Table_2_Neuromusculoskeletal Simulation Reveals Abnormal Rectus Femoris-Gluteus Medius Coupling in Post-stroke Gait.pdf

Post-stroke gait is often accompanied by muscle impairments that result in adaptations such as hip circumduction to compensate for lack of knee flexion. Our previous work robotically enhanced knee flexion in individuals post-stroke with Stiff-Knee Gait (SKG), however, this resulted in greater circumduction, suggesting the existence of abnormal coordination in SKG. The purpose of this work is to investigate two possible mechanisms of the abnormal coordination: (1) a reflex coupling between stretched quadriceps and abductors, and (2) a coupling between volitionally activated knee flexors and abductors. We used previously collected kinematic, kinetic and EMG measures from nine participants with chronic stroke and five healthy controls during walking with and without the applied knee flexion torque perturbations in the pre-swing phase of gait in the neuromusculoskeletal simulation. The measured muscle activity was supplemented by simulated muscle activations to estimate the muscle states of the quadriceps, hamstrings and hip abductors. We used linear mixed models to investigate two hypotheses: (H1) association between quadriceps and abductor activation during an involuntary period (reflex latency) following the perturbation and (H2) association between hamstrings and abductor activation after the perturbation was removed. We observed significantly higher rectus femoris (RF) activation in stroke participants compared to healthy controls within the involuntary response period following the perturbation based on both measured (H1, p 0.05) when the perturbation was removed. The RF-GMed coupling suggests an underlying abnormal coordination pattern in post-stroke SKG, likely reflexive in origin. These results challenge earlier assumptions that hip circumduction in stroke is simply a kinematic adaptation due to reduced toe clearance. Instead, abnormal coordination may underlie circumduction, illustrating the deleterious role of abnormal coordination in post-stroke gait.