The functional neuroanatomy of bipolar disorder: a consensus model
Article first published online: 25 MAY 2012
© 2012 John Wiley and Sons A/S
Volume 14, Issue 4, pages 313–325, June 2012
How to Cite
Strakowski, S. M., Adler, C. M., Almeida, J., Altshuler, L. L., Blumberg, H. P., Chang, K. D., DelBello, M. P., Frangou, S., McIntosh, A., Phillips, M. L., Sussman, J. E. and Townsend, J. D. (2012), The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disorders, 14: 313–325. doi: 10.1111/j.1399-5618.2012.01022.x
- Issue published online: 25 MAY 2012
- Article first published online: 25 MAY 2012
- Received 28 October 2011, revised and accepted for publication 18 March 2012
- bipolar disorder;
- functional magnetic resonance imaging (fMRI);
- prefrontal cortex
Strakowski SM, Adler CM, Almeida J, Altshuler LL, Blumberg HP, Chang KD, DelBello MP, Frangou S, McIntosh A, Phillips ML, Sussman JE, Townsend JD. The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disord 2012: 14: 313–325. © 2012 The Authors. Journal compilation © 2012 John Wiley & Sons A/S.
Objectives: Functional neuroimaging methods have proliferated in recent years, such that functional magnetic resonance imaging, in particular, is now widely used to study bipolar disorder. However, discrepant findings are common. A workgroup was organized by the Department of Psychiatry, University of Cincinnati (Cincinnati, OH, USA) to develop a consensus functional neuroanatomic model of bipolar I disorder based upon the participants’ work as well as that of others.
Methods: Representatives from several leading bipolar disorder neuroimaging groups were organized to present an overview of their areas of expertise as well as focused reviews of existing data. The workgroup then developed a consensus model of the functional neuroanatomy of bipolar disorder based upon these data.
Results: Among the participants, a general consensus emerged that bipolar I disorder arises from abnormalities in the structure and function of key emotional control networks in the human brain. Namely, disruption in early development (e.g., white matter connectivity and prefrontal pruning) within brain networks that modulate emotional behavior leads to decreased connectivity among ventral prefrontal networks and limbic brain regions, especially the amygdala. This developmental failure to establish healthy ventral prefrontal–limbic modulation underlies the onset of mania and ultimately, with progressive changes throughout these networks over time and with affective episodes, a bipolar course of illness.
Conclusions: This model provides a potential substrate to guide future investigations and areas needing additional focus are identified.