Clinical Psychiatry ICD-11 · K.Ragimov · 2026
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6A23

Acute and transient psychotic disorder

ICD-10F23Acute and transient psychotic disorders
DSM-5-TRF23Brief Psychotic Disorder

1. Definition and nosology

Acute and transient psychotic disorder (ICD-11: 6A23; DSM-5-TR: F23 Brief Psychotic Disorder) — a disorder characterized by rapid onset (a few days to weeks), psychotic symptoms (delusions, hallucinations, disorganized speech, grossly disorganized behavior), short duration, and full recovery to premorbid functional level.

Characteristic features:

  • Rapid onset — The full clinical picture develops within 2 weeks;
  • Polymorphic (multiform) symptoms — delusions, hallucinations, and emotional fluctuations together.
  • Short duration — in DSM-5-TR at least 1 day but < 1 month, in ICD-11 < 3 months;
  • Full functional recovery — patient fully returns to premorbid level.

2. History

  • Magnan V. (1893) — The term “bouffée délirante” describes acute-onset, short-lived polymorphic psychotic episodes in France.
  • Wernicke K., Kleist K., Leonhard K. (1900–1957) — The concept of “cycloid psychoses” — from the German psychiatric school; rapid onset and favorable prognosis.
  • Scandinavian school — “psychogenic psychosis” — Strömgren E. (1940) — psychosis in the context of stress or trauma.
  • DSM-III (1980) — “Brief Reactive Psychosis” — requiring a stress factor.
  • DSM-IV (1994) and DSM-5 (2013) — stressor criterion has been removed (remains as a qualifier); term ‘Brief Psychotic Disorder’.
  • ICD-11 (2019) — term “Acute and transient psychotic disorder” retained; 3-month duration; polymorphic symptomatology emphasized.

3. Epidemiology

  • Annual incidence: 3.9–9.6 per 100,000 (Castagnini A., Berrios G.E. Eur Arch Psychiatry Clin Neurosci 2009 review).
  • Sex: Relatively frequent in women (1.5–2:1) — especially in postpartum context.
  • Age of onset: 20–35 years; slightly later than schizophrenia.
  • Cultural and geographic: frequency higher in low- and middle-income countries (Susser E. et al. Arch Gen Psychiatry 1994 meta-analysis of 10 country studies).
  • Postpartum onset — belongs to the category of postpartum psychosis (6E21).
  • Diagnostic persistence and conversion: 30–50% of patients are re-diagnosed with schizophrenia, schizoaffective disorder, or bipolar disorder on long-term follow-up (Castagnini A. et al. Schizophr Res 2013).

4. Etiology and pathogenesis

4.1 Genetic factors

  • Schizophrenia and bipolar disorder partially share genetic risk.
  • Risk increases when psychotic or affective disorder is present in family history.

4.2 Triggers and stress

  • Acute psychosocial stress (death, displacement, natural disaster) — identified in a significant proportion of patients; indicated as a stress qualifier in DSM-5-TR.
  • Postpartum period — hormonal and sleep disturbances.
  • Substance use — cannabis, amphetamine, hallucinogens — can trigger a psychotic episode, but substance-induced psychosis is coded as a separate category if the substance is specified.
  • Short-term sleep deprivation, intense emotional tension.

4.3 Neurobiological mechanisms

  • Temporary hyperactivity of the dopaminergic system — in the context of stress, cortisol or hormonal changes.
  • Central mechanisms similar to schizophrenia, but shorter-term and potentially reversible.

5. Clinical features

5.1 Classic presentation

  • Rapid onset — from premorbid normal function to full psychotic picture within days or weeks.
  • Polymorphic (variable) symptoms — delusions (persecution, relationship, religious), hallucinations (auditory, visual, cenesthetic), disorganized speech.
  • Emotional fluctuation — acute fear, ecstasy, panic, bewilderment.
  • Consciousness is clear (if consciousness is impaired, delirium should be excluded).
  • Behavior — odd, disorganized; sometimes with catatonic components.

5.2 ICD-10 subtypes (F23.0–F23.2)

  • F23.0 Acute polymorphic psychotic disorder — without schizophrenia symptoms;
  • F23.1 Acute polymorphic psychotic disorder — with schizophrenia symptoms;
  • F23.2 Acute schizophrenia-like psychotic disorder — Schneider first-rank symptoms dominant.

5.3 Course

Typical course — peak achieved within 2–4 weeks, then gradual or rapid subsidence. Full recovery — within 1 month (DSM-5-TR) or 3 months (ICD-11). Persisting beyond this period results in a change of diagnosis to schizophreniform (DSM-5-TR F20.81, 1–6 months) or schizophrenia.

