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: 10684682
• 负责人: Joshua Mccall
• 金额: $ 5.27万
• 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/10684682
• 关键词: Address; Age; Agreement; 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 Development; Language Disorders; Lesion; Maps; Measures; Medial; Mediator; 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; behavior measurement; cingulate cortex; cognitive control; disability; flexibility; frontal lobe; improved; language impairment; language processing; neural; non-verbal; novel therapeutic intervention; prospective; recruit; stroke-induced aphasia; targeted treatment; theories; verbal; 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/概要 据估计，每年有18万例失语症（一种后天性语言障碍）新发病例，其中大部分是中风引起的。 患有失语症的中风幸存者在说话时经常出错，并且在检测他们的语言时通常受损。 言语错误。成功地监测一个人的语音错误，称为语音错误监测（SEM） 改善有效的沟通，因此是治疗的重要预期目标。然而，针对 SEM治疗目前很困难，因为在失语症中SEM的认知和神经介质很差， 明白这项建议解决了我们对失语症SEM的理解中的两个主要空白： 失语症中SEM较差的认知控制（目的1），以及负责SEM的功能性脑网络， 失语症患者（Aim 2）。 迄今为止，关于失语症SEM的研究主要集中在语言特异性介质的作用，例如， 听觉理解，假设差的SEM是由特定领域的言语或语言缺陷造成的。 尽管研究人员同意SEM依赖并招募认知控制，但认知控制也会受损， 虽然认知控制缺陷与失语症有关，但认知控制缺陷是否会导致SEM损伤仍不清楚。这一拟议 本研究探讨了认知控制能力的不同方面，以发现它们作为SEM中介的作用。我们 预测语言相关的认知控制不良有助于失语症的SEM受损。神经 失语症中SEM损伤的介质几乎未被探索，但来自健康参与者的证据表明， 支持前扣带皮层（ACC）作为自我监控的关键区域。由于ACC很少 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，由于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50名失语症患者和50名年龄 匹配的控制，使用言语错误监测的措施，认知控制任务的表现， 口语词汇产生和理解的测量。语言网络将被映射在个人 受试者使用已知可靠激活个体语言网络的经验证的功能性MRI任务 失语症患者，静息状态数据将用于确定ACC和语言之间的连接 区域涉及错误监视性能。假设是：（1）语言相关的认知 控制以及非语言认知控制评分将与SEM相关，以及（2）SEM将 与剩余语言网络到ACC的连接有关。这项研究将阐明行为和 神经介质的扫描电镜，这可能成为未来的治疗目标，纳入扫描电镜。