In this section the emphasis is directed to other entrapment syndromes.

Etiology

The compressed segment is in a specific location on the nerve as determined by the local anatomy, i.e. where the nerve traverses a tunnel bound by bone and fibrous tissue or where the nerve passes from one compartment to another. Changes in the tissue consistency that surrounds the nerve can precipitate entrapment. Trauma with direct injury or callus formation after fracture also has been implicated. Systemic diseases that have been associated with entrapment include hypothyroidism, acromegaly, rheumatoid arthritis, osteoarthritis, giant-cell arteritis, and amyloidosis. An anatomic variant, such as an accessory muscle, arterial aneurysm, or congenitally small tunnel, can precipitate an entrapment neuropathy as well. Compression of the posterior interosseous nerve, for example, has been described with hemihypertrophy and with a lipoma in the region of the elbow. There are cases with compression of the median nerve by a lipoma in the deep palmar space and compression of the ulnar nerve by a schwannoma in the cubital tunnel.

Occupational causes of neuropathy are common. Carpal tunnel syndrome has been reported as an overuse syndrome in persons who employ sign language for the deaf. The carpal tunnel syndrome has been observed in patients with paraparesis who use crutches for walking. Compression of the ulnar nerve in Guyon's canal is seen in cyclists. Compression of the ulnar nerve is legendary in patients who spend long hours leaning their elbows on bars.

The probable cause of entrapment neuropathy is a decrease in the neural blood supply. The nerve receives its blood supply from the mesoneurium, which is flexible and permits continuing perfusion as the extremity moves. Venous obstruction caused by compression increases intrafascicular pressure. This, in turn, decreases perfusion, which leads to edema. A vicious cycle ensues. An ingrowth of fibroblasts and scar ultimately results. This adds to the vicious cycle of worsening hypoxia. Diabetes, which compromises the blood supply, places the nerve at an additional risk of compression and repetitive injury. Compression and atrophy can be so long-standing that end organ fibrosis may result. In this situation, decompression of the nerve will not improve the neurologic symptoms.

The electrodiagnostic findings in any entrapment neuropathy depend on a number of variables including (1) the timing of the study, (2) the severity of the injury, and particularly (3) the relative amounts of demyelination and axonal loss. In the experience of a competent electrodiagnostician, normal findings are rarely identified as abnormal. Conversely, electrodiagnostic evaluations may be inadequate to identify minor injuries to nerves. This situation can occur in proximal demyelinating lesions when conduction studies cannot be obtained above and below the suspected lesion due to technical limitations. In addition, false-negative results or inconclusive results may occur because of premature testing. Complete expression of an abnormality may require up to 7 days for motor nerve conduction. 9- 10 days for sensory conduction, and 3 weeks for needle examination of muscle; however, electrodiagnostic studies are useful to diagnose other syndromes, such as proximal lesions, multiple lesions, or lesions that accompany diabetes mellitus.

Differential Diagnosis

Strict criteria should be used to diagnose entrapment neuropathies. It is regular to see patients with spondylotic myelopathy and radiculopathy who have undergone unnecessary carpal tunnel surgery. The peak age for both conditions is the same, and many of these patients have electrical evidence of carpal tunnel syndrome.

Radiculopathy involving the C8 nerve root can be confused with ulnar neuropathy. When the patient has thenar atrophy as well as involvement of the ulnar nerve, a C8 nerve root lesion should be suspected strongly. A double crush syndrome is when cervical or thoracic outlet compression worsens median or ulnar entrapment. It is unusual for a patient to have more than one lesion. A high index of suspicion, the unique symptoms and physical findings, the results of electrodiagnostic studies, and, when necessary, cervical spine imaging should lead to the correct diagnosis.

Internal Neurolysis

The value of internal neurolysis at the time of decompression has long been debated. Mackinnon and colleagues documented an improved electrical and morphologic recovery with neurolysis compared to decompression alone in a rat model. In a clinical paper, however, Mackinnon and colleagues demonstrated that although neurolysis is a safe procedure, it does not provide clinical benefit in patients who have had carpal tunnel surgery. Neurolysis of a nerve whose diameter is diminished by a circumferentially thickened and scarred epineurium may improve nutrition and permit nerve expansion during healing. Nevertheless, neurolysis is not necessary for all patients undergoing carpal tunnel surgery or with compressed nerves. Performance of internal neurolysis in every carpal tunnel operation courts disaster. The decision on whether or not to perform a neurolysis depends on the observation of the nerve in the operating room. If the nerve remains narrowed after the surgical decompression or if intraneural scarring is present, neurolysis should be done. Patients who present with recurrent symptoms could have neurolysis. After neurolysis, the fascicles, even if atrophic, will be obvious and not hidden in thick epineurium.

