Abstract
Functional abnormalities of segmental spinal cord neurons likely contribute to the patho genesis of spasticity following stroke. Identification of dysfunctional circuit elements responsible for spasticity could lead to rational pharmacotherapy for this set of motor dis orders. The purpose of this study was to clarify the role of the spinal recurrent inhibito ry pathway in the development of spasticity: to seek clinico-electrophysiological corre lations between objective signs signifying increased spinal excitability and the level of recurrent inhibition acting on spinal segmental circuitry. The study population was lim ited to patients with recent motor strokes, and testing was done longitudinally during the development of spasticity. Recurrent inhibition was approximated by the conditioned H' response of Bussel and Pierrot-Desseiligny. Ratios of amplitudes of soleus H-reflex to conditioned H' responses were computed for patients who were tested at least twice dur ing the early post-stroke period. On initial testing, there were absent H' responses in the affected limbs of the patients, compared to healthy controls, indicating a supranor mal level of activity of Renshaw cells. In two patients, serial testing revealed a progres sive and sustained increase of the H' response amplitude in the affected limb coincident with development of hyperreflexia. Therefore, in at least some patients, decreased recur rent inhibition paralleling clinical detection of spasticity may indicate a pathogenetic of spasticity. If this trend is supported in larger studies, these data provide a rationale for specific antispastic pharmacological therapy targeted to the Renshaw cell early in the post-stroke period. This preliminary study demonstrates the importance of a longitudi nal'testing design in studies seeking to understand pathophysiological mechanisms of spasticity.