ICD-116A23	ACUTE AND TRANSIENT PSYCHOTIC DISORDER Acute and transient psychotic disorder
ICD-10F23	Acute and transient psychotic disorders
DSM-5-TRF23	Brief Psychotic Disorder

1. Definition and nosology

Acute and transient psychotic disorder (ICD-11: 6A23 Acute and Transient Psychotic Disorder; 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 — Full clinical picture formation within 2 weeks;
• Polymorphic (multiform) symptoms — delusions, hallucinations, and emotional fluctuations together.
• Short term — in DSM-5-TR < 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 “cyclic 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” — with requirement of 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 / 100 000 (Castagnini A., Berrios G.E. Curr Psychiatry Rep 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. Soc Psychiatry Psychiatr Epidemiol 1998 meta-analysis of 10 country studies).
• Postpartum onset — belongs to the category of postpartum psychosis (6E20 / 6A23.x).
• Perseverance 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. Aetiology 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-weeks.
• Polymorphic (variable) symptoms — delusions (persecution, relationship, religious), hallucinations (auditory, visual, cenesthetic), disorganized speech.
• Emotional fluctuation — acute fear, ecstasy, panic, bewilderment.
• No alterations in consciousness (except delirium).
• Behavior — odd, disorganized; sometimes with catatonic components.

5.2 ICD-11 subtypes

• Polymorphic psychotic disorder — without schizophrenia symptoms;
• Polymorphic psychotic disorder — with schizophrenia symptoms;
• Acute psychotic disorder like schizophrenia — 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 leads to diagnosis transition 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; < 3 months persists.

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

6.2 Source-specific clarifications

• DSM-5-TR (F23): qualifiers — “With marked stressor(s)” (with an acute stressor), “Without marked stressor”, “With postpartum onset” (within 4 weeks of birth).
• ICD-11 (6A23): Three subtypes – polymorphic (without/with schizophrenia symptoms) and schizophrenia-like. Postpartum onset is assigned to the separate code 6E20.
• Stress factor “It is not a criterion, but a qualifier — compulsory in DSM-IV” 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 elapsed).

6.4 Differential diagnosis

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 first episode psychosis protocol (see 6A20 §7.2):

• Absolute: complete blood count, liver/kidney, 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 — recommended in first episode (NICE CG178); especially with atypical presentation or neurological signs.
• EEG — rule out seizures, atypical clinical presentation.
• EKG — before starting antipsychotic.
• Lumbar puncture — suspected autoimmune encephalitis (atypical psychosis + motor symptoms + female age).

8. Treatment

8.1 General principles

1. Urgent assessment and hospitalization if necessary — for safety of 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; discontinuation based on first episode not standard — individual assessment.
5. In stress-induced context — psychosocial support, CBT-based stress management.
6. In postpartum onset — as a medical emergency; risk of child homicide and suicide is high; hospitalization, mother-child co-hospitalization conditions are preferred; see chapter 6E20.
7. ECT — in refractory severe cases, with catatonic features, safest option 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 Source-specific clarifications

• NICE CG178 (Psychosis): first episode psychosis guidelines — low-dose atypical antipsychotic first line; 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.

Treatment methods

1. Early Intervention Services (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. Acute and transient patients also included in EIP programs.
2. Cognitive Behavioral Therapy for psychosis (CBTp — Cognitive Behavioural 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 relapse early markers, family communication training. Pharoah Cochrane 2010.
4. Electroconvulsive Therapy (ECT) — Effective with catatonic features, severe pharmacotherapy resistance, during pregnancy. NICE TA59. UK ECT Review Group Lancet 2003.
5. PANSS, BPRS — Standardized assessment of psychotic severity.

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’, depends on individual strength”

Why it is widespread: Time 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 alone — 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: “Acute psychosis is as dangerous as postpartum psychosis / no, it always resolves on its own”

Clinical logic: every acute psychotic episode warrants urgent medical evaluation. Postpartum onset risk especially high (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-IV ‘Brief Reactive Psychosis’, a stressor was a criterion, but in DSM-5-TR and ICD-11 not a criterion but a qualifier — 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 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 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 or contraindicated — its calming effect is illusory, 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 episode; 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, 2018 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. Curr Psychiatry Rep 2009;11(4):237–247.
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. Soc Psychiatry Psychiatr Epidemiol 1998;33(10):485–490.
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).