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

    loading  Checking for direct PDF access through Ovid


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<0.01). Controls revealed task-dependent modulation of motor evoked responses (MEPs) between isometric and dynamic contractions in MG, but not SOL while the MED and LOW groups failed to modulate MEPs. SICF revealed no differences between muscles, contraction type, or groups. In SO, controls revealed attenuation of SICI during movement. Stroke survivors revealed a progressive reduction in SICI during isometric PF across functional level while SICI increased during dynamic PF, resulting in a pattern reversal between controls and LOW (p=0.02).Conclusion: Deficits in dynamic PF post-stroke appear to be driven by changes in SICI rather than SICF, suggesting dysregulation of GABA-A. Impaired intracortical inhibition could reduce PF capacity by interfering with selective muscle recruitment during dynamic tasks.

    loading  Loading Related Articles