Akbas Tunc, Neptune Richard R, Sulzer James
Walker Department of Mechanical Engineering, University of Texas at Austin, Austin, TX, United States.
Front Neurol. 2019 Apr 2;10:301. doi: 10.3389/fneur.2019.00301. eCollection 2019.
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, < 0.001) and simulated (H1, = 0.022) activity. Simulated RF and gluteus medius (GMed) activations were correlated only in those with SKG, which was significantly higher compared to healthy controls (H1, = 0.030). There was no evidence of synergistic coupling between any combination of hamstrings and hip abductors (H2, > 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.
中风后的步态通常伴随着肌肉损伤，这会导致诸如髋关节外展等适应性变化，以补偿膝关节屈曲不足。我们之前的研究通过机器人辅助增强了中风后患有僵膝步态（SKG）个体的膝关节屈曲，然而，这导致了更大程度的外展，表明SKG中存在异常协调。这项研究的目的是探究异常协调的两种可能机制：（1）股四头肌和外展肌拉伸之间的反射耦合，以及（2）自主激活的膝关节屈肌和外展肌之间的耦合。我们使用了之前收集的九名慢性中风参与者和五名健康对照在步态摆动前期行走时有无施加膝关节屈曲扭矩扰动情况下的运动学、动力学和肌电图测量数据，进行神经肌肉骨骼模拟。通过模拟肌肉激活来补充测量的肌肉活动，以估计股四头肌、腘绳肌和髋外展肌的肌肉状态。我们使用线性混合模型来探究两个假设：（H1）扰动后非自主期（反射潜伏期）内股四头肌和外展肌激活之间的关联，以及（H2）扰动消除后腘绳肌和外展肌激活之间的关联。基于测量（H1，<0.001）和模拟（H1，=0.022）活动，我们观察到在扰动后的非自主反应期内，中风参与者的股直肌（RF）激活明显高于健康对照。模拟的RF和臀中肌（GMed）激活仅在患有SKG的个体中相关，与健康对照相比显著更高（H1，=0.030）。当扰动消除时，没有证据表明腘绳肌和髋外展肌的任何组合之间存在协同耦合（H2，>0.05）。RF - GMed耦合表明中风后SKG中存在潜在的异常协调模式，可能起源于反射。这些结果挑战了早期的假设，即中风中的髋关节外展仅仅是由于脚趾离地间隙减小而产生的运动学适应。相反，异常协调可能是外展的基础，说明了异常协调在中风后步态中的有害作用。
