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: 8770743
• 负责人: Xiaogang HU
• 金额: $ 7.65万
• 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 2016-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8770743
• 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; 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）：肌肉无力是半球中风后限制运动功能的主要损伤之一。导致肌肉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瘫痪肌肉的运动神经元重新神经支配。目前，我们对中风后运动单位结构变化程度的了解受到与肌内记录技术相关的限制，这些技术既具有侵入性又效率低下。最近开发出了一种用于运动单位分析的新型表面肌电图（sEMG）记录和分解技术，并在神经系统完整的个体中进行了测试。该系统采用独特的表面电极，非侵入性且高效，有可能同时产生大量运动单位。因此，该提案的目的是 1) 量化中风后麻痹肌肉运动单位大小减少的程度和频率。 2) 建立中风幸存者瘫痪肌肉运动神经元神经支配的强有力标记。我们将记录 32 名中风幸存者在指定力量水平的等长收缩期间的麻痹性和对侧第一背侧骨间肌的 sEMG 信号，我们还将记录 32 名神经系统完整的年龄匹配对照受试者的 sEMG 信号。我们将使用新颖的 sEMG 分解算法提取单个运动单元放电活动，并使用尖峰触发平均技术估计运动单元形状特征。为了实现目标 1，我们将计算关键运动单位动作电位 (MUAP) 参数，包括峰峰值幅度、持续时间和均方根值，以估计运动单位大小。为了实现目标 2，我们将量化 MUAP 的多相特性（即峰值数量）作为运动神经元神经支配的估计。我们还将检查运动单位的结构变化与运动损伤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，瘫痪肌肉的运动单位尺寸减小，并且中风后瘫痪肌肉中 MUAP 的多相变化（即大量峰值）也更加明显。拟议的研究将提供有关周围运动单位结构变化在肌肉无力中的作用的重要信息。这里使用的新颖的非侵入性技术将提供一种有效的方法来系统地检查运动单位特征的变化，并有可能作为一种诊断工具来区分中风中肌肉无力的中枢和外周起源。因此，拟议的工作可以为差异化靶向康复治疗提供理论依据，并有可能最大限度地提高中风幸存者的功能恢复。我