Catatonia
A motor syndrome with many causes, one test-and-treat move, and a lethal variant
Recognizing catatonia
Definition. Catatonia is a psychomotor syndrome diagnosed when at least 3 of 12 DSM-5 features are present. It is a syndrome rather than a final diagnosis, so every case demands a search for the underlying cause. Because a mute patient cannot report symptoms, the signs must be elicited actively: move each limb to feel for resistance, leave the arm raised to test for catalepsy, and scratch your own head in view to test for echopraxia.
| Feature | What the examiner sees |
|---|---|
| Stupor | No spontaneous movement and no meaningful response to the surroundings |
| Catalepsy | Keeps a position the examiner imposes, even against gravity |
| Waxy flexibility | Limbs yield to repositioning with slight, even resistance |
| Posturing | Holds an odd position spontaneously for long periods |
| Mutism | Little or no speech despite intact language ability |
| Negativism | Resists or does the opposite of requests |
| Mannerisms and stereotypy | Exaggerated versions of normal actions; repetitive purposeless movements |
| Agitation and grimacing | Purposeless excitement unrelated to surroundings; fixed odd facial expressions |
| Echolalia and echopraxia | Copying the examiner's words or movements |
Bush-Francis scale. The Bush-Francis Catatonia Rating Scale grades 23 signs for severity; its first 14 items form a screening tool, and 2 or more positive items suggest catatonia. Rescoring after a lorazepam challenge and during treatment documents the response.
Causes and workup
Psychiatric causes. Bipolar disorder and major depression cause more catatonia than schizophrenia, a common misconception on exams; other psychotic disorders and autism spectrum disorder are further associations. DSM-5 codes catatonia as a specifier of a mental disorder, as catatonic disorder due to another medical condition, or as unspecified catatonia.
Medical causes. Suspect one when there is no psychiatric history, abnormal vital signs, or fluctuating consciousness. Important causes are anti-NMDA receptor encephalitis, nonconvulsive status epilepticus, other encephalitides, strokes and structural lesions, metabolic derangements such as hyponatremia and hepatic encephalopathy, lupus, and drug-related states, notably benzodiazepine withdrawal.
Anti-NMDA receptor encephalitis. Typically a young woman develops a psychiatric prodrome (insomnia, agitation, psychosis), then catatonia, orofacial dyskinesias, seizures, autonomic instability, and hypoventilation. CSF antibodies confirm it; pelvic ultrasound or MRI looks for an ovarian teratoma, and treatment is tumor removal plus immunotherapy.
Workup. Check vital signs, CK, CBC, electrolytes including sodium, glucose, renal and liver function, ammonia, TSH, and a urine drug screen. Obtain an EEG to exclude nonconvulsive status epilepticus, which can look identical to catatonia. Add MRI and lumbar puncture with anti-NMDAR antibodies when the picture is atypical or there is no psychiatric history.
Treatment
- Score and stabilizeBush-Francis score, vital signs, CK, labs, and EEG; stop antipsychotics.
- Lorazepam challengeLorazepam 1–2 mg IV, then rescore within minutes; clear improvement supports the diagnosis and predicts response.
- Scheduled lorazepamTitrate upward, often to high daily doses, while the underlying disorder is treated.
- ECTIf benzodiazepines fail after several days, or urgently for malignant catatonia or dangerous refusal of food and fluids.
Expected response. Most patients improve with lorazepam, those with mood disorders more reliably than those with schizophrenia. A negative first challenge does not exclude catatonia; repeat the dose or give a scheduled trial before calling it a failure. ECT is highly effective, including in benzodiazepine-resistant cases.
Malignant catatonia and complications
Malignant catatonia. Fever, autonomic instability (tachycardia, labile blood pressure, diaphoresis), altered consciousness, and a rising CK signal a life-threatening form that requires ICU care, high-dose lorazepam, and early ECT. It is clinically hard to separate from neuroleptic malignant syndrome, which many regard as a drug-induced form of the same process.
| Feature | Malignant catatonia | NMS |
|---|---|---|
| Onset | Catatonic signs precede the fever | After starting or raising a dopamine blocker |
| Findings | Fever, rigidity, autonomic swings, altered consciousness, ↑ CK | Same |
| Treatment | High-dose lorazepam, early ECT | Stop the drug, cooling and fluids, lorazepam, dantrolene or bromocriptine; ECT if refractory |
Hold antipsychotics during catatonia. High-potency agents such as haloperidol can deepen catatonia or precipitate NMS, and catatonia itself is a risk factor for NMS. When psychosis later needs treatment, reintroduce a second-generation antipsychotic cautiously while watching for rigidity, fever, and a rising CK.
Complications of immobility. Refusal to eat or drink and prolonged immobility cause dehydration and malnutrition (treat with IV fluids and nasogastric feeding), venous thromboembolism, aspiration pneumonia, pressure ulcers, contractures, rhabdomyolysis with AKI, and urinary retention. Pulmonary embolism is a recognized cause of sudden death, so give heparin or LMWH prophylaxis unless contraindicated, reposition regularly, and involve physical therapy early.