Schizophrenia

ICD-10F20	Schizophrenia
DSM-5-TRF20.9	Schizophrenia

1. Definition and nosology

Schizophrenia — a psychotic disorder characterized by significant disturbance in thought, perception, affect, and behavior, accompanied by at least one month of active-phase symptoms and typically a chronic course. In the ICD-11 classification it is placed under code 6A20 in the group ‘Schizophrenia and other primary psychotic disorders’ (6A20–6A2Z).

Nosologically, it is a primary psychotic disorder — meaning psychotic symptoms are not fully explained by another medical condition, substance effect, or affective disturbance. Schizoaffective disorder (6A21), schizotypal disorder (6A22), acute and transient psychotic disorder (6A23) and delusional disorder (6A24) are coded separately.

2. History

The modern concept of schizophrenia has passed through four main stages:

• Kraepelin (1899) — “dementia praecox” (early dementia) — a disorder characterized by persistent cognitive decline that begins in early adulthood.
• Bleuler (1911) — The term “schizophrenias” (meaning “split mind,” but not in the sense of “dual personality”); the “4A” symptoms (loosening of associations, affect, ambivalence, autism) are taken as fundamental.
• Schneider (1959) — “first-rank symptoms” (audible thoughts, commentary hallucinations, thought withdrawal, sense of control) accepted as diagnostic priority; this approach is reflected in DSM-III and ICD-10.
• DSM-5 (2013) and ICD-11 (2019) — subtypes (paranoid, hebephrenic, catatonic, simple) have been abolished (clinical utility and validity not proven, variable over time); Schneider’s first-rank symptoms have been downgraded to equal status with other symptoms; additionally, ICD-11 applies a dimensional approach — 6A25 symptom domains (positive, negative, depressive, manic, psychomotor, cognitive) and 6A20.x Course qualifiers.

Main changes compared with ICD-10 (F20): elimination of subtypes, elimination of the special status of Schneiderian symptoms, retention of the 1-month duration criterion, but, unlike DSM-5-TR, it has no 6-month total-illness duration requirement.

3. Epidemiology

Prevalence and incidence

• Lifetime prevalence: 0.3–0.7% (Saha S. et al. PLoS Med 2005, systematic review, 188 studies, 46 countries).
• Annual incidence: 15.2 per 100,000 (McGrath J.J. et al. BMC Med 2004 meta-analysis).
• Geographic and cultural variability exists, but the core incidence rate remains within a certain range.

Sex and age

• Male : female ratio ~1.4 : 1; age at onset: males 18–25, females 25–35 (Aleman A. et al. Arch Gen Psychiatry 2003).
• In women, a second incidence peak is observed after menopause (associated with the reduction of the neuroprotective effect of estrogen).
• Onset in childhood is rare (<1% of all cases); a first diagnosis after the age of 50 is uncommon.

Comorbidity and mortality

• Substance use disorder — comorbid ~50% (especially tobacco, cannabis, alcohol).
• Depression — comorbid in 25–80% over the course.
• Suicide: Lifetime risk ~5–10% (Hor K., Taylor M. J Psychopharmacol 2010); the highest risk is within the first 5 years.
• Overall mortality: 2–4 times higher compared to the population (Olfson: SMR 3.7); expected lifespan is approximately 10–20 years shorter (Hjorthøj C. et al. Lancet Psychiatry 2017 — 14.5 years; Laursen T.M. et al. Annu Rev Clin Psychol 2014) — mainly cardiovascular diseases, metabolic syndrome, tobacco use.

4. Etiology and pathogenesis

4.1 Genetic factors

Heritability 60–80% (Sullivan P.F. et al. Arch Gen Psychiatry 2003, twin meta-analysis). Monozygotic twin concordance ~50%, dizygotic ~15%, general population risk ~1%. One parent with schizophrenia — child risk ~10%; both parents — ~40%.

Polygenic nature: GWAS studies have identified over 200 risk loci (Trubetskoy V. et al. Nature 2022, n>76,000 cases). There is no single “schizophrenia gene” — the risk is made up of hundreds of small-effect variants and copy number variations (CNV) — 22q11.2 deletion (~25-fold increased risk), 16p11.2, NRXN1 deletions.

