Brain, Vol. 126, No. 3, 610-622,
March 2003
© 2003 Guarantors of Brain
doi: 10.1093/brain/awg056
Rostral anterior cingulate cortex dysfunction during error processing in schizophrenia
1 Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada, 2 Division of Psychiatry, School of Community Health Sciences, University of Nottingham, Nottingham, UK and 3 Department of Psychiatry, Institute of Living, Yale University School of Medicine, New Haven, CT, USA
Correspondence to: Peter F. Liddle, Division of Psychiatry, School of Community Health Sciences, A Floor, South Block, Queen’s Medical Centre, Nottingham NG7 2UH, UK E-mail: peter.liddle{at}nottingham.ac.uk
Previous research has demonstrated that patients with schizophrenia have an impaired ability to monitor erroneous responses to stimuli internally. Event-related potential (ERP) studies of error-eliciting tasks indicate that, in healthy adults, the commission of an erroneous response is associated with a fronto-centrally distributed negative voltage component termed the error negativity (Ne) or error-related negativity (ERN). In patients with schizophrenia, the Ne/ERN elicited by errors of commission (EoC) is reduced in amplitude compared with that elicited in healthy participants. Functional MRI (fMRI) studies and source localization analyses of ERP data in healthy participants suggest that EoC are associated with activity in the rostral anterior cingulate cortex (ACC). Using event-related fMRI, we examined the brain activity associated with EoC in a group of 10 patients with schizophrenia and 16 matched healthy participants. Patients were stable, partially remitted, medicated out-patients recruited from the community. Participants performed a Go/NoGo task variant that was shown previously to elicit a reduced Ne/ERN during EoC in patients with schizophrenia relative to healthy participants, as well as robust rostral ACC activation during EoC in healthy participants. Patients with schizophrenia were characterized by relative underactivity in the rostral ACC compared with healthy participants. There was also evidence for more widespread underactivity in the limbic system. In contrast to these regions of relative hypoactivity, patients with schizophrenia demonstrated hyperactivity relative to healthy participants in bilateral parietal cortex during both EoC and correctly rejected NoGo trials. Our results are consistent with previous ERP research demonstrating functional abnormalities during error processing in schizophrenia. In light of the role of the rostral ACC and other limbic structures in mediating affective and motivational behaviour, our results suggest there may be a disturbed affective or motivational response to the commission of errors in schizophrenia.
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