Neurophysiological insights into sit-to-stand post stroke.

Introduction: Stroke often results in the loss of ability to stand-up independently or to perform the transfer with compensatory movement patterns. While neurological disorders are associated with sit-to-stand disability, the neurophysiological mechanisms underlying the movement and the impact of injury at brain level remain poorly understood. Methods: Stroke participants ( Results: Kinematic data confirms post-stroke participants take significantly longer to complete a sit-to-stand transfer compared to healthy controls but maintain the same kinematic movement phases and temporal muscle activation patterns. EMG data indicates stroke survivors stand up using largely the same temporal muscle activation patterns, however they exhibit delayed peak activity of the vastus lateralis and biceps femoris compared to healthy controls. EEG data reveal stroke survivors demonstrate variable event-related spectral perturbation patterns and reduced event-related synchronization/de-synchronization in the alpha and beta frequency bands and increased asymmetry between brain hemispheres when compared to healthy controls. Conclusion: EMG data supports the wider literature that confirms stroke survivors stand up using the same temporal muscle activation patterns compared to healthy controls, however peak activity of the vastus lateralis and biceps femoris are delayed. EEG data add new knowledge to our understanding of the central control of sit-to-stand transfers in a stroke population, highlighting differences in cortical activity from healthy controls, notably in ERSP patterns during sit to stand phases and in brain hemisphere asymmetry. Findings have relevance as a potential biomarker for stroke functional recovery and indicate that BCI-based applications of sit to stand may need to be trained individually in stroke survivors as they demonstrate variable cortical activation patterns compared to healthy controls.