4.2 Neurodevelopmental model

Schizophrenia as a neurodevelopmental disorder — accepted (Weinberger D.R. Arch Gen Psychiatry 1987; Murray R.M., Lewis S.W. BMJ 1987). Disturbance in early brain development (intrauterine and early postnatal) leads to clinical manifestation at a young age. Evidence:

• Premorbid cognitive deficits and motor delays — documented from childhood.
• Synaptic pruning (during puberty) is excessive — reduction in cortical gray matter mass.
• Already documented brain structural changes in the first episode (not a mediator — a marker).

4.3 Environmental risk factors

• Obstetric complications — hypoxia, infection, fetal growth restriction (Cannon M. et al. Am J Psychiatry 2002 meta-analysis, OR ~2).
• Maternal viral infections during pregnancy (influenza, herpes) — increase risk by 2–7 times (Brown A.S. Schizophr Bull 2006).
• Cannabis use during adulthood — increases psychosis risk 2–3 times, even with early and high THC doses (Marconi A. et al. Schizophr Bull 2016 meta-analysis).
• Growing up in urban environments, migration, social isolation, childhood trauma — moderate increase in risk (van Os J. et al. Nature 2010 review).
• Paternal age 45+ — associated with increased risk of new mutations (Malaspina D. Arch Gen Psychiatry 2001).

4.4 Neurobiological mechanisms

• Dopamine hypothesis (updated): mesolimbic dopamine hyperactivity → positive symptoms; mesocortical hypoactivity → negative and cognitive symptoms (Howes O.D., Kapur S. Schizophr Bull 2009).
• Glutamate NMDA hypofunction: Ketamine and PCP produce schizophrenia-like symptoms via NMDA blockade; this places the glutamate system as the second key mechanism (Olney J.W., Farber N.B. Arch Gen Psychiatry 1995).
• GABAergic interneurons: Parvalbumin-positive interneuron dysfunction in the prefrontal cortex leads to working memory impairment.
• Structural changes: a decrease in cortical gray matter volume (particularly prefrontal and superior temporal cortex), ventricular enlargement, hippocampal volume reduction (Haijma S.V. et al. Schizophr Bull 2013, meta-analysis n>18,000).
• Inflammation theory: Elevated CRP, IL-6, and microglia activation documented in first episodes (Khandaker G.M. et al. Lancet Psychiatry 2015).

5. Clinical features

Symptom domains (ICD-11 / 6A25)

Positive symptoms

Delusion (persecutory, referential, grandiose, control), hallucinations (most typical auditory — commentary or dialogue), formal thought disorder (disorganized speech, neologisms, “word salad”), grossly disorganized behavior.

Negative symptoms

Affective flattening, avolition (loss of motivation), alogia (poverty of speech), anhedonia, social withdrawal. A major factor in functional impairment; responds poorly to pharmacotherapy.

Cognitive symptoms

Working memory, attention, executive function, semantic and verbal memory impairments. Present in 75–85% of patients (Heinrichs R.W., Zakzanis K.K. Neuropsychology 1998 meta-analysis).

Depressive and manic symptoms

Affective episodes are widespread in the course of schizophrenia; if the affective episode does not explain the psychotic symptoms, the diagnosis of schizophrenia remains.

Psychomotor symptoms

Catatonic components (mutism, negativism, waxy flexibility, stereotypy), agitation, retardation.

Stages of illness

1. Premorbid phase — discrete cognitive and social deficits starting from childhood (clinical schizophrenia is not yet present).
2. Prodromal phase — months-years; social withdrawal, unusual experiences, depressive symptoms, subclinical psychotic symptoms.
3. Acute (first) psychotic episode — manifest positive symptoms; average age 18–25 (in males).
4. Stabilization and residual phases — residual symptoms, functional impairment, relapse episodes.

The “1/3 principle” (Hegarty J.D. et al. Am J Psychiatry 1994 review)

• 1/3 patients — good functional recovery.
• ~1/3 — residual symptoms, partial functional recovery.
• ~1/3 — severe chronic course, requires continuous support.

