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High-Intensity Gait Training With Functional Electrical Stimulation Enhances Corticospinal Excitability of Paretic Ankle Muscles in Individuals Post-Stroke.

Created on 10 Dec 2025

Authors

Vyoma Parikh, Anjali Sivaramakrishnan, Justin Liu, Jiang Xu, Catherine F Mason, Trisha M Kesar

Published in

Neural plasticity. Volume 2025. Pages 5529427. Epub Dec 01, 2025.

Abstract

High-intensity readmill training (FAST) and functional electrical stimulation (FES) are both evidence-supported interventions that improve gait function post-stroke, but their neural mechanisms are unclear. Here, we tested the hypothesis that FAST-FES training, which incorporates task-specific sensorimotor stimulation to paretic ankle muscles, would induce greater upregulation of lesioned corticospinal tract (CST) excitability compared to dose-matched training without FES in individuals post-stroke.
In this repeated-measures crossover study, 11 participants >6 months post-stroke (66.25 ± 8.15 years, six females) received FAST-FES or FAST gait training protocols (comprising three training sessions) in a randomized order, with an intervening >3-week washout period. FES was applied to the paretic dorsi- and plantar-flexor muscles during the paretic swing and terminal stance phases of gait, respectively. CST excitability was measured before and after each training protocol from bilateral tibialis anterior and soleus muscles in three different test positions: sit-rest, sit-active, and quiet standing.
We found a significant main effect of intervention on training-induced change in motor evoked potential (MEP) amplitude (p=0.02). Post hoc comparisons revealed that FAST-FES caused a larger training-induced increase in MEPs than FAST training (p=0.01). FAST-FES did not affect CST excitability of the nonlesioned hemisphere, with no significant changes in MEP amplitude of the nonparetic ankle muscles.
FAST-FES training increased corticospinal excitability in paretic ankle muscles without upregulating nonparetic ankle corticospinal drive, suggesting preferential induction of neuroplasticity in the lesioned CST.

PMID:
41368651
Bibliographic data and abstract were imported from PubMed on 10 Dec 2025.

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