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    Investigating The Neurocognitive Mechanisms of Error Monitoring in Aphasia

    Cover for Investigating The Neurocognitive Mechanisms of Error Monitoring in Aphasia
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    View/Open: McCall_georgetown_0076D_15139.pdf (2.2MB) Bookview

    Creator
    McCall, Joshua
    Advisor
    Turkeltaub, Peter E
    Friedman, Rhonda B
    Abstract
    Speech error monitoring (SEM) is critical for effective communication, and is especially important in aphasia, a language impairment commonly caused by stroke. The present dissertation employs three studies to investigate the behavioral deficits and brain lesions that reduce SEM in aphasia. The first study characterized cognitive control impairments in aphasia. The aim was to distinguish semantic control from phonological control and identify their contribution to aphasic deficits. Using a novel task paradigm, the study confirmed that people with aphasia can have impairments in semantic and phonological control relative to matched neurotypical participants. Furthermore, semantic control impairments appeared to contribute to semantic deficits in aphasia. The second study investigated the behavioral deficits and brain lesions that affect SEM of phonological versus semantic errors. Mixed effects generalized linear models examined whether deficits in speech, language, and cognitive control reduce monitoring of phonological and semantic errors. Support vector regression (SVR) lesion symptom mapping analyses identified lesions that selectively reduce SEM of phonological errors relative to semantic errors. The results indicate deficits in motor speech as well as lesions to the motor cortex selectively reduce phonological SEM. Additionally, the results indicate deficits in auditory comprehension selectively reduce semantic SEM. Across both error types, the results indicate semantic control deficits reduce SEM. The third study investigated critical fiber tract connections supporting SEM. Connections were mapped across entire brains using diffusion-weighted images. SVR connectome-based lesion symptom mapping identified connections that, when lesioned, reduce SEM. The results indicated that SEM was reduced by lesioned connections between posterior medial frontal cortex (pMFC) and brain regions that support speech production and comprehension, as well as executive function. This dissertation highlights the importance of cognitive control and the pMFC in SEM, and suggests that there are distinct neurocognitive substrates for SEM of phonological versus semantic errors. Specifically, SEM of phonological errors appears to rely on motor speech abilities, and SEM of semantic errors on speech comprehension. Future clinical approaches and research on SEM may benefit from considering phonological SEM separately from semantic SEM, as well as the role of cognitive control in SEM.
    Description
    Ph.D.
    Permanent Link
    http://hdl.handle.net/10822/1064679
    Date Published
    2022
    Subject
    Aphasia; Cognitive Control; Connectivity; Lesion-Symptom Mapping; Speech Error Monitoring; Stroke; Neurosciences; Neurosciences;
    Type
    thesis
    Publisher
    Georgetown University
    Extent
    227 leaves
    Collections
    • Graduate Theses and Dissertations - Neuroscience
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    Georgetown University Seal
    ©2009 - 2023 Georgetown University Library
    37th & O Streets NW
    Washington DC 20057-1174
    202.687.7385
    digitalscholarship@georgetown.edu
    Accessibility