Delineating abnormal coordination patterns in post-stroke gait : a multidisciplinary approach
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Stroke is the largest cause of long-term disability in U.S. where majority of the survivors experience impairments such as muscle weakness, spasticity and abnormal coordination. Stiff-Knee gait (SKG) is an incessant disability defined by the reduced knee flexion during swing. The abnormal neuromuscular mechanisms governing the interactions between impairments during SKG is still not clear. This work attempts to reveal the causal relationship between the specific influences of different impairments on post-stroke gait. Specifically, it delineates the underlying neuromuscular mechanisms behind observed increased hip abduction in SKG. The results indicate that hip abduction is part of an abnormal coordination pattern, instead of a presumed compensation for reduced knee flexion. This result is supported by previous work observing coupled knee flexion and hip abduction motions during SKG following pre-swing knee flexion torque perturbations. I hypothesized the underlying mechanism behind excessive hip abduction is due to an involuntary mechanism between quadriceps and abductor muscles which is initiated by quadriceps hyperreflexia. The results obtained from neuromusculoskeletal modeling and simulation suggest an involuntary coupled response between estimated rectus femoris (RF) and gluteus medius (GMed) activations following simulated peak RF fiber stretch velocity, suggesting an abnormal cross-planar reflex coupling initiated by excessive RF stretch reflex response. We have elicited RF reflex responses in SKG to identify the association between RF hyperreflexia and severity of the SKG excluding the influence of increased voluntary RF activity. Our results indicate a strong negative correlation between RF H-reflex response and reduced peak knee flexion angle in SKG, revealing the distinctive influence of spasticity in SKG. This novel framework delineates the abnormal neuromuscular mechanisms behind the excessive hip abduction in post-stroke gait using biomechanics, neuromusculoskeletal simulations and neurophysiological perturbations. The results obtained from this dissertation could improve lower-limb interventions for gait rehabilitation following stroke by introducing quantified measures of abnormal coordination in SKG and improve the development of subject-specific assistive technology targeting impairments to restore healthy gait.