6. Diagnosis

6.1 Unified diagnostic criteria (DSM-5-TR · ICD-11 consensus points)

A. Presence of one or more psychotic symptoms:

  1. Delusions;
  2. Hallucinations;
  3. Disorganized speech;
  4. Grossly disorganized or catatonic behavior.

(At least one of 1, 2, or 3 must be present.)

B. Duration of the episode:

  • DSM-5-TR: ≥ 1 day, < 1 month, then full recovery to premorbid functional level.
  • ICD-11: full syndrome forms within 2 weeks; persists for less than 3 months.

C. Exclusions — not fully explained by affective disorder with psychotic features, schizophrenia, schizoaffective disorder, substance-induced psychosis, organic psychosis.

6.2 Differences between sources

  • DSM-5-TR (F23): qualifiers — “With marked stressor(s)” (with an acute stressor), “Without marked stressor”, “With peripartum onset” (during pregnancy or within 4 weeks of birth).
  • ICD-11 (6A23): No symptom subtypes; by course 6A23.0 – first episode, 6A23.1 – multiple episodes. Postpartum psychosis is assigned to the separate code 6E21.
  • Stress factor — not a criterion but a qualifier; was compulsory in DSM-III-R’s “Brief Reactive Psychosis.”

6.3 Diagnostic algorithm

  1. Clinical interview + information from relatives — onset dynamics, premorbid function.
  2. Structured interview (SCID-5, MINI).
  3. Severity scales — PANSS, BPRS.
  4. Toxicology screening (mandatory) — to rule out substance-induced psychosis.
  5. Physical and neurological examination.
  6. Laboratory: complete blood count, liver, kidney, electrolytes, glucose, TSH, B12, syphilis, HIV.
  7. EEG and brain MRI — first episode or atypical clinical presentation.
  8. In postpartum context — thyroid function mandatory.
  9. Assessment of suicide and child harm risk (in postpartum conditions).
  10. Monitoring — may vary based on diagnosis duration (after 1 or 3 months have elapsed).

6.4 Differential diagnosis

DisorderDistinguishing features
Schizophrenia (6A20)Duration ≥ 1 month (ICD-11) / ≥ 6 months (DSM-5-TR general); residual symptoms.
Schizoaffective disorder (6A21)An affective episode is present during a significant portion of the total illness duration.
Schizophreniform disorder (DSM-5-TR; ICD-10-CM F20.81)DSM-5-TR — 1–6 months; ICD-11 — no separate code.
Bipolar I with psychotic features (6A60.x)In the context of a manic episode.
Postpartum psychosis (6E21)Within about 6 weeks postpartum (ICD-11; DSM-5-TR: 4 weeks), typically in the first 2 weeks; high risk of infanticide and maternal suicide — medical emergency.
Substance-induced psychosisClear temporal relationship with substance (cannabis, amphetamine, hallucinogen); toxicology screening.
Secondary psychotic syndrome (6E61)Associated with organic cause (autoimmune encephalitis, lupus, paraneoplastic encephalitis).
DeliriumAlteration in consciousness; attentional fluctuation; organic cause.
Dissociative episodeIn trauma context; social withdrawal predominates.

7. Examination and assessment

7.1 Clinical scales

  • PANSS, BPRS — psychotic severity.
  • HAM-D, YMRS — assessment of affective components.
  • C-SSRS — suicide risk.
  • GAF/PSP — functional level.

7.2 Laboratory investigations

According to the first-episode psychosis protocol (see 6A20 §7.2):

  • Mandatory: complete blood count, liver and kidney function, glucose, electrolytes, TSH, B12, folate, toxicology screening, HIV, syphilis, pregnancy test, prolactin.
  • If organic psychosis is suspected — anti-NMDA-R antibodies (CSF), ANA, lupus panel, paraneoplastic antibody panel, ammonia, ceruloplasmin.
  • In postpartum context — TSH (postpartum hypothyroidism possible).

7.3 Instrumental investigations

  • Brain MRI — appropriate in first episode (NICE: when indicated); especially with atypical presentation or neurological signs.
  • EEG — rule out seizures, atypical clinical presentation.
  • ECG — before starting antipsychotic.
  • Lumbar puncture — suspected autoimmune encephalitis (atypical psychosis, dyskinesia, seizures, altered consciousness).

