Investigating the Neurocognitive Mechanisms of Error Monitoring in Aphasia

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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.