Default mode network abnormalities in bipolar disorder and schizophrenia

Öngür, Dost; Lundy, Miriam; Greenhouse, Ian; Shinn, Ann K.; Menon, Vinod; Cohen, Bruce M.; Renshaw, Perry F.

doi:10.1016/j.pscychresns.2010.04.008

« Previous Next »Psychiatry Research: Neuroimaging
Volume 183, Issue 1 , Pages 59-68, 30 July 2010

Default mode network abnormalities in bipolar disorder and schizophrenia

Dost Öngür
- McLean Hospital, Belmont, MA and Harvard Medical School, Boston, MA, United States
- Corresponding author. AB320, McLean Hospital, 115 Mill St., Belmont, MA 02478, United States. Tel.: +1 617 855 3922; fax: +1 617 855 2895.
Miriam Lundy
- Yale University School of Nursing, New Haven, CT, United States
- These authors contributed equally to this work.
Ian Greenhouse
- Department of Neuroscience, University of California San Diego, La Jolla, CA, United States
- These authors contributed equally to this work.
Ann K. Shinn
- McLean Hospital, Belmont, MA and Harvard Medical School, Boston, MA, United States
Vinod Menon
- Department of Psychiatry and Behavioral Sciences and Program in Neuroscience, Stanford University School of Medicine, Stanford, CA, United States
Bruce M. Cohen
- McLean Hospital, Belmont, MA and Harvard Medical School, Boston, MA, United States
Perry F. Renshaw
- The Brain Institute, University of Utah School of Medicine, Salt Lake City, UT, United States

Received 15 November 2009; received in revised form 6 April 2010; accepted 10 April 2010.

Abstract

The default-mode network (DMN) consists of a set of brain areas preferentially activated during internally focused tasks. We used functional magnetic resonance imaging (fMRI) to study the DMN in bipolar mania and acute schizophrenia. Participants comprised 17 patients with bipolar disorder (BD), 14 patients with schizophrenia (SZ) and 15 normal controls (NC), who underwent 10-min resting fMRI scans. The DMN was extracted using independent component analysis and template-matching; spatial extent and timecourse were examined. Both patient groups showed reduced DMN connectivity in the medial prefrontal cortex (mPFC) (BD: x=−2, y=54, z=−12; SZ: x=−2, y=22, z=18). BD subjects showed abnormal recruitment of parietal cortex (correlated with mania severity) while SZ subjects showed greater recruitment of the frontopolar cortex/basal ganglia. Both groups had significantly higher frequency fluctuations than controls. We found ventral mPFC abnormalities in BD and dorsal mPFC abnormalities in SZ. The higher frequency of BOLD signal oscillations observed in patients suggests abnormal functional organization of circuits in both disorders. Further studies are needed to determine how these abnormalities are related to specific symptoms of each condition.