Bipolar Affective Disorder

Bipolar affective disorder (BPAD) is a chronic, episodic mood disorder defined by recurrent episodes of mania/hypomania and depression with inter-episode recovery. It is one of the highest-yield psychiatry topics for NEET PG — expect questions on Bipolar I vs II, manic episode criteria, lithium therapeutics/toxicity, and ECT indications.

Definition & core concepts

Bipolar disorder is a mood (affective) disorder characterised by at least one episode of elevated, expansive or irritable mood (mania or hypomania), usually alternating with depressive episodes. The "bi-polar" refers to the swing between the two emotional poles. It is distinguished from unipolar depression (only depressive episodes) by the presence of a high (manic/hypomanic) pole.

Key descriptors:

• Mania — severe mood elevation lasting ≥1 week (or any duration if hospitalisation required), causing marked impairment, psychosis, or hospitalisation.
• Hypomania — milder elevation lasting ≥4 consecutive days, no marked impairment, no psychosis, no hospitalisation.
• Mixed features — manic and depressive symptoms occurring simultaneously.
• Euthymia — the normal, stable inter-episode mood state.

High-yield: A single manic episode is sufficient to diagnose Bipolar I disorder — a depressive episode is NOT required. This is a favourite trap.

Classification

Type	Defining episode(s)	Depression needed?	Psychosis	Functional impact
Bipolar I	≥1 manic episode	No	May occur	Marked / hospitalisation
Bipolar II	≥1 hypomanic + ≥1 major depressive episode	Yes (mandatory)	Never in hypomania	Mild–moderate
Cyclothymia	Chronic subthreshold highs & lows for ≥2 yrs (1 yr in children)	Subthreshold only	No	Mild, fluctuating
Rapid cycling	≥4 mood episodes / 12 months	—	—	Poorer prognosis

High-yield: If a patient ever has a full manic episode, the diagnosis is Bipolar I, regardless of how many depressive episodes occurred. Bipolar II requires hypomania + major depression and crucially has never had a full manic episode.

Cyclothymia is the bipolar analogue of dysthymia/persistent depressive disorder: chronic mood instability that never reaches the threshold for a full manic or major depressive episode, persisting ≥2 years with symptom-free intervals no longer than 2 months.

Epidemiology & etiology

• Lifetime prevalence ~1% (Bipolar I); equal sex distribution for Bipolar I, slight female predominance in Bipolar II and rapid cycling.
• Earliest onset among major mood disorders — typically late teens to early 20s (mean ~20–25 yrs); earlier onset than unipolar depression.
• Highest heritability of all psychiatric disorders — concordance ~40–70% in monozygotic twins; strong family history.

High-yield: Bipolar disorder has the strongest genetic loading among mood disorders. Monozygotic concordance far exceeds dizygotic.

Pathophysiology (exam-relevant)

• Monoamine hypothesis — relative excess of noradrenaline/dopamine in mania; deficiency in depression.
• Dopaminergic overactivity underlies manic psychosis (explains efficacy of antipsychotics).
• Kindling phenomenon — episodes become more frequent/autonomous over time, justifying early mood stabiliser prophylaxis.
• Antidepressant monotherapy can precipitate a manic switch — a classic clinical pearl.

Clinical features

Manic episode — diagnostic criteria

Core: a distinct period of abnormally elevated, expansive, or irritable mood AND increased goal-directed activity/energy, lasting ≥1 week, with ≥3 of the following (≥4 if mood is only irritable):

Mnemonic — DIG FAST:

1. D — Distractibility
2. I — Indiscretion / Impulsivity (excessive pleasurable risky activity — spending, sex, driving)
3. G — Grandiosity / inflated self-esteem
4. F — Flight of ideas / racing thoughts
5. A — Activity increase / psychomotor Agitation
6. S — Sleep decreased (reduced need for sleep, not insomnia)
7. T — Talkativeness / pressured speech

High-yield: Decreased need for sleep (feeling rested after 2–3 hours) is one of the most specific and earliest markers of an emerging manic episode.

Additional manic features: psychomotor over-activity, over-familiarity, disinhibition, increased libido, grandiose or persecutory delusions, and mood-congruent psychotic features. Severe mania may present with confusion ("delirious mania") or catatonia.

Hypomanic episode

Same symptom menu but ≥4 days, observable change in functioning, no marked impairment, no psychosis, no hospitalisation. The patient is often more productive — which is why insight is poor and patients rarely present voluntarily.

Bipolar depression

Clinically resembles major depression but more often features:

• Atypical features — hypersomnia, hyperphagia, leaden paralysis
• Psychomotor retardation
• Earlier onset, more episodes, higher psychosis/suicide risk
• Brief, abrupt episodes

High-yield: Atypical depressive features (hypersomnia + hyperphagia + psychomotor retardation) plus a young patient with episodic illness should raise suspicion for bipolar depression rather than unipolar — important because antidepressant monotherapy is contraindicated.