6. Diagnosis

6.1 Unified diagnostic criteria (DSM-5-TR · ICD-11 · NICE CG178 consensus)

A. Active-phase symptoms — at least 2 of the following must have persisted for ≥ 1 month; at least one must be from (1)–(3):

1. Delusion
2. Hallucinations
3. Formal thought disorder / disorganized speech
4. Grossly disorganized or catatonic behavior
5. Negative symptoms (affective flattening, avolition, alogia)

B. Functional impairment — significant decline in one or several areas of work, relationship or self-care.

C. Exclusions — psychoactive substance effects and organic causes (toxicology screening, brain imaging, lab tests) must be excluded.

D. Affective differentiation — affective episode does not fully explain psychotic symptoms (schizoaffective disorder or affective disorder with psychotic features excluded).

6.2 Differences between sources

• DSM-5-TR (F20.9) additional requirement: total duration of illness ≥6 months (1 month active + prodromal and/or residual). In the context of autism spectrum or speech disorder — schizophrenia is coded only when clear delusions or hallucinations are additionally present.
• Difference in ICD-11 (6A20): ≥ 1 month of active symptoms is sufficient, overall 6-month requirement is not necessary. Subtypes have been abolished; instead 6A25 symptom domains and 6A20.x course qualifiers (.0 first episode, .1 multiple episodes, .2 continuous, .Z unspecified; 5th character: 0 symptomatic, 1 partial, 2 full remission) are coded.
• NICE CG178 practice requirement: The diagnosis is clinical, but may be supported by structured interview and severity scale (NICE does not require this); first episode: ECG and baseline metabolic indicators (glucose, HbA1c, lipids, prolactin) are mandatory, brain MRI — when indicated.

6.3 Diagnostic algorithm

1. Clinical interview (patient + at least one informed relative).
2. Structured diagnostic interview (SCID-5 or MINI).
3. Severity assessment (initial PANSS or BPRS score).
4. Physical and neurological examination.
5. Toxicology screening (urine) and substance use history.
6. Mandatory laboratory tests (see § 7.2 below).
7. Brain MRI (at first episode).
8. Differential diagnosis (§ 6.4).
9. Comorbidity and suicide risk assessment (C-SSRS).
10. Functional level assessment (GAF or PSP).

6.4 Differential diagnosis

7. Examination and assessment

7.1 Clinical interview and scales

• Structured interview: SCID-5 (for DSM-5), MINI (short, accessible in clinical practice).
• Severity scales (gold standard): PANSS (30 items, 7-point scale), BPRS (18 items), SANS/SAPS (negative/positive separately), CGI-S.
• Functional level: GAF (DSM-IV), PSP (Personal and Social Performance Scale).
• Suicide risk: C-SSRS (Columbia-Suicide Severity Rating Scale).
• Cognitive assessment: MATRICS Consensus Cognitive Battery (MCCB) — research and specialized clinics.

7.2 Laboratory investigations

Mandatory in first episode: Complete blood count, liver and kidney function tests, fasting glucose and HbA1c, lipid profile, TSH and T4, vitamin B12 and folate, toxicology screening (cannabis, amphetamine, opioid, cocaine, PCP, MDMA), HIV and syphilis serology, pregnancy test (in females), baseline prolactin level.

Selective (based on clinical suspicion): EEG (rule out seizure or delirium), anti-NMDA-R antibodies (CSF — atypical presentation), ceruloplasmin and 24-hour urine copper (suspected Wilson’s disease), homocysteine (suspected organic cause).

7.3 Instrumental investigations

• Brain MRI (T1, T2, FLAIR) — appropriate at first episode (NICE: when indicated).
• ECG — before starting antipsychotic (baseline QTc).
• Brain CT — when MRI is unavailable.

