Abstract TP144: Intracortical Circuits Reveal Muscle- and Task-specific Dysfunction Contributing to Weakness Following Stroke

• Published in: Stroke (1970) 2016-02, Vol.47 (suppl_1)
• Main Authors: Little, Virginia L, Walker, Eric R, Patten, Carolynn
• Format: Article
• Language: English
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/str.47.suppl_1.tp144

Abstract only Introduction: Weakness is a prominent clinical manifestation following stroke. While central factors, including activation impairment, contribute to hemiparetic weakness, specific mechanisms remain poorly understood. Here we probed functioning of the corticospinal pathway and intracortical circuits mediating dynamic force production. Hypothesis: We hypothesized that impairments of intracortical inhibition and excitation contribute to deficits in plantarflexor (PF) force production capacity following stroke. Methods: We studied 19 chronic stroke survivors (age: 66.0±9.6 yrs; chronicity: 77.3±60.9 mo) and 7 controls (age: 61.3±9.7 yrs) and used the Short Physical Performance Battery to group stroke survivors by functional ability (i.e., HIGH, MED, LOW). We obtained peak isometric PF force during a series of maximal voluntary contractions. Single and paired pulse transcranial magnetic stimulation (TMS) was delivered over the ipsilesional hemisphere during isometric and dynamic PF contractions to assess corticomotor excitability, short intracortical inhibition (SICI), and short intracortical facilitation (SICF). Results: Peak isometric force (p=0.04) and cortical excitability in both medial gastrocnemius (MG) and soleus (SO) were progressively reduced across functional levels post-stroke (p’s