Mania vs Hypomania — quick comparison

Feature	Mania	Hypomania
Duration	≥1 week	≥4 days
Impairment	Marked	None/mild
Psychosis	May be present	Never
Hospitalisation	Often	Never (by definition)
Diagnosis implied	Bipolar I	Bipolar II (with MDD)

Diagnosis & investigations

Bipolar disorder is a clinical diagnosis (DSM-5 / ICD-11) based on longitudinal history and mental status examination. There is no confirmatory lab test. Investigations are to exclude organic mimics and establish a baseline before starting mood stabilisers.

**Diagnostic approach → ** History (episodic course, family history) → Mental status examination → rule out substance use & medical causes → baseline investigations before drug therapy → screen suicide risk.

Baseline / pre-treatment work-up:

• Lithium — renal function (urea, creatinine, eGFR), thyroid function (TFT), calcium, ECG, pregnancy test; baseline weight.
• Valproate — LFTs, CBC (platelets), weight, pregnancy test.
• General — TFT (hypothyroidism mimics depression; hyperthyroidism mimics mania), serum electrolytes, urine drug screen, B12.

High-yield: Always exclude organic causes of mania — hyperthyroidism, steroids, stimulants/cocaine/amphetamine, frontal lobe lesions, multiple sclerosis, neurosyphilis, and antidepressant-induced switch.

Management

Acute mania — drug of choice

First-line for acute mania: a mood stabiliser (lithium or valproate) and/or a second-generation antipsychotic (olanzapine, risperidone, quetiapine, aripiprazole), often in combination for severe mania.

**Acute mania algorithm → ** Ensure safety/admit if needed → stop any antidepressant → start antipsychotic ± lithium/valproate → add short-term benzodiazepine (lorazepam) for agitation/sleep → ECT if refractory, severe, pregnant, or life-threatening.

• Valproate acts faster than lithium and is preferred in mixed episodes and rapid cyclers.
• Lithium is best for classic/euphoric mania and has the strongest anti-suicidal evidence.

Bipolar depression

• First-line: Quetiapine, lurasidone, olanzapine-fluoxetine combination (OFC), or lamotrigine.
• Lamotrigine is the agent best at preventing the depressive pole (poor anti-manic efficacy).
• Avoid antidepressant monotherapy — risk of manic switch and cycle acceleration; if used, always cover with a mood stabiliser.

Maintenance / prophylaxis — drug of choice

High-yield: Lithium is the gold-standard, drug of choice for long-term prophylaxis of bipolar disorder and the only agent with robust anti-suicidal properties.

Drug	Best for	Therapeutic level	Key toxicity / caution
Lithium	Prophylaxis, euphoric mania, anti-suicidal	Acute 0.8–1.2; maint 0.6–1.0 mmol/L	Narrow index; renal/thyroid; Ebstein anomaly
Valproate	Mixed states, rapid cycling, acute mania	~50–100 µg/mL	Hepatotoxicity, NTD/teratogen, PCOS, weight
Lamotrigine	Depressive pole prophylaxis	Not routinely monitored	SJS/TEN — slow titration
Carbamazepine	Refractory/rapid cycling	4–12 µg/mL	Enzyme inducer, agranulocytosis, SIADH

Lithium — the high-yield drug

• Mechanism: inhibits inositol monophosphatase (inositol-depletion hypothesis) and GSK-3β; not a sedative.
• Excretion: purely renal; reabsorbed in proximal tubule alongside sodium.
• Therapeutic range (maintenance): 0.6–1.0 mmol/L; acute mania up to 1.2 mmol/L. Toxicity begins >1.5 mmol/L; severe/life-threatening >2.0 mmol/L.
• Sampled as a 12-hour trough (morning level, 12 h post-dose).

High-yield: Lithium has a narrow therapeutic index. Sodium depletion (low-salt diet, dehydration), thiazide diuretics, ACE inhibitors/ARBs, and NSAIDs all raise lithium levels and precipitate toxicity. (Mnemonic: "TAN" — Thiazides, ACEi/ARB, NSAIDs.)

Lithium toxicity — clinical staging

Early/mild: coarse tremor, nausea, vomiting, diarrhoea, lethargy. Moderate: confusion, ataxia, dysarthria, myoclonus, nystagmus. Severe (>2.5 mmol/L): seizures, gross tremor, renal failure, coma, cardiac arrhythmia, death.

**Toxicity management → ** Stop lithium → IV normal saline (volume + sodium repletion) → monitor levels/electrolytes/ECG → haemodialysis if level >4.0 (or >2.5 with symptoms/renal failure). There is no specific antidote.

