The functional neuroanatomy of bipolar disorder: A consensus model

Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0559, USA.
Bipolar Disorders (Impact Factor: 4.97). 06/2012; 14(4):313-25. DOI: 10.1111/j.1399-5618.2012.01022.x
Source: PubMed


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.
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.
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.
This model provides a potential substrate to guide future investigations and areas needing additional focus are identified.

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Available from: Andrew Mark Mcintosh, Apr 04, 2014
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    • "We focussed on regions identified as abnormal in prior functional studies from this cohort as we considered these may be associated with abnormal structural connectivity. Furthermore, our selection does include some of the most commonly implicated regions in the literature, such as the amygdala and prefrontal regions (Strakowski et al., 2012; Wessa et al., 2014). "
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    09/2015; 234(1). DOI:10.1016/j.pscychresns.2015.08.004
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    • "Vascular lesions of the thalamus may be accompanied by behavioral changes that resemble symptoms of BD, including abnormal energy (apathy or motor hyperactivity), psychomotor acceleration, mood swings, social inadequacy, and psychotic manic states (Schmahmann, 2003; Carrera and Bogousslavsky , 2006; De Witte et al., 2011). Thus, our finding of decreased thalamus GM in BD patients compared with HC is consistent with the theory that thalamus may be involved in the neurocircuitry responsible for the clinical manifestations of BD (Strakowski et al., 2012). "
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