Characterizing Lower Extremity Neurophysiological Responses to Sensory Augmentation after Stroke

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PROJECT SUMMARY/ABSTRACT After a stroke, walking ability can be compromised, which can lead to reduced quality of life and decreased ability to perform activities of daily living. Post-stroke walking recovery is mediated by nervous system reorganization (e.g., neuroplasticity), however our understanding of these processes related to improvements in walking function are limited due to the neurophysiological complexity of walking itself. Additionally, current practices of assessing stroke- impacted neuroplasticity are heavily focused on the motor system. Of keen interest is the integration of sensory and motor systems (e.g., sensorimotor integration-SMI), which are necessary for initiating, sustaining, and coordinating walking while providing continuous feedback on body state and actions. Additionally, impaired sensation post-stroke can lead to lower extremity dysfunction, balance problems, and falls, highlighting the need to investigate the effects of stroke on SMI in relation to walking function and recovery. Given the importance of SMI in walking, the capacity for these sensorimotor networks to exibit plastic changes may be a crucial mediator for improvements in walking funciton, thus necessitating relevant methods of assaying sensorimotor plasticity. To address this gap in knowledge, in the F99 Phase (Aim 1) I will characterize lower extremity sensorimotor plasticity in individuals post-stroke. I will specifically target the connections between the primary sensory cortex (S1) and and the primary motor cortex (M1) using paired associative stimulation (PAS), a novel method of assaying sensorimotor plasticity. PAS is based on the Hebbian principle of associative plasticity, in that repetitive stimulation of pre- and post-synaptic neurons within S1 and M1 leads to increased synaptic efficacy, evidenced by rapid and long-lasting increases in transcranial magnetic stimulation-induced muscle responses, or motor evoked potential (MEP) amplitude. We intend to account for individual differences in SMI by adjusting the timing between stimuli, and measuring the time it takes the electrical stimulation to reach S1, via somatosensory evoked potentials. Changes in MEP amplitude following PAS are thought to reflect the induced associative plasticity between S1 and M1, and are shown to be reflective of upper extremity function, with limited work done in the lower extremities. Therefore, we hypothesize that individualized PAS protocols, will facilitate increases in MEP amplitude, and changes will be associated with clinical measures of walking function. In the K00 Phase (Aim 2), I will pursue advanced training in post-stroke sensory and motor reorganization via multi- modal techniques to understand walking and balance recovery. I will seek out postdoctoral mentorship that will allow me to build on my predoctoral work by acquiring advanced electrophysiological and neuroimaging skills. I will also focus on individualized assessments and the identification of mechanisms underlying the response to treatment between individuals over the course of rehabilitation. The F99/K00 will help facilitate my path to independence through research training and career development, enroute to my long-term goal of becoming an independent researcher at an academic medical center. The proposed work and career direction aim to inform lower extremity rehabilitation efforts by providing functional and structural neural correlates of recovery.