Abstract

Objective To investigate if, following stroke, sustained involuntary activity after voluntary contraction (e.g., grip) of the long finger flexor muscles of the paretic hand is attributable to augmented serotonin release from brainstem pathways, affecting excitability of spastic motoneurons. Methods This single-dose placebo-controlled study examined whether a serotonin receptor (5-HT2) antagonist, cyproheptadine hydrochloride, could reduce delay in muscle relaxation of a key paretic long finger flexor muscle immediately after grip for persons with stroke. Time to initiate the long finger flexor muscle contraction, grip and pinch strengths, and clinical hand function scores (the Action Research Arm Test and the Box and Block Test) were also assessed. Results Cyproheptadine hydrochloride reduced mean delays in finger relaxation ( n = 13; from 7.2 to 4.1 s; SEM = 1.2 s; p = .026) in comparison to placebo, while leaving grip and pinch strengths and time to initiate the muscle contraction largely unaffected. Reduction in the relaxation time alone did not lead to increased clinical hand function scores. Conclusions The findings support the supposition that monoaminergic brainstem pathways may be disinhibited following stroke, thereby resulting in increased delays in muscle relaxation. Significance Treatments to reduce delay in muscle relaxation may facilitate hand rehabilitation in persons with stroke.

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