8. Treatment

8.1 General principles

  1. Urgent assessment and hospitalization if necessary — for the safety of the patient or others.
  2. First-line: atypical antipsychotic at low dose — risperidone 1–4 mg, olanzapine 5–15 mg, quetiapine 200–600 mg, aripiprazole 5–15 mg.
  3. In acute agitation — oral lorazepam 1–2 mg + oral disintegrating olanzapine 5–10 mg; intramuscular — olanzapine 10 mg im or aripiprazole 9.75 mg im, if necessary haloperidol 5 mg + lorazepam 2 mg im (classic).
  4. Duration — antipsychotic typically 3–6 months (after remission), then gradual reduction and monitoring; there is no standard discontinuation protocol after a first episode — individual assessment required.
  5. In stress-induced context — psychosocial support, CBT-based stress management.
  6. In postpartum onset — as a medical emergency; risk of infanticide and maternal suicide is high; hospitalization, mother-child co-hospitalization conditions are preferred; see chapter 6E20–6E2Z.
  7. ECT — in refractory severe cases, with catatonic features, one of the safe options during pregnancy.
  8. Long-term follow-up — 30–50% of patients transition to long-term psychotic disorder; monthly in the first year, then quarterly.

8.2 Treatment methods

  1. Early Intervention in Psychosis (EIP — Early Intervention in Psychosis) — Multidisciplinary care for first psychotic episode over 3 years — low-dose pharmacotherapy, CBTp, family intervention, employment support. RAISE (Kane J.M. et al. Am J Psychiatry 2016) RCT. Patients with acute and transient psychotic disorder are also included in EIP programs.
  2. Cognitive Behavioral Therapy for psychosis (CBTp — Cognitive Behavioral Therapy for psychosis) — Re-evaluation of psychotic symptoms in “thought–emotion–behavior” formulation. NICE CG178 §1.3.7.1.
  3. Family Psychoeducation — Support for patient after episode, recognition of early relapse markers, family communication training. Pharoah Cochrane 2010.
  4. Electroconvulsive Therapy (ECT) — Effective for catatonic features, severe pharmacotherapy resistance, during pregnancy. NICE TA59. UK ECT Review Group Lancet 2003.
  5. PANSS, BPRS — Standardized assessment of psychotic severity.

8.3 Differences between sources

  • NICE CG178 (Psychosis): first-episode psychosis guidelines — low-dose first-line atypical antipsychotic; early intervention services (EIP) involvement; psychosocial intervention combined.
  • APA Practice Guideline 2021 (Schizophrenia): There is no specific algorithm for acute and transient psychotic disorder; principles of first-episode psychosis.
  • NICE CG192 (Antenatal and postnatal mental health): Postpartum psychosis is a medical emergency — hospital admission, atypical antipsychotic + benzodiazepine, ECT in refractory cases.

9. Prognosis

Good prognostic factors

  • Very rapid onset and short duration.
  • Clear stress trigger.
  • Premorbid good functional level.
  • Presence of an affective component.
  • Polymorphic symptomatology (without schizophrenia symptoms).
  • Absence of family psychotic history.
  • No cannabis or other substance use.

Poor prognostic factors

  • Schizophrenia-like symptoms (Schneider first-rank).
  • Absence of stress trigger.
  • Gradual onset.
  • Premorbid functional impairment.
  • Schizophrenia in family history.
  • Substance use.

Follow-up targets

  • Long-term follow-up is critical — 30–50% transition to schizophrenia, schizoaffective, or bipolar; monthly in the first year, then quarterly formal monitoring.
  • Recognition of relapse markers (sleep disturbance, social withdrawal, unusual experiences).
  • Gradual reduction and discontinuation of antipsychotic dose — individual decision (relapse risk vs side effects).
  • Comorbid substance use and trauma intervention.
  • In postpartum cases — high recurrence risk in subsequent pregnancies, prophylactic treatment plan.

10. Myths and misconceptions

10.1 Etiology and conceptual myths

Myth 1: “Acute and transient psychosis is ‘just a psychological breakdown’ that depends on individual strength”

Why it is widespread: Temporal correlation with stress and short-term course appears to support “psychological” explanation.

Clinical and biological rationale: Stress is a trigger factor, but not an explanation on its own — not all stressed individuals experience psychosis. Genetic and neurobiological vulnerability exists. Castagnini 2013 evidence — 30–50% of patients transition to schizophrenia, schizoaffective or bipolar disorder; this indicates neurobiological vulnerability.

Real clinical step: Stress management and psychotherapeutic support are important, but antipsychotic treatment should not be delayed.