8. Treatment

8.1 General principles (NICE CG178 · APA 2021 · WFSBP 2015 · Maudsley 14e consensus)

1. Multimodal approach — pharmacotherapy + psychosocial intervention + systemic support. Pharmacotherapy alone is not sufficient for functional recovery.
2. Collaborative decision-making with the patient (shared decision making) — medication, dose, and side effect profile are discussed; adherence begins at this stage.
3. Atypical antipsychotic in first episode preferred — low dose, gradual titration. In a first episode, the lower half of the standard dose may be sufficient.
4. Effect assessment — Partial response in 2–4 weeks, full response at adequate dose expected in 4–6 weeks. If no response, the medication is changed.
5. Monotherapy — antipsychotic polypharmacy increases the side-effect burden, and evidence of benefit is weak; clozapine + second antipsychotic may be an exception.
6. Treatment-resistant schizophrenia (TRS) — failure to respond to two different antipsychotics at adequate doses and durations (each at least 6 weeks, up to 8 weeks in poor response) — clozapine should be initiated.
7. Maintenance treatment — at least 1–2 years after first episode, long-term/lifetime after multiple episodes. Discontinuing the antipsychotic sharply raises relapse risk: at one year relapse was 27% on drug versus 64% on placebo (Leucht S. et al. Lancet 2012, 65 trials, n=6493; RR 0.40).
8. Psychosocial intervention — CBTp and family intervention should be offered to all patients (NICE CG178 — strong recommendation).
9. Systematic monitoring — metabolic parameters, EPS, prolactin, ECG.
10. LAI (long-acting injectable) — in cases of adherence issues or patient preference; better outcome in relapse prevention after first episode (Tiihonen J. et al. JAMA Psychiatry 2017).

8.2 Pharmacotherapy — first-line antipsychotics

Mechanism, dose, evidence, and side effect profile for each medication.

Typical (first generation) antipsychotics — haloperidol 5–20 mg/day, chlorpromazine 200–800 mg/day, flupentixol 6–18 mg/day, zuclopenthixol 25–150 mg/day. Effective for positive symptoms, but high risk of EPS and tardive dyskinesia, and weak effect on negative symptoms — not superior when atypical antipsychotics are available.

Note on the mechanism: The primary mechanism of all antipsychotics is mesolimbic D2 receptor antagonism (in atypicals, additional 5-HT2A antagonism — contributes to the reduction of negative symptoms and EPS). 60–80% D2 occupancy is the therapeutic range; >80% increases EPS risk. Below 60% the effect is insufficient (Kapur S., Mamo D. Prog Neuropsychopharmacol Biol Psychiatry 2003).

8.3 Treatment-resistant schizophrenia and clozapine

Clozapine — The most effective evidence-based medication in TRS (Kane J. et al. Arch Gen Psychiatry 1988 initial RCT; Siskind D. et al. Br J Psychiatry 2016 meta-analysis). 30–60% of TRS patients respond to clozapine.

Advantages: low D2 occupancy (40–60%), but strong effect on various receptors (D4, 5-HT2A, M1, α1); fewer EPS, better effect on negative symptoms; reduces suicide (FDA indication).

Initiation protocol: starting dose 12.5 mg; gradually increase to 200–450 mg/day (max 900 mg/day). Complete blood count + white cell differential — weekly for first 18 weeks, then every 2 weeks for up to 1 year, then monthly. ANC ≥ 2.0 × 10⁹/L — green zone (treatment continues); 1.5–2.0 × 10⁹/L — warning zone, monitor twice weekly; < 1.5 × 10⁹/L — red zone, clozapine stopped immediately (UK SmPC scheme; see Appendix A.1). In benign ethnic neutropenia the thresholds are 0.5 × 10⁹/L lower.

Clozapine side effects and management:

• Agranulocytosis (~0.8%, mortality 5%) — blood count monitoring.
• Myocarditis — especially within the first 4 weeks; troponin, ECG.
• Constipation — risk of ileus and perforation; prophylactic laxative.
• Hypersalivation, sedation — dose-dependent.
• Seizures — the risk rises at doses above 600 mg/day; EEG monitoring.
• Metabolic syndrome — high; regular monitoring.

Clozapine discontinuation — important clinical point: sudden cessation causes rebound psychosis (more severe than original symptoms), cholinergic rebound (nausea, vomiting, diarrhea) and adrenergic rebound (agitation, insomnia). In agranulocytosis clozapine is stopped immediately — the patient is switched to another antipsychotic in an inpatient setting with low agranulocytosis risk. For planned discontinuation — 10–25% dose reduction every 1–2 weeks.

