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KMID : 0860920150170010007
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Journal of the Korean Association EMG-Electrodiagnostic Medicine
2015 Volume.17 No. 1 p.7 ~ p.13
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Pathophysiology of Compression or Enterapment Neuropathy
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Kwon Ki-Han
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Abstract
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Compression peripheral neuropathy is relatively common but its pathophysiology in human has not been well known because of the likelihood of permanent nerve damage in vivo human experiments. Many animal models have developed to understand the pathophysiology of compression neuropathy. According to the many animal models and a few human studies, compression neuropathy involves abnormality of intraneural microcirculation, axonal transport and connective tissue (mesoneurium, epineurium, perineurium, endonurium) as well as nerve fiber itself. Low magnitude nerve compression of short duration can initiate neural structural changes which persist for at least one month. Chronic nerve compression with loose ligatures or short tubes around nerve for about weeks or months caused a break-down in blood nerve barrier and perineurial edema, followed by epineurial and perineurial fibrosis, demyelination and finally Wallerian degeneration. Recent studies tell us that compression neuropathy is likely to be a combination of Schwann cell mechanosensitivity to shear stress and acute and/or chronic ischemia. Responding to shear stress, Schwann cells decrease myelin sickness and increase in number and make phenotype switching of neurons of DRG (dorsal root ganglion) by GDNF (glial fiber neurotrophic factor) expression.
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KEYWORD
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compression neuropathy, pathophysiology, Schwann cell
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