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.
Abnormal mechanisms of antisaccade generation in schizophrenia patients and unaffected biological relatives of schizophrenia patients
Article first published online: 16 JUL 2010
Journal compilation © 2010 Society for Psychophysiological Research. No claim to original US government works
Volume 48, Issue 3, pages 350–361, March 2011
How to Cite
Kang, S. S., Dionisio, D. P. and Sponheim, S. R. (2011), Abnormal mechanisms of antisaccade generation in schizophrenia patients and unaffected biological relatives of schizophrenia patients. Psychophysiology, 48: 350–361. doi: 10.1111/j.1469-8986.2010.01074.x
- Issue published online: 9 FEB 2011
- Article first published online: 16 JUL 2010
- (Received July 13, 2009; Accepted April 30, 2010)
- Eye-movement control;
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.