SPROUTING AS A CAUSE OF SPASTICITY

Abstract

Monkey and cat spinal cords were transected and potentials were recorded from opposite pairs of dorsal roots and from the surface of the cord above the entrance zone of each at intervals of 9 days to 5 months after various unilateral cord lesions. The previously unoperated side served as control. Lesions were checked histologically and counts were made of the number of afferent fibers crossing the dorsal columns and sweeping into the dorsal horn on each side. All types of lesion produced significant increase in fiber count on the side of the lesion. Lesions of over 3 weeks'' duration, except those confined to the dorsal columns, gave significant increase in the size of the presynaptic potential associated with activity of afferent terminations in response to single dorsal root volleys. Increase in internuncial potentials never significantly exceeded that in afferent terminal potential and occasionally fell below it. Synapse time of interneurons increased upon the spastic side. Degeneration studies demonstrated an increase in distribution of afferents on the side of hemisection. It is concluded that sprouting of afferent terminals to fill gaps left by degeneration of descending tracts is a major cause of the spasticity of paraplegia. This occurs in normal fibers following degeneration of neighboring axons. Lesions confined to the dorsal columns induce sprouting in the absence of descending degeneration, but under these conditions the sprouts fail to develop functional connections.