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: 10052892
• 负责人: James Sulzer
• 金额: $ 43.61万
• 依托单位: UNIVERSITY OF TEXAS AT AUSTIN
• 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/10052892
• 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; Hyperactive behavior; 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; 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，许多损害发展，影响行走能力。我们缺乏一个清晰的认识 这些损伤的特征及其与步行能力受损的关系。例如，我们应用 外骨骼膝关节屈曲，以帮助中风后膝关节屈曲减少的患者。辅助改善膝关节 屈曲，但令人惊讶地恶化了代偿运动，如髋关节外展。初步分析显示 这种帮助引起了过度兴奋的股四头肌反射活动。此外，股四头肌反应是 仅在中风后个体中与髋外展肌异常协调。这些结果质疑 关于哪些运动是补偿性的，哪些是由于神经损伤的传统观念。因此，在本发明中， 中风后恢复功能性步态的关键差距是表征以下因素之间的相互联系： 生物力学问题和神经损伤。我们的新方法是将联合收割机最先进的方法结合起来， 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、过度兴奋反射活动和异常协调。临床意义在于 有针对性的干预措施的基础，如反射调制和神经智能外骨骼， 与受损的脊髓回路相互作用在我们的初步工作中将表明，我们有多年的 使用反射刺激、机器人技术和计算机技术表征卒中后步态障碍的经验 使我们小组有资格参与这个项目的独特方法。 本建议的目的是建立生物力学和神经生理机制 中风后潜在的病理步态。在目标1中，我们确定髋关节外展是否是对 通过比较中风患者减少膝关节屈曲，以诱导健康人相似的步行模式， 个体肌肉激活模式和肢体内协调将提供证据， 中风后神经控制的差异。在目标2中，我们使用反射神经生理学方法来探索后 中风个体的反射协调模式。我们希望发现过度活跃的股四头肌反射 与膝关节屈曲受损有关。我们还希望展示反射活动之间的相互关系 在四头肌和外展肌中，正如我们的模型所预测的那样，代表着异常的协调。在目标3中， 我们在步态中使用基于复杂的成对外周神经刺激的反射调节协议， 技术.这些方法将为研究反射异常的脊髓机制提供依据 可能导致中风后步态受损的行为。这一全面的测试程序 结合生物力学和神经生理学，揭示中风后步态障碍的新知识。 这些结果将对我们对神经肌肉损伤的理解产生广泛的影响， 开发用于治疗的靶向疗法。