Median Nerve

The more proximal median compression syndromes can produce pain, neurologic deficit, or both. The compression can occur above the elbow at the ligament of Struthers or below the elbow by the pronator teres muscle (Figure 1A,B,C).

Fig-1

Entrapment at Ligament of Struthers

The ligament of Struthers, which should not be confused with the arcade of Struthers (which produces ulnar neuropathy), is located 5 cm proximal to the medial epicondyle. The median nerve and brachial artery both pass beneath this ligament. Nerve compression at the ligament of Struthers usually produces a syndrome of pain and local tenderness. The anterior interosseous nerve branch of the median nerve can be compressed at the ligament of Struthers, with resultant motor neuropathy. This phenomenon is unusual. The electrodiagnostic findings demonstrate a reduced or absent median sensory potential. With a predominantly demyelinating lesion, conduction velocity may be slowed across the involved segment with a normal conduction velocity below. Conduction study motor amplitudes will be reduced after axon loss, regardless of the site of stimulation. With demyelination, however, motor amplitudes are abnormal only with stimulation above the site of the lesion. With any amount of axon loss, denervation will be evident in all median innervated muscles of the hand and forearm. Section of the ligament effectively relieves symptoms.

Pronator Syndrome

Radial Nerve

Compression neuropathies of the radial nerve produce clinical syndromes dependent on the level of compression (Figures 3 and 4). The lesion in the proximal arm is rarely spontaneous but is associated with trauma, most commonly fracture of the humerus. "Saturday night palsy" results from compression of the radial nerve when the patient sleeps heavily with the posterior arm resting against a firm edge. The patient presents with wristdrop and an inability to extend the fingers. This condition usually is associated with sensory loss because of the high level of the nerve injury. Of patients who present with radial nerve palsy. 80% recover spontaneously; therefore, exploration is not performed early in most instances. If the palsy is associated with fracture of the humerus, however, early surgery may be appropriate. When the nerve is explored, it should be freed from the bone fragments or callus and reanastomosed when divided.

In patients with demyelinating lesions of the radial nerve at the middle to proximal humerus, results of conduction studies distal to the lesion are normal. Studies performed proximal to the lesion will show a reduced or slowed motor response compared with stimulation distal to the lesion. In patients with axonal lesions, radial motor and sensory amplitudes are reduced and denervation is found in all radial muscles innervated distal to the triceps muscle. Changes on electromyography are not observed until 3 weeks after the injury.

The radial nerve curves around the posterior humerus in the spiral groove and enters the anterior aspect of the arm, 10 cm proximal to the lateral epicondyle, by passing through the lateral intermuscular septum. The radial nerve passes anterior to the radiohumeral joint where it divides into superficial and deep branches. The superficial branch proceeds distally, deep to the brachioradialis muscle, to provide sensation to the dorsum of the first web space in the hand. The deep branch spirals around the neck of the radius, passing between the two heads of the supinator muscle, to enter the posterior aspect of the arm as the posterior interosseous nerve (Figure 4A). The deep branch supplies the extensor muscles of the wrist, hand, and thumb except for the extensor carpi radialis longus muscle, which is innervated by a branch from the radial nerve before it enters the supinator muscle.

Fig-3	Fig-4

Radial Tunnel Syndrome

The clinical syndrome associated with compression of the deep branch of the radial nerve has been called the radial tunnel syndrome. It may be confused with tennis elbow. The radial tunnel syndrome, however, produces a deep somatic ache in the extensor muscles, usually exacerbated by exercise, without sensory or motor symptoms. Four potential sites of compression exist: (1) by fibrous bands anterior to the radial head (Figure 4B), (2) by vessels of the leash of Henry that pass over the radial nerve to supply the brachioradialis muscle, (3) by the tendinous margin of the extensor carpi radialis brevis muscle, and (4) by the arcade of Frohse, which is the sharp ligamentous margin of the superficial head of the supinator muscle (Figure 4C). The latter is the most common site of compression. This sharp edge is not present in the fetus. It is fibrotendinous in 30% of limbs. The arcade of Frohse forms in response to repeated rotary movements of the arm. This syndrome in the dominant arm in 89% of patients. Most patients have a history of repetitive trauma, such as is observed in bricklayers, pipe fitters, machine operators, orchestra conductors, and tennis players. Other causes of compression may be tumor, lipoma, synovial proliferation in rheumatoid arthritis, or fracture of the head of the radius.

