ICD-116A40	CATATONIA ASSOCIATED WITH ANOTHER MENTAL DISORDER Catatonia associated with another mental disorder
ICD-10F06.1	Organic catatonic disorder
DSM-5-TRF06.1	Catatonia Associated With Another Mental Disorder (Catatonia Specifier)

1. Definition and nosology

Catatonia (ICD-11: 6A40 Catatonia Associated with Another Mental Disorder; 6A41 Catatonia Induced by Substances or Medications; 6E69 Secondary Catatonia Syndrome; DSM-5-TR: F06.1 Catatonia) — syndrome of complex disturbance in psychomotor, behavioral and autonomic functions. Not an independent disorder — clinical syndrome on background of another psychiatric or medical condition.

DSM-5-TR — catatonia is no longer a subtype of schizophrenia (that status was abolished); can be coded in the context of affective disorders, neurodevelopmental disorders, organic conditions, and substance-induced states.

2. History

• Kahlbaum K. (1874) — “Die Katatonie oder das Spannungsirresein” — catatonia as a separate syndrome.
• Kraepelin (1899) — catatonia integrated as ‘dementia praecox’ subtype.
• Bleuler (1911) — retained within schizophrenia category.
• 1970s–1980s — Taylor, Fink — catatonia's widespread presence in affective disorders and reconfirmation as a general syndrome.
• DSM-5 (2013) and ICD-11 (2019) — catatonia formalized as transnosological syndrome; schizophrenia subtype status abolished.

3. Epidemiology

• 7–15% of patients admitted to psychiatric hospital have catatonic symptoms (Fink M., Taylor M.A. Catatonia 2003).
• Catatonia is most prevalent in affective disorders (especially bipolar manic and depressive episodes).
• In schizophrenia, 10–20% of patients exhibit catatonic features during the course.
• Organic catatonia — autoimmune encephalitis (especially anti-NMDA-R, anti-LGI1), electrolyte disturbances, uremic and hepatic encephalopathy, sepsis, neurosyphilis, neuromuscular disease context.
• Persistent clinical overlap with Neuroleptic Malignant Syndrome (NMS) — some researchers consider them the same spectrum.

4. Aetiology and pathogenesis

• GABA-ergic system hypofunction — the rapid clinical effect of lorazepam (within hours) supports this; GABA-A receptor dysfunction is the central mechanism.
• Dopamine dysregulation — neuroleptic-induced catatonia and within the spectrum of NMS; antipsychotic discontinuation cholinergic and adrenergic rebound.
• Glutamate NMDA dysregulation — autoimmune anti-NMDA-R encephalitis presents a classic catatonic presentation.
• Genetic — predisposition associated with affective disorders.

5. Clinical features

DSM-5-TR criteria — at least 3 of 12 symptoms:

1. Stupor — psychomotor activity absence, unresponsiveness to surroundings.
2. Catalepsy — maintaining posture against passive induction.
3. Waxy flexibility — posture induced by the examiner is maintained as though moulded in wax.
4. Mutism — absence of speech or significant reduction.
5. Negativism — opposition to instructions or external stimuli.
6. Posturing — involuntary spontaneous posture maintenance (against gravity).
7. Mannerism — strange caricature of ordinary behaviors.
8. Stereotypy — purposeless repetitive movements.
9. Agitation — independent of external stimuli.
10. Grimacing — facial muscle expressions.
11. Echolalia — repetition of others' speech.
12. Echopraxia — repetition of others' actions.

Severity forms

• Retarded (stuporous) catatonia — motor reduction, mutism dominant; majority of cases.
• Excited (manic) catatonia — high agitation, autonomic disturbance, hyperthermia.
• Malignant catatonia — hyperthermia with excited form, autonomic instability, high CPK, mortality risk – coincides with NMS; emergency medical condition.

6. Diagnosis

6.1 Unified diagnostic criteria

DSM-5-TR — ≥3 of 12 features; ICD-11 — same clinical features across different categories.

6.2 Diagnostic tests

• Lorazepam challenge test: 1–2 mg IV/IM lorazepam → significant reduction of catatonic signs within 10–30 minutes confirms the diagnosis (Bush G. et al. Acta Psychiatr Scand 1996).
• Bush-Francis Catatonia Rating Scale (BFCRS) — 23-item standardized scale; first 14 items screening (≥ 2 signs — positive).

6.3 Etiological investigation (mandatory)

1. Complete blood count, liver/renal, electrolytes (Na, K, Ca, Mg, P), glucose, ammonia, CPK, troponin, thyroid, B12.
2. Toxicology screening.
3. Syphilis, HIV.
4. Brain MRI.
5. EEG — rule out non-convulsive status epilepticus.
6. Lumbar puncture — suspected encephalitis / autoimmune encephalitis (anti-NMDA-R, anti-LGI1 antibodies).
7. ANA, lupus panel.

6.4 Differential diagnosis

7. Examination and assessment

• BFCRS — baseline ratings and monitoring.
• The above laboratory and instrumental examinations — an etiological search.
• Autonomic function (blood pressure, pulse, temperature, urine output) — especially in malignant form.
• Comorbid mood disorder and psychotic symptom assessment (later, when patient can speak).

