Organic Mood & Psychotic Disorders
Psychiatry · Organic · lean revision notes
Organic Mood & Psychotic Disorders
Secondary psychiatric syndromes caused by a demonstrable medical, structural, endocrine, metabolic, or toxic insult to the brain — rather than a primary "functional" illness. The exam loves the frontal vs temporal lobe personality split, the endocrine mimics (thyroid, Cushing), and the neuropsychiatric red flags of HIV, SLE and Wilson's disease.
High-yield: Any psychiatric presentation that is new-onset after age 40, has atypical features, abnormal vitals/neuro signs, clouded sensorium, or visual hallucinations should make you hunt for an organic cause before labelling it schizophrenia or primary mood disorder.
1. Definition & Classification
An organic mental disorder is a behavioural or psychological syndrome arising from a measurable cerebral dysfunction, primary (e.g., tumour, stroke) or secondary (systemic disease affecting the brain). ICD-10 groups these in F06 ("Other mental disorders due to brain damage and dysfunction and to physical disease"). DSM-5 abandoned the word "organic" and uses the phrase "due to another medical condition", but NEET PG still uses the classic terminology.
| ICD-10 code | Organic syndrome |
|---|---|
| F06.0 | Organic hallucinosis |
| F06.1 | Organic catatonic disorder |
| F06.2 | Organic delusional (schizophrenia-like) disorder |
| F06.3 | Organic mood (affective) disorder |
| F06.4 | Organic anxiety disorder |
| F06.5 | Organic dissociative disorder |
| F06.7 | Mild cognitive disorder |
| F07.0 | Organic personality disorder |
High-yield: Organic hallucinosis = persistent/recurrent hallucinations (classically visual or auditory) in clear consciousness, no dominant delusion or mood change. The prototype is alcoholic hallucinosis and peduncular hallucinosis (vivid, Lilliputian visual hallucinations from midbrain/thalamic lesions).
Functional vs Organic — the discriminating features
| Feature | Favours organic | Favours functional (primary) |
|---|---|---|
| Age of onset | >40 yrs, or very early childhood | 15–35 yrs |
| Consciousness | Often clouded/fluctuating | Clear |
| Hallucination type | Visual, tactile, olfactory | Auditory |
| Course | Fluctuating, diurnal variation | More steady |
| Neuro signs | Present (focal deficits, seizures) | Absent |
| Cognition | Disoriented, poor memory | Usually intact |
| Family history | Often absent | Often positive |
2. Etiology & Pathophysiology
A useful screening mnemonic for organic/secondary causes — "VITAMINS-D":
- Vascular (stroke, vasculitis)
- Infective (HIV, neurosyphilis, encephalitis)
- Traumatic (TBI, subdural)
- Autoimmune (SLE, anti-NMDA receptor encephalitis)
- Metabolic (hepatic/renal/electrolytes, Wilson's)
- Idiopathic/Inflammatory
- Neoplastic (frontal/temporal tumours, paraneoplastic limbic encephalitis)
- Structural / Substance (drugs, alcohol, steroids)
- Degenerative & Endocrine (thyroid, Cushing, Addison, parathyroid)
The unifying pathophysiology is disruption of fronto-subcortical and limbic circuits: lesions of the dorsolateral prefrontal cortex impair executive function, orbitofrontal lesions disinhibit, mesial frontal/anterior cingulate lesions cause apathy, and temporal-limbic irritation generates psychosis and affective change.
3. Lesion-based clinical features (the core NEET PG zone)
Frontal lobe syndromes — three classic sub-syndromes
- Orbitofrontal (disinhibited) syndrome → impulsivity, social disinhibition, jocularity (Witzelsucht = inappropriate facetiousness/punning), poor judgement, emotional lability. The textbook eponym is Phineas Gage.
- Dorsolateral (dysexecutive) syndrome → impaired planning, poor abstraction, perseveration, reduced verbal fluency, poor set-shifting (fails Wisconsin Card Sorting Test).
- Medial frontal / anterior cingulate (apathetic) syndrome → abulia, akinetic mutism, profound apathy.
High-yield: Frontal lobe lesions classically cause primitive reflexes (grasp, snout, palmomental, glabellar tap), perseveration, and utilisation behaviour, with relatively preserved memory early on. Lack of insight is characteristic.
