Brain Health and Aphasia Recovery

摘要 失语症患者之间的语言障碍差异很大。我们的神经生物学 基于中风损伤的模型只能部分解释失语症状。我们假设 卒中损伤外残留脑组织的完整性是重要的，但尚未完全认识到， 失语症严重程度和恢复的决定因素。 众所周知，心血管危险因素会导致累积的广泛性脑损伤。 通过小血管疾病(SVD)。在失语症文献之外，SVD一直被强烈地与 认知储备差，对各种形式的神经损伤的恢复力降低。中风幸存者患有 失语症通常有心血管危险因素，通常表现为SVD。然而， 在我们的康复模型中，SVD通常不被考虑在内，即使残留的脑组织 负责克服功能丧失的问题。因此，病变外较高程度的SVD可能 导致更严重的失语症状和更少的康复机会，因为补偿能力的降低 中风伤。我们的目标是直接检验这一假设。 我们建议评估失语症是如何由卒中病变结合残脑形成的。 正直。神经成像(脑核磁共振)是解决这个问题的理想选择。SVD由以下部分组成 微血管病理性缺血性改变和微出血。SVD引起的缺血性改变可以是 通过使用T2加权和T2-FLAIR图像的白质高强度测量，以及 可以使用磁化率加权图像来评估微出血。SVD优先影响白人 物质和弥散磁共振成像可以提供脑白质微结构完整性的额外测量，以及它们 与整个脑神经网络结构(大脑连接体)的关系。 利用我们在卒中后病变症状标测、白质和连接体成像方面的经验 我们建议对失语症的神经生物学和SVD的影响进行全面的研究。我们的项目将在 国际SVD评估指南(报告血管变化的标准 神经成像-奋力)，它将开发一种创新的多模式机器学习方法，以完全 评估大脑的完整性。 大脑完整性和语言测量将在慢性(项目1)和急性 (方案2)失语症康复。行为和语言评估将由项目4指导。 神经成像核心，我们将开发和分发一种多模式神经成像方法来量化严重程度 和SVD的位置。 具体目标1将纵向评估SVD的独立影响，控制脑损伤， 关于急性和慢性症状，以及急性和慢性语言康复。《特定目标2》将评估 通过评估SVD和中风的影响探讨SVD导致语言障碍的机制 结缔组织神经网络结构的损害、联合长程白质纤维的丢失及其 与语义、词汇-语义、词汇-语音、语音/语音缺陷的关系。

Abstract Language impairments can vary considerably between individuals with aphasia. Our neurobiological models based on the stroke lesion can only partly explain the aphasic symptoms. We hypothesize that the integrity of the residual brain tissue outside the stroke lesion is an important, but not yet fully appreciated, determinant of aphasia severity and recovery. It is well recognized that cardiovascular risk factors lead to cumulative widespread brain damage through small vessel disease (SVD). Outside the aphasia literature, SVD has been strongly associated with poor cognitive reserve and reduced resiliency to various forms of neurological injury. Stroke survivors with aphasia typically have cardiovascular risk factors and they commonly exhibit SVD. However, the impact of SVD is not usually taken into account in our models of recovery, even though the residual brain tissue is responsible for overcoming the loss of function. It follows that higher degrees of SVD outside the lesion may lead to worse aphasic symptoms and less chances of recovery due to reduced capacity to compensate for the stroke injury. Our goal is to directly test this hypothesis. We propose to evaluate how aphasia is shaped by the stroke lesion in combination with residual brain integrity. Neuroimaging (brain MRI) is ideally suited to address this problem. SVD is composed of microangiopathic ischemic changes and microhemorrhages. The ischemic changes from SVD can be measured through white matter hyper intensities using T2-weighted and T2-FLAIR images, and the microhemorrhages can be assessed using susceptibility-weighted images. SVD preferentially affects white matter and diffusion MRI can provide additional measures of white matter microstructural integrity and their relationship with the whole brain neuronal networks architecture (the brain connectome). Using our experience with post-stroke lesion symptom mapping, white matter and connectome imaging we propose a comprehensive study of the neurobiology and impact of SVD in aphasia. Our project will build on international guidelines for SVD assessment (The STandards for ReportIng Vascular changes on nEuroimaging - STRIVE) and it will develop an innovative multimodal machine learning approach to fully assess brain integrity. Brain integrity and language measures will be assessed in the context of chronic (Project 1) and acute (Project 2) aphasia recovery. The behavioral and linguistic assessments will be guided by Project 4. With the neuroimaging core, we will develop and distribute a multimodal neuroimaging approach to quantify the severity and location of SVD. Specific Aim 1 will longitudinally assess the independent impact of SVD, controlling for the brain lesion, on acute and chronic symptoms, as well as acute and chronic language recovery. Specific Aim 2 will evaluate the mechanisms by which SVD leads to language impairments by assessing the impact of SVD and stroke lesions on connectome neural network architecture, loss of associative long-range white matter fibers and its relationship with semantic, lexical-semantic, lexical-phonological, phonological/phonetic deficits.