Long-term lithium adverse effects (mnemonic — "LITHIUM")

• L — Leukocytosis (benign)
• I — Insipidus (nephrogenic diabetes insipidus — polyuria/polydipsia)
• T — Tremor (fine tremor; coarse tremor = toxicity)
• H — Hypothyroidism / Hyperparathyroidism
• I — Increased weight
• U — Upset stomach / GI
• M — Metallic taste, Memory issues; teratogenic — Ebstein anomaly (atrialised RV) in 1st trimester

Routine monitoring: lithium level every 3–6 months; TFT and renal function every 6–12 months.

ECT in bipolar disorder

High-yield: ECT indications in BPAD — severe/treatment-refractory mania, life-threatening manic exhaustion / delirious mania, pregnancy, catatonia, high suicide risk, severe psychotic/refractory bipolar depression, and patient who cannot wait for drugs to act. ECT is highly effective and rapid in both poles.

Complications

• Suicide — bipolar disorder carries one of the highest suicide rates of any psychiatric illness; risk highest in depressive and mixed states.
• Mixed states and rapid cycling (worsened by antidepressants and hypothyroidism).
• Substance use disorders (very common comorbidity), alcohol misuse.
• Psychosocial: financial ruin, legal problems, relationship breakdown from manic indiscretions.
• Treatment complications: lithium-induced CKD/diabetes insipidus/hypothyroidism, valproate-induced PCOS and teratogenicity, lamotrigine SJS.
• Antidepressant-induced manic switch and treatment-emergent rapid cycling.

Key differentials

Differential	Distinguishing point
Unipolar depression	No history of mania/hypomania; antidepressants safe
Schizoaffective disorder	≥2 weeks of psychosis without prominent mood symptoms
Schizophrenia	Mood-incongruent psychosis dominates; chronic deterioration
ADHD	Chronic (not episodic), childhood onset, no euphoria/grandiosity
Borderline PD	Mood shifts in hours, interpersonally triggered, chronic emptiness
Substance-induced	Temporal link to stimulants/steroids; resolves on cessation
Cyclothymia	Subthreshold, never reaches full episode threshold
Organic / secondary mania	Hyperthyroidism, frontal lesion, MS, neurosyphilis

High-yield: In schizoaffective disorder, psychotic symptoms must persist for ≥2 weeks in the absence of a major mood episode — this is the line that separates it from psychotic bipolar disorder, where psychosis occurs only during mood episodes.

Recently asked / exam angle

• Bipolar I vs II distinction — "single manic episode = Bipolar I" and "Bipolar II needs hypomania + major depression but never full mania."
• Lithium therapeutic level — maintenance 0.6–1.0 mmol/L; toxicity >1.5; dialysis cut-offs.
• Drugs that raise lithium levels — thiazides, NSAIDs, ACE inhibitors/ARBs (image/clinical vignette of toxicity after starting an NSAID).
• Lithium teratogenicity — Ebstein's anomaly.
• Lithium mechanism — inositol monophosphatase / GSK-3β inhibition.
• Drug of choice in pregnancy / refractory mania / catatonia — ECT.
• Mood stabiliser for the depressive pole — lamotrigine (and its SJS warning + slow titration).
• Valproate preferred in mixed episodes and rapid cyclers; valproate + PCOS + neural tube defects.
• Most specific early symptom of mania — decreased need for sleep.
• Mood disorder with strongest genetic loading / earliest onset — bipolar disorder.
• DIG FAST mnemonic for manic criteria.
• Antidepressant monotherapy precipitating manic switch — single-best-answer vignettes.

Rapid revision

1. One manic episode = Bipolar I; depression not required.
2. Bipolar II = hypomania + major depression, never a full manic episode.
3. Mania ≥1 week; hypomania ≥4 days; cyclothymia ≥2 years subthreshold.
4. Manic criteria: DIG FAST (≥3, or ≥4 if mood only irritable).
5. Decreased need for sleep = earliest, most specific manic sign.
6. Lithium = DOC for prophylaxis and the only proven anti-suicidal agent.
7. Lithium maintenance level 0.6–1.0 mmol/L; toxicity >1.5 mmol/L; dialysis if >4.0.
8. Lithium levels raised by Thiazides, ACEi/ARB, NSAIDs (TAN) and dehydration/low salt.
9. Lithium toxicity → coarse tremor, ataxia, confusion, seizures; treat with IV saline ± dialysis (no antidote).
10. Lithium teratogenicity → Ebstein's anomaly; long-term → hypothyroidism, nephrogenic DI.
11. Valproate for mixed states/rapid cycling; lamotrigine for the depressive pole (watch SJS).
12. ECT for refractory/life-threatening mania, pregnancy, catatonia, high suicide risk; avoid antidepressant monotherapy (manic switch).