Tennis Elbow

In discussing the broad diagnosis of tennis elbow, a range of disorders from lateral epicondylitis to severe extensor weakness, they included the radial tunnel syndrome. On examination, tenderness is present over the lateral epicondyle of the humerus or just distal to the radial head where the nerve travels into the supinator muscle. A typical increase in pain occurs when extension of the middle finger is resisted. This maneuver will tighten the origins of the extensor carpi radialis brevis muscle and further compress the nerve. Injury to the origin of the extensor carpi radialis brevis tendon at the lateral epicondyle is related to epicondylitis-the classic tennis elbow. Local injection with lidocaine and a corticosteroid provides only temporary relief of symptoms.

Results of electrodiagnostic studies may demonstrate delays in motor latencies from the spiral groove to the medial border of the extensor digitorum communis muscle, but they are frequently normal. For patients whose neuropathy does not respond to avoidance of trauma, use of splints, and administration of anti-inflammatory medications, surgical exploration with decompression of the superficial radial nerve is indicated.

Posterior Interosseous Nerve Syndrome

The syndrome of the posterior interosseous nerve differs from the radial tunnel syndrome in that the predominant symptoms and findings are motor rather than pain or sensory loss. The arcade of Frohse is the major constricting structure. Severe weakness of the radial innervated muscles exists with inability to extend the fingers at the metacarpophalangeal joint. The wrist dorsiflexes in a dorsoradial direction because of paralysis of the extensor carpi ulnaris and the extensor digitorum communis muscles. The brachioradialis, extensor carpi radialis longus, extensor carpi radialis brevis, and supinator muscles are not weak because these muscles are innervated by branches that arise before the point at which the radial nerve enters the arcade of Frohse. In this syndrome, pain and local tenderness are followed by progressive motor loss. When sensory loss is present, a more proximal lesion must be considered.

The electrodiagnostic findings of an axonal injury to the posterior interosseous nerve consist of normal radial sensory studies. Normal or reduced amplitude of the radial motor response occurs when recording from a distal radial nerve innervated muscle. Denervation will be found in all radial nerve innervated muscles excluding the triceps, brachioradialis, extensor carpi radialis longus, extensor carpi radialis brevis, and anconeus muscles.

For patients with the posterior interosseous nerve syndrome with significant motor findings, surgical exploration is indicated. For patients with a less severe clinical course, rest, the use of splints, and the administration of anti-inflammatory medications are indicated.

Wartenberg's Syndrome

Wartenberg's syndrome is a rare syndrome that results from the compression of the superficial radial nerve in the forearm. This syndrome is characterized by pain in the proximal forearm and hypoesthesia over the dorsal thumb. No weakness is present. The compression is usually caused by trauma or wearing a tight band or watch. Electrodiagnostic findings of a superficial radial neuropathy consist solely of a diminished or absent radial nerve sensory response.

Suprascapular Nerve Entrapment Neuropathy The suprascapular nerve is a mixed peripheral nerve that provides motor innervation to the supraspinatus and infraspinatus muscles (Figure 5). The nerve has no cutaneous distribution but provides sensory supply to the posterior capsule of the shoulder joint. The syndrome of suprascapular nerve compression includes aching in the posterior aspect of the shoulder with weakness and ultimately atrophy of the muscles involved. Weakness and atrophy produce difficulty in lifting the arm overhead and weakness of external rotation. Wasting of the infraspinatus muscle is obvious because less tissue overlies the infraspinatus muscle. The lack of involvement of the deltoid and rhomboid muscles differentiates this lesion from a C5 nerve root lesion.  nerve. The suprascapular nerve begins as a branch from the upper trunk of the brachial plexus and runs parallel and lies deep to the inferior belly of the omohyoid muscle. It travels deep to the trapezius muscle and through the suprascapular notch into the supraspinous fossa. In the notch the suprascapular ligament compresses the
	Fig-5
The suprascapular artery passes superficial to the ligament. In the supraspinous fossa, the remainder of the nerve curves around the lateral margin of the spine to enter the infraspinous fossa. The suprascapular notch is a continuum between a widely patent notch and a bony foramen. The smaller notch is more likely to be involved with entrapment neuropathy. The sling effect in which the nerve is compressed by the sharp inferior edge of the ligament. Plain roentgenography of the scapula, visualizing the notch, may be helpful in establishing the diagnosis. Repetitive trauma has been implicated in the origin of this neuropathy, although it is observed in patients with isolated trauma, condition in a person who used poorly fitted crutches with excess shoulder depression and an exaggerated swing. Conduction studies of the suprascapular nerve are not accomplished readily. Denervation in the supraspinatus and infraspinatus muscles, sparing the cervical paraspinal, deltoid, and rhomboid muscles. is consistent with this diagnosis. Surgical release of the nerve should be performed early. Relief of pain is prompt, but that motor function returns slower.

