Role of corticomotor drive to walking recovery and responses to functional electrical stimulation in stroke survivors

Date
2016
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Publisher
University of Delaware
Abstract
Despite current standard rehabilitation efforts, walking deficits that contribute to limitations in activity and participation in individuals with chronic stroke persist. Recent developments in a noninvasive brain stimulation technology, transcranial magnetic stimulation (TMS), provide an opportunity to investigate neurophysiologic components underlying post-stroke motor recovery by quantifying the strength of corticomotor connectivity to specific muscles. There is evidence that the balance of corticomotor drive to paretic and nonparetic upper extremities of stroke survivors is related to motor function, can be changed through rehabilitation, and can predict functional outcomes in response to intervention. However, neurophysiologic mechanisms underlying lower extremity motor recovery are unknown and our understanding of rehabilitation effects on cortical factors that could influence post-stroke walking ability is poor. The overall purpose of this project was to investigate corticomotor factors underlying lower extremity clinical (aim 1) and biomechanical (aim 2) walking function following stroke. Additionally, we sought to determine the effectiveness of a single session of rehabilitation utilizing gait training with functional electrical stimulation (FES) to induce changes in corticomotor behavior that, if improved, could promote positive changes in biomechanical walking impairments (aim 3). The results of this study indicate that balance of corticomotor drive to the paretic and nonparetic lower extremities is critical to the level of walking function achieved by individuals with chronic stroke. Our results suggest that both the lesioned and nonlesioned motor cortices play a role in post-stroke walking recovery. This can be evidenced by the origins of corticomotor asymmetry stemming from both reduced corticomotor drive to the paretic leg and enhanced corticomotor drive to the nonparetic leg in stroke survivors with poor walking recovery. These patterns of corticomotor asymmetry are different between resting and active motor states and more severely affect the ankle plantarflexor muscles than the dorsiflexor muscles. The balance of corticomotor drive between limbs affected post-stroke walking biomechanical function, as we found that corticomotor symmetry to plantarflexor muscles determined the propulsive strategy that stroke survivors used to achieve their fastest walking speeds. Critically, findings of this project further demonstrated that a single session of gait rehabilitation utilizing FES could promote corticomotor balance to plantarflexors that was positively related to improvements in biomechanical gait impairments. Together, these findings offer new insights into neurophysiologic mechanisms underlying post-stroke walking ability and identify specific cortical mechanisms that may be targeted through rehabilitation to produce positive changes in biomechanical walking function in stroke survivors.
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