bipolar II disorder

**DSM-5-TR criteria** - ≥1 current or past hypomanic episode: elevated/expansive/irritable mood plus increased energy/activity lasting ≥4 consecutive days, with ≥3 of the DIG FAST symptoms (Distractibility, Indiscretion/risky behavior, Grandiosity, Flight of ideas, Activity increase, Sleep decreased need, Talkativeness). Hypomania is observable by others but does NOT cause marked functional impairment, does NOT require hospitalization, and has NO psychosis. - ≥1 current or past major depressive episode: ≥2 weeks of ≥5 SIG E CAPS symptoms, including depressed mood or anhedonia. - NO lifetime manic episode (that would make it bipolar I). Mania is ≥7 days, or any duration if hospitalization is required, with marked impairment or psychosis. - Symptoms are not better explained by schizoaffective disorder or another psychotic disorder, and are not due to a substance or medical condition.

**Bipolar I vs II vs cyclothymia** - Bipolar I: ≥1 manic episode. Depression is common but not required. - Bipolar II: hypomania plus major depression. Psychosis during a mood episode would suggest mania or severe depression, not hypomania. - Cyclothymic disorder: ≥2 years (1 year in children and adolescents) of numerous hypomanic and depressive symptoms that do not meet full episode criteria. - A switch to mania makes the diagnosis bipolar I. An antidepressant-induced switch is classically a risk, especially with antidepressant monotherapy.

**Epidemiology and pathophysiology** - Onset is typically late teens to mid-20s. Women may be more commonly affected than in bipolar I (which is ~1:1), and rapid cycling is more common in women. - Strong genetic component (heritability ~60-85%). Implicated pathways include dysregulated monoamines (dopamine, serotonin, norepinephrine), glutamate and GABA signaling, circadian rhythm disruption, and HPA axis dysregulation.

**Clinical significance** - Patients usually seek care during depression, not hypomania. Screen every depressed patient for past hypomania or mania, family history of bipolar disorder, early onset, atypical features (hypersomnia, hyperphagia), and recurrent episodes. - High suicide risk, comparable to or higher than bipolar I. Also high rates of comorbid anxiety, substance use, ADHD, and borderline personality disorder. - The depressive burden is greater than in bipolar I, so patients spend more time depressed than hypomanic. - Rule out secondary causes: substances (stimulants, steroids), hyperthyroidism, and neurologic disease.

**Management** - Acute bipolar depression: quetiapine (first-line), lurasidone, lumateperone, or cariprazine. Lithium and lamotrigine are options. Avoid antidepressant monotherapy because of the risk of switching or rapid cycling. - Maintenance: lithium (strong anti-suicide evidence), lamotrigine (particularly effective for preventing depressive episodes), or quetiapine. - Lithium: narrow therapeutic index. Adverse effects include tremor, nephrogenic diabetes insipidus, hypothyroidism, and teratogenicity (Ebstein anomaly). Toxicity is increased by NSAIDs, ACE inhibitors, thiazides, and dehydration. Monitor levels, renal function, and TSH. - Lamotrigine: risk of Stevens-Johnson syndrome, which requires slow titration. Dose is reduced with valproate. Valproate is teratogenic (neural tube defects). - Psychotherapy (CBT, interpersonal and social rhythm therapy, psychoeducation) is a helpful adjunct. ECT is an option for severe or refractory depression.

**High-yield pearls** - Hypomania: ≥4 days, no marked impairment, no psychosis, no hospitalization. - If a vignette describes a depressed patient with prior periods of decreased need for sleep and high energy but no major impairment, think bipolar II. - Bipolar II is not a "milder" form of bipolar I because the depressive morbidity and suicide risk are substantial.