8.4 LAI (long-acting injectable) options

8.5 Management of acute psychomotor agitation

• Oral (preferred): lorazepam 1–2 mg + olanzapine 5–10 mg oral disintegrating tablet, or risperidone 1–2 mg oral solution.
• Intramuscular: olanzapine 10 mg IM, or aripiprazole 9.75 mg IM, or haloperidol 5 mg + lorazepam 2 mg im (classic).
• Attention: Olanzapine im + benzodiazepine parenteral — risk of respiratory depression; should not be used concurrently.

8.6 Management of side effects

Extrapyramidal symptoms (EPS):

Metabolic side effect: Body weight, waist circumference, blood pressure — monthly for the first 6 months, then every 6 months; fasting glucose, HbA1c, lipids — at baseline, 12 weeks, then annually. Intervention: diet and physical activity counseling, metformin (in overweight), switching antipsychotic to a metabolically neutral agent (aripiprazole, lurasidone).

Hyperprolactinemia: high risk — risperidone, paliperidone, amisulpride, typical antipsychotics; low risk — aripiprazole, quetiapine, clozapine. In symptomatic cases (galactorrhea, amenorrhea, sexual dysfunction, osteoporosis) — change the medication.

Neuroleptic Malignant Syndrome (NMS) — a medical emergency (mortality up to 10%): Clinical tetrad — hyperthermia, muscle rigidity, altered consciousness, autonomic instability. Lab: CK > 1000, leukocytosis, myoglobinuria. Intervention: immediate discontinuation of antipsychotic, intensive care support, dantrolene, bromocriptine, ECT if necessary.

8.7 Special conditions

• Pregnancy: complete discontinuation of the antipsychotic increases relapse risk. As a class, antipsychotics do not meaningfully increase the risk of congenital malformations (Huybrechts K.F. et al. JAMA Psychiatry 2016, 1.3 million pregnancies); the possible exception is risperidone (about 26% higher risk, needs confirmation). The choice is individual: a drug that works is usually continued.
• Older adults: EPS, orthostatic hypotension, sensitivity to anticholinergic effects; low dose, quetiapine or risperidone preferred; refer to Beers Criteria.
• Comorbid substance use: smoking cessation support, cannabis cessation, concurrent treatment of alcohol dependence (naltrexone, acamprosate).

8.8 Source-specific clarifications

• NICE CG178: Early Intervention in Psychosis (EIP) — intensive multidisciplinary support in the first 3 years; clozapine is the recommended option after failure of two antipsychotics.
• APA 2021: maintenance treatment duration after first episode 2–5 years; cognitive remediation and supported employment are strongly recommended for functional recovery.
• WFSBP 2015: equivalent dose ranges and adequate duration (4–6 weeks) before medication change; LAI effective in relapse prevention.
• Maudsley 14e (2021): Detailed protocol for clozapine titration, side effect management, and reasons for polypharmacy.
• AR Ministry of Health Clinical Protocol (2009): Atypical antipsychotic first-line; conventional neuroleptics when an atypical antipsychotic is unavailable. General algorithm aligns with NICE/APA.

