema with scattered lymphocytes.
4. Signs and symptoms
a. Pain and paresthesias of the palm involving the wrist and/or palmar aspect of the thumb, index finger, long finger, and the radial half of the ring finger
b. Feelings of clumsiness, weakness, night pain, and hypesthesia are also possible.
c. Long-standing disease will lead to thenar atrophy.
d. Provocative maneuvers include the Tinel sign (percussion over the nerve that produces electric sensation distally in the distribution of the nerve) and a positive Phalen maneuver (wrist flexion with the elbow in extension for up to 60 seconds produces paresthesias).
e. The most sensitive maneuver is the carpal compression test, in which direct compression for 60 seconds over the volar aspect of the forearm at the level of or slightly proximal to the wrist crease elicits distal paresthesias; sensation along the radial aspect of the palm should be normal because the palmar cutaneous branch of the median nerve does not travel within the carpal canal.
5. Electrophysiologic changes
a. Distal motor latency >4.0 ms or asymmetry of 1.0 ms between hands
b. Distal sensory latency >3.5 ms or asymmetry of 0.5 ms between hands
c. Amplitude <20 μm and end stage has fibrillation potentials and positive sharp waves in the thenar muscles
6. Treatment
a. Includes nonsteroidal anti-inflammatory drugs (NSAIDs) and a static splint to maintain the wrist in neutral, especially when the EMG/NCV study results are negative
b. Steroid injections are controversial; can provide relief if short duration of symptoms. If no improvement following steroid injection, then carpal tunnel release may not be as effective.
c. Surgery
i. Open or endoscopic release
ii. Potential advantage of endoscopic treatment is reduced likelihood of postoperative pillar pain; potential disadvantage is the higher risk of complications during the early portion of the learning curve for the surgeon.
iii. Incomplete release of transverse carpal ligament is the most common reason for persistent symptoms following surgery, especially with endoscopic carpal tunnel release.
iv. Complications after endoscopic carpal tunnel release may include ulnar nerve injury, common digital nerve laceration, or laceration of the superficial arch.
D. Proximal median nerve entrapment
1. Overview
a. C5-T1 nerve root involvement, which in the forearm supplies the pronator teres (PT), flexor carpi radialis, palmaris longus (PL), FDS, and the radial half of the FDP
b. Martin-Gruber connections are anomalies in which the median and ulnar nerves communicate in the proximal forearm. There are four patterns:
i. Median 
ulnar median muscles of the hand
ii. Median ulnar ulnar muscles of the hand
iii. Ulnar median median muscles of the hand
iv. Ulnar median ulnar muscles of the hand
2. Possible causes of compression include the ligament of Struthers, which connects the supracondylar process of the distal humerus with the medial epicondyle, humerus fractures, and muscle anomalies.
3. Pronator syndrome—Potential sites of compression include the lacertus fibrosus, PT, ligament of Struthers, proximal arch on the undersurface of the FDS, and arcade of vessels.
a. Signs and symptoms—Pain and tenderness in the volar aspect of the forearm, activity-induced paresthesias, and hyperesthesias in the thumb, index finger, and radial side of the ring finger. May have Tinel sign, muscle weakness, and positive compression test. Pain provoked by full elbow flexion against resistance (lacertus fibrosus as the offending structure), resistive forearm pronation (PT is the offending structure), resistive digital flexion of the middle finger (FDS is the offending structure). EMG/NCV study results are often inconclusive.
b. Treatment includes splinting, NSAIDs, and avoidance of forearm rotation. Surgery includes curved incision at the proximal forearm and the release of all four potential sites of compression.
4. Anterior interosseous nerve compression syndrome—Motor nerve that branches from the median nerve 4 to 6 cm distal to the elbow, supplying the radial half of the FDP, the FPL, and the pronator quadratus.
a. Signs and symptoms—Ill-defined forearm pain, inability to make a circle with index finger and thumb ("O" sign), weakness of pronation with elbow flexion (
Figure 1). May occur spontaneously or after repetitive motion. EMG may show denervation of FPL, pronator quadratus.
b. Possible etiologies—Nerve may be compressed by the deep head of the PT, the origin of the FDS, the flexor carpi radialis, accessory muscles that connect the FDS to the FDP, or the Gantzer muscle (accessory head of the FPL).
c. Surgical treatment is indicated if motor function does not recover after 3 months. Treatment includes release of superficial arch of FDS, lacertus fibrosus, detachment of superficial head of PT, ligation of any crossing vessels, and removal of any potential space-occupying lesions.
