Altered Motor Function & Force Feedback After Spinal Cord Injury

后肢的伸肌积极参与重量支撑和行走活动。 这些肌肉通过抑制性的、依赖于力的通路广泛地连接， 一系列功能性行为的成功执行，包括运动。这些 反射通路被认为起源于高尔基体腱器官， 并促进运动过程中关节间协调。这些联系的权重 对照组之间存在差异，动物在静止时去大脑，但服从近端到远端的梯度 在跑步机上行走。这一发现表明了这些反射的强度和分布 通路以任务依赖的方式受到调节。我们的初步数据， 动物表明，脊髓半切改变了正常分布和一个主导的 出现远端到近端的抑制梯度。有这种病变的动物不表现出折刀 抑制，这是一种由高尔基体腱器官以外受体介导的现象， 脊髓背侧的双侧损伤强度和分布的变化 我们观察到的力反馈与肢体僵硬度降低和 在运动任务中的体重接受-这两个问题都是在人类身上看到的， 脊髓损伤（SCI）。这些发现为潜在机制提供了新的见解 导致损伤后运动功能的破坏。我们的指导假设是：SCI- 诱导的力反馈失调导致强烈的抑制， 近端肌肉，并在重量支撑期间导致肢体刚度不足 运动的阶段。目前的应用程序已经从两个跨部门的协作工作发展而来， 建立了实验室，汇集了SCI，可塑性，力反馈和电机方面的专业知识 控制拟议的研究旨在了解和映射力反馈的变化 SCI后的控制，表征步态亚阶段的相关变化，其中抑制力 反馈被认为在不同的运动任务中是最活跃的，并决定了 白色物质束可以调节负责力反馈的脊髓回路。数据 将与现有的实验室数据库进行比较 包含来自控制去大脑制剂的力反馈结果。总体而言， 这些研究将阐明破坏这种体内控制系统对 性能，提供关键的机械洞察力可能是必不可少的设计最 为SCI患者和其他神经系统疾病患者提供有效的康复计划， 为开发测试人体力反馈的新方法奠定基础

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