[Pathogenesis of acute and chronic compression neuropathy].

The purpose of this study was to clarify the morphological changes in the cell body following acute, and chronic, nerve compression injuries. One hundred and fifty-eight adult male Wistar rats were used for the experiments. Acute compression was produced by clamping the sciatic nerve (ca. 1.3 mm diameter) using a stainless steel Micro-Tube-Clamp (1.6 mm-width and an internal diameter of 1.0 mm). To produce chronic entrapment neuropathy, we used Mackinnon-Dellon's procedure, in which a 1.0 cm length of Silastic tube with an internal diameter of 1.51 mm was wrapped around the nerve trunk. The morphological and functional changes in the nerve trunks were then studied. Histological examinations and morphometric measurements of the nerve cell bodies in the L5 dorsal root ganglion were also carried out for up to 15 months after the procedure. Degeneration of large myelinated nerve fibers, interfascicular edema, interruption of the blood-nerve barrier and a delay in the fast orthodromic axonal transport were found as early as 1 day after clamping, a decreased in the motor nerve conduction velocity on the third day, and a thickening in the perineurium after 1 week. In the chronic experiment, these changes were found at 4, 4, 2, 8, 8, and at 2 months after wrapping, respectively. A significant change in the nuclear eccentricity was morphometrically discovered in both types of nerve compressions-on the third day after clamping, and at 6 months after wrapping. In addition, dispersion of Nissl substance, dislocation of cell organelles and an increase in the number of cytoskeletons were observed in the somata. Acute and chronic nerve compression induced morphologic changes in the nerve cell body as well as in the peripheral nerve fibers. These findings suggested that compression of the peripheral nerve fiber changed the metabolic activity of the nerve cell body. We concluded that compression neuropathy affected the whole neuron including the nerve cell body.