Synopsis
Recognise dopamine-related hyperthermic rigidity, stop the precipitant, prevent renal and cardiorespiratory injury, and distinguish neuroleptic malignant syndrome from serotonin toxicity, catatonia, infection and seizures.
- Neuroleptic malignant syndrome is an idiosyncratic