CORTICAL PLASTICITY--LEARNING ORIGINS OF HUMAN DISABILITY

皮质可塑性--学习人类残疾的起源

• 批准号: 6314151
• 负责人: MICHAEL M MERZENICH
• 金额: $ 14.32万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-05-01 至 2001-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6314151
• 关键词: Aotus; behavior test; behavioral /social science research tag; cerebral cortex; chordate locomotion; computer data analysis; disease /disorder model; dystonia; electrophysiology; experience; learning; method development; motor cortex; nervous system disorder; neural information processing; neural plasticity; neuroanatomy; psychomotor function; sensorimotor system; sensory cortex; tendon injury

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.

我们研究的总体目的是建立一个基础 理解皮质可塑性的贡献的科学 并学习人类的起源和表达 神经残疾，并利用新的理解来指导 修复疗法。 在这个项目中，我们将研究皮质 由重复，刻板印象，认知上引起的塑料变化 重要的运动练习产生一致的传入 降解肌肉和皮肤皮质表示的输入 皮质中的传入信息。 我们将进一步记录 紧急重复应变损伤的神经病学（RSI）包括 该行为产生的手（FDH）的局灶性障碍 训练并关联培训生成的大脑脱不同 运动和反馈感官信息的表示 控制运动运动发展的运动 功能障碍。 我们将定义经验的关系 - 诱导Si和Mi的变化，疼痛的发作和进展 和手臂上的炎症，并确定是否疼痛 发作a）启用或放大，或b）可以通过动态触发， 副皮质代表性降解。 我们将确定 诱导的塑料运动和感觉皮质变化是否 字段在姿势上是特定的，这是紧急的签名特征 局灶性障碍。 我们将确定是否以及如何 姿势菌株可能有助于RSI/FDH创世纪。 最后，我们 应评估这个灵长类动物模型中的补救培训策略 访问行为策略以重新分化皮质 感官传入和动作的表示 由RSI/FDH诱导行为降低。 这项研究应导致我们对我们的看法的根本变化 皮质可塑性和对慢性神经系统的学习贡献 疾病，可能会对发展产生重大影响 对于这个非常大的补救治疗疗法， 不断增长的患者组。