Combining neurophysiology and biomechanics to delineate post-stroke gait impairments

结合神经生理学和生物力学来描述中风后步态障碍

• 批准号: 10599625
• 负责人: James Sulzer
• 金额: $ 38.82万
• 依托单位: CASE WESTERN RESERVE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2020
• 资助国家: 美国
• 起止时间: 2020-08-01 至 2025-07-31
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/10599625
• 关键词: Abnormal coordination; Address; Affect; Age; Behavior; Belief; Biomechanics; Complex; Computing Methodologies; Couples; Coupling; Data; Development; Educational Intervention; Exhibits; Financial compensation; Gait; Goals; H-Reflex; Hip region structure; Homosynaptic Depression; Human; Hyperactivity; Hyperreflexia; Impairment; Individual; Intelligence; Internet; Intervention; Knee; Knowledge; Lead; Link; Methods; Modeling; Motion; Motor Neurons; Muscle; Muscle Weakness; Musculoskeletal; Nervous System Trauma; Neurologic; Neuronal Plasticity; Neurotransmitters; Orthotic Devices; Pathologic; Pattern; Pelvis; Peripheral Nerve Stimulation; Persons; Phase; Physical therapy; Plant Roots; Procedures; Protocols documentation; Reflex action; Research; Robotics; Role; Self-Help Devices; Soleus Muscle; Spinal; Stimulus; Stroke; Techniques; Testing; Walking; Work; abnormal reflex; base; clinically significant; conditioning; conventional therapy; exoskeleton; experience; experimental study; femoral nerve; foot; improved; innovation; kinematics; multidisciplinary; multimodality; neuromuscular; neurophysiology; neuroregulation; novel; novel strategies; post stroke; presynaptic; prevent; quadriceps muscle; rectus femoris; relating to nervous system; response; side effect; spinal reflex; stem; stretch reflex; targeted treatment; treatment planning; working group

PROJECT SUMMARY Following stroke, numerous impairments develop that affect walking ability. We lack a clear understanding of what characterizes these impairments and their relation to impaired walking ability. For example, we applied exoskeletal knee flexion to assist those with reduced knee flexion post-stroke. The assistance improved knee flexion but surprisingly worsened compensatory motions such as hip abduction. Preliminary analysis indicated that the assistance elicited hyperexcitable quadriceps reflex activity. Additionally, the quadriceps response was abnormally coordinated with hip abductor muscles only in post-stroke individuals. These results question traditional beliefs regarding which motions are compensatory and which are due to neural impairment. Thus, the critical gap to restoring functional gait post-stroke is characterizing the interconnection between biomechanical issues and neural impairments. Our novel approach is to combine state-of-the-art methods in biomechanics and neurophysiology to develop cause-and-effect models of the interconnection between gait kinematics, hyperexcitable reflex activity and abnormal coordination. The clinical significance is the groundwork for targeted interventions such as reflex modulation and neurally intelligent exoskeletons that interact with the impaired spinal circuitry. It will be shown in our preliminary work that we have years of experience characterizing post-stroke gait impairments using reflex stimulation, robotics and computational methods that uniquely qualify our group for this project. The objective of this proposal is to establish the biomechanical and neurophysiological mechanisms underlying pathological gait post-stroke. In Aim 1, we determine whether hip abduction is a compensation for reduced knee flexion by comparing people with stroke to induced similar walking patterns in healthy individuals. Muscle activation patterns and intralimb coordination will provide evidence towards fundamental differences in neural control after stroke. In Aim 2, we use reflex neurophysiological methods to probe post- stroke individuals’ reflex coordination patterns. We expect to find that hyperactive quadriceps reflexes are associated with impaired knee flexion. We additionally expect to show the interrelation between reflex activity in the quadriceps and the abductors as predicted by our models representing abnormal coordination. In Aim 3, we use reflex conditioning protocols during gait based on sophisticated paired peripheral nerve stimulation techniques. These methods will provide evidence of the spinal mechanisms at the root of abnormal reflex behavior that likely underlie impaired gait post-stroke. Together this comprehensive testing procedure incorporates biomechanics and neurophysiology to reveal new knowledge of post-stroke gait impairment. These results will have broad impact on our understanding of neuromuscular impairments and enable the development of targeted therapies for treatment.

项目摘要 中风后，会产生许多影响步行能力的障碍。我们对 这些障碍及其与步行能力受损的关系的特征。例如，我们应用了 外骨骼的膝盖屈曲，以帮助减少膝盖屈曲的人。援助改善了膝盖 屈曲，但令人惊讶的是，补偿性动作（例如髋关节绑架）。初步分析 援助引起了六头肌反射活性。另外，股四头肌的响应是 仅在后击中的个体中与髋关节绑架肌肉协调。这些结果问题 关于哪些运动是补偿性的传统信念，哪些是由于神经损害。那， 恢复势势恢复功能差距的关键差距是表征 生物力学问题和神经障碍。我们的新方法是将最新方法结合在 生物力学和神经生理学，以开发步态之间相互联系的因果模型 运动学，过度锻炼反射活性和异常协调。临床意义是 针对目标干预措施的基础工作，例如反射调制和中性智能外骨骼 与受损的脊柱回路相互作用。我们的初步工作将显示我们多年 使用反射刺激，机器人技术和计算表征后触摸后的损伤表征后的经验 唯一使我们的小组符合该项目的方法。 该建议的目的是建立生物力学和神经生理机制 基础病理步态后冲程。在AIM 1中，我们确定髋关节绑架是否是对 通过比较中风的人与诱发的健康步行模式来减少膝盖屈曲 个人。肌肉激活模式和INTALIMB协调将提供基本的证据 中风后神经控制的差异。在AIM 2中，我们使用反射神经生理方法来探测 - 中风个人的反射协调模式。我们希望发现多动股四头肌反射是 与膝盖屈曲受损有关。我们还期望显示反射活动之间的相互关系 在AIM 3中， 我们基于复杂的配对外周神经刺激在步态过程中使用反射调节方案 技术。这些方法将提供异常反射根源的脊柱机制的证据 行程后触摸后可能受损的行为。一起这个全面的测试程序 结合生物力学和神经生理学，以揭示触摸后步态障碍的新知识。 这些结果将对我们对神经肌肉障碍的理解产生广泛的影响，并使 开发有针对性的治疗疗法。