E. Cubital tunnel syndrome
1. Overview
a. The ulnar nerve (C8-T1) originates from the medial cord of the brachial plexus. It supplies the flexor carpi ulnaris, the ulnar half of the FDP in the forearm, the two ulnar lumbricals, all dorsal and palmar interossei, the adductor pollicis, the deep head of the flexor pollicis brevis, and the hypothenar musculature.
b. Cutaneous branches include the palmar branch for hypothenar skin and a dorsal branch for the dorsoulnar side of the hand and ulnar two digits (crosses palmar-dorsal distal to the ulnar styloid).
c. Volume of canal maximum in extension to 45° flexion and decreases by 50% with flexion as the canal changes from oval to slit-like.
2. Potential sites of compression: arcade of Struthers (medial intermuscular septum), medial epicondyle, roof of cubital tunnel (arcuate ligament), Osborne fascia (proximal fascial band between the two heads of the flexor carpi ulnaris), proximal flexor profundus arch
3. Possible etiologies: repetitive use of vibrating tools, playing musical instruments, tourniquet use, intra-operative malpositioning, cubitus varus and valgus deformity, adhesions, burns and heterotopic ossification, space-occupying lesions (ganglion, lipoma, osteochondroma), and arthritis
[Figure 1. Clinical photograph of a patient with anterior interosseous nerve compression or paralysis. Note the inability to flex at the interphalangeal joint of the thumb and the distal interphalangeal joint of the index finger.]
4. Signs and symptoms
a. Paresthesias, night pain, pain; all exacerbated with elbow flexion and shoulder abduction
b. Abducted little finger (Wartenberg sign) with an ulnar nerve injury proximal to wrist, due to unopposed pull of the extensor digiti minimi and weakness of the third palmar interosseous
c. NCV studies show slowing across the elbow, low amplitudes of sensory nerve action potential, and CMAP.
d. Thumb interphalangeal (IP) flexion during attempted key pinch (Froment sign) and thumb metacarpophalangeal hyperextension laxity during attempted key pinch (Jeanne sign) is sometimes seen.
5. Differential diagnosis—Includes C8 or T1 radiculopathy, thoracic outlet syndrome, Pancoast tumor, and double crush syndrome.
6. Treatment includes NSAIDs and night elbow extension splinting.
7. Surgery options
a. Ulnar nerve release from cubital tunnel
b. Medial epicondylectomy
c. Anterior transposition procedures, including subcutaneous, submuscular, and intramuscular transposition. Anterior transposition is believed to improve oxygen supply to the nerve by improving intrinsic intraneural circulation.
[
Figure 2. Intraoperative photograph showing a ganglion in the ulnar tunnel causing isolated compression of the motor branch of the ulnar nerve.]
The medial antebrachial cutaneous nerve is at risk.
F. Ulnar nerve entrapment at wrist (Guyon canal)
1. Canal is defined by the flexor retinaculum and the muscles of the hypothenar eminence as the floor of the canal, the pisiform and the pisohamate ligament as the ulnar boundary, the hook of the hamate as the radial border of the canal, and the roof of the canal as the fibrous arcade that connects the hook of the hamate and the pisiform (the volar carpal ligament).
2. The ulnar nerve divides into the superficial sensory and the deep motor branches within the canal.
a. Zone I is the area proximal to the bifurcation of the nerve.
b. Zone II includes the deep motor branch to just beyond the fibrous arch of the hypothenar muscles.
c. Zone III involves only the superficial branch or the sensory component.
3. The deep motor branch supplies the intrinsics, including the flexor pollicis brevis, except the remaining thenar muscles and the radial two lumbricals.
4. Etiology
a. May be space-occupying lesions (ganglion, lipoma in zone I or II), repeated trauma, ulnar artery thrombosis or aneurysm (zone III), hook of the hamate fracture, pisiform dislocation, inflammatory arthritis, fibrous band, congenital bands, or bony anomalies (Figure 2).
b. Allen test and Doppler studies are helpful for diagnosis of arterial issues; CT scans are helpful to evaluate hook of the hamate fractures.
