Abstract
The basic pathophysiology of nerve compression injuries is complex and it is important to consider the microanatomy of the neuron and the peripheral nerve. The clinical stages of nerve compression lesions can be related to changes in intraneural microcirculation and nerve fiber structure; alterations in vascular permeability, with subsequent formation of edema; and deterioration of nerve function observed in experimental studies. The double-crush and reversed double-crush syndromes are related to disturbances in axonal transport induced by compression, followed by morphologic and functional changes in the nerve cell bodies. An underlying neuropathy in subjects can make the peripheral nerves more susceptible to compression injuries.
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