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Title page for ETD etd-07182012-091223

Type of Document Dissertation
Author Thakkar, Katharine Natasha
URN etd-07182012-091223
Title Inhibition and monitoring of saccadic eye movements in schizophrenia
Degree PhD
Department Psychology
Advisory Committee
Advisor Name Title
Sohee Park Committee Chair
Andrew Tomarken Committee Member
Jeffrey Schall Committee Member
Stephan Heckers Committee Member
  • schizophrenia
  • eye movements
  • response inhibition
  • response monitoring
  • corollary discharge
Date of Defense 2012-05-29
Availability unrestricted
Cognitive dysfunction is a core feature of schizophrenia, but the precise nature of these deficits has yet to be delineated. The goal of the following series of experiments was to advance our understanding of two particular cognitive functions related to control of action in schizophrenia, response inhibition and response monitoring, using two experimental paradigms that are firmly grounded in neurophysiology research and mathematical modeling, the saccadic countermanding and double-step tasks. Results indicated abnormalities in the control of action in patients with schizophrenia. Patients demonstrated replicable impairments in the efficiency of response inhibition. In addition, abnormal response monitoring was observed in two ways. First, across two studies, patients showed an exaggerated response to an unexpected cue requiring them to inhibit; their reaction times were more influenced by the immediately preceding trial. Second, patients showed evidence for fauly response monitoring by their difficulties with rapid, online adjustments of behavior. Compared to controls, they had fewer and slower error corrections and they failed to appropriately use feed-forward signals to predict the future position of the eye, putativley reflecting altered corollary discharge signals. These monitoring abnormalities were related to positive symptom severity. Finally, there was evidence for heritability of response inhibition impairments, with slower response inhibition observed in healthy relatives of schizophrenic patients. Further, both exaggerated trial history effects and slower response inhibition varyed as a function of psychosis-proneness, with the performance of bipolar patients falling between that of schizophrenia patients and controls. Combined, results shed further light on the cognitive profile of schizophrenia and lead to neurobiologically constrained hypotheses about the etiology of cognitive dysfunction. Additionally, these data contribute significantly to cognitive neuropsychiatric theories of some of the more bizarre and pathognomonic symptoms of the disease.
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