Objective This critical review appraises neuroimaging findings in bipolar disorder in emotion processing, emotion regulation, and reward processing neural circuitry, to synthesize current knowledge of the neural underpinnings of bipolar disorder, and provide a neuroimaging research “roadmap” for future studies. Method We examined findings from all major studies in bipolar disorder that used fMRI, volumetric analyses, diffusion imaging, and resting state techniques, to inform current conceptual models of larger-scale neural circuitry abnormalities in bipolar disorder Results Bipolar disorder can be conceptualized in neural circuitry terms as parallel dysfunction in bilateral prefrontal cortical (especially ventrolateral prefrontal cortical)-hippocampal-amygdala emotion processing and emotion regulation neural circuitries, together with an “overactive” left-sided ventral striatal-ventrolateral and orbitofrontal cortical reward processing circuitry, that result in characteristic behavioral abnormalities associated with bipolar disorder: emotional lability, emotional dysregulation and heightened reward sensitivity. A potential structural basis for these functional abnormalities are gray matter decreases in prefrontal and temporal cortices, amygdala and hippocampus, and fractional anisotropy decreases in white matter tracts connecting prefrontal and subcortical regions. Conclusion Neuroimaging studies of bipolar disorder clearly demonstrate abnormalities in neural circuitries supporting emotion processing, emotion regulation and reward processing, although there are several limitations to these studies. Future neuroimaging research in bipolar disorder should include studies adopting dimensional approaches; larger studies examining neurodevelopmental trajectories in bipolar disorder and at-risk youth; multimodal neuroimaging studies using integrated systems approaches; and studies using pattern recognition approaches to provide clinically useful, individual-level data. Such studies will help identify clinically-relevant biomarkers to guide diagnosis and treatment decision-making for individuals with bipolar disorder.

Interpersonal and social rhythm therapy appears to add to the clinical armamentarium for the management of bipolar I disorder, particularly with respect to prophylaxis of new episodes.

Objective The prevalence of suicide attempts (SA) in bipolar II disorder (BPII), particularly in comparison to the prevalence in bipolar I disorder (BPI), is an understudied and controversial issue with mixed results. To date, there has been no comprehensive review of the published prevalence data for attempted suicide in BPII. Methods We conducted a literature review and meta-analysis of published reports that specified the proportion of individuals with BPII in their presentation of SA data. Systematic searching yielded 24 reports providing rates of SA in BPII and 21 reports including rates of SA in both BPI and BPII. We estimated the prevalence of SA in BPII by combining data across reports of similar designs. To compare rates of SA in BPII and BPI, we calculated a pooled odds ratio (OR) and 95% confidence interval (CI) with random-effect meta-analytic techniques with retrospective data from 15 reports that detailed rates of SA in both BPI and BPII. Results Among the 24 reports with any BPII data, 32.4% (356 /1099) of individuals retrospectively reported a lifetime history of SA, 19.8% (93 /469) prospectively reported attempted suicide, and 20.5% (55 /268) of index attempters were diagnosed with BPII. In 15 retrospective studies suitable for meta-analysis, the prevalence of attempted suicide in BPII and BPI was not significantly different: 32.4% and 36.3%, respectively (OR = 1.21, 95% CI: 0.98–1.48, p = 0.07). Conclusion The contribution of BPII to suicidal behavior is considerable. Our findings suggest that there is no significant effect of bipolar subtype on rate of SA. Our findings are particularly alarming in concert with other evidence, including (i) the well-documented predictive role of SA for completed suicide and (ii) the evidence suggesting that individuals with BPII use significantly more violent and lethal methods than do individuals with BPI. To reduce suicide-related morbidity and mortality, routine clinical care for BPII must include ongoing risk assessment and interventions targeted at risk factors.

Most patients met the diagnostic criteria for conditions for which there are proven treatments; however, inaccurate diagnosis proved common. This barrier to optimal treatment could be ameliorated with the use of structured interviews for common diagnoses. Scores on social/interpersonal measures support the premise that DSM symptoms provide only part of the relevant information about patients' conditions.

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