Lower Extremity Long-Latency Reflexes Differentiate Walking Function After Stroke

Abstract

The neural mechanisms of walking impairment after stroke are not well characterized. There is a need for a neurophysiologic marker that can unambiguously differentiate functional status and potential for walking recovery. The long-latency reflex (LLR) is a supraspinally-mediated response that integrates sensorimotor information during movement. It is hypothesized that lower extremity LLRs contribute to regulation of motor output during walking in healthy individuals. The goal of the present study was to assess the relationship between lower extremity LLRs, measures of supraspinal drive, and walking function. Thirteen 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 four 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. This 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 responses allow for unambiguous differentiation between individuals post-stroke and are associated with multiple measures of motor function. 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.