MODELS OF NORMAL & POSTSTROKE HEMISPHERIC INTERACTIONS

描述(申请人摘要)：虽然众所周知，半球 中风可以扰乱非病变大脑半球的功能，机制 对于这种颠覆，人们知之甚少。因此，《公约》的具体目标是 拟开展的研究工作有：1)建立半球的计算机模型 相互作用和不对称性，用它们来系统地研究因素 对功能偏侧化的影响；2)研究急性脑缺血的影响。 这些模型中的局灶性病变，确定影响恢复的因素和 他们可能如何被操纵以最大限度地恢复。因此，这项工作将 介绍一种研究半球的新的计算方法 卒中的专门化和经颧骨错位补充了更多 传统的人体和动物实验工作。 在这项研究中创建的神经模型将由配对的、 涉及感觉运动任务的相互连接的半球区域和 语言任务。虽然从生物现实中简化了，但这些 计算模型基于公认的大脑皮层原理。 连通性、动力性和可塑性。它们将被用来检查哪一个 提出了几个当代关于脑出血生物学机制的假说 半球专业化在测试中会产生功能偏侧化 一个详细的计算大脑模型。具体来说，我们将审查 在大小、连通性、兴奋性、可塑性等方面的不对称性 对半球区域进行模拟，并对其作用进行不同假设 穹隆(抑制性与兴奋性等)。选定的版本 然后，这些模型将受到模拟急性局灶性病变的影响 不同大小和位置的S评估哪些模型假设和损害 会导致经膝盖骨错位。我们将特别强调 确定可以变化的模型要素，以最大限度地提高损伤后的效果 恢复。 据我们所知，这是开发计算模型的第一次尝试 大脑半球的特化和经颧骨的分裂。初步 仿真结果清楚地证明了所提出工作的可行性。 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卒中后恢复，并可能提示 中风患者的新闻治疗理念。

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.