8.9 Treatment methods

1. Cognitive Behavioral Therapy for psychosis (CBTp — Cognitive Behavioral Therapy for psychosis) — Re-evaluation of psychotic symptoms within “thought–emotion–behavior” formulation; patient addresses hallucinations and delusions with reality testing, behavioral experiments, and search for alternative explanations. Standard course — 16+ individual sessions, 6–12 months. Effect: small-to-medium effect on positive symptoms (Grade A in NICE), improvement in functional level (Wykes T. et al. Schizophr Bull 2008, n=2284 meta-analysis; NICE CG178 § 1.3.7.1).
2. Family Intervention — Psychoeducation, communication training and problem-solving in families with high expressed emotion (EE). Patient + at least one family member, 10+ sessions, 3–12 months. Effect: reduces relapse risk by ~20%, reduces hospitalization (Pharoah F. et al. Cochrane Database Syst Rev 2010;(12):CD000088, n>3500). NICE CG178 § 1.3.7.2.
3. Cognitive Remediation — Computer- or trainer-based structured cognitive exercises — attention, working memory, executive function, social cognition. 20–40 sessions, 2–3 times per week. Effect: small-medium improvement in cognitive indicators, transfers to functional level only when applied together with psychosocial rehabilitation (Wykes T., Huddy V., Cellard C., McGurk S.R., Czobor P. Am J Psychiatry 2011;168(5):472–485, meta-analysis n=2104).
4. Supported Employment / Individual Placement and Support (IPS) — Direct support in real workplaces — “place-then-train” principle (starting job search without prior preparation stage). Personal job coordinator, finding a job based on individual interest and ability, on-site support. Effect: more than half enter competitive employment (20% in control groups) — Drake R.E., Bond G.R., Goldman H.H. et al. Health Aff (Millwood) 2016;35(6):1098–1105. NICE CG178 § 1.3.7.3.
5. Early Intervention in Psychosis (EIP — Early Intervention in Psychosis) — Intensive multidisciplinary care over 3 years following first psychotic episode — low-dose pharmacotherapy, CBTp, family intervention, employment support, peer support. RAISE RCT and OPUS RCT (Kane J.M. et al. Am J Psychiatry 2016; Petersen L. et al. BMJ 2005; Marshall M., Rathbone J. Cochrane Database Syst Rev 2011) — EIP superior to standard care, reduces relapse, improves functional level. NICE CG178 § 1.4.
6. Assertive Community Treatment (ACT) — Multidisciplinary team (psychiatrist, clinical psychologist, social worker, peer specialist) provides intensive support to the patient in the community (at home, workplace); 24/7 accessibility, low patient/staff ratio (~10:1). Target: patients with high risk of rehospitalization and homelessness. Effect: reduces hospital days, increases residential stability (Marshall M., Lockwood A. Cochrane 2011).
7. PANSS / BPRS — Severity scales — PANSS (Positive and Negative Syndrome Scale) — 30 items, 7-point scale; BPRS (Brief Psychiatric Rating Scale) — 18 items. Quantitative assessment of psychotic symptoms based on structured interview. For initial assessment and treatment monitoring in clinical practice. Kay S.R., Fiszbein A., Opler L.A. Schizophr Bull 1987;13(2):261–276 (PANSS); Overall J.E., Gorham D.R. Psychol Rep 1962;10:799–812 (BPRS).

9. Prognosis

Good prognostic factors

• Brief untreated period (DUP < 6 months)
• Acute onset, clear stressor
• Premorbid good function
• Predominance of positive symptoms (few negative symptoms)
• Presence of an affective component
• Good social support, family cooperation
• Early intervention and adherence

Poor prognostic factors

• Gradual onset, long prodrome
• Early age of onset (childhood or early adolescence)
• Premorbid functional impairment (from childhood)
• Predominance of negative symptoms
• Severity of cognitive deficit
• Substance use (especially cannabis, amphetamine)
• Non-adherence, social isolation
• DUP > 1 year

Follow-up targets

• Clinical stability and relapse prevention (antipsychotic adherence, consideration of LAI).
• Metabolic and cardiovascular risk management (a major contributor to mortality).
• Functional recovery — employment, independent living, social relationships.
• Comorbid substance use, depression, suicide risk monitoring.
• Strengthening family and community support systems.

10. Myths and misconceptions

10.1 Etiology myths

Myth 1: “Schizophrenia is attributed to spirit or demonic possession”

Why it is widespread: Historical-religious context — psychosis in medieval Europe explained as ‘demonic possession’; the subjectively extraordinary nature of hallucinations reinforces this; in communities with limited access to psychiatric services, family first consults religious leader.

Clinical and biological rationale: Schizophrenia is associated with measurable neurobiological markers — reduction in cortical gray matter volume (Haijma S.V. Schizophr Bull 2013, meta-analysis n>18,000), mesolimbic dopamine hyperactivity (Howes O.D. Schizophr Bull 2009), 60–80% heritability (Sullivan P.F. 2003). Dose-proportional effect of D2 receptor antagonist antipsychotics supports the specificity of the pharmacological mechanism. ‘Possession’ concept cannot be tested at these levels and is not open to falsification.

