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.

项目摘要拟议项目的长期目标是了解脊髓的复杂起源损伤（SCI）诱发肌肉减少，萎缩，无力和肌肉缩水，通常导致有限联合运动的范围和内在肌肉机械性能的渐进变化。特别是我们的拟议的研究计划依赖于几种最近开发的新型表面雷电图（EMG）技术调查有关脊柱损伤后尾动神经元变性的有争议的概念。使用电动机单位编号索引测量和高密度表面EMG记录和处理技术，我们将确定运动单位结构和瘫痪肌肉的功能变化，可能是由于尾部引起的可以通过三个特定目标捕获运动神经元变性。即，我们计划评估是否在那里是使用运动单位数量的脊柱损伤的运动神经元变性的证据瘫痪的肌肉（AIM 1），并使用记录的自发性EMG活性在瘫痪的肌肉中（目标2）。此外，我们将检查运动单位动作电势传播模式的变化和神经区域，作为运动神经元损失的标志和随后的肌肉纤维瘫痪肌肉，因此为脊柱损伤提供了运动神经元变性的次要证据（AIM 3）。这这项研究中使用的方法无创，可能方便使用，并提供有价值的信息除了基于针的EMG和其他常规电生理方法提供的内容之外。来自这些新颖的方法将增强我们对潜在运动神经元病理生理学的理解科学堕落。这将为制定康复策略和设备的制定提供指导恢复正常肌肉功能。这项研究的发现还具有重要的临床价值诊断和治疗脊柱损伤，改善结果测量并帮助评估药物或疗法。