Temporal lobe & limbic syndromes
- Temporal lobe epilepsy (TLE) / mesial temporal sclerosis → the most epileptogenic and "psychiatric" lobe.
- Inter-ictal psychosis of epilepsy: schizophrenia-like psychosis with preserved affect and personality (unlike true schizophrenia), often after years of TLE; left-sided foci favour psychosis.
- Post-ictal psychosis with a lucid interval of 1–7 days after a seizure cluster.
- Geschwind syndrome (inter-ictal personality of TLE): hyperreligiosity, hypergraphia, hyposexuality, viscosity ("stickiness"), and intensified emotionality.
- Klüver–Bucy syndrome (bilateral temporal/amygdala damage — HSV encephalitis, trauma): hyperorality, hypersexuality, placidity, hypermetamorphosis (compulsive exploration), visual agnosia (psychic blindness).
High-yield — Frontal vs Temporal personality change (most repeated table):
| Frontal lobe | Temporal lobe | |
|---|---|---|
| Behaviour | Disinhibition / apathy | Psychosis, religiosity |
| Affect | Labile, euphoric (Witzelsucht) | Deepened emotionality, viscosity |
| Memory | Working memory poor; episodic relatively spared early | Episodic/verbal memory impaired |
| Hallmark | Primitive reflexes, perseveration | Geschwind syndrome, déjà vu, automatisms |
| Hallucinations | Less common | Olfactory ("uncinate fits"), gustatory, complex visual |
| Eponym | Phineas Gage | Klüver–Bucy, Geschwind |
High-yield: Olfactory hallucinations ("uncinate fits" — usually unpleasant, burnt-rubber smell) localise to the medial temporal lobe (uncus) and strongly suggest a temporal focus/tumour, not primary psychiatric illness.
4. Endocrine causes (commonly tested mimics)
Thyroid
- Hypothyroidism → depression, psychomotor slowing, poor memory; severe untreated disease → "myxoedema madness" (agitation, paranoid psychosis, hallucinations).
- Hyperthyroidism / thyrotoxicosis → anxiety, restlessness, mania-like agitation; in the elderly, apathetic thyrotoxicosis mimics depression. Thyroid storm can produce frank delirium/psychosis.
High-yield: Always order TSH in any new mood disorder, treatment-resistant depression, or rapid-cycling bipolar disorder — subclinical hypothyroidism is a classic reversible contributor.
Cushing's syndrome / steroid effects
- Endogenous Cushing's → depression is the commonest psychiatric feature (~50–60%), plus irritability, anxiety, cognitive impairment.
- Exogenous steroids → dose-dependent; euphoria/mania more common with exogenous steroids, depression and psychosis at higher doses ("steroid psychosis"); risk rises sharply above ~40 mg/day prednisolone.
Others
- Addison's disease → apathy, depression, fatigue, occasionally psychosis.
- Hyperparathyroidism / hypercalcaemia → "stones, bones, groans, psychiatric moans" — depression, lethargy, psychosis.
- Phaeochromocytoma → paroxysmal anxiety/panic with headache, palpitations, sweating (think when "panic attacks" come with surging BP).
- Hypoglycaemia & hyponatraemia → acute confusion, behavioural change.
5. Systemic & infective neuropsychiatric syndromes
HIV
- HIV-associated neurocognitive disorder (HAND) — spectrum from asymptomatic neurocognitive impairment → mild neurocognitive disorder → HIV-associated dementia (subcortical dementia: psychomotor slowing, apathy, memory loss).
- Mania ("AIDS mania") and depression are frequent.
- Always exclude opportunistic CNS infection (toxoplasmosis, cryptococcus, PML) and CNS lymphoma before attributing symptoms to HAND.
Systemic lupus erythematosus (SLE)
- Neuropsychiatric SLE (NPSLE) — wide spectrum: cognitive dysfunction (commonest), psychosis, mood disorder, seizures, lupus cerebritis, chorea.
- Lupus psychosis is part of the 1997 ACR classification criteria.
