Entrapment Neuropathies

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Chapter 33 Entrapment Neuropathies

Some peripheral nerves, irrespective of whether they are motor, sensory, or of mixed type, pass through narrow, constricted areas in the arms or legs. Under certain circumstances, these nerves are susceptible to compression at these sites,13 and this compression can eventually clinically manifest as entrapment neuropathy.46 Entrapment of nerves usually occurs as they pass beside a joint, such as the elbow, wrist, or hip and only very occasionally elsewhere in the limbs. This, along with the fact that entrapment neuropathy seldom occurs in the head or trunk, suggests that repetitive motion is a major factor that precipitates entrapment in an anatomically constricted segment.

Two types of physical constrictions predispose to entrapment neuropathy. The first type (Fig. 33.1A) is a fibro-osseous tunnel. The space available for the nerve within the tunnel becomes constricted either because the contents of the tunnel become larger or hypertrophic, as when a patient with tenosynovitis has carpal tunnel syndrome, or because the walls of the tunnel encroach upon the tunnel’s lumen, as when fractured fragments of a carpal bone displace into the carpal canal. Compression of a nerve in a tunnel is an example of static compression. The second type (Fig. 33.1B) involves dynamic compression of the nerve as it passes through a fibrotendinous arcade. The nerve is flanked by two bellies of a muscle that under static conditions do not compress the nerve. When they contract, however, they cause a shutter-like closure of the arcade, compressing the nerve. For example, this can occur at the arcade of Frohse in the supinator muscle, the two heads of the flexor carpi ulnaris at the entrance to the cubital tunnel, or the two heads of the flexor digitorum sublimis forming the “sublimis bridge.”

Pathology of Nerve Compression7

The pathophysiological changes following nerve compression821 are dependent on the degree, rate, and duration of compression. Loss of function of the nerve as a result of compression is manifested clinically by motor paralysis, paresthesia, or numbness. In physiological terms, mild and brief compression produces a transient and reversible conduction block within the nerve. Sustained compression over a long period causes structural changes. Not all components of the nerve are equally susceptible to a given degree of compression. Nerve fibers that have a greater amount of epineurium compared to the nerve fascicles are less susceptible to compression than those with larger fascicles and scanty epineurium (Fig. 33.2). Also, within a given nerve, not all fibers undergo degenerative changes to the same extent. The superficially located fibers tend to bear the brunt of the compression, while the central fibers are relatively spared. Large, heavily myelinated fibers subserving light touch and motor function are more sensitive to compressive changes than unmyelinated fibers subserving pain sensation.

Impediment to microvascular flow appears to be a major factor in the pathophysiology of nerve impingement.7 Capillary blanching and venular obstruction herald progressive compression. This leads to nerve ischemia, which in turn leads to endothelial impairment and progressive edema; the edema compounds the ischemia and swelling of the nerve (Fig. 33.3). Critical swelling of a nerve within the constraints of its surroundings may lead to further nerve compression, a phenomenon that can be called a mini-compartmental syndrome.

Nerve compression blocks axonal transport. The antegrade transport from the nerve cell to the axon toward the synapse can be divided into fast and slow components; the fast component carries the membrane-associated materials and the slow components carry the cytoskeletal proteins. Nerve compression impedes both the fast and slow components of the antegrade flow, resulting in a swelling of the nerve proximal to the compression as a result of the damming up of the moving axoplasm within the fibers. Thus, the distribution of cytoskeletal elements, axolemma constituents, and the transmitter substances required for synaptic conduction are all impaired by a block of antegrade flow. Retrograde axonal flow from the synaptic level to the cell body of the nerve is similarly blocked by compression of the nerve. This results in a loss of transfer of neuronotropic factors to the nerve cell body. The impairment of retrograde axonal transport results in certain changes in the nerve cell body comparable to those that occur after peripheral nerve section (wallerian degeneration). Thus, changes noted in the cell body are an eccentric nucleus, dispersion of Nissl substance (chromatolysis), and a decrease in nuclear and whole cell volumes. The overall result of the impediment to axoplasmic flow is impaired membrane permeability and conduction block.

