Altered Motor Function & Force Feedback After Spinal Cord Injury

运动功能改变

• 批准号: 9894867
• 负责人: DENA R. HOWLAND
• 金额: $ 57.87万
• 依托单位: UNIVERSITY OF LOUISVILLE
• 依托单位国家: 美国
• 财政年份: 2017
• 资助国家: 美国
• 起止时间: 2017-04-01 至 2022-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9894867
• 关键词: Acute; Animals; Area; Behavior; Bilateral; Chest; Data; Data Collection; Databases; Decerebrate State; Decerebration procedure; Development; Distal; Dorsal; Extensor; Feedback; Felis catus; Gait; Goals; Golgi Targeting; Golgi Tendon Organs; Human; Immunohistochemistry; Injury; Joints; Laboratories; Lateral; Leg; Lesion; Limb structure; Link; Locomotion; Maps; Mediating; Methods; Modeling; Motor; Movement; Muscle; Normal Statistical Distribution; Pathway interactions; Pattern; Performance; Phase; Preparation; Procedures; Production; Publishing; Recovery; Reflex action; Rehabilitation therapy; Research; Silver; Spinal; Spinal Cord; Spinal cord injury; Stains; System; Testing; Time; Walking; Weight; Work; base; design; experimental study; force feedback; gait examination; gait rehabilitation; injured; innovation; insight; kinematics; locomotor tasks; motor control; motor disorder; nervous system disorder; novel; preservation; programs; receptor; relating to nervous system; response; spinal tract; treadmill; white matter

Extensor muscles of the hind limbs are actively involved in weight support and walking activities. These muscles are extensively linked by inhibitory, force dependent pathways which contribute to the successful execution of a range of functional behaviors, including locomotion. These reflex pathways are thought to arise from Golgi tendon organs and are believed to regulate limb stiffness and promote inter-joint coordination during movements. Weightings of these linkages vary across control, decerebrate animals when quiescent, but obey a proximal to distal gradient during stepping on a treadmill. This finding indicates the strength and distribution of these reflex pathways are subject to modulation in a task-dependent manner. Our preliminary data in animals suggest that spinal cord hemisection alters the normal distribution and a dominant distal-to-proximal inhibitory gradient emerges. Animals with this lesion do not exhibit clasp-knife inhibition, a phenomenon mediated by receptors other than Golgi tendon organs and that results from bilateral injury to the dorsal half of the spinal cord. Changes in the strength and distribution of force feedback that we have observed is correlated with diminished limb stiffness and poor weight acceptance during locomotor tasks – both of which are problems seen in humans with spinal cord injuries (SCIs). These findings provide new insight into potential mechanisms contributing to disruption of motor function following injury. Our guiding hypothesis is: SCI- induced force-feedback dysregulation results in strong inhibition directed toward proximal muscles and contributes to inadequate limb stiffness during weight support phases of movement. The current application has evolved from collaborative work across two established laboratories, bringing together expertise in SCI, plasticity, force feedback and motor control. The proposed studies are designed to understand and map changes in force feedback control following SCI, characterize associated changes in gait subphases where inhibitory force feedback is thought to be most active across diverse locomotor tasks, and determine which white matter tracts may modulate spinal circuitry responsible for force feedback. Data generated in the proposed projects will be compared with an existing laboratory database containing force feedback findings from control decerebrate preparations. Overall, findings from these studies will explicate the impact of disrupting this intralimb control system on performance, provide critical mechanistic insight likely to be essential for design of the most effective rehabilitation programs for those with SCIs and other neurological disorders, and lay groundwork for development of a new method for testing force feedback in humans

后肢的伸肌积极参与体重支撑和步行活动。 这些肌肉通过抑制性，依赖力途径广泛联系 成功执行一系列功能行为，包括运动。这些 反射途径被认为是由高尔基肌腱器官引起的，被认为可以调节肢体 僵硬并促进运动过程中的关节间协调。这些联系的权重 在静止时在对照中，脑杂交动物变化，但服从远端到远端梯度 在踏上跑步机期间。这一发现表明这些反射的强度和分布 途径以任务依赖性方式受到调制。我们的初步数据 动物表明脊髓半分裂改变了正态分布和主导性 远端到抑制性梯度出现。这种病变的动物不存在扣刀 抑制作用，一种由高尔基肌腱器官以外的接收器介导的现象，结果 从双侧损伤到脊髓的背侧一半。强度和分布的变化 我们观察到的力反馈与肢体刚度的降低相关 运动任务期间的体重接受 - 这两者都是在人类中看到的问题 脊髓损伤（SCIS）。这些发现为潜在机制提供了新的见解 受伤后导致运动功能的破坏。我们的指导假设是： 诱导的力反馈失调导致针对的强烈抑制 近端肌肉并导致体重支撑期间的肢体刚度不足 运动阶段。当前的应用程序已经从两个的协作工作中演变 已建立的实验室，将SCI，可塑性，力量反馈和电动机的专业知识汇集在一起 控制。拟议的研究旨在理解和映射力反馈的变化 SCI之后的控制，在抑制力的情况下表征相关的变化 反馈被认为是在潜水员运动任务中最活跃的，并确定哪个 白质区可能会调节负责力反馈的脊柱回路。数据 将在拟议项目中生成的现有实验室数据库中生成 包含来自控制双脑部制剂的力反馈发现。总体而言，发现 这些研究将阐明破坏这种内部INTALIMB控制系统对 性能，提供可能对设计最重要的关键机理见解 为患有SCI和其他神经系统疾病的人有效的康复计划，并进行 开发新方法来测试人类反馈的基础