High-yield: In a young woman with new psychosis + arthralgia/rash/cytopenias, check ANA, anti-dsDNA, anti-ribosomal-P (associated with lupus psychosis), and antiphospholipid antibodies. Distinguish lupus cerebritis from steroid-induced psychosis — a recurring clinical dilemma.
Wilson's disease (hepatolenticular degeneration)
- Autosomal recessive ATP7B mutation → copper accumulation in liver, basal ganglia, cornea.
- Psychiatric symptoms (personality change, mood disorder, psychosis) are the presenting feature in up to a third and notoriously delay diagnosis in young adults.
- Neuro: tremor ("wing-beating"), dysarthria, dystonia, parkinsonism, drooling, risus sardonicus.
High-yield — Wilson's workup flow: Suspect (young person + psychiatric + extrapyramidal/liver signs) → slit-lamp for Kayser–Fleischer rings → low serum ceruloplasmin + high 24-h urinary copper → raised hepatic copper / genetic ATP7B confirms. MRI shows the "face of the giant panda" sign in the midbrain. Drug of choice: chelation — D-penicillamine (add pyridoxine) or trientine; zinc for maintenance/asymptomatic; avoid neuroleptics where possible (worsen extrapyramidal features).
6. Diagnosis & investigation of choice
A stepwise organic screen for new/atypical psychiatric presentation:
- History & MSE → onset, course, sensorium, drug/alcohol, systemic symptoms.
- Bedside cognitive test → MMSE / MoCA; assess orientation and attention (clouding = delirium).
- First-line bloods → CBC, electrolytes, calcium, glucose, RFT, LFT, TSH, B12/folate, VDRL.
- Targeted serology → HIV, ANA/anti-dsDNA (if SLE suspected), serum ceruloplasmin (if young + EPS).
- Neuroimaging → MRI brain is the investigation of choice for structural causes (tumour, MS, limbic encephalitis); CT if acute/contraindication.
- EEG → suspected TLE, encephalitis, or to confirm delirium (diffuse slowing); temporal spikes in TLE.
- CSF / autoimmune antibodies → anti-NMDA receptor antibodies (young woman, psychosis + seizures + dyskinesia + autonomic instability — search for ovarian teratoma), paraneoplastic panel.
High-yield: MRI brain is the single best structural investigation; EEG is the key test pointing to temporal lobe epilepsy or encephalitis; anti-NMDA-receptor encephalitis is the must-not-miss cause of acute psychosis in a young woman (treat with immunotherapy + tumour removal, not just antipsychotics).
7. Management / drug of choice
General principle: treat the underlying cause — much of organic psychiatry is potentially reversible.
- Symptomatic psychosis/agitation: prefer high-potency, low-anticholinergic antipsychotics in low doses (e.g., haloperidol for acute agitation; risperidone/quetiapine for ongoing). Use cautiously — organic brains are sensitive to side effects and delirium.
- Avoid strongly anticholinergic agents (worsen confusion) and use the lowest effective dose.
- Organic mood disorder: SSRIs for depression; mood stabilisers if manic — but correct the medical driver (steroids, thyroid) first.
- Steroid psychosis: taper/reduce the steroid; short course of antipsychotic (olanzapine/haloperidol); lithium can be prophylactic in those needing continued steroids.
- Catatonia (organic or functional): benzodiazepine (lorazepam) challenge first-line; ECT if refractory or malignant catatonia.
- TLE psychosis: optimise anti-epileptics; cautious low-dose antipsychotic (some lower seizure threshold — clozapine and chlorpromazine are the worst offenders).
- Wilson's: chelation as above.
High-yield: In delirium (the commonest acute organic syndrome), the management priority is identify and treat the cause + supportive measures; if pharmacological control is needed, low-dose haloperidol is standard, benzodiazepines are first-line specifically for alcohol/sedative withdrawal delirium, and antipsychotics should be avoided in Lewy body dementia and Parkinson's (use quetiapine/clozapine if essential).
8. Complications
- Misdiagnosis as primary psychiatric illness → delayed treatment of a reversible/curable disease (e.g., Wilson's, NPSLE, hypothyroidism, B12 deficiency, neurosyphilis).
- Antipsychotic-induced worsening (extrapyramidal crisis in Wilson's, neuroleptic sensitivity in Lewy body dementia, lowered seizure threshold in TLE).