Thoracic Outlet Syndrome The thoracic outlet syndrome is a controversial subject. In some institutions, it is diagnosed and treated so often that one would think it constitutes a menace to public health. In other institutions, it is rarely diagnosed. Before the controversy is discussed, the conventionally held views regarding anatomy, symptoms, findings, and treatment are described. The brachial neurovascular bundle goes through the thoracic outlet to enter the arm. The thoracic outlet is divided into the intrascalene triangle, the costoclavicular space, and the subcoracoid tunnel. Most cases of neurovascular compression occur in the first portion by an anomalous first rib or by fibromuscular bands running from the tip of an incomplete rib or a prominent C7 transverse process to the scalene tubercle of the first rib. Other acquired conditions that can compress the brachial plexus should be kept in mind, such as fracture with callus formation, aneurysms of the subclavian artery, and tumors (most commonly a Pancoast tumor). Wilbourn described five clinical syndromes. The first is a major arterial syndrome. This syndrome is associated with a bony anomaly, such as a cervical rib. The arterial wall is damaged and poststenotic dilatation occurs. Thrombus may be found in the vessel, disposing to distal emboli and Reynaud's phenomenon. This condition may constitute a surgical emergency.
	Fig-6
The second is a minor arterial syndrome. Eighty percent of adults reduce or obliterate their radial pulse when they elevate, abduct, and externally rotate their arm. Using photo­plethysmography during provocative tests in normal subjects. Considerable but asymptomatic arterial obstruction in 60% of subjects and bilateral obstruction in 33 % of subjects is noted. The third is the venous obstruction syndrome. Spontaneous thrombosis of the subclavian or axillary vein may be observed in young adults after vigorous repetitive activity of the upper extremity. Cyanosis, swelling, and aching of the limb occur. The brachial plexus is not involved. The classification of this syndrome as a type of a thoracic outlet syndrome may not be correct.  The fourth is the true neurogenic thoracic outlet syndrome. The major component in this syndrome is weakness and wasting of the intrinsic muscles of the hand. This syndrome is also associated with intermittent aching in the medial forearm and is the only widely accepted thoracic outlet syndrome. The pathologic finding is usually the fibrous band from a rudimentary cervical rib to the first rib that compresses the lower trunk of the brachial plexus. In 75 % of patients, all of the intrinsic muscles are weak and wasted. The thenar muscles are most severely wasted because the lower trunk plexopathy most severely affects median nerve fibers to the thenar eminence. Rarely will a patient with true neurogenic thoracic outlet syndrome have reduced ulnar sensory amplitude as well as reduced median and ulnar motor amplitude on the affected side. Median, ulnar, and radial nerve innervated muscles, which are also innervated by the lower trunk and medial cord of the brachial plexus, will be denervated. Treatment is surgical removal of the offending band, The prognosis for the wasted muscle of the hand is poor. The last group is termed by Wilbourn, as the "disputed neurogenic thoracic outlet syndrome." Most operations are performed for this group. Wilbourn, believes that the criteria for surgery are usually broad and poorly defined. This pain syndrome is without anatomic or physiologic changes. No objective clinical or laboratory findings exist. Results of electrodiagnostic studies are normal. No evidence is present to suggest that serious neural compression will occur if the condition is not treated. The incidence of documented neurosis and litigation is high in this group of patients. A moratorium should be placed on surgery for patients with the disputed thoracic outlet syndrome; a significant complication rate associated with the operation. Postoperative evaluations by an independent neurologist reported persistence of symptoms in the face of the surgeon's report of excellent results. In the thoracic outlet syndrome, as well as in the other entrapment neuropathies, careful evaluation of the history and physical examination and results of electrodiagnostic studies should permit proper selection of patients for treatment and performance of the appropriate surgical procedures.