Using surface electromyography to assess motor unit structural change post stroke

描述(申请人提供)：肌肉无力是大脑半球中风后限制运动功能的主要损害之一。导致肌肉无力的一个机制是运动单位的结构变化，包括肌纤维直径缩小、肌纤维丢失，甚至瘫痪肌肉的运动轴突丢失和运动神经元再支配。目前，我们对中风后这种运动单位结构变化的程度的了解受到与肌肉内记录技术相关的限制，这些技术既有创伤性又效率低下。最近开发了一种用于运动单位分析的新的表面肌电(SEMG)记录和分解技术，并在神经功能正常的个体中进行了测试。该系统利用一种独特的非侵入性和高效的表面电极，潜在地同时产生大量的电机单元。因此，这项建议的目的是：1)量化中风后瘫痪肌肉运动单位大小减少的程度和频率。2)建立卒中幸存者偏瘫肌肉运动神经元再支配的可靠标记物。我们将记录32名中风幸存者在特定力量水平下等长收缩时偏瘫和对侧第一骨间背侧肌的表面肌电信号，也将记录32名神经功能正常的年龄匹配的对照组的表面肌电信号。我们将使用新的表面肌电信号分解算法提取单个运动单元的放电活动，并使用尖峰触发平均技术估计运动单元的形状特征。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，以估计运动单位的大小。为了达到目标2，我们将量化MUAP的多相特性(即峰值的数量)，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与运动损伤严重程度之间的关系。我们假设，由于纤维尺寸减小和肌肉纤维丢失，偏瘫肌肉中的运动单位尺寸减小，并且MUAP中的多相变化(即，更多的峰值)在中风后的偏瘫肌肉中也更明显。这项拟议的研究将提供有关外周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，并可能作为一种诊断工具来区分中风肌肉无力的中枢性和外周性起源。因此，这项拟议的工作可以为不同目标的康复治疗提供理论基础，有可能最大限度地促进中风幸存者的功能恢复。我

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