Evidence: WHO mhGAP Intervention Guide v2.0 — schizophrenia recognized as a medical condition. APA Resource Document on Religious/Spiritual Commitments (2018): religious practice may complement treatment, but cannot replace it.

Real clinical step: Antipsychotic initiation should not be delayed. Respecting family’s religious-cultural beliefs preserves therapeutic alliance — allowing exorcism rituals to replace antipsychotic treatment results in delayed treatment and poor prognosis (Marshall M. et al. Arch Gen Psychiatry 2005 — DUP > 1 year is a poor prognostic marker).

Myth 2: “Schizophrenia is a result of poor upbringing or a ‘cold mother’”

Why it is widespread: In the 1940s–1960s, influence of the psychoanalytic school (Fromm-Reichmann F. — concept of ‘schizophrenogenic mother’); the family-blaming model remained dominant in clinical practice for a long time.

Clinical and biological rationale: Heritability 60–80% — in children adopted away from biological family, risk mainly associated with diagnosis of biological parents, and in high genetic risk family dysfunction increases it (Heston L.L. Br J Psychiatry 1966; Tienari P. et al. Br J Psychiatry 2004 — Finland adoptive study). High emotional expression (EE) in family increases relapse risk, but it is not a primary etiology; it is a course modulator.

Evidence: APA, AAP, NICE — the concept of ‘schizophrenogenic mother’ has been abandoned by the scientific community.

Real clinical step: Family intervention (see “Treatment methods”) — based not on blaming, but on psychoeducation and communication training.

Myth 3: “Schizophrenia = split personality”

Why it is widespread: Etymological fallacy — mistranslation of “schizo” (split) + “phrenia” (mind) as “split personality”; mass culture (film, literature) reinforces false images.

Clinical and biological rationale: Bleuler’s 1911 term described a disruption of the mind’s internal coherence (splitting of associations), not the existence of separate personalities. “Double personality” is a distinct disorder: Dissociative Identity Disorder (6B64), with a completely different etiology (childhood trauma) and clinical manifestations.

Evidence: WHO ICD-11 — schizophrenia (6A20) and DID (6B64) are coded as separate disorders.

Myth 4: “People with schizophrenia are dangerous and aggressive”

Why it is widespread: Mass media particularly emphasizes a history of psychosis in violent incidents — reports attract attention, but the base rate is not presented.

Clinical and biological rationale: People with schizophrenia are more likely to become victims of violence (Maniglio R. Acta Psychiatr Scand 2009 systematic review — victimization ratio 2.3–140 times higher depending on crime type). The risk of violence is increased only in a specific, narrow context: untreated acute paranoid delusions + concurrent substance use (Fazel S. et al. PLoS Med 2009 meta-analysis). Minimal difference compared to population in treated, stable patients.

Evidence: Violence committed by persons with a diagnosis of schizophrenia constitutes less than 5% of all violence in society (Fazel S., Grann M. Am J Psychiatry 2006).

Real clinical step: Stigma impedes psychosocial recovery; psychoeducation for family and community is critically important.

10.2 Harmful “treatment” methods

Myth 5: “Exorcism or religious ritual can replace an antipsychotic”

Why it is widespread: Fear of antipsychotic side effects; greater accessibility of social support within religious communities; stigma of psychiatric care.

Risk: Each additional month of Duration of Untreated Psychosis (DUP) worsens long-term functional prognosis (Marshall M. et al. Arch Gen Psychiatry 2005, n=3700 meta-analysis). In patients with DUP > 1 year, remission rate significantly decreases. High risk of suicide in untreated acute episode.

Evidence: NICE CG178, WHO mhGAP — antipsychotic treatment should not be delayed; religious-cultural support may be applied in parallel.

