CORTICAL PLASTICITY--LEARNING ORIGINS OF HUMAN DISABILITY

我们研究的总体目标是创建一个基础 了解皮质可塑性贡献的科学 以及学习人类的起源和表达方式 神经功能障碍，并用这种新的理解来指导 补救疗法。在这个项目中，我们将研究大脑皮质 由重复、刻板印象、认知引起的可塑性变化 产生重合传入的重要动作练习 降低肌肉和皮肤的皮质表示的输入 大脑皮层的传入信息。我们将进一步记录 急诊反复劳损(RSI)的神经学包括 由这种行为引起的手局灶性肌张力障碍(FDH) 训练，以及相关训练产生的大脑去分化 运动和反馈感觉信息的表征 运动控制对感觉运动进展的影响 功能障碍。我们将定义经验的关系-- SI和MI在疼痛发生和发展中的诱导变化 和手臂的炎症，并决定是否疼痛 开始a)使能或放大，或b)可以由动态触发， 帕累尔皮质代表性退化。我们将决定 是否诱发运动和感觉皮质的可塑性改变 字段是事后特定的，这是Emerent的标志性特征 局灶性肌张力障碍。我们将决定是否以及如何 体位性劳损可能与RSI/FDH的发生有关。最后，我们 将在这个灵长类动物模型中评估补救训练策略， 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 被RSI/FDH诱导的行为降解。 这项研究应该会从根本上改变我们看待 皮质可塑性和学习对慢性神经病学的贡献 疾病，并可能对发展产生重大影响 对于这个非常大的和更有效的补救疗法 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.