Neurocognitive Mechanisms of Sentence Production Impairment in Aphasia

项目总结 卒中后失语症(PSA-G)以一系列症状(句子支离破碎， 功能词法错误，动词缺乏，语速慢)，但现有的理论和语言 干预措施侧重于个别症状。这种单一症状的理论和干预重点导致 功能性沟通方面的收益有限。这项研究的长期目标是改善临床 对PSA-G的干预效果。作为迈向这一目标的第一步，该项目的目标是推进 通过解决两个关键差距，建立了PSA-G的理论框架。第一个差距是在机械方面 理解词汇、语法、运动和认知过程如何协同工作以实现流利 句子的产生以及如何在PSA-G中分解这一点。第二个鸿沟是对神经的理解。 句子制作计划如何随着时间的推移正常展开的潜在机制，以及什么至关重要 与卒中后失语的其他变体相比，时空变化导致PSA-G，主要表现为 词汇-语义缺陷(PSA-LS)。中心假设是无语法语言产生的原因是 形态合成和音素运动过程的神经动力学的时空变化，导致 在发音规划点上的累积处理瓶颈。这种协作式处理瓶颈 语法错误模型将以两个具体目标进行测试。具体目标1将阐明相对贡献 失语症患者句法和非句法过程对句子产生的影响 路径建模框架。这一目标的预期结果是更好地理解 失语症候群背后的不同语言过程中的哪种延迟会损害流利的句子 一般在失语症中产生，更具体地说在PSA-G和PSA-LS中产生。具体目标2将决定 不同语言缺陷的句子产生的神经机制。 脑磁图(MEG)将被用来比较时间进程和功能连接的变化 在要求日益苛刻的形态句法生产中，关键的周边和对侧句法中枢 任务。这一目标的预期结果是一个时空特定的句子产生的神经模型 神经典型、PSA-G和PSA-LS扬声器。这项研究的意义在于，它将在经验上推动 建立了句子生成的多维模型，这将为进一步发展奠定基础 针对失语症的有针对性和有效的语言干预。它还将有助于更好地 对神经退行性失语症的语法错误的认识。该项目的创新方面包括：a 新的多维理论框架，融合了音位的非句法维度 规划、处理能力和速度以及神经生理动力学；PSA- G组和PSA-LS组；同时肌电对口语的脑磁图分析 测量。

PROJECT SUMMARY Post-stroke agrammatic aphasia (PSA-G) is characterized by a cluster of symptoms (fragmented sentences, errors in functional morphology, a dearth of verbs, and slow speech rate), yet extant theories and language interventions focus on individual symptoms. This single-symptom theoretical and intervention focus results in limited gains in functional communication. The long-term goal of this research is to improve the clinical effectiveness of interventions for PSA-G. As a first step towards this goal, this project’s objective is to advance the theoretical framework of PSA-G by addressing two critical gaps. The first gap is in the mechanistic understanding of how lexical, grammatical, motoric, and cognitive processes work together to enable fluent sentence production and how this breaks down in PSA-G. The second gap is in the understanding of neural mechanisms underlying how sentence production planning normally unfolds over time and what crucial spatiotemporal alterations give rise to PSA-G versus other variants of post-stroke aphasia with predominantly lexico-semantic deficits (PSA-LS). The central hypothesis is that agrammatic language production results from spatiotemporal alterations in the neural dynamics of morphosyntactic and phonomotor processes, causing a cumulative processing bottleneck at the point of articulatory planning. This Synergistic Processing Bottleneck Model of Agrammatism will be tested with two specific aims. Specific Aim 1 will elucidate the relative contribution of syntactic and non-syntactic processes towards sentence production in aphasia by using speed metrics and a path modeling framework. The expected outcomes of this aim are an improved understanding of the extent to which delays in different linguistic processes underlying the agrammatic symptom cluster impair fluent sentence production in aphasia generally, and in PSA-G versus PSA-LS more specifically. Specific Aim 2 will determine the neural mechanisms underlying sentence production across language deficit profiles. Magnetoencephalography (MEG) will be used to compare alterations in timecourse and functional connectivity of key perilesional and contralesional syntactic hubs across increasingly demanding morphosyntactic production tasks. The expected outcome of this aim is a spatiotemporally specified neural model of sentence production in neurotypical, PSA-G, and PSA-LS speakers. The significance this research is that it will forward an empirically established multidimensional model of sentence production, which will lay the foundation for developing more targeted and effective language interventions for agrammatic aphasia. It will also contribute to a better understanding of agrammatism in neurodegenerative aphasias. The innovative aspects of this project include: a novel multidimensional theoretical framework that incorporates non-syntactic dimensions of phonomotor planning, processing capacity and speed, and neurophysiological dynamics; direct comparisons between PSA- G and PSA-LS groups; and MEG analysis of spoken language with simultaneous electromyographic measurement.