Using surface electromyography to assess motor unit structural change post stroke

使用表面肌电图评估中风后运动单位结构变化

• 批准号: 8845633
• 负责人: Xiaogang HU
• 金额: $ 5.12万
• 依托单位: REHABILITATION INSTITUTE OF CHICAGO D/B/A SHIRLEY RYAN ABILITYLAB
• 依托单位国家: 美国
• 财政年份: 2014
• 资助国家: 美国
• 起止时间: 2014-06-01 至 2015-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8845633
• 关键词: Action Potentials; Address; Age; Algorithms; Architecture; Atrophic; Axon; Biopsy Specimen; Caliber; Characteristics; Clinic; Clinical; Contralateral; Denervation; Diagnosis; Diagnostic; Dorsal; Electrodes; Electromyography; Ensure; Fiber; Financial compensation; Frequencies; Health; Image; Impairment; Individual; Injury; Intramuscular; Isometric Contraction; Knowledge; Lead; Methods; Motor; Motor Neurons; Mus; Muscle; Muscle Fibers; Muscle Weakness; Neurons; Outcome; Outcomes Research; Paresis; Pattern; Peripheral; Phase; Plant Roots; Procedures; Process; Property; Recovery of Function; Rehabilitation therapy; Research; Role; Severities; Shapes; Side; Signal Transduction; Skin; Specific qualifier value; Stroke; Surface; Survivors; System; Techniques; Testing; Work; axonal sprouting; base; design; loss of function; motor function improvement; motor impairment; neuromuscular; novel; post stroke; reinnervation; targeted treatment; tool

DESCRIPTION (provided by applicant): Muscular weakness is one of the major impairments limiting motor function following a hemispheric stroke. One mechanism that can contribute to muscle weakness is the structural changes of the motor unit, including reduction of fiber diameter, muscle fiber loss, and even motor axon loss and motoneuron reinnervation of paretic muscles. Currently, our knowledge of the extent of such motor unit structural change post-stroke is limited by the constraints associated with intramuscular recording techniques, which are both invasive and inefficient. A novel surface electromyogram (sEMG) recording and decomposition technique for motor unit analysis has recently been developed and tested in neurologically intact individuals. The system utilizes a unique surface electrode that is non-invasive and efficient, potentially yielding a large number of motor units simultaneously. Accordingly, the aims of this proposal are 1) To quantify the degree and frequency of the reduction in motor unit size in paretic muscle post-stroke. 2) To establish robust markers of motoneuron reinnervation in paretic muscle of stroke survivors. We will record the sEMG signals of both paretic and contralateral first dorsal interosseous muscles of 32 stroke survivors during isometric contractions at specified force levels, and we will also record the sEMG of 32 neurologically intact age-matched control subjects. We will extract single motor unit discharge activities using the novel sEMG decomposition algorithm, and estimate motor unit shape characteristics using the spike triggered averaging techniques. To address Aim 1, we will calculate key motor unit action potential (MUAP) parameters, including peak-peak amplitude, duration, and root mean squared values, as estimates the motor unit size. To address Aim 2, we will quantify the polyphasic properties (i.e., the number of peaks) of the MUAP as an estimate of motoneuron reinnervation. We will also examine the association between the structural changes in motor units and the severity of motor impairment. We hypothesize that the motor unit size in the paretic muscle is reduced, because of fiber size reduction and muscle fiber loss, and that the polyphasic changes (i.e., a larger number of peaks) in the MUAP are also more visible in the paretic muscle following a stroke. The proposed research will provide important information regarding the role of peripheral motor unit structural changes in muscle weakness. The novel and non-invasive techniques used here will provide an efficient way to systematically examine changes in motor unit characteristics, and can potentially serve as a diagnostic tool to distinguish central vs. peripheral origins of muscle weakness in stroke. The proposed work can thus provide a rationale for differentially targeted rehabilitation therapies with a potential to maximize functional recovery of stroke survivors. i

描述（由申请人提供）：肌无力是半球卒中后限制运动功能的主要障碍之一。导致肌无力的一种机制是运动单位的结构变化，包括纤维直径减小、肌纤维损失、甚至运动轴突损失和麻痹肌肉的运动神经元再支配。目前，我们对中风后这种运动单元结构变化的程度的了解受到与肌内记录技术相关的约束的限制，肌内记录技术是侵入性的且效率低下。一种新的表面肌电图（sEMG）的记录和分解技术的运动单元分析最近已开发和测试在神经功能完好的个人。该系统采用独特的表面电极，是非侵入性和有效的，可能产生大量的运动单位同时。因此，本建议的目的是1）量化中风后轻瘫肌肉中运动单位尺寸减小的程度和频率。2)建立脑卒中幸存者瘫痪肌肉运动神经元再支配的可靠标记。我们将记录32名中风幸存者在指定力量水平下等长收缩期间的麻痹和对侧第一背侧骨间肌的sEMG信号，我们还将记录32名神经功能完好的年龄匹配对照受试者的sEMG。我们将使用新的表面肌电信号分解算法提取单个运动单位放电活动，并使用尖峰触发平均技术估计运动单位的形状特征。为了解决目标1，我们将计算关键的运动单位动作电位（MUAP）参数，包括峰-峰幅度、持续时间和均方根值，以估计运动单位大小。为了解决目标2，我们将量化多相特性（即，峰的数目）作为运动神经元再支配的估计。我们还将研究运动单位的结构变化和运动障碍的严重程度之间的关联。我们假设，由于纤维尺寸减小和肌纤维损失，轻瘫肌肉中的运动单位尺寸减小，并且多相变化（即，更大数量的峰）在中风后的麻痹肌肉中也更明显。这项研究将为外周运动单位结构变化在肌无力中的作用提供重要信息。这里使用的新的和非侵入性的技术将提供一种有效的方法来系统地检查运动单元特征的变化，并可能作为一种诊断工具，以区分中央与外周起源的中风肌肉无力。因此，拟议的工作可以提供一个理由，差异有针对性的康复治疗的潜力，以最大限度地恢复中风幸存者的功能。我