5. Signs and symptoms
a. Clawing of ring and little fingers, Froment sign (flexion of the IP joint rather than adduction of thumb when holding a piece of paper), Wartenberg sign (abduction posture of little finger).
b. Rare to have pronounced clawing with cubital tunnel syndrome; to differentiate between the two, cubital tunnel syndrome has sensory deficit on the dorsum of the hand, motor deficit of the extrinsic ulnar-innervated muscles, Tinel sign at the elbow, and positive elbow flexion test.
c. Symptoms vary based on the site of compression with zones I through III. If the deep ulnar motor nerve is compressed, the patient will have normal hypothenar muscle function and weak function of the first dorsal interosseous.
6. Treatment
a. Nonsurgical—Wearing padded gloves, avoidance of offending provocative actions, splinting, and NSAIDs.
b. Surgery—Release of the hypothenar muscle origin, removal of any space-occupying lesions, and exploration of the entire ulnar nerve in the canal.
V. Radial Nerve Compression Syndromes
A. Anatomy
1. Radial nerve (C5-8) supplies triceps, brachioradialis, extensor carpi radialis longus (ECRL), anconeous, and radial half of brachialis.
2. Posterior interosseous nerve supplies the supinator, extensor carpi radialis brevis (ECRB), extensor digitorum communis, abductor pollicis longus, extensor indicis proprius, and extensor pollicis longus.
B. Proximal compression
1. Etiologies—Humerus fracture, tourniquet palsy, or prolonged postural compression.
2. Signs and symptoms—Weakness of elbow extension and forearm supination, loss of wrist/digit/thumb extension.
3. Treatment—Recovery is usually spontaneous; if no recovery by 3 to 4 months, neurolysis, nerve grafting, or tendon transfers should be considered.
C. Compression at the elbow—Radial nerve divides proximal to the elbow with direct branches to the ECRL, brachioradialis, and occasionally ECRB; the nerve divides into a superficial sensory branch and the posterior interosseous nerve.
1. Posterior interosseous nerve (PIN) compression syndrome
a. Etiologies—May be idiopathic or result from repetitive forearm motion, Monteggia fracture-dislocation, radial head fracture-dislocations, synovitis, blunt trauma, or space-occupying lesions (lipoma or ganglion). Offending anatomic structures include the proximal edge of the supinator (arcade of Frohse), fibrous edge of ECRB, the arcade of vessels from the radial recurrent artery (leash of Henry), and fibrous bands.
b. Signs and symptoms—Patient presents most often with weakness and pain and difficulty extending the metacarpophalangeal joints of the fingers and thumb because the posterior interosseous nerve innervates the ECRB, supinator, extensor carpi ulnaris, extensor digitorum communis, extensor indicis proprius, extensor digiti quinti, abductor pollicis longus, extensor pollicis longus, and extensor pollicis brevis. No sensory changes because the posterior interosseous is a pure motor nerve. Wrist extension occurs with ERCL (no ECRB or extensor carpi ulnaris), so radial deviation occurs with wrist extension; must differentiate between PIN compression and tendon rupture in rheumatoid patients (in the latter, the tenodesis effect is lost).
c. Treatment—Initial treatment is nonsurgical and includes splinting and avoidance of provocative behavior. This may be followed by decompression of the arcade of Frohse, release of the distal edge of the supinator, release of the fibrous edge of the ECRB, ligation of the arcade of vessels from the radial recurrent artery (leash of Henry), and release of fibrous bands superficial to the radiocapitellar joint. Patients may continue to improve for up to 18 months postoperatively.
2. Radial tunnel syndrome
a. Etiologies—Same structures may be responsible as for posterior interosseous neuropathy, but no muscle paralysis is seen on physical examination.
b. Signs and symptoms—Deep, aching pain in the dorsoradial forearm that radiates from the lateral elbow to the dorsal aspect of the wrist. Physical examination reveals tenderness in the mobile wad over the supinator arch, paresthesias in the dorsal first web space, pain with resistive supination with the arm and wrist in extension, and pain with passive pronation with wrist flexion.
c. Diagnosis—EMG/NCV study results are inconclusive. The diagnosis may be made with injection. The primary differential diagnosis is lateral epicondylitis, but the two conditions often coexist.
d. Treatment—Similar to posterior interosseous neuropathy.
D. Compression at the wrist
1. Definition—Sensory radial nerve compression (Wartenberg sign or cheiralgia).
2. Etiology—Often caused by direct blows, handcuffs, tight cast, external fixator pins, or tight watchband. Fascia between brachioradialis and ECRL tendons may compress the nerve; repetitive wrist flexion and ulnar deviation may exacerbate the symptoms.
