MODELS OF NORMAL & POSTSTROKE HEMISPHERIC INTERACTIONS

描述（申请人的摘要）：虽然众所周知，半球形的 中风可以破坏非病变半球的功能， 对这种破坏的了解很少。 因此， 建议的研究是：1）开发大脑半球的计算机模型 相互作用和不对称性，利用它们来系统地研究因素 影响功能的偏侧化，2）研究急性 这些模型中的局灶性病变，影响恢复的决定因素， 如何操纵它们来最大限度地恢复 因此，这项工作将 介绍一种新的计算方法来研究半球 脑卒中中的专业化和跨胼胝体神经联系不能， 传统的人类和动物实验。 在这项研究中创建的神经模型将包括成对的， 涉及感觉运动任务的相互连接的半球区域和 语言任务。 虽然从生物现实简化，这些 计算模型是基于普遍接受的原则， 连通性、动态性和可塑性。 它们将被用来检查 一些当代的假说关于生物学机制， 大脑半球特化产生功能偏侧化， 一个详细的计算大脑模型 具体来说，我们将研究 的大小、连接性、兴奋性、可塑性等不对称 模型半球区域和不同的假设的作用， 胼胝体（抑制性与兴奋性等）。的选择版本 然后，这些模型将经受模拟的急性局灶性损伤， 不同的尺寸和位置，以评估哪些模型假设和病变 导致胼胝体神经联系不能。 将特别强调 识别可以变化以最大化损伤后的模型特征 复苏 据我们所知，这是第一次尝试发展计算模型 大脑半球的特殊化和胼胝体神经联系不能。 初步 模拟结果清楚地表明了拟议工作的可行性。 这些模型将允许系统地探索潜在的机制 大脑半球功能不对称和中风后恢复，并可能表明 中风患者的治疗理念。

DESCRIPTION (Applicant's Abstract): While it is well known that hemispheric strokes can disrupt function of the non-lesioned hemisphere, the mechanisms of this disruption are poorly understood. Accordingly, the specific aims of the proposed research are 1) to develop computer models of hemispheric interactions and asymmetries, using them to systematically study factors influencing laterlization of function, and 2) to study the effects of acute focal lesion sin these models, determining factors influencing recovery and how they might by manipulated to maximize recovery. Thus, this work will introduce a new computational approach to studying hemispheric specialization and transcallosal diaschisis in stroke that complements more traditional human and animal experimental work. The neural models created in this research will consist of paired, interconnected hemispheric regions involving sensorimotor tasks and a linguistic task. Although simplified from biological reality, these computational models are based on generally accepted principles of cortical connectivity, dynamics and plasticity. They will be used to examine which of several contemporary hypotheses about the biological mechanisms of hemispheric specialization produce functional lateralization when tested in a detailed computational brain model. Specifically, we will examine asymmetries in the size, connectivity , excitability, plasticity, etc. of model hemisphere regions and different assumptions about the role of the corpus callosum (inhibitory versus excitatory, etc.). Selected versions of these models will then be subjected to simulated acute focal lesions of varying sizes and location s to assess which model assumptions and lesions lead to transcallosal diaschisis. Particular emphasis will be placed on identifying model features that can be varied to maximize post-lesion recovery. To our knowledge, this is the first attempt to develop computational models of hemispheric specialization and transcallosal diaschisis. Preliminary simulations have clearly demonstrated the feasibility of the proposed work. These models will allow systematic exploration of the mechanisms underlying hemispheric functional asymmetries and post-stroke recovery, and may suggest news therapeutic concepts for stroke patients.