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Abnormal mechanisms of antisaccade generation in schizophrenia patients and unaffected biological relatives of schizophrenia patients

Authors

  • Seung Suk Kang,

    1. Department of Psychology, University of Minnesota, Twin Cities, Minnesota
    2. Department of Psychiatry, University of Minnesota, Twin Cities, Minnesota
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  • Daphne P. Dionisio,

    1. Department of Psychology, University of Minnesota, Twin Cities, Minnesota
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  • Scott R. Sponheim

    1. Department of Psychology, University of Minnesota, Twin Cities, Minnesota
    2. Department of Psychiatry, University of Minnesota, Twin Cities, Minnesota
    3. Veterans Affairs Medical Center, Minneapolis, Minnesota
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  • We thank Monica Calkins, Ph.D., Clayton Curtis, Ph.D., and Kevin Haroian for assistance in task design and implementation. Kathryn A. McGuire, Ph.D., John. J. Stanwyck, Sarah M. Sass, and Robb Hunter assisted with task implementation and data acquisition, and Carly Smitkowski assisted in scoring the eye movement data. We are also grateful to Jennifer McDowell, Ph.D., for consultation and guidance during the processing and quantification of eye movement data. This work was supported by grants from the Department of Veterans Affairs Medical Research Service, the National Institutes of Mental Health (5R24MH069675) to Scott Sponheim, as well as by the Mental Illness and Neuroscience Discovery (MIND) Institute and the Mental Health Patient Service Line at the Veterans Affairs Medical Center, Minneapolis, Minnesota.

Address correspondence to: Scott R. Sponheim, Ph.D., Minneapolis VA Medical Center (116B), One Veterans Drive, Minneapolis, MN 55417. E-mail: sponh001@umn.edu

Abstract

Although errant saccadic eye movements may mark genetic factors in schizophrenia, little is known about abnormal brain activity that precedes saccades in individuals with genetic liability for schizophrenia. We investigated electrophysiological activity preceding prosaccades and antisaccades in schizophrenia patients, first-degree biological relatives of schizophrenia patients, and control subjects. Prior to antisaccades, patients had reduced potentials over lateral prefrontal cortex. Smaller potentials were associated with worse antisaccade performance. Relatives also exhibited reduced pre-saccadic potentials over lateral frontal cortex but additionally had reduced potentials over parietal cortex. Both patients and relatives tended toward increased activity over orbital frontal cortex prior to saccades. Results are consistent with lateral prefrontal dysfunction marking genetic liability for schizophrenia and underlying deficient saccadic control.

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