3. Signs and symptoms—Paresthesias in the dorsoradial aspect of the hand with ill-defined pain in the forearm and wrist.
4. Diagnosis—Diagnostic wrist block may temporarily relieve the pain. Must differentiate from de Quervain tenosynovitis or intersection syndrome.
5. Treatment—Includes wrist splint, avoidance of offending activities, and, rarely, surgery. When performed, surgery involves a longitudinal incision, neurolysis, and release of fascia between the brachioradialis and the ECRL.
VI. Thoracic Outlet Syndrome
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A. |
Anatomy—The cervicothoracobrachial passage consists of an interscalene triangle, costoclavicular space, and coracopectoral tunnel. |
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B. |
Possible etiologies—The following may cause compression: cervical rib, vertebral transverse process, anomalous insertion of the scalenes, fibromuscular bands, clavicular and first rib malunion, repetitive shoulder use, and certain athletic activities including weightlifting, rowing, and swimming. |
|
C. |
Signs and symptoms 1. Vascular symptoms—arterial ischemia, venous congestion, and Raynaud phenomenon 2. Neurologic symptoms a. Sensory and motor dysfunction b. Upper plexus involves C5-C7 and localized to the lateral arm, occiput, and scapula. c. Lower plexus C8-T1 syndrome localized to scapular, axillary, medial arm, and forearm areas. |
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D. |
Incidence—More common in women. |
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E. |
Symptoms and clinical diagnosis 1. Vague symptoms with equivocal EMG/NCV studies. 2. Diagnosis often made with positive provocative tests including Adson, hyperabduction, and costoclavicular maneuvers 3. Noninvasive vascular studies and angiography identify the vascular form of thoracic outlet syndrome. |
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G. |
Treatment 1. Initial treatment includes activity modification and physical therapy to strengthen the shoulder girdle muscles. 2. If intractable pain, neurologic deficit, or persistent vascular insufficiency is present, surgery is an option; procedures include scalenotomy, scalenectomy, and excision of cervical or first rib (through transaxillary approach). |
VII. Neuropathies of the Shoulder
A. Suprascapular nerve entrapment
1. C5-C6 nerve roots take almost a direct course across the posterior triangle of the nerve to supply the supraspinatus and infraspinatus muscles.
2. Pathology may result from fractures, blunt trauma, traction lesions, repetitive motion with resistive exercise, or encroachment from space-occupying lesions (eg, ganglia) at either the suprascapular notch or the spinoglenoid notch.
3. The suprascapular nerve passes through the suprascapular notch below the superior transverse scapular ligament, and the suprascapular artery (branch of the thyrocervical trunk of the subclavian artery) passes above the ligament.
4. If the nerve is entrapped at the spinoglenoid notch, only the infraspinatus is affected.
5. Signs and symptoms include posterior lateral shoulder pain, suprascapular notch tenderness, muscle weakness of shoulder external rotation, and abduction.
6. Treatment
a. Nonsurgical treatment includes muscle strengthening.
b. Surgery involves releasing the suprascapular notch using a posterior approach and enlarging the bony notch.
B. Musculocutaneous nerve compression (C5-C7)
1. Overview—Originates from the lateral cord and supplies the coracobrachialis, biceps brachii, half of the brachialis, and the sensory aspect of the lateral antebrachial cutaneous nerve.
2. Etiologies—May be compressed within the substance of the coracobrachialis secondary to shoulder dislocation, after surgical procedures (most frequently injured with shoulder surgical approach), and, rarely, distally, where the nerve emerges from the biceps tendon.
3. Signs and symptoms—Weakness of elbow flexion, muscle weakness, tenderness, and lateral arm hypesthesias.
4. Treatment—Usually nonsurgical; surgery to release the nerve is necessary only very rarely.
C. Long thoracic nerve entrapment (C5-C7)
1. Overview—The long thoracic nerve is susceptible to traction injuries with shoulder depression, direct blow, or prolonged hyperabduction of the arms with elbows flexed. This nerve supplies the serratus anterior (maintains scapula position) and assists the trapezius with shoulder elevation.
2. Signs and symptoms—Patients present with dull shoulder pain, weakness, scapular winging when arms push against resistance, and pain with arm elevation.