With acute and severe compression one observes a characteristic sequential invagination or telescoping of the myelin sheath (Fig. 33.4). The polarity of invagination is reversed at the edges of the compression. With chronic compression, segmental demyelination occurs within the compressed segments, accounting for the slowing of conduction velocity of the nerve. In the early phases, the nerve fibers distal to the compression show normal morphology. With sustained compression, axolysis occurs within the compressed segment, leading to distal wallerian degeneration.

The Entrapment Syndromes

The entrapment sites, the nerves involved at each site, and the corresponding syndromes are listed in Table 33.1. This chapter will cover the most common entrapment syndromes: carpal tunnel syndrome, cubital tunnel syndrome, meralgia paresthetica, suprascapular nerve entrapment, and tarsal tunnel syndrome. Some patients can develop multiple entrapment neuropathies.23

Carpal Tunnel Syndrome24

The carpal tunnel syndrome2527 is the most common entrapment neuropathy encountered in clinical practice. It results from compression of the distal median nerve within the carpal tunnel, located in the proximal part of the palm of the hand.28 The carpal tunnel is bounded dorsally by the carpal bones and ventrally by the transverse carpal ligament. The carpal bones form a shallow trough that is converted into a tunnel by the carpal ligament. The contents of the tunnel are the median nerve and tendons of the long flexor muscles (see Fig. 33.1A). Any lesion affecting the synovial sheath tends to compromise the cross-sectional diameter of the carpal canal and may induce compressive neuropathy.29 Recent studies that include magnetic resonance imaging (MRI) and computed tomography (CT) scans show that patients with carpal tunnel syndrome tend to have small carpal canals. The small size of the carpal canal, measured by the decrease in its cross-sectional diameter, is a congenital or developmental phenomenon.30 Its small size in women may account for their higher incidence of carpal tunnel syndrome.

Clinical Features31

Women are more commonly affected than men, by a ratio of 7:3. Most patients are middle-aged at the onset of symptoms. The predominant symptom is an aching, burning, tingling, numb sensation in the hand, ordinarily in the lateral half of the hand and the outer three or four digits.32 Frequently there may be an aching pain in the proximal forearm or even in the arm up to the shoulder and it can lead to confusion with cervical radiculopathy. Patients typically wake up at night with increased pain, and they may shake their hand to obtain relief. The symptoms are often bilateral. With severe or advanced compression patients complain of weakness of grip and a tendency to drop things.

In the early stages of the syndrome, at which time most patients are seen in contemporary practice, there are few objective findings. Two mechanical tests can be performed. Tinel’s sign may be elicited by lightly tapping over the median nerve at the wrist crease, which results in a tingling in the distribution of the median nerve if positive. Phalen’s test consists of asking the patient to flex the wrist to 90 degrees for about 60 seconds, which will precipitate paresthesia in the distribution of the median nerve if positive.3335 Neither test is conclusive and both results are often absent. Perception of light touch, pinprick, and two-point discrimination in the tips of the fingers in the median nerve distribution may be impaired. In advanced cases there may be atrophy of the thenar muscles, especially in the abductor pollicis brevis. A recently proposed scratch collapse test for evaluation of carpal and cubital canal syndrome may be a significant addition for clinicians but it needs to be evaluated by independent reviewers.36

The clinical history, especially of nocturnal pain, is usually the most reliable diagnostic clue. There are several local and systemic risk factors that precipitate the symptoms of carpal tunnel syndrome (Table 33.2).3744

TABLE 33.2 Risk Factors in the Pathogenesis of Carpal Tunnel Syndrome

Local Factors Systemic Factors
Increased volume of the contents of the carpal canal

Reduction in the capacity of the carpal canal

Other local factors

Increased susceptibility of nerves to pressure

Factors unique to women

Inflammatory and autoimmune disorders

Metabolic disorders


The most important diagnostic tests are electromyography and study of nerve conduction velocity.45 The earliest and most significant finding is the prolongation of sensory latency due to demyelination. The sensory evoked response will show diminution of amplitude and may even be absent. Motor latency abnormalities occur late in the course of the disease. Needle electromyography may show loss of motor unit potentials and the presence of denervation potentials in the median-innervated muscles in the thenar eminence due to axonal loss. Clinically it corresponds to the impairment of two-point discrimination.