Investigating the Neurocognitive Mechanisms of Error Monitoring in Aphasia

研究失语症错误监测的神经认知机制

基本信息

批准号：
10472051
负责人：
Joshua Mccall
金额：
$ 5.18万
依托单位：
GEORGETOWN UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-09-08 至 2025-09-07
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10472051
关键词：
Address Age Anterior Aphasia Attention Behavioral Brain Brain region Clinical Cognitive Cognitive deficits Communication Comprehension Cross-Sectional Studies Data Electroencephalography Felis catus Functional Magnetic Resonance Imaging Funding Future Goals Impairment Individual Language Language Disorders Lesion Maps Measures Medial Mediator of activation protein Methods Modeling Monitor Names Neurocognitive Neurologist Participant Patient-Focused Outcomes Patients Performance Persons Production Psyche structure Research Research Personnel Research Project Grants Research Training Residual state Rest Role Speech Statistical Models Stroke Testing Training United States National Institutes of Health auditory comprehension base behavior measurement cingulate cortex cognitive control disability flexibility frontal lobe improved language impairment language processing prospective recruit relating to nervous system stroke-induced aphasia targeted treatment theories virtual white matter

项目摘要

Abstract/Summary Stroke causes most of the estimated 180,000 yearly new cases of aphasia, an acquired language impairment. Stroke survivors with aphasia often make errors when speaking, and are generally impaired at detecting their speech errors. Successful monitoring of one’s speech errors, referred to as Speech Error Monitoring (SEM) improves effective communication, and thus is an important prospective target for therapy. However, targeting SEM in therapy is currently difficult because the cognitive and neural mediators of SEM in aphasia are poorly understood. This proposal addresses two major gaps in our understanding of SEM in aphasia: the role of cognitive control in poor SEM in aphasia (Aim 1), and the functional brain networks responsible for SEM in people with aphasia (Aim 2). To date, research on SEM in aphasia has focused on the role of language-specific mediators, e.g., auditory comprehension, assuming that poor SEM results from a domain-specific speech or language deficit. Although researchers agree that SEM relies on and recruits cognitive control, which is also impaired in aphasia, it remains unknown whether cognitive control deficits contribute to SEM impairments. This proposed study probes different aspects of cognitive control abilities to discover their role as mediators of SEM. We predict that poor language-related cognitive control contributes to impaired SEM in aphasia. The neural mediators of SEM impairments in aphasia are virtually unexplored, but evidence from healthy participants supports the anterior cingulate cortex (ACC) as a region critical for self-monitoring. Since the ACC is rarely lesioned in people with aphasia, and is part of a dynamic network that interacts with many brain regions, we predict that poor SEM results from stroke-induced disruption of communication between the language network and the ACC. This prospective cross sectional study will gather data on 50 individuals with aphasia and 50 age matched controls, using measures of error monitoring in speech, performance on cognitive control tasks, and measures of spoken word production and comprehension. Language networks will be mapped in individual subjects using a validated functional MRI task known to reliably activate the language network in individuals with aphasia, and resting-state data will be used to determine if connectivity between the ACC and language regions relates to error-monitoring performance. The hypotheses are that (1) both language-related cognitive control as well as non-language cognitive control scores will be associated with SEM, and (2) SEM will be associated with connectivity of residual language networks to the ACC. This study will elucidate behavioral and neural mediators of SEM, which may become targets for future treatments that incorporate SEM.

摘要/总结每年估计有 18 万例新发失语症（一种获得性语言障碍），其中大部分是由中风引起的。患有失语症的中风幸存者在说话时经常犯错误，并且通常无法察觉自己的声音。言语错误的成功监控，称为言语错误监控（SEM）。改善有效的沟通，因此是治疗的重要前瞻性目标。 SEM 在治疗中目前很困难，因为 SEM 在失语症中的认知和神经介质很差该提案解决了我们对 SEM 在失语症中的理解的两个主要差距：失语症 SEM 的认知控制能力差（目标 1），以及负责 SEM 的功能性大脑网络失语症患者（目标 2）。迄今为止，对失语症 SEM 的研究主要集中在语言特定中介的作用上，例如，听觉理解，假设较差的 SEM 是由于特定领域的言语或语言缺陷造成的。尽管研究人员一致认为 SEM 依赖并招募认知控制，但认知控制在以下情况下也会受到损害：失语症，目前尚不清楚认知控制缺陷是否会导致 SEM 损伤。研究探讨了认知控制能力的不同方面，以发现它们作为 SEM 中介者的作用。预测与语言相关的认知控制不良会导致失语症的 SEM 受损。失语症 SEM 损伤的调节因素实际上尚未被探索，但来自健康参与者的证据支持前扣带皮层 (ACC) 作为自我监控的关键区域，因为 ACC 很少见。在失语症患者中受损，并且是与许多大脑区域相互作用的动态网络的一部分，我们预测较差的 SEM 是由中风引起的语言网络之间的沟通中断造成的和 ACC。这项前瞻性横断面研究将收集 50 名 50 岁失语症患者的数据匹配控制，使用言语错误监控措施，认知控制任务的表现，以及口语产生和理解的测量将被映射到个人中。受试者使用经过验证的功能性 MRI 任务，已知能够可靠地激活个体的语言网络患有失语症，静息态数据将用于确定 ACC 和语言之间的连接是否假设是（1）两者都与语言相关的认知。控制以及非语言认知控制分数将与 SEM 相关，并且 (2) SEM 将与残余语言网络与 ACC 的连接相关。这项研究将阐明行为和行为。 SEM 的神经介质，可能成为未来结合 SEM 治疗的目标。