BACKGROUND: Schizophrenia subjects demonstrate difficulties on tasks requiring saccadic inhibition, despite normal refixation saccade performance. Saccadic inhibition is ostensibly mediated via prefrontal cortex and associated cortical/subcortical circuitry. The current study tests hypotheses about the neural substrates of normal and abnormal saccadic performance among subjects with schizophrenia. METHODS: Using functional magnetic resonance imaging, blood oxygenation level-dependent (BOLD) data were recorded while 13 normal and 14 schizophrenia subjects were engaged in refixation and antisaccade tasks. RESULTS: Schizophrenia subjects did not demonstrate the increased prefrontal cortex BOLD contrast during antisaccade performance that was apparent in the normal subjects. Schizophrenia subjects did, however, demonstrate normal BOLD contrast associated with refixation saccade performance in the frontal and supplementary eye fields, and posterior parietal cortex. CONCLUSIONS: Results from the current study support hypotheses of dysfunctional prefrontal cortex circuitry among schizophrenia subjects. Furthermore, this abnormality existed despite normal BOLD contrast observed during refixation saccade generation in the schizophrenia group.
BACKGROUND:Schizophrenia subjects demonstrate difficulties on tasks requiring saccadic inhibition, despite normal refixation saccade performance. Saccadic inhibition is ostensibly mediated via prefrontal cortex and associated cortical/subcortical circuitry. The current study tests hypotheses about the neural substrates of normal and abnormal saccadic performance among subjects with schizophrenia. METHODS: Using functional magnetic resonance imaging, blood oxygenation level-dependent (BOLD) data were recorded while 13 normal and 14 schizophrenia subjects were engaged in refixation and antisaccade tasks. RESULTS:Schizophrenia subjects did not demonstrate the increased prefrontal cortex BOLD contrast during antisaccade performance that was apparent in the normal subjects. Schizophrenia subjects did, however, demonstrate normal BOLD contrast associated with refixation saccade performance in the frontal and supplementary eye fields, and posterior parietal cortex. CONCLUSIONS: Results from the current study support hypotheses of dysfunctional prefrontal cortex circuitry among schizophrenia subjects. Furthermore, this abnormality existed despite normal BOLD contrast observed during refixation saccade generation in the schizophrenia group.
Authors: Kara A Dyckman; Adrian K C Lee; Yigal Agam; Mark Vangel; Donald C Goff; Jason J S Barton; Dara S Manoach Journal: Schizophr Res Date: 2011-08-09 Impact factor: 4.939
Authors: Rajeev S Ramchandran; Dara S Manoach; Mariya V Cherkasova; Kristen A Lindgren; Donald C Goff; Jason J S Barton Journal: Exp Brain Res Date: 2004-07-29 Impact factor: 1.972
Authors: Dara S Manoach; Adrian K C Lee; Matti S Hämäläinen; Kara A Dyckman; Jesse S Friedman; Mark Vangel; Donald C Goff; Jason J S Barton Journal: Biol Psychiatry Date: 2013-02-04 Impact factor: 13.382
Authors: M Steffens; C Neumann; A-M Kasparbauer; B Becker; B Weber; M A Mehta; R Hurlemann; U Ettinger Journal: Psychopharmacology (Berl) Date: 2018-10-24 Impact factor: 4.530