Brain dynamics of lexical retrieval after left hemisphere stroke

左半球卒中后支持词汇提取的脑动力学研究 本研究旨在探讨慢性脑卒中患者词汇提取的脑动力学支持。 由于左半球（LH）病变引起的失语症。因LH而出现卒中诱发性失语的患者 损害经常经历主要的词汇检索困难。然而，词汇提取能力并不等同于 在这些病人中。这种变化的一个可能的解释是，词汇检索需要 由不同的神经区域支配的多种认知成分。特别是， 左侧前额叶皮层（LPFC）的损伤通常可以立即识别他们试图识别的单词。 比如说，在几个选项或目标词的开头之间进行选择时。左侧病变患者 后颞叶皮层（pLTC）可能在识别正确的单词时有困难，即使给他们这个单词。 因此，LPFC和pLTC可能在词汇提取、词汇激活和 因此，LPFC与pLTC卒中后的选择和脑网络重组可能不同- 诱发病变。域一般认知控制过程已被提出在恢复中发挥作用 中风引起的失语症然而，一般认知控制机制在多大程度上 LH卒中后的词汇提取尚不清楚。本项目旨在阐明这些问题。在 特别地，所提出的研究将检验支持词汇检索的时空动力学 在LH卒中后，当病变包括LPFC与pLTC时， 可以进行控制。我们的主要假设是，LPFC周围病变的患者 而pLTC则不会表现出更有效的领域-一般认知控制 在词汇提取机制比病变患者包围pLTC。的组合 新的理论和方法的方法将被用于沿着完善的任务，评估 词汇提取和领域一般认知控制。目标1将调查LPFC损坏的影响 对比pLTC对词汇提取的影响，以推断这些区域在词汇激活和选择中的因果作用， 建立和新颖的行为模型。目标2将决定是否以及何时 与对照组相比，LPFC或pLTC病变患者的控制PFC区域参与词汇提取。 匹配的控制使用空间增强头皮脑电图（EEG）。最后，目标3将检查 如果这些群体之间的词汇提取能力的差异是由大脑的差异造成的， 使用EEG衍生的功能连接测量的连接性。造成的个人和社会成本 中风后的词汇提取中断是相当可观的。这些研究的结果将提供关键的一步 了解脑动力学支持中风诱发失语症的词汇检索。这些结果可能 从而导致临床工具的词汇检索能力的评估。

Brain dynamics supporting lexical retrieval after left hemisphere stroke This proposal examines the brain dynamics supporting lexical retrieval in patients with chronic stroke-induced aphasia due to left-hemisphere (LH) lesions. Patients presenting with stroke-induced aphasia due to LH damage often experience major lexical retrieval difficulties. Lexical retrieval abilities are, however, not equally compromised in these patients. One possible explanation for this variability is that lexical retrieval requires multiple cognitive components that are subserved by different neural regions. In particular, patients with lesions to the left lateral prefrontal cortex (LPFC) can often immediately recognize the word they are trying to say when given a choice between a few options or the onset of the target word. Patients with lesions in the left posterior temporal cortex (pLTC) may have trouble recognizing the correct word even when it is given to them. The LPFC and pLTC may therefore play different roles in subprocesses of lexical retrieval, lexical activation and selection, and brain network reorganization may consequently be different after LPFC versus pLTC stroke- induced lesions. Domain-general cognitive control processes have been proposed to play a role in recovery from stroke-induced aphasia. However, the degree to which domain-general cognitive control mechanisms are engaged in lexical retrieval following LH stroke is unclear. This project seeks to shed light on these issues. In particular, the proposed research will examine the spatio-temporal dynamics supporting lexical retrieval following LH stroke when lesions encompass the LPFC versus the pLTC, and how domain-general cognitive control may be engaged. Our main hypothesis is that patients with lesions encompassing the LPFC but not the pLTC will show more efficient engagement of domain-general cognitive control mechanisms in lexical retrieval than patients with lesions encompassing the pLTC. A combination of novel theoretical and methodological approaches will be used along with well-established tasks that assess lexical retrieval and domain-general cognitive control. Aim 1 will investigate the impact of damage to the LPFC versus pLTC on lexical retrieval to infer the causal roles of these regions in lexical activation and selection using established and novel behavioral modeling. Aim 2 will determine if and when domain-general cognitive control PFC regions are involved in lexical retrieval in patients with LPFC or pLTC lesions in comparison with matched-controls using spatially-enhanced scalp electroencephalography (EEG). Finally, Aim 3 will examine if differences in lexical retrieval abilities between these groups are subserved by differences in brain connectivity using EEG-derived functional connectivity measures. The personal and societal cost caused by lexical retrieval disruption after stroke is considerable. The results of these studies will provide a key step toward understanding brain dynamics supporting lexical retrieval in stroke-induced aphasia. These results may in turn lead to clinical tools for the assessment of lexical retrieval abilities.