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: 10222742
• 负责人: James Sulzer
• 金额: $ 39.08万
• 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 2022-06-05
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10222742
• 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; 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.

项目概要 中风后，会出现许多影响行走能力的损伤。我们缺乏清晰的认识 这些障碍的特征及其与行走能力障碍的关系。例如，我们应用了 外骨骼膝关节屈曲，以帮助中风后膝关节屈曲减少的患者。辅助改善膝盖 屈曲，但令人惊讶的是代偿性运动（例如髋部外展）恶化。初步分析表明 援助引起了股四头肌反射活动的过度兴奋。此外，股四头肌的反应是 仅在中风后个体中与髋关节外展肌异常协调。这些结果提出疑问 传统观念认为哪些运动是代偿性的，哪些运动是由于神经损伤造成的。因此， 中风后恢复功能性步态的关键差距是表征之间的相互联系 生物力学问题和神经损伤。我们的新颖方法是将最先进的方法结合起来 生物力学和神经生理学开发步态之间相互联系的因果模型 运动学、过度兴奋的反射活动和异常协调。其临床意义在于 为反射调节和神经智能外骨骼等有针对性的干预措施奠定基础 与受损的脊髓回路相互作用。我们的前期工作将表明我们有多年的经验 使用反射刺激、机器人技术和计算来表征中风后步态障碍的经验 使我们团队有资格参与该项目的独特方法。 该提案的目的是建立生物力学和神经生理学机制 中风后潜在的病理步态。在目标 1 中，我们确定髋部外展是否是对 通过比较中风患者来减少膝关节弯曲，以诱导健康人相似的步行模式 个人。肌肉激活模式和肢体内协调将为基本原理提供证据 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究后 中风个体的反射协调模式。我们期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 正如我们的模型所预测的，股四头肌和外展肌代表异常协调。在目标 3 中， 我们在步态期间使用基于复杂的配对周围神经刺激的反射调节方案 技术。这些方法将为异常反射根源的脊柱机制提供证据 可能是中风后步态受损的行为。综合这个全面的测试程序 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，并使 开发针对治疗的靶向疗法。