Compressed segment of nerve is in a specific location 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 oedema. 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.
Strict criteria should be used to diagnose entrapment neuropathies. In many cases, the patients having 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 in which cervical or thoracic outlet compression can overlap with 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.
The value of internal neurolysis at the time of decompression still in debate. 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. Phalen stated that performance of internal neurolysis in every carpal tunnel operation courts disaster. Peimer who favours neurolysis, believes that it is important to evaluate the intraneural pathologic findings. 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 should have neurolysis. After neurolysis, the fascicles, even if atrophic, will be obvious and not hidden in thick epineurium. I am in full agreement with Phalen, that neurolysis during carpal tunnel release, even contraindicated in simple compression, because the fascicles will be later exposed to further scar formation and subsequently lesser degree of improvement. Even, if the nerve is hypotrophied, then neurolysis will only increase the surgical trauma. This manoeuvre must be kept to certain cases, when a mass is suspected inside the 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.
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.
The pronator syndrome is characterized by mild to moderate pain in the forearm. The pain increases with movement of the elbow, with repeated supination and pronation, and with repeated use of the grip. Loss of dexterity in the hand, mild weakness, and median nerve paresthesia occur. Numbness may be present, not only in the fingers, but also in the thenar region of the palm because of involvement of the palmar cutaneous nerve that branches distal to the site of compression. These symptoms resemble carpal tunnel syndrome, but the symptoms of paresthesia while sleeping are absent. The pain in the forearm and the local tenderness can be reproduced by resisted pronation. Tinel's sign may be present over the nerve. The anatomic level of compression is within the substance of the pronator teres muscle. The median nerve with the brachial artery lies between the two heads of the pronator teres and passes deep to the fibrous origin of the flexor digitorum superficialis muscle. Compression may be caused by the thickened lacertus fibrosus, by a hypertrophied pronator muscle, or by a tight fibrous band of the flexor digitorum superficialis muscle. Results of electrodiagnostic studies are often normal. When results are abnormal, they parallel the findings in patients with the ligament of Struthers syndrome except that no denervation is present in the pronator teres muscle.
Treatment of patients with the pronator syndrome is initially conservative with administration of anti-inflammatory medication and use of splints. An attempt is made to eliminate precipitating events. Should these measures be ineffective, surgery should provide good results. The lacertus fibrosus is released and the median nerve is translocated to a subcutaneous position anterior to the pronator teres muscle. The nerve should be exposed from the distal upper arm to the middle forearm. The median nerve and its major branches should be visualized. Care should be taken to preserve the branches of the medial cutaneous nerve of the forearm. Injury to this nerve can produce a painful neuroma.
Anterior Interosseous Nerve Syndrome
The anterior interosseous nerve separates from the main median nerve approximately 8 cm distal to the lateral epicondyle. It gives off a sensory branch to the wrist joint and provides motor innervation to the flexor pollicis longus muscle, the flexor digitorum profundus muscle of the index and middle fingers, and the pronator quadratus muscles. The site of compression is slightly more distal in the mass of the pronator teres muscle than that for the pronator syndrome. The compression is caused by the tendinous origin of the deep head of the pronator teres muscle, which crosses the anterior interosseous nerve at its origin from the parent median nerve. An enlarged bicipital bursa has also been described as the causative agent. Whereas pain and tenderness are present in the forearm of patients with the anterior interosseous nerve syndrome, the predominant symptoms and objective findings are motor. When untreated, the pain often resolves. Motor loss then follows. Characteristically, an abnormal pinch is produced because of the inability to flex the interphalangeal joint of the thumb. Results of nerve conduction studies typically are normal in patients with the anterior interosseous nerve syndrome. Results of needle electromyography indicate denervation restricted to the three muscles innervated by the nerve. Occasional patients may present clinically with the anterior interosseous nerve syndrome and with electrodiagnostic proof of a more proximal lesion of the median nerve. Presumably, the fascicles destined to become the anterior interosseous nerve are affected more selectively in this situation. The surgical exposure for patients with this syndrome is similar to that for the pronator syndrome.
In addition to the ulnar nerve compression found at the cubital tunnel, ulnar neuropathies can be caused by compression at the arcade of Struthers and in Guyon's canal. Because the sensory symptoms are located on the medial aspect of the hand and arm, it is necessary to be certain that the condition is not caused by a C8 nerve root or lower brachial plexus lesion.
Arcade of Struthers
The arcade of Struthers is located where the ulnar nerve passes through the medial intermuscular septum into the posterior compartment. The arcade is a fibrous septum that is located 8 cm proximal to the medial epicondyle. It is present in only 70% of patients. The arcade of Struthers is rarely a site of primary compression. It may, however, become important following an anterior transposition of the nerve as a proximal tether impinging on the nerve. It is important to release the band when transposing the nerve to prevent this secondary compression.
Guyon's canal is found on the medial aspect of the wrist. The anterior border of Guyon's canal is the volar carpal ligament, whereas the posterior border is the transverse carpal ligament. Within the canal, the ulnar nerve runs with the ulnar artery and vein and divides into motor and sensory branches. The distal lesion affects only the motor branch, and the more proximal lesion affects both the motor and the sensory branch. Because the motor branch is deeply placed and tethered as it passes around the hook of the hamate bone, it is prone to compressive lesions. Spaceoccupying lesions, such as ganglia, produce compression as does chronic occupational trauma in cyclists and in persons who use their hands as hammers. Space-occupying lesions may be encountered in patients with fracture of the pisiform bone or hook of the hamate bone. Pure motor paresis produces a claw hand as a result of intrinsic weakness and separation of the fourth and fifth fingers (Wartenberg's sign). Mixed nerve compression produces paresthesia and sensory loss as well as the typical claw hand.
Electrodiagnostic findings again depend on whether the lesion is predominantly axonal or demyelinating. With demyelinating lesions, slowing of motor and sensory latencies across the wrist may be expected, particularly when sensory studies are performed by the palmar technique, and the motor conductions are performed while recording from the first dorsal interosseous muscle. In axonal lesions, motor and sensory amplitudes are reduced and denervation is found in the ulnar muscles of the hand. Reduced amplitude of the dorsal cutaneous branch of the ulnar nerve or denervation in the ulnar muscles of the forearm implies the existence of a lesion proximal to the wrist. When the patient's condition does not respond to the use of splints and the administration of anti-inflammatory medications, the canal should be explored. Surgery in this instance usually is indicated earlier than in patients with other compression neuropathies because of the motor involvement. Both superficial and deep branches of the nerve within the canal should be explored carefully. Any mass within the canal, such as a ganglion cyst or a displaced hook of the hamate bone, should be removed.
Compression neuropathies of the radial nerve produce clinical syndromes dependent on the level of compression. 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 me radial nerve when the patient sleeps heavily with the posterior arm resting against a firm edge. The patient presents with wrist drop 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. 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.
Radial Tunnel Syndromes
The clinical syndromes associated with compression of the deep branch of the radial nerve has been called the radial tunnel syndromes. It may be confused with tennis elbow. The radial tunnel syndromes, however, produce 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, (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. 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. 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.
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 manoeuvre 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 syndromes 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 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. 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. 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 nerve. 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 shape of 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. 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, such as in football players and sports related with hammering and throwing a baseball. 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. Release of the nerve should be performed early. Relief of pain is prompt, but that motor function returns slower.
The 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 Raynaud's phenomenon. This condition may constitute a surgical emergency. 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, a considerable but asymptomatic arterial obstruction in 60% of subjects and bilateral obstruction in 33% of subjects. 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.