- Progression to permanent cognitive impairment / dementia if untreated.
- Self-harm and aggression from disinhibition or psychosis.
- Neuroleptic malignant syndrome and malignant catatonia — life-threatening, can be hard to distinguish (both → hyperthermia, rigidity, autonomic instability, raised CPK).
9. Key differentials
- Delirium vs dementia vs primary psychosis — see table.
- Organic vs functional psychosis — see Section 1 table.
- Lupus cerebritis vs steroid psychosis — timing relative to steroid dose, other lupus activity markers, anti-ribosomal-P.
- Frontotemporal dementia (behavioural variant) vs late-onset primary psychiatric disorder.
- Anti-NMDA receptor encephalitis vs acute schizophrenia/NMS.
| Feature | Delirium | Dementia | Primary psychosis |
|---|---|---|---|
| Onset | Acute (hours–days) | Insidious (months–yrs) | Variable |
| Consciousness | Clouded, fluctuating | Clear (until late) | Clear |
| Attention | Markedly impaired | Relatively preserved early | Usually preserved |
| Course | Fluctuating, worse at night (sundowning) | Progressive, stable over a day | Steady |
| Hallucinations | Visual common | Variable | Auditory |
| Reversibility | Often reversible | Usually irreversible | — |
| EEG | Diffuse slowing | Variable | Normal |
Recently asked / exam angle
- Frontal vs temporal lobe personality change — repeatedly asked: Witzelsucht & primitive reflexes (frontal) vs Geschwind/Klüver–Bucy & uncinate fits (temporal).
- Phineas Gage — image/eponym question pointing to orbitofrontal disinhibition.
- Klüver–Bucy syndrome features and its localisation (bilateral temporal/amygdala), commonest cause HSV encephalitis.
- Wilson's disease — young adult with psychiatric symptoms + tremor; investigation of choice (slit-lamp KF rings, low ceruloplasmin, high urinary copper), drug of choice (penicillamine), MRI "panda" sign.
- Anti-NMDA receptor encephalitis — young woman, psychosis + seizures + orofacial dyskinesia; look for ovarian teratoma.
- Steroid-induced psychiatric effects — euphoria/mania most common; dose threshold.
- Cushing's — commonest psychiatric symptom is depression.
- Organic hallucinosis / peduncular hallucinosis and alcoholic hallucinosis (clear consciousness).
- Apathetic thyrotoxicosis in the elderly mimicking depression.
- Geschwind syndrome triad — hyperreligiosity, hypergraphia, hyposexuality.
Rapid revision
- Organic = think when onset >40, clouded sensorium, visual/olfactory hallucinations, focal neuro signs, no family history.
- Frontal lobe: disinhibition (orbitofrontal, Witzelsucht, Phineas Gage), dysexecutive (dorsolateral, Wisconsin card sort), apathetic/abulic (medial) + primitive reflexes.
- Temporal lobe: psychosis (often left foci), Geschwind (hyperreligiosity, hypergraphia, hyposexuality, viscosity), uncinate fits = olfactory hallucinations.
- Klüver–Bucy: hyperorality, hypersexuality, placidity, hypermetamorphosis, visual agnosia — bilateral temporal, classically HSV encephalitis.
- Cushing's → depression; exogenous steroids → euphoria/mania, psychosis at high dose.
- Always check TSH in new/resistant mood disorder; elderly apathetic thyrotoxicosis mimics depression.
- Wilson's: young + psychiatric + tremor → KF rings, ↓ceruloplasmin, ↑24-h urinary copper, MRI "panda" sign; treat with D-penicillamine/trientine/zinc.
- NPSLE psychosis: young woman, check ANA/dsDNA/anti-ribosomal-P; differentiate from steroid psychosis.
- Anti-NMDA encephalitis: psychosis + seizures + dyskinesia + autonomic instability → hunt for ovarian teratoma; treat with immunotherapy.
- MRI = best structural test; EEG flags TLE/encephalitis; delirium → low-dose haloperidol (benzodiazepine for withdrawal delirium).
- Catatonia: lorazepam challenge first, ECT if refractory/malignant.
- Organic hallucinosis = persistent hallucinations in clear consciousness (alcoholic & peduncular types).