3. Treatment—Recovery is usually spontaneous with bracing. Rarely, requires pectoralis major transfer.
D. Spinal accessory nerve palsy
1. Definition—Condition affecting the cranial nerve that supplies the sternocleidomastoid and the trapezius.
2. Etiologies—Injury caused by direct blow, wrestling accident, acromioclavicular dislocations, iatrogenic injury after radical neck dissection, and heavy loads applied to the shoulder.
3. Symptoms—Feelings of heaviness in the arms, dull shoulder pain, trapezius muscle atrophy, drooping shoulder girdle, lateral displacement of the scapula.
4. Treatment—Usually resolves spontaneously unless the etiology is a postsurgical palsy, which may require neurolysis, nerve repair, or grafting. If the condition has been present for an extended period of time, scapula may be stabilized with fascia lata to the ribs or spinal processes, or the rhomboids and levator muscles may be transferred laterally into the scapula.
E. Axillary nerve compression (quadrilateral space syndrome)
1. Definition—Compression of nerve and posterior circumflex humeral artery. This nerve supplies the teres minor and deltoid muscles.
2. Etiologies—May be idiopathic or traumatic (most commonly following anterior glenohumeral dislocation), or may occur in throwing athletes.
3. Signs and symptoms—May present as shoulder pain, paresthesias in the arm, point tenderness over the quadrilateral space. Provocative pain and paresthesias with shoulder abduction, elevation, and external rotation for 1 minute.
4. Diagnosis—Angiography demonstrates arterial occlusion when shoulder abducted beyond 60°.
5. Treatment—Includes avoidance of provocative maneuvers and surgical release of the teres minor and transverse fibrous bands.
Top Testing Facts
1. Sensory potentials are unaffected by lesions proximal to the dorsal root ganglion even if there is a sensory loss.
2. Positive sharp waves and fibrillations do not appear for 3 to 5 weeks after a nerve lesion, and they remain until the lesion is resolved or the muscle becomes fibrotic. May also appear with first-degree muscle disorders such as muscular dystrophy.
3. Fasciculation potentials are caused by the spontaneous discharge of groups of muscle fibers within the muscle and are common with amyotrophic lateral sclerosis, progressive spinal muscle atrophy, and degenerative diseases of the anterior horn such as poliomyelitis and syringomyelia.
4. The most sensitive physical examination test for carpal tunnel syndrome is the carpal compression test (altered sensation/pain in the area distal to the site of compression).
5. Martin-Gruber connections are median-to-ulnar motor interconnections in the proximal forearm that innervate the median (most common) or ulnar muscles in the hand.
6. Complications after endoscopic carpal tunnel release may include ulnar nerve injury, common digital nerve laceration, or laceration of the superficial arch.
7. Ulnar nerve entrapment at the wrist (Guyon canal) may be caused by space-occupying lesions (ganglion, lipoma in zone I or II), repeated trauma, ulnar artery thrombosis or aneurysm (zone III), hook of the hamate fracture, pisiform dislocation, inflammatory arthritis, fibrous band, congenital bands, or bony anomalies.
8. Posterior interosseous nerve compression syndrome may be idiopathic or result from repetitive forearm motion, Monteggia fracture-dislocation, radial head fracture-dislocations, blunt trauma, or space-occupying lesions (lipoma or ganglion).
9. The same anatomic structures may be responsible for radial tunnel syndrome as for posterior interosseous neuropathy, but in patients with radial tunnel syndrome, no muscle paralysis is seen on physical examination.
10. If the suprascapular nerve is entrapped at the spinoglenoid notch, only the infraspinatus is affected.
Bibliography
Brown RA, Gelberman RH, Seiler JG III, et al: Carpal tunnel release: A prospective, randomized assessment of open and endoscopic methods. J Bone Joint Surg Am 1993;75:1265-1275.
Gelberman RH, Aronson D, Weisman MH: Carpal-tunnel syndrome: Results of a prospective trial of steroid injection and splinting. J Bone Joint Surg Am 1980;62:1181-1184.
Gelberman RH, Eaton RG, Urbaniak JR: Peripheral nerve compression. Instr Course Lect 1994;43:31-53.
Gelberman RH, Pfeffer GB, Galbraith RT, Szabo RM, Rydevik B, Dimick M: Results of treatment of severe carpal-tunnel syndrome without internal neurolysis of the median nerve. J Bone Joint Surg Am1987;69:896-903.