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Bipolar II disorder: a state‐of‐the‐art review
Author(s) -
Berk Michael,
Corrales Asier,
Trisno Roth,
Dodd Seetal,
Yatham Lakshmi N.,
Vieta Eduard,
McIntyre Roger S.,
Suppes Trisha,
Agustini Bruno
Publication year - 2025
Publication title -
world psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 15.51
H-Index - 93
eISSN - 2051-5545
pISSN - 1723-8617
DOI - 10.1002/wps.21300
Bipolar II disorder (BD‐II) is currently identified by both the DSM‐5 and ICD‐11 as a distinct subtype of bipolar disorder, defined by at least one depressive episode and at least one hypomanic episode, with no history of mania. Despite its prevalence and impact, the literature on BD‐II remains relatively sparse. This paper provides a comprehensive overview of the available research and current debate on the disorder, including its diagnostic criteria, clinical presentations, comorbidities, epidemiology, risk factors, and treatment strategies. Patients with BD‐II often present with recurrent depressive episodes, which outnumber hypomanic episodes by a ratio of 39:1. The condition is therefore often misdiagnosed as major depressive disorder and treated with antidepressant monotherapy, which may worsen its prognosis. The recognition of BD‐II is further complicated by the overlap of its symptoms with other disorders, in particular borderline personality disorder. Although BD‐II is often perceived as a less severe form of bipolar disorder, evidence suggests significant functional and cognitive impairment, accompanied by an elevated risk of suicidal behavior, including a rate of completed suicide at least equivalent to that observed in bipolar I disorder (BD‐I). Psychiatric comorbidities, in particular anxiety and substance use disorders, are common. The disorder is associated with a high prevalence of numerous physical comorbidities, with a particularly high risk of comorbid cardiovascular diseases. Various genetic and environmental risk factors have been identified. Inflammation, circadian rhythm dysregulation and mitochondrial dysfunction are being studied as potential pathophysiological mechanisms. Current treatment guidelines, often extrapolated from BD‐I and depression research, may not fully address the unique aspects of BD‐II. Nevertheless, substantial evidence supports the value of some pharmacological treatments – primarily mood stabilizers and atypical antipsychotics – augmented by psychoeducation, cognitive behavioral or interpersonal and social rhythm therapy, and lifestyle interventions. Further research on BD‐II should be a priority, in order to refine diagnostic criteria, identify potentially modifiable risk factors, and develop targeted interventions.

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