Myth 2: “Non-postpartum acute psychosis is safe and always resolves on its own”

Clinical logic: every acute psychotic episode warrants urgent medical evaluation. The risk is especially high with postpartum onset (infant homicide ~4%, maternal suicide). Non-postpartum acute transient episodes also carry suicide and violence risk — patient’s delusional content and behavioral control should be assessed.

Myth 3: “Presence of a stressor is a condition for diagnosis”

Evidence: In DSM-III-R ‘Brief Reactive Psychosis’, a stressor was a criterion, but in DSM-5-TR and ICD-11 it is a qualifier, not a criterion — acute psychotic episodes without a stressor are also diagnostically possible.

10.2 Misguided treatment approaches

Myth 4: “Acute psychosis resolves on its own, treatment can be delayed”

Clinical logic and evidence: Marshall M. et al. Arch Gen Psychiatry 2005 — as the duration of untreated psychosis (DUP) lengthens, long-term prognosis worsens. Even in a transient episode, early antipsychotic intervention is crucial for shortening the duration of symptoms and reducing complications.

Myth 5: “An acute psychotic patient can be left alone — they can control themselves”

Evidence: In acute psychotic episodes, the patient’s reality testing is impaired, and self-care, food and fluid intake, and personal safety cannot be maintained. Hospital admission or 24/7 supervision is usually required.

Myth 6: “In acute transient psychosis, exorcism or religious ritual can replace antipsychotics”

Evidence: similar to schizophrenia — prognosis worsens as DUP lengthens; religious-cultural support can be provided in parallel but does not replace antipsychotic treatment.

10.3 Ineffective or harmful approaches

Myth 7: Acute psychosis is a “spiritual emergency” or “transition to higher consciousness”; treatment is harmful

Why it is widespread: Stan Grof and the ‘transpersonal psychology’ movement reinterpret psychotic experiences as ‘spiritual awakening’.

Clinical logic and evidence: This approach is not accepted in modern clinical practice and evidence-based psychiatry. Psychotic symptoms cause real distress to the patient and pose risk; refusal of treatment leads to poor clinical outcome (DUP extension).

Myth 8: “Cannabis can calm an acute psychotic episode”

Evidence: Cannabis is a psychosis trigger and is contraindicated — its calming effect is illusory, and it indirectly exacerbates symptoms; contraindicated in clinical practice.

Myth 9: “Vitamins, omega-3, valerian, St John’s Wort are effective in acute psychosis”

Evidence: These complementary interventions have not demonstrated efficacy in acute psychotic episodes; St John’s Wort reduces antipsychotic levels via cytochrome P450 induction (interaction).

Myth 10: “Hypnotherapy or psychoanalytic deep therapy can be used in acute psychosis”

Evidence: In acute psychotic episodes, deep psychoanalytic intervention may disorganize the patient; at this stage, supportive therapy, structure, and safety are important, deep intervention is not.

11. Sources

  1. WHO. ICD-11 for Mortality and Morbidity Statistics. 6A23 Acute and transient psychotic disorder. 2024.
  2. American Psychiatric Association. DSM-5-TR. Washington DC: APA Publishing; 2022.
  3. NICE Clinical Guideline 178. Psychosis and schizophrenia in adults: prevention and management. 2014, 2019 update.
  4. NICE Clinical Guideline 192. Antenatal and postnatal mental health: clinical management and service guidance. 2014, 2020 update.
  5. American Psychiatric Association. Practice Guideline for the Treatment of Patients with Schizophrenia, 3rd ed. 2021.
  6. Castagnini A., Berrios G.E. Acute and transient psychotic disorders (ICD-10 F23): a review from a European perspective. Eur Arch Psychiatry Clin Neurosci 2009;259(8):433–443.
  7. Castagnini A., Bertelsen A., Berrios G.E. Diagnosis of acute and transient psychotic disorders 12 years after admission: a follow-up study. Schizophr Res 2013;143(1):198–203.
  8. Susser E., Wanderling J. Epidemiology of nonaffective acute remitting psychosis vs schizophrenia. Arch Gen Psychiatry 1994;51(4):294–301.
  9. Marshall M., Lewis S., Lockwood A. et al. Association between duration of untreated psychosis and outcome. Arch Gen Psychiatry 2005;62(9):975–983.
  10. Kane J.M., Robinson D.G., Schooler N.R. et al. Comprehensive versus usual community care for first-episode psychosis (RAISE). Am J Psychiatry 2016;173(4):362–372.
  11. NICE Technology Appraisal 59. Guidance on the use of electroconvulsive therapy. 2003 (reviewed).

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