Chronic Nerve Compression

Ischemia and endoneurial edema also contribute to the pathology of nerves that sustain chronic compression; modest pressure magnitudes develop, such as occurs with median nerve compression in the carpal tunnel and ulnar neuropathy at the elbow. The ischemic hypothesis has focused on the transperineurial vascular system. This includes an intrafascicular circulation, composed mostly of capillaries running longitudinally within the endoneurium and an extrafascicular network within the epineurium, composed predominantly of venules and arterioles. The extrinsic vessels penetrate the relatively rigid perineurium to anastomose with the intrinsic circulation, and it is this transperineurial vessel network that may be particularly susceptible to focal compression, especially because these vessels traverse the perineurium at oblique angles.

These transperineurial vessels, especially the venules, are vulnerable to constriction caused by endoneurial edema and elevated (intrinsic) endoneurial fluid pressure. Constriction of these vessels causes venous congestion, endoneurial capillary leakage, and elevated endoneurial fluid pressures. These effects introduce metabolic disturbances to the microenvironment, with subsequent damage to the peripheral nerve anatomy and nerve function. Thus chronic external compression may induce ischemia and endoneurial edema with concomitantly elevated endoneurial fluid pressures. These two effects impair nerve function by altering the metabolic microenvironment as well as contributing to nerve injury by further constricting transperineurial venules. Thus a precarious cycle of venous congestion, ischemia, and metabolic disturbances is initiated that eventually leads to a “miniature compartment syndrome.”

In cases of median neuropathy at the wrist (i.e., carpal tunnel syndrome), it is thought that carpal tunnel pressures may rise to abnormal levels, increasing the endoneurial fluid pressure and thereby impairing the transperineurial microcirculation. Carpal tunnel pressure and consequently endoneurial fluid pressures probably rise significantly at night in the setting of carpal tunnel syndrome because the limb venous return is impeded by limb posture and reduced limb movement. Endoneurial edema due to other causes, for instance, diabetes, further increases nerve susceptibility to compression.

Moderately elevated pressures also disturb axonal transport. Retrograde axonal transport is critical for communication with the nerve cell body. Fast and slow anterograde axonal transport may also be reversibly impaired after compression. The blocking of axonal transport with compression is a graded effect, related to the magnitude and duration of compression. For example, the susceptibility to entrapment in diabetic polyneuropathy may be in part due to the combination of widespread endoneurial edema (diabetes) and focal (entrapment) impairment of axonal flow.

The gliding capacity of a peripheral nerve is another important factor inherent to chronic compression neuropathies. This is particularly relevant at common sites of entrapment, such as the wrist and elbow. Gliding of nerves is necessary during movement of limbs and is made possible by conjunctiva-like adventitia that allow longitudinal excursion of a nerve trunk. Restriction of glide may occur with extraneural and intraneural fibrosis, especially at sites of entrapment, inducing nerve stretch lesions, edema, inflammation, and further fibrosis. Stretch may contribute to nerve injury at common sites of entrapment, although it is unlikely to be the major factor in injury and is likely overshadowed by the consequences of direct pressure and perhaps ischemia.

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