Motor Function after Stroke

中风后的自然恢复通常是不完全的，这使得中风后残疾成为一种可能。 非常普遍的问题。新的治疗方法正在开发中，以减少患者的残疾， 中风的慢性期这些疗法旨在改善行为状态，而不是通过急性 挽救组织，而是通过改变存活到慢性期的大脑元素的功能。 这种恢复性方法有可能达到高比例的中风受试者。 有限的指导可用于此类治疗的最佳处方。患者中 慢性平台期，其特征表明， 治疗，这表明赤字，而不是固定的？为了解决这个问题，108名患者 在过去20周内中风且运动状态达到平台期的患者， 在多个领域进行评估，包括人口统计学、临床、放射学、脑成像， 神经生理学和遗传学的测量。为期3周的标准化手臂运动疗法 随后，将重新检查与手臂运动功能相关的临床评估。 本研究假设，使用行为检查预测治疗反应的能力 (the在这种情况下选择患者的通常方法）通过添加 几项措施，特别是脑损伤和功能。分析还将确定一个伤害 阈值指示哪些患者可能或不可能通过治疗改善。其他 分析将集中在一个拟议的模型学习废用：能力，以确定这些病人 那些在中风中幸存下来的大脑区域使用不足的人将有助于慢性中风治疗。 一个特别感兴趣的指标是BDNF基因型。BDNF val 66 met多态性是 目前在大约1/4的人，已与某些减少 皮质可塑性的措施，并可能是特别重要的预测， 自发和治疗诱导的中风恢复。这将在108例患者中进行评价 治疗研究，以及9个研究中心150例患者的自发恢复研究。 残疾影响中风患者多年。一些新的治疗方法集中在 中枢神经系统修复可能会改善这种情况。然而，最佳的方法来应用这些 治疗方法尚不清楚，特别是选择那些最有可能对 疗法拟议研究的总体假设是，表征CNS损伤和 功能将提供神经生物学的见解，有助于最佳地应用恢复疗法， 人类中风患者这些知识应有助于减少残疾， 适当针对中风患者。

Spontaneous recovery after stroke is generally incomplete, making post-stroke disability a highly prevalent problem. New therapies are in development to reduce disability in patients in the chronic phase of stroke. Such therapies aim to improve behavioral status not by acutely salvaging tissue but by changing function in brain elements that survive to the chronic phase. This restorative approach has the potential to reach a high fraction of subjects with stroke. Limited guidance is available for optimal prescription of such therapies. Among patients in the chronic plateau phase, which characteristics suggest potential for reducing disability with therapy, and which suggest that deficits are instead fixed? To address this issue, 108 patients who have had a stroke in the last 20 weeks and whose motor status has reached a plateau will be evaluated, in multiple domains, including demographic, clinical, radiological, brain mapping, neurophysiological, and genetic measures. A 3-week course of standardized arm motor therapy will follow, after which clinical assessments related to arm motor function will be rechecked. This study hypothesizes that the ability to predict treatment response using behavioral exam (the usual means of selecting patients in this context) is substantially improved with addition of several measures, particularly of brain injury and function. Analyses will also define an injury threshold that indicates which patients are, or are not, likely to improve with therapy. Other analyses will focus on a proposed model of learned disuse: the ability to identify those patients who are underusing brain regions that survived the stroke would aid chronic stroke therapies. One measure of particular interest is BDNF genotype. The BDNF val66met polymorphism is present in approximately 1/4th of people, has been associated with reduction in certain measures of cortical plasticity, and might be of particular importance to predicting both spontaneous and therapy-induced stroke recovery. This will be evaluated in the 108 patient therapy study, as well as a study of spontaneous recovery in 150 patients across 9 sites. Disability affects stroke patients for many years. A number of new therapies focused on CNS repair might improve this situation. However, optimal approach to applying these therapies is unclear, particularly the issue of selecting those patients most likely to respond to therapy. The overall hypothesis of the proposed study is that characterizing CNS injury and function will provide neurobiological insights useful for optimally applying restorative therapies to human patients with stroke. Such knowledge should facilitate reducing disability in appropriately targeted patients with stroke.