Background: The ability to elicit a rapid, reactive step to recover balance after a postural destabilization is paramount to fall prevention. In response to a given balance perturbation magnitude, people after stroke display impaired spatiotemporal stepping kinematics. Yet, spatiotemporal stepping kinematics at individualized perturbation magnitudes after stroke and the underlying neural correlates remain unknown. Here, we tested whether stepping kinematics differ in people after stroke at individualized balance perturbation magnitudes and further examined neuromechanical mechanisms underlying impaired stepping kinematics after stroke. Methods: 16 participants with chronic (>6mo.) stroke and 16 age-matched controls underwent standing balance perturbations at individualized step threshold, the perturbation magnitude that elicited unintentional steps in approximately 50% of trials. We quantified the spatiotemporal kinematics of the first reactive step and weight-bearing asymmetry immediately prior to the perturbation onset. Cortical N1s, perturbation-evoked brain responses reflecting cortical processing for balance control, were extracted from Cz signals and identified as the most negative local minimum (100-300ms). Results: While there were no group-level differences in step duration, step velocity, and step trajectory, people with stroke showed delayed step initiation (Cohen d= 0.89, p=0.02) and termination latencies (Cohen d= 0.81, p=0.03). Delayed step initiation latencies after stroke correlated with lower clinical balance function (e.g., miniBEST score; r= -0.67, p=0.004) and delayed cortical responses (r=0.58, p=0.02) but not weight-bearing asymmetry (p>0.86). Conclusions: The relationships between delayed step initiation, lower clinical balance function, and slower cortical responses suggests cortical processing speed may be a limiting factor for post-stroke balance function and identifies neuromechanical targets for fall prevention.
Tsai et al. (Fri,) studied this question.