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

• 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
• 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

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/摘要 中风导致大多数估计的18万年新的失语症病例，这是一种被收到的语言障碍。 失语症的中风冲浪者在讲话时通常会出错，并且通常会受到损害 语音错误。成功监视语音错误，称为语音错误监控（SEM） 改善有效的沟通，因此是治疗的重要前瞻性靶标。但是，定位 SEM在治疗中目前很难 理解。该提议解决了我们对SEM的理解中的两个主要差距： 贫困SEM的认知控制（AIM 1），以及负责SEM的功能性脑网络 失语症的人（AIM 2）。 迄今为止，对失语症中的SEM的研究集中于语言特定的介体的作用，例如 听觉理解，假设SEM较差源于特定于领域的语音或语言防御。 尽管研究人员同意，SEM依赖并招募认知控制，这也受到了损害 失语症，认知控制是否定义有助于SEM障碍，尚不清楚。这提出了 研究问题的认知控制能力的不同方面，以发现其作为SEM介体的作用。我们 预测与语言相关的认知控制差会导致失语症中的SEM受损。神经 失语症中SEM障碍的介体几乎是出乎意料的，但是健康参与者的证据 支持前扣带回皮层（ACC）是自我监测至关重要的区域。因为ACC很少 失语症患者的病变，是与许多大脑区域互动的动态网络的一部分，我们 预测SEM不良导致中风引起的语言网络之间的沟通中断 和ACC。 这项前瞻性横断面研究将收集有关50名失语和50岁年龄的人的数据 使用语音中的错误监控，认知控制任务的性能以及 口语产生和理解的度量。语言网络将在个人中映射 使用经过验证的功能性MRI任务的受试者已知可靠地激活个人语言网络 失语症和静止状态数据将用于确定ACC和语言之间的连接是否存在 与错误监控性能有关的区域。假设是（1）两个与语言有关的认知 控制以及非语言认知控制评分将与SEM相关联，（2）SEM将是 与剩余语言网络与ACC的连通性有关。这项研究将阐明行为和 SEM的神经介质可能成为纳入SEM的将来治疗的靶标。