Lower extremity long-latency reflexes differentiate walking function after stroke.

Abstract

The neural mechanisms of walking impairment after stroke are not well characterized. Specifically, there is a need for understanding the mechanisms of impaired plantarflexor power generation in late stance. Here, we investigated the association between two neurophysiologic markers, the long-latency reflex (LLR) response and dynamic facilitation of antagonist motor-evoked responses, and walking function. Fourteen individuals with chronic post-stroke hemiparesis and thirteen healthy controls performed both isometric and dynamic plantarflexion. Transcranial magnetic stimulation (TMS) assessed supraspinal drive to the tibialis anterior. LLR activity was assessed during dynamic voluntary plantarflexion and individuals post-stroke were classified as either LLR present (LLR+) or absent (LLR-). All healthy controls and nine individuals post-stroke exhibited LLRs, while five did not. LLR+ individuals revealed higher clinical scores, walking speeds, and greater ankle plantarflexor power during walking compared to LLR- individuals. LLR- individuals exhibited exaggerated responses to TMS during dynamic plantarflexion relative to healthy controls. The LLR- subset revealed dysfunctional modulation of stretch responses and antagonist supraspinal drive relative to healthy controls and the higher functioning LLR+ individuals post-stroke. These abnormal physiologic responses allow for characterization of individuals post-stroke along a dimension that is clinically relevant and provides additional information beyond standard behavioral assessments. These findings provide an opportunity to distinguish among the heterogeneity of lower extremity motor impairments present following stroke by associating them with responses at the nervous system level.