Reflex Hyperexcitability Persists During Voluntary Muscle Activation Following Stroke

Stroke is a leading cause of disability in the United States, disrupting neural pathways that contribute to smooth, controlled movement. The short-latency spinal stretch reflex is one such pathway, and its task-dependent modulation facilitates both movement execution and posture maintenance. Much of this modulation can be explained by voluntary muscle activation; the reflex increases with activation of the agonist muscle (i.e. agonist facilitation) and, at least during movement, decreases with activation of antagonist muscles (i.e. antagonist inhibition). While stretch reflex hyperexcitability post-stroke is well-documented when individuals are instructed to relax, how reflexes behave during active tasks remains less understood. Specifically, it is unknown how stroke affects agonist facilitation and antagonist inhibition of the short-latency stretch reflex. In this study, we tested the hypotheses that stroke alters the effects of agonist and antagonist muscle activation on the stretch reflex and that alterations correlate with impairment, as determined by Fugl-Meyer score. We recorded muscle background and short-latency stretch reflex activity using electromyography from individuals with chronic stroke and healthy controls during a postural task in which participants generated varying levels of co-contraction at the elbow. We found that the effects of muscle activation are intertwined: antagonist activity inhibits agonist facilitation of the stretch reflex. Overall, agonist facilitation increases after stroke while antagonist inhibition remains unchanged; neither effect correlates with impairment. Post-stroke increases in agonist facilitation reveal that the post-stroke stretch reflex is increasingly heightened with agonist activation, highlighting persistent stretch reflex differences during active tasks and motivating future work on functional implications.