Altered Motor Function & Force Feedback After Spinal Cord Injury

后肢伸展肌肉积极参与重量支持和行走活动。 这些肌肉广泛地由抑制性的、力依赖的通路连接在一起。 一系列功能行为的成功执行，包括运动。这些 反射通路被认为起源于高尔基体肌腱器官，并被认为调节肢体 僵硬，并促进运动中关节间的协调。这些链接的权重 在对照中变化，在静止时去掉动物的大脑，但服从近端到远端的梯度 在踩着跑步机的时候。这一发现表明了这些反射的强度和分布。 通路以一种任务相关的方式受到调制。我们的初步数据在 动物表明，脊髓半横断改变了正态分布和显性 远端至近端出现抑制梯度。患有这种病变的动物不会表现出卡片刀。 抑制，一种由高尔基肌腱器官以外的受体介导的现象，并导致 从双侧损伤到脊髓后半部。力量和分布的变化 我们观察到的力反馈与肢体僵硬和不良相关 运动任务中的体重承受性--这两种情况在人类中都存在 脊髓损伤(SCI)。这些发现为潜在的机制提供了新的见解 导致受伤后运动功能的中断。我们的指导性假设是：SCI- 诱导性力反馈失调导致强抑制作用 近端肌肉，并在负重支持过程中导致肢体僵硬不足 运动的阶段。当前的应用程序已经从跨两个应用程序的协作工作发展而来 现有的实验室，汇集了脊髓损伤、可塑性、力反馈和运动方面的专业知识 控制力。拟议的研究旨在了解和绘制力反馈中的变化 脊髓损伤后的对照，表征步态亚相的相关变化，其中抑制力 反馈被认为是在不同的运动任务中最活跃的，并决定了 白质束可能调制负责力反馈的脊髓回路。数据 在拟议项目中生成的数据将与现有的实验室数据库进行比较 包含来自对照去大脑准备的力反馈结果。总体而言，来自 这些研究将阐明破坏这种肢体内部控制系统对 性能，提供关键的机械洞察力，这可能是设计最重要的 为那些患有SCI和其他神经疾病的人提供有效的康复计划，并 为开发一种新的人体力反馈测试方法奠定基础

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