Chronic nerve root compression. Pathophysiologic mechanism of nerve root dysfunction.

摘要

STUDY DESIGN. The pathophysiologic changes of the spinal nerve root caused by chronic compression were assessed in the lumbar spine of the adult dog. METHODS. The seventh lumbar nerve root was banded with a Silastic tube 5 mm long and a 3 mm internal diameter, which is slightly larger than the diameter of the nerve root. Histologic and electrophysiologic studies as well as assessment of the blood-nerve barrier function in the nerve root were conducted at 24 hours through 12 months. RESULTS. The earliest findings were thickening of the dura mater and arachnoid membrane around the affected nerve root corresponding to the alteration of the blood-nerve barrier in the nerve root after 1 month. After 3 months, large myelinated fibers decreased in number and small newly formed fibers increased in the periphery of the fascicle. At 6 months, endoneurial fibrosis and Wallerian degeneration of nerve fibers became obvious. Compound action potentials and sensory nerve conduction velocity decreased by 3 and 12 months, respectively. Decrease in amplitude of the compressed action potential was identical to the period of decrease in large myelinated fibers, and nerve conduction velocity did not decrease as long as some large myelinated fiber remained until 12 months after tubing. CONCLUSION. Intraradicular edema caused by alteration of the blood-nerve barrier is the most important factor in the nerve root dysfunction due to chronic compression.