Shift from Unilateral to Bilateral Sensory-Motor Connectivity in Chronic Hemiparetic Stroke

抽象的。中风后出现的异常运动协同作用是中风患者的主要限制。 通过将随意运动限制为刻板的肌肉共激活来恢复独立功能 模式.屈曲协同作用的最终表现限制了手臂/手的功能，如伸展和手的张开; 并且还被报道与过度活跃的牵张反射或痉挛有关。先前的研究发现， 屈曲协同和痉挛与对侧降皮质的募集有关， 延髓脊髓径路然而，体感系统如何适应这种运动使用的变化， 通路和适应性感觉反馈对麻痹手臂的异常运动控制的作用仍然存在 大部分未知。从麻痹手臂传递躯体感觉的上行感觉通路 在受损半球的初级感觉皮层的对侧。然而，我们的初步数据显示， 表明，在表达屈曲协同和痉挛的个体中，这种感觉信息是 随后转移到对侧半球，这是一个可能支持 偏瘫性中风的异常运动模式。本研究的总体目标是研究 这种适应不良的半球体感“转变”的病理生理学及其与上半球的关系 偏瘫中风后的肢体运动障碍。结果将导致更好地理解 异常肢体协同作用和痉挛通过关闭感觉运动回路，这应该提供一种新的手段 通过其治疗性地预防和减轻上肢运动损伤的出现和表现， 中风之后拟议的研究旨在测试我们特定目标中的以下关键假设： 单侧运动性中风后，躯体感觉处理的半球移位提供感觉反馈 来支持运动系统中不适应的半球移位。这种大脑半球的感觉转移不仅 影响意志运动控制，这有助于屈曲协同作用的表达（目标1），但 也是牵张反射的经皮质回路，其与过度活跃的牵张反射（或痉挛状态）有关。 以及长潜伏期牵张反射的增加的起始延迟（Aim 2）。此外，大脑半球的感觉 移位，作为受伤大脑中神经可塑性的结果，可以在没有运动输出的情况下发生;并且这种感觉 移位可以指示运动缺陷的程度（目标3）。通过测试这些假设，拟议的研究将 提高我们对感觉反馈在中风后运动障碍中的作用的理解。这应该允许 从新的感官角度确定更多受损个体的运动缺陷， 难以执行运动任务的急性/亚急性患者。此外，在此过程中获得的知识 这项研究将促进未来开发有针对性的、假设驱动的治疗干预措施， 在恢复过程中减少适应不良的跨半球感觉-运动连接，从而促进运动 功能，而不诱导异常协同作用和痉挛损伤。

Abstract. The emergence of abnormal movement synergies following a stroke presents a major limitation to the recovery of independent function by constraining voluntary movements to stereotypical muscle coactivation patterns. The resulting expression of the flexion synergy limits arm/hand function, like reaching and hand opening; and has also been reported to be linked to hyperactive stretch reflexes or spasticity. Previous studies found that flexion synergy and spasticity are associated with the recruitment of contralesional descending cortico- bulbospinal pathways. However, how the somatosensory system adapts to this change in the use of motor pathways and the role of adaptive sensory feedback to the abnormal motor control of the paretic arm remain largely unknown. The ascending sensory pathways that convey somatosensation from the paretic arm project contralaterally to the primary sensory cortex in the lesioned hemisphere. Our preliminary data, however, suggests that, in individuals that express the flexion synergy and spasticity, this sensory information is subsequently transferred to the contralesional hemisphere, a process that may support the manifestation of the abnormal movement patterns in hemiparetic stroke. The overall goal of the proposed research is to examine the pathophysiology of this maladaptive hemispheric somatosensory “shift” and its relationship to the upper limb motor impairments following a hemiparetic stroke. The results will lead to a greater understanding of abnormal limb synergies and spasticity by closing the sensorimotor loop, which should provide a novel means by which to therapeutically prevent and mitigate the emergence and expression of upper limb motor impairments, following a stroke. The proposed research aims to test the following key hypotheses in our specific aims: Following a unilateral motor stroke, a hemispheric shift in somatosensory processing provides sensory feedback to support the maladaptive hemispheric shift in the motor system. This hemispheric sensory shift not only influences volitional movement control which contributes to the expression of the flexion synergy (Aim 1), but also the transcortical loop of the stretch reflex that is related to the hyperactive stretch reflexes (or spasticity) and the increased onset delay of the long-latency stretch reflex (Aim 2). Furthermore, the hemispheric sensory shift, as a result of neuroplasticity in an injured brain, can occur in the absence of motor output; and this sensory shift can indicate the extent of motor deficits (Aim 3). By testing these hypotheses, the proposed research will improve our understanding of the role of sensory feedback in post-stroke motor impairments. This should allow for the determination of motor deficits from a new sensory perspective for more impaired individuals or acute/subacute patients who have difficulty performing motor tasks. Furthermore, the knowledge gained in this study will facilitate the future development of targeted, hypothesis-driven therapeutical interventions that aim at reducing maladaptive cross-hemispheric sensory-motor connectivity during recovery thus, promoting motor function without inducing abnormal synergy and spasticity impairments.