Axon regeneration after decompression of the conus medullaris.

Abstract

The effect of acute spinal stenosis (simulating fracture) and decompression of stenosis on axon regeneration was evaluated in an animal model. Clinical function and quantitative histomorphometry were used to gain insight into the clinicopathologic effects of acute spinal stenosis and decompression. Decompression of extrinsic compression after thoracolumbar fractures has been suggested to maximize recovery of neurologic function. Clinical studies seem to support this, but the histologic results of decompression are poorly understood. Experimental spinal stenosis was created in 5 female beagle dogs, followed by decompression in three of the beagles at 6 weeks. Clinical function and histologic appearance were analyzed using a monoclonal antibody to neurofilaments. Stenosis consistently produced significant neurologic deficit and axon degeneration within motor roots distal to the stenosis. Decompression resulted in improved neurologic function and a tendency for the axons to return to normal number and volume based on quantitative histomorphometry. This study provides an animal model and functional and histologic data that support the use of decompression of acute spinal stenosis of 50% or more canal compromise at the level of the conus medullaris and a neurologic deficit. This may be seen clinically in thoracolumbar fractures.