Comparison of muscle coordination between individuals post-stroke and kinematically constrained walking
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Abnormal motor coordination affects motor function following stroke, yet we lack a complete characterization of how such abnormal coordination affects movements such as gait. Previous research found that post-stroke gait exhibited fewer movement primitives, or muscle modules, than healthy individuals, suggesting abnormal coordination may affect gait function. However, aside from abnormal coordination, the reduced number of modules could also be due to compensations in response to other impairments such as increased muscle tone and spasticity. Our previous research compared gait in those with post-stroke Stiff-Knee Gait (SKG) to healthy individuals with kinematically constrained knee flexion. While healthy individuals compensated with pelvic obliquity, those with post-stroke SKG also exhibited greater hip abduction, suggesting the motion may be related to neural impairments such as abnormal coordination. We hypothesize that abnormal coordination, not the compensations due to restricted ranges of motion induced by other impairments, is associated with reduced gait function. In this experiment, we compared muscle coordination patterns emerging from healthy individuals with and without restricted knee kinematics to a cohort of individuals post-stroke, both with and without SKG. We predicted the number of muscle modules would be fewer than healthy individuals with similar gait kinematics and found that mechanical knee restriction reduced the number of modules similar to those with post-stroke SKG in walking. Constraining healthy motions resulted in similar muscular coordination patterns to unrestricted gait suggesting the robustness of muscle recruitment despite a kinematic perturbation. The composition of modules in the pre-swing phase between those with SKG and the mechanically restricted group differed (Spearman’s ρ = -0.024), whereas comparisons between post-stroke individuals without SKG (NSKG) and the healthy group were similar (Spearman’s ρ = 0.833). We found those with SKG relied less on hamstrings than healthy counterparts, suggesting an altered motor command beyond adaptation. Muscle coordination patterns in constrained motions during gait were not similar to SKG while the NSKG group showed greater similarity to normal walking. Thus, our data suggests that abnormal coordination may play a greater role in SKG than those without SKG. The results of this comparison will help develop more accurate interventions for clinical treatment.