8. Treatment

8.1 General principles (BAP 2023 · Fink-Taylor protocol)

1. STOP antipsychotics — particularly typical and high D2 antagonists (haloperidol, risperidone high dose) — can enhance catatonia, transform into malignant form.
2. Lorazepam first-line — 1–2 mg IM/IV, titration based on initial response; typical effective dose 6–24 mg/day; some patients require 30+ mg. ~70–80% patients respond (Sienaert P. et al. Front Psychiatry 2014 review).
3. ECT — refractory cases (lorazepam non-response within 48–72 hours), malignant catatonia — first-line, life-saving measure. NICE TA59 — strong recommendation in catatonia.
4. Etiological treatment — parallel: if against a background of affective disorder, mood stabilizer (lithium); in schizophrenia context — atypical antipsychotic (clozapine or quetiapine less risky) cautiously with lorazepam.
5. In autoimmune catatonia — immunotherapy (IV steroid, IVIG, plasmapheresis, second-line rituximab).
6. Supportive treatment — hydration, nutrition (NG tube necessary), DVT prophylaxis, skin care, aspiration pneumonia prophylaxis.
7. In malignant catatonia — ICU; aggressive hydration, dantrolene, bromocriptine, ECT.

8.2 Source-specific clarifications

• BAP 2023 (British Association for Psychopharmacology) Catatonia Consensus Guidelines — lorazepam is first-line; ECT is for refractory or malignant cases; avoid or use antipsychotics with extreme caution.
• Fink M., Taylor M.A. Catatonia: A Clinician's Guide (2003) — classic protocol; lorazepam test and high-dose lorazepam therapy.
• NICE TA59 — ECT open recommendation in catatonia.

Treatment methods

1. Bush-Francis Catatonia Rating Scale (BFCRS) — 23-item scale; first 14 items screening (≥ 2 positive); 23 items severity. Bush G. et al. Acta Psychiatr Scand 1996.
2. Lorazepam challenge test — reduction of catatonic signs within 10–30 min after 1–2 mg IM/IV lorazepam administration confirms diagnosis and guides therapy plan. Bush G. et al. 1996.
3. Electroconvulsive Therapy (ECT) — Gold standard in catatonia; UK ECT Review Group Lancet 2003 evidence base; NICE TA59. Typically 6–12 sessions, bilateral target.
4. Immunotherapy (in autoimmune catatonia) — IV methylprednisolone 1 g/day × 5 days → IVIG and/or plasmapheresis; in refractory cases rituximab, cyclophosphamide. Graus F. et al. Lancet Neurol 2016 autoimmune encephalitis protocol.

9. Prognosis

• Lorazepam and/or ECT response — most patients achieve full recovery within days to weeks.
• High relapse if etiological disorder is untreated.
• Complications — aspiration pneumonia from prolonged stupor, DVT, dehydration, skin ulcers.
• Malignant catatonia — mortality 10–20% (if untreated).
• Monitoring — in etiological disorder context; recognition of relapse markers.

10. Myths and misconceptions

Myth 1: “Catatonia is a subtype of schizophrenia”

Evidence: DSM-5 (2013) and ICD-11 (2019) — catatonia as a transnosological syndrome; schizophrenia subtype status abolished. More frequent in the context of affective disorders (Fink & Taylor 2003).

Myth 2: “Catatonic patient should be treated with antipsychotics”

Evidence: An antipsychotic may worsen catatonia and precipitate the malignant form. First-line — lorazepam, then ECT. Antipsychotic if needed for the etiological disorder, cautiously with lorazepam; atypical preferred (clozapine or quetiapine).

Myth 3: “A catatonic patient has lost consciousness or is in a coma”

Evidence: Most catatonic patients are fully aware of surroundings — mutism and psychomotor impairment are not loss of consciousness. Patient remembers everything after episode. Staff conversations near patient should be cautious.

Myth 4: “Catatonia is a rare or historical condition, absent in modern psychiatry”

Evidence: 7–15% of patients admitted to psychiatric hospitals have catatonic symptoms (Fink & Taylor 2003); the syndrome is recognised far less often than it occurs.

Myth 5: “Lorazepam only sedates, does not provide ‘true’ treatment”

Evidence: Lorazepam targets the core mechanism of catatonic syndrome (GABAergic hypofunction); ~70–80% of patients experience dramatic and rapid clinical recovery.

Myth 6: “ECT is dangerous and outdated in catatonia”

Evidence: ECT is the gold standard for catatonia, NICE TA59 clear recommendation; life-saving in malignant catatonia.

Myth 7: The patient must be forced to talk — breaking the psychological barrier

Evidence: Mutism is biologically rooted, not psychological “resistance”; demanding it increases the patient's distress and is not therapeutic.

11. Sources

1. WHO. ICD-11. 6A40 Catatonia. 2024.
2. APA. DSM-5-TR. 2022.
3. Rogers J.P., Pollak T.A., Begum N. et al. Catatonia: demographic, clinical and laboratory associations. Psychol Med 2023 (BAP Guidelines).
4. Fink M., Taylor M.A. Catatonia: A Clinician's Guide to Diagnosis and Treatment. Cambridge Univ Press; 2003.
5. Bush G., Fink M., Petrides G. et al. Catatonia. I. Rating scale and standardized examination. Acta Psychiatr Scand 1996;93(2):129–136.
6. Sienaert P., Dhossche D.M., Vancampfort D. et al. A clinical review of the treatment of catatonia. Front Psychiatry 2014;5:181.
7. Graus F. et al. A clinical approach to diagnosis of autoimmune encephalitis. Lancet Neurol 2016;15(4):391–404.
8. NICE TA59. Guidance on the use of electroconvulsive therapy. 2003 (reviewed).
9. UK ECT Review Group. Lancet 2003;361(9360):799–808.