Determining the effects of increased demands for voluntary adjustments on the neuromuscular control of walking post-stroke

确定自愿调整需求增加对中风后行走神经肌肉控制的影响

• 批准号: 10596397
• 负责人: Natalia Sanchez
• 金额: $ 15.16万
• 依托单位: CHAPMAN UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2023
• 资助国家: 美国
• 起止时间: 2023-06-01 至 2025-05-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10596397
• 关键词: Age; Agonist; Awareness; Behavior; Biofeedback; Brain Stem; Chronic; Clinical; Clinical Trials; Compensation; Cues; Data; Disabled Persons; Educational Intervention; Environment; Foundations; Future; Generations; Goals; Impairment; Individual; Interruption; Intervention; Joints; Kinetics; Length; Lesion; Lower Extremity; Measures; Mediating; Modification; Motor; Movement; Muscle; Nervous System Trauma; Neural Pathways; Participant; Pathway interactions; Pattern; Persons; Protocols documentation; Recovery; Rehabilitation therapy; Research; Research Priority; Residual state; Resources; Speed; Stroke; Testing; Time; Torque; Training; Visual; Walking; Work; antagonist; clinical decision-making; comparison control; design; gait rehabilitation; hemiparetic stroke; indexing; insight; kinematics; motor control; motor impairment; neural; neuroimaging; neuromuscular; neuroregulation; novel strategies; post stroke; primary outcome; response; restoration; stroke survivor; therapy design; treadmill; treatment response; verbal; walking intervention; walking rehabilitation

Abstract The goal of this proposal is to determine the effects of explicitly driven or implicitly driven walking modifications on muscle activation patterns and co-contraction post-stroke. This work is significant, as studies have shown that muscle activation patterns after neurologic injury cannot generate walking kinematics comparable to those seen in neurotypical individuals; this finding implies that to attain true walking recovery after neurologic injury, interventions should aim to restore the muscle activations underlying walking behaviors. Here, we first explore muscle activations during walking using biofeedback to guide explicit modification of walking patterns, which is a common approach used in clinical and research interventions for walking retraining. We hypothesize that explicit walking modifications might be detrimental at a muscle activation level as they engage cortical pathways for voluntary control that have been interrupted by the stroke lesion, resulting in increased muscle co-contraction. Co-contraction hinders true recovery as it impairs the ability to selectively control different segments during walking, resulting in overreliance on compensatory patterns. We will also explore muscle activation patterns during implicit walking modifications. We will use external modifications in the walking environment, mainly split-belt adaptation followed by tied belt walking, to assess if implicit modifications of walking that rely less on cortical neural control are associated with levels of co-contraction comparable to neurotypical controls—an indication that implicitly-mediated modifications could be a more effective approach to restore muscle activation patterns during walking post-stroke. In this study, we will assess co-contraction during walking in people post-stroke as they reduce asymmetry in step lengths guided by explicit biofeedback (Aim 1) or implicitly following split-belt adaptation and washout (Aim 2). Our central hypothesis is that given differences in the neural control of explicitly- vs. implicitly-mediated walking modifications, we will observe greater levels of co-contraction with interventions that rely on explicit compared to implicit control. Supplementing this central hypothesis, we also predict that co-contraction will be associated with motor impairment, and in more impaired individuals co-contraction will be exacerbated by explicit modifications given the reliance on lesioned cortical pathways. Our results will identify the tasks and conditions that can reduce co- contraction to promote restoration of neuromuscular control post-stroke. This proposal aligns with the NCMRR research priority to develop objective markers of treatment response and functional progress that predict rehabilitation treatment response and enable the tailoring of interventions to the needs, abilities, and resources of the person with disability.

摘要 这个建议的目标是确定显式驱动或隐式驱动的步行修改的效果 中风后的肌肉激活模式和协同收缩。研究表明，这项工作意义重大 神经损伤后的肌肉激活模式不能产生与那些 在神经典型个体中可见;这一发现意味着为了在神经损伤后获得真正的行走恢复， 干预措施应旨在恢复步行行为背后的肌肉激活。在这里，我们首先探索 在步行过程中使用生物反馈来指导明确修改步行模式，这是 这是临床和研究干预中用于行走再训练的常用方法。我们假设 明确的步行改变可能在肌肉激活水平上是有害的，因为它们涉及皮层神经元， 自愿控制的途径已被中风病变中断，导致肌肉增加 共收缩。共同收缩阻碍了真正的复苏，因为它损害了选择性控制不同的能力。 在步行过程中的节，导致过度依赖代偿模式。我们还将探索肌肉 在隐式步行修改期间的激活模式。我们将在行走中使用外部修改 环境，主要是分裂带适应，然后是系带行走，以评估是否隐含的修改， 较少依赖皮质神经控制的行走与协同收缩水平相关， 神经典型对照-暗示介导的修饰可能是更有效的方法 恢复中风后行走时的肌肉激活模式。在这项研究中，我们将评估共同收缩 在中风后的人行走过程中，由于他们在明确的生物反馈指导下减少了步长的不对称性， (Aim 1）或隐含地遵循分裂带适应和洗脱（目标2）。我们的核心假设是， 显式与隐式介导的步行修改的神经控制的差异，我们将观察 与内隐控制相比，依赖外显控制的干预措施的共同收缩程度更高。 补充这一中心假设，我们还预测，共同收缩将与运动 在更多受损的个体中，共同收缩将因明确的修改而加剧， 对受损皮层通路的依赖我们的研究结果将确定任务和条件，可以减少co- 收缩以促进中风后神经肌肉控制的恢复。本提案与NCMRR保持一致 优先研究开发治疗反应和功能进展的客观标志物， 康复治疗反应，并使干预措施能够适应需求，能力和资源 残疾人的权利。