Motor impairment related changes in muscles properties in chronic stroke

 描述（由申请人提供）：手臂功能受损是中风幸存者慢性残疾的主要原因。已经开发了许多治疗方法来促进手臂功能的恢复，目标是中风引起的运动障碍，例如轻瘫、痉挛和导致不自主肘、腕关节功能障碍的独立关节控制的丧失。 以及在举起手臂时手指弯曲（即，屈曲协同作用）。然而，我们对 肌肉如何适应这些损伤随着时间的推移是不清楚的，在这个节骨眼上，也不清楚肌肉特性的变化如何影响瘫痪手臂的功能使用。因此，我们建议确定瘫痪手臂的骨骼肌结构变化的程度，由于持续的突出屈曲协同作用，瘫痪，以及相关的瘫痪上肢废用。随后，我们建议证明这些继发性肌肉骨骼变化的能力，以产生功能性手臂运动的影响，通过使用新的模拟相结合的手臂和手的运动。我们假设，屈曲协同作用，轻瘫，和慢性废用的麻痹上肢，中风的结果，诱导被动和主动肌肉特性的实质性变化，从而限制了产生功能性手臂运动的能力，即使从大脑的正常神经驱动将被恢复。在目标1中，我们建议调查异常屈曲协同作用和被动刚度增加之间的关系，导致中风患者手臂姿势更加屈曲。在目标2中，我们提出表征肌肉结构参数的变化（即，肌束和肌节长度以及肌肉体积），并确定与年龄匹配的健全个体的任何结构偏差对最大等长力产生能力的影响，如通过计算肌肉生理横截面积所指示的，肌肉生理横截面积是个体肌肉产生力的能力的标准解剖学测量。最后，作为目标3的一部分，我们建议采用最先进的正向动力学模拟技术，使用上肢模型，集成了手臂和手，以确定在何种程度上改变肌肉特性（目标1和2）和异常肌肉协同激活模式（目标1）帐户的严重限制，在功能使用的上肢慢性偏瘫中风的个人经历。提出的研究的基本原理是，确定慢性偏瘫卒中后偏瘫上肢功能使用中肌肉特性改变的确切作用将允许设计更有效的康复干预措施。这将通过突出各种肌肉骨骼变化的相对重要性来改变临床医生治疗偏瘫上肢康复的方式，这些肌肉骨骼变化与提出的治疗方法相结合。测量工具提供了设计和测试疗法的手段，以减少或防止中风后肌肉的有害变化。

 DESCRIPTION (provided by applicant): Impaired arm function is a major cause of chronic disability among stroke survivors. A number of treatment approaches have been developed to facilitate the recovery of arm function, targeting stroke induced motor impairments such as paresis, spasticity and losses of independent joint control that result in involuntary elbow, wrist and finger flexion while lifting the arm (i.e., the flexion synergy). However, our understanding of how muscle adapts to these impairments over time is not clear at this juncture nor how changes in muscle properties impact the functional use of the paretic arm. Therefore, we propose to determine the extent of structural changes in the skeletal muscles of the paretic arm due to the persistence of a prominent flexion synergy, paresis, and the associated disuse of the paretic upper limb. Subsequently, we propose to demonstrate the effects of these secondary musculoskeletal changes on the ability to generate functional arm movements by using novel simulations of combined arm and hand motion. We postulate that the flexion synergy, paresis, and the chronic disuse of the paretic upper limb that results from the stroke, induce substantial changes in both passive and active muscle properties, thus limiting the ability to generate functional arm movements, even if normal neural drive from the brain would be restored. In Aim 1, we propose to investigate the relationship between the abnormal flexion synergy and increases in passive stiffness that result in more flexed arm postures in individuals with stroke. In Aim 2 we propose to characterize changes in muscle architectural parameters (i.e., fascicle and sarcomere length, and muscle volume) following stroke and determine the effect of any structural deviations from age-matched able-bodied individuals on maximum isometric force generation ability, as indicated by calculating muscle physiological cross-sectional area, a standard anatomical measure of an individual muscle's ability to generate force. Finally, as part of Aim 3 we propose to employ state-of-the-art forward dynamics simulation techniques using an upper limb model that integrates the arm and hand to determine the extent to which altered muscle properties (Aims 1 & 2) and abnormal muscle co-activation patterns (Aim 1) account for the severe limitations in functional use of the upper limb experienced by individuals with chronic hemiparetic stroke. The rationale that underlies the proposed research is that determining the exact role of altered muscle properties on functional use of the paretic upper limb following chronic hemiparetic stroke will allow for the design of more effective rehabilitation interventions This will change the way clinicians approach the rehabilitation of the paretic upper limb by highlighting the relative importance of the various musculoskeletal changes which combined with the proposed measurement tools provide the means to design and test therapies to reduce or prevent detrimental changes in muscle following stroke.