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Degeneration of motoneurons caudal to spinal lesion

脊髓病变尾部运动神经元变性

基本信息

批准号：
8412990
负责人：
WILLIAM Zev RYMER
金额：
$ 18.67万
依托单位：
REHABILITATION INSTITUTE OF CHICAGO D/B/A SHIRLEY RYAN ABILITYLAB
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-02-01 至 2014-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8412990
关键词：
Action Potentials Acute Amyotrophic Lateral Sclerosis Articular Range of Motion Atrophic Cervical spinal cord injury Cessation of life Chronic Clinical Contracture Data Development Diagnosis Diagnostic Disease Disease Progression Electric Stimulation Electrodes Frequencies Functional disorder Goals Hand Knowledge Lesion Longitudinal Studies Measurement Measures Mechanics Mediating Methods Motor Motor Neurons Movement Muscle Muscle Fibers Muscle Weakness Muscle fasciculation Muscle function Needles Neurologic Outcome Paralysed Paresis Pattern Pharmaceutical Preparations Prevalence Process Property Quadriplegia Rehabilitation device Relative (related person)Research Rest Skeletal Muscle Spastic Spinal Spinal Injuries Spinal cord injury Spinal cord injury patients Structure Surface Techniques Testing Time abstracting base density effective therapy improved indexing motor impairment nerve supply novel rehabilitation strategy reinnervation restoration white matter damage

项目摘要

Project Abstract The long-term goals of the proposed project are to understand the complicated origins of the spinal cord injury (SCI) induced muscle paresis, atrophy, weakness, and muscle contractures that often result in a limited range of joint motion and progressive changes in intrinsic muscle mechanical properties. In particular, our proposed research plan relies on several recently developed novel surface electromygram (EMG) techniques to investigate controversial concepts about caudal motoneuron degeneration after a spinal injury. Using motor unit number index measurements and high-density surface EMG recording and processing techniques, we will determine whether motor unit structure and function changes of paralyzed muscles, potentially due to caudal motoneuron degeneration, can be captured via three specific aims. Namely, we plan to assess whether there is evidence for motoneuron degeneration caudal to spinal injury using estimates of motor unit numbers in paralyzed muscles (Aim 1), and using the recorded spontaneous EMG activities in resting paralyzed muscles (Aim 2). In addition, we will examine alterations in motor unit action potential propagation patterns and innervation zones, as a marker of motoneuron loss and subsequent muscle fiber reinnervation in paralyzed muscles, thus providing secondary evidence for motoneuron degeneration caudal to spinal injury (Aim 3). The methods used in this study are noninvasive, potentially convenient to use, and offer valuable information beyond that provided by needle-based EMG and other routine electrophysiological methods. The findings from these novel methods will enhance our understanding of the pathophysiology of potential motoneuron degeneration in SCI. This will provide guidance for the development of rehabilitation strategies and devices for restoration of normal muscle functions. The findings from this study also have important clinical value for the diagnosis and treatment of spinal injury, improve outcome measurements, and help evaluate the effects of medication or therapies.

项目摘要该项目的长期目标是了解脊髓的复杂起源损伤（SCI）引起的肌肉麻痹、萎缩、虚弱和肌肉挛缩，通常导致有限的关节活动范围和内在肌肉力学特性的渐进性变化。特别是我们提出的研究计划依赖于最近开发的几种新的表面肌电图（EMG）技术探讨脊髓损伤后尾侧运动神经元变性的争议性概念。使用电机单位数指数测量和高密度表面肌电图记录和处理技术，我们将确定是否运动单位的结构和功能的变化麻痹的肌肉，可能是由于尾部运动神经元退化，可以通过三个特定的目标来捕获。也就是说，我们计划评估是否有是脊髓损伤后运动神经元变性的证据，使用运动单位数量的估计，瘫痪肌肉（目的1），并使用记录的自发EMG活动，在休息瘫痪肌肉 (Aim 2）。此外，我们将研究运动单位动作电位传播模式的改变，神经支配区，作为运动神经元丢失和随后的肌纤维再支配的标记，肌肉，从而提供脊髓损伤尾侧运动神经元变性的次要证据（目的3）。的本研究中使用的方法是非侵入性的，使用方便，并提供有价值的信息这超出了基于针的EMG和其他常规电生理学方法所提供的。的结果这些新方法将增强我们对潜在运动神经元病理生理学的理解。 SCI的退化。这将为制定康复策略和设备提供指导，恢复正常的肌肉功能。本研究的发现对临床应用也有重要价值。脊柱损伤的诊断和治疗，改善结果测量，并帮助评估药物或治疗。