Compression Neuropathies

Acute neuropathies tend to manifest more with predominant motor manifestations, for instance, peroneal neuropathy—a footdrop, and radial neuropathy—a wristdrop; sensory disturbances are relatively mild. Entrapment neuropathies usually present with paresthesias (tingling) predating focal weakness by months and often years, as well as overshadowing it. Median neuropathies at the wrist initially are characterized by hand tingling at night or with various hand activities, particularly driving; only later in the course does weakness of the thumb, particularly the abductor pollicis brevis, become evident. Diabetes mellitus, myxedema, or, rarely, hereditary neuropathy with liability to pressure palsy makes nerves more susceptible to compression injury.

Peripheral nerves are made up of many myelinated and unmyelinated nerve fibers originating from either the anterior horn cell (motor) or the posterior root ganglia (sensory) and traveling the nerve’s entire length. Nerve fibers are organized into fascicles, of which there are many within one peripheral nerve. Elements contained within the fascicles represent the endoneurium. The perineurium, a protective sheath of connective tissue, surrounds each fascicle. Schwann cells concentrically wrap their cytoplasmic processes around axons many times, creating the myelinated nerve fiber. Each nerve segment is associated with one adjacent Schwann cell. When many Schwann cells are lined up contiguously, the entire nerve fiber becomes myelinated. An internode consists of one myelinated segment. Nodes of Ranvier represent areas lacking myelin, thus interrupting the internodal sections and containing high concentrations of voltage-gated sodium channels. Juxtaparanodal and paranodal regions are distinctive myelin folds at internode edges containing high concentrations of voltage-gated potassium channels. These areas are integral to conduction of action potentials down the axon.

ACUTE NERVE COMPRESSION

When nerve tissues are subjected to mechanical compression, some of the compressed tissues are displaced to sites of lower pressure. This is especially the case for acute compression neuropathies, such as proximal radial neuropathy (“Saturday night palsy”) and neuropathies secondary to tourniquet compression. With acute nerve compression, damage is concentrated at the compression edges. The predominant injury at this level implies that the pressure gradient itself, rather than the absolute pressure, is the critical factor for acute compression neuropathy.

In the setting of experimental acute compression, the earliest histopathologic change seen within just a few hours is an invagination of one paranodal segment into its adjacent paranode. Directed toward the uncompressed tissue, paranodal myelin, tethered to the axon, may be grossly distorted, resulting in invagination on one side and passive stretching on the other side. Longitudinal movement of the axon relative to the Schwann cell accompanies the paranodal myelin alterations. In extreme cases, myelin lamellae may be ruptured. These findings are reminiscent of intussusception of the bowel, suggesting that that the pressure gradient between compressed and uncompressed nerve provides definitive forces causing axoplasm extrusion “similar to toothpaste from a tube.”

The sequential events of acute, focal compression initially include an early combined extrusion of endoneurial fluid (i.e., the fluid between fibers), axonal fluid, and cytoskeletal elements, and subsequently distortion of myelin and Schwann cell elements. A second slower phase is attributed to further endoneurial and axonal fluid extrusion, paranodal disruption, Schwann cell cytoplasm extrusion, and displacement of other tissue elements. Additional damage (e.g., of the cytoskeletal network) may occur at more extreme pressures or with protracted compression. Nodes of Ranvier are frequently obscured or lengthened because of displaced paranodal myelin.

Classic nerve conduction studies provide a means to measure the magnitude of the nerve action potential conduction block as well as focal conduction slowing. These findings correlate with the degree and duration of compression. Focal ischemia may also contribute in some compression neuropathies, particularly in combination with the direct effects of pressure. Transient nerve block, for instance, when a limb “goes to sleep” for a few seconds, may be related to modest external pressures, and/or may be primarily caused by focal ischemia because no recognizable structural nerve pathology has been convincingly demonstrated. For more severe cases of acute compression, nerve fiber remyelination may occur weeks to months after resolution of the acute compression.

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