# Biomechanical and neural mechanisms of post-stroke gait training

> **NIH NIH R01** · EMORY UNIVERSITY · 2020 · $609,184

## Abstract

Stroke induces a cascade of neurophysiologic changes in cortical and spinal circuits that result in 
biomechanical gait impairments (reduced paretic propulsion, footdrop) and gait dysfunction (reduced speed). 
While increasing gait speed is a major goal of stroke gait rehabilitation, targeting walking speed as a primary 
gait rehabilitation outcome without regard to biomechanical and neural mechanisms fails to meet the emerging 
standards of precision medicine, which is the future of rehabilitation research. Thus, here, we will confirm a 
novel theoretical framework regarding neurobiological (top-­down) and biomechanics (bottom-­up) 
mechanisms of how 2 gait treatments improve walking speed post-­stroke. Fast treadmill walking (Fast), a well-­
studied and clinically-­used intervention, improves gait speed. However, Fast-­induced speed improvements in 
people post-­stroke may occur at the cost of inter-­limb asymmetry, energy inefficiency, and maladaptive 
neuroplasticity. Recent work has demonstrated that combining Fast with functional electrical stimulation 
(FastFES) not only leads to improvements in gait speed but also reduces energy cost (EC) of stroke gait. 
Because reduced EC is crucial for sustaining faster gait speeds and promoting community activity, 
biomechanical factors influencing EC post-­stroke merit more in-­depth study. Building upon knowledge gained 
from previous FastFES work and our preliminary data, Aim 1 will test our hypothesis that in contrast to Fast, 
FastFES promotes greater use of the paretic leg for forward propulsion, thereby improving inter-­limb 
biomechanical asymmetry, which we hypothesize reduces EC. Gait rehabilitation essentially involves retraining 
the central nervous system. Our lack of understanding of neuroplasticity mechanisms underlying gait 
interventions continues to be a barrier to improving gait rehabilitation outcomes. Aim 2 will determine, for the 
first time, if and how FastFES and Fast modulate excitability of neural circuits impacted by stroke and 
implicated in locomotor control. Stroke leads to decrease in lesioned motor cortex (M1) excitability and 
corticospinal tract (CST) output, and elevated spinal reflex excitability. New findings from our lab suggest that 
unlike Fast, FastFES enhances lesioned CST and M1 excitability, restoring more normal CST output. FastFES 
and Fast also differ in their effects on spinal excitability. Like most gait treatments, Fast and FastFES must 
contend with high inter-­individual variability in treatment responses (a subset of participants are “non-­
responders”). Aim 3 will address whether baseline measures or short-­term changes in neurophysiological 
biomarkers (CST and spinal excitability) can predict long-­term training-­effects. Results from our mechanism-­
focused clinical investigation will elucidate how, why, and for whom Fast and FastFES induce clinical benefits. 
The overall impact of this work will be future development of cutting-­edge gait treat...

## Key facts

- **NIH application ID:** 9988469
- **Project number:** 5R01HD095975-02
- **Recipient organization:** EMORY UNIVERSITY
- **Principal Investigator:** Trisha Kesar
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $609,184
- **Award type:** 5
- **Project period:** 2019-08-02 → 2024-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9988469

## Citation

> US National Institutes of Health, RePORTER application 9988469, Biomechanical and neural mechanisms of post-stroke gait training (5R01HD095975-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/9988469. Licensed CC0.

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