Myth 6: “‘Insulin coma therapy’ and ‘lobotomy’ — old treatments are still secretly used in hospitals”

Reality: Insulin coma therapy (Sakel 1933) and prefrontal lobotomy (Moniz 1936, Freeman 1945) were widely used in the 1950s, but were abandoned due to lack of comparative evidence of effectiveness and severe side effects following the introduction of antipsychotics (chlorpromazine 1952). These methods are not used in modern clinical practice. ECT (electroconvulsive therapy) is different — evidence-based, used for modern indications for catatonia (NICE TA59) and in refractory schizophrenia (APA).

10.3 Ineffective methods or those delaying primary treatment

Myth 7: “Mega-doses of vitamin B3 (niacin) cure schizophrenia (orthomolecular psychiatry)”

Why it is widespread: Hoffer and Osmond in the 1950s proposed the niacin mega-dose theory based on single case report studies; the alternative medicine movement continues to support this approach.

Evidence: APA Task Force (Lipton M.A. et al. 1973) and subsequent RCTs — vitamin B3 or other vitamin mega-doses have no effect on schizophrenia symptoms. Niacin mega-dose can cause liver damage and hyperuricemia.

Myth 8: “Cannabis (especially CBD) cures schizophrenia”

Why it is widespread: Exaggerated media presentation of preliminary studies on CBD’s antipsychotic effect; marketing by the medical cannabis industry.

Reality: THC (primary psychoactive component of cannabis) increases psychosis risk two- to threefold (Marconi A. et al. Schizophr Bull 2016 meta-analysis). Preliminary RCTs on CBD (McGuire P. et al. Am J Psychiatry 2018) showed modest effect, but evidence base is insufficient to replace standard antipsychotics.

Evidence: NICE CG178, APA 2021 — CBD is not a standard recommendation for schizophrenia treatment; THC-containing cannabis is contraindicated.

Myth 9: Antipsychotics destroy the brain, turn you into a “zombie”; lifelong use is harmful

Why it is widespread: Severe EPS side effects of early typical antipsychotics; patient experiences shared on social media.

Biological logic: Structural changes associated with antipsychotic use exist (Ho B.C. et al. Arch Gen Psychiatry 2011), but these should be compared with: untreated schizophrenia itself causes faster cortical volume reduction (Cahn W. et al. Arch Gen Psychiatry 2002). Antipsychotic discontinuation sharply increases relapse risk — 64% at one year versus 27% (Leucht S. Lancet 2012), relapse itself exerts neurotoxic effects.

Evidence: Tiihonen J. et al. (Lancet 2009 — Finland; JAMA Psychiatry 2017 — Sweden) registry studies: continuous antipsychotic use reduces mortality and hospital admissions.

Real clinical step: Medication selection based on side effect profile, dose titration, and response to patient complaints is handled through shared decision-making with the patient.

Myth 10: “Schizophrenia is incurable, lifelong illness, recovery is impossible”

Reality: Hegarty 1/3 principle (Am J Psychiatry 1994) — approximately 1/3 of patients achieve good functional recovery; this rate increases, especially with Early Intervention in Psychosis (EIP) (Kane J.M. et al. Am J Psychiatry 2016 — RAISE RCT). “Clinical recovery” and “personal recovery” (Recovery model) are distinguished — a patient can build a meaningful life even without complete symptom remission.

Real clinical step: The prognosis is individual; early intervention, adherence, family support and psychosocial rehabilitation significantly increase recovery chances.

Myth 11: “Acupuncture, homeopathy, valerian are effective as substitutes for antipsychotics”

Evidence: Cochrane reviews (Rathbone J. Cochrane 2007 — acupuncture; Ernst E. reviews — homeopathy) — no evidence of efficacy in schizophrenia. Complementary methods can be applied as adjuncts (stress management, sleep hygiene), but do not replace antipsychotics.

11. Sources

1. WHO. ICD-11 for Mortality and Morbidity Statistics (Version 2024). 6A20 Schizophrenia. icd.who.int
2. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). Washington, DC: American Psychiatric Association Publishing; 2022.
3. NICE Clinical Guideline 178. Psychosis and schizophrenia in adults: prevention and management. 2014, 2019 update. nice.org.uk/guidance/cg178
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