CORTICAL PLASTICITY--LEARNING ORIGINS OF HUMAN DISABILITY

我们研究的总体目标是建立一个基础 理解大脑皮层可塑性的科学 学习人类语言的起源和表达 神经系统残疾，并使用新的理解来指导 补救疗法。 在这个项目中，我们将研究 可塑性变化引起的重复，刻板，认知 重要的运动练习产生一致的传入 降低肌肉和皮肤的皮质表征的输入 皮层的传入信息 我们将进一步记录 紧急重复性劳损（RSI）的神经病学，包括 由这种行为产生的手部局部肌张力障碍（Fdh） 训练和相关训练产生的大脑去分化 运动和反馈感觉信息的表征 控制运动到感觉运动的进展 功能障碍 我们将定义经验的关系- 引起SI和MI的变化对疼痛的发作和进展 以及手臂上的炎症，并确定是否疼痛 起始a）使能或放大，或B）可以由动态触发， parralel皮质代表性退化。 我们将决定 是否诱导了运动和感觉皮层的可塑性变化 场域是姿态特定的，这是突现的标志性特征 局部肌张力障碍 我们将决定是否以及如何 姿势性劳损可能是RSI/FDh的发生原因之一。 最后我们 将评估在这个灵长类动物模型中的补救训练策略， 来获取重新分化大脑皮层的行为策略 感觉传入和运动的表征， 通过RSI/FDh诱导行为降解。 这项研究应该导致我们如何看待 皮质可塑性和学习对慢性神经系统疾病的影响 疾病，并可能对发展产生重大影响， 更有效的补救疗法， 不断增长的患者群体。

An overall objective of our research is to create a foundation science for understanding the contributions of cortical plasticity and learning to the origins of, and the expressions of human neurological disability, and to use that new understanding to guide remediation therapies. In this project, we shall study cortical plastic changes induced by repetitive, stereotyped, cognitively important movement exercises generating coincident afferent inputs that degrade the cortical representations of muscle and skin afferent information in the cortex. We shall further document the neurology of emergent repetitive strain injuries (RSI) including focal dystonias of the hand (Fdh) generated by this behavioral training, and relate training-generated de-differentiation of brain representations of movements and feedback sensory information controlling movements to the progression of sensorimotor dysfunction. We shall define the relationship of experience- induced changes in SI and MI to the onset and progression of pain and inflammation in the arm, and determine whether or not pain onset a) enables or amplifies, or b) could be triggered by dynamic, parralel cortical representational degradation. We shall determine whether induced plastic changes in motor and sensory cortical fields are posturally specific, which is signature feature of emergent focal dystonias. We shall determine whether or not and how postural strain might contribute to RSI/FDh genesis. Finally, we shall evaluate remediation training strategies in this primate model, to access behavioral strategies for redifferentiating cortical representations of sensory afferents and movements that have been degraded by RSI/FDh-inducing behaviors. This study should lead to a fundamental change in how we view cortical plasticity and learning contributions to chronic neurological disease, and could have a major impact on the development of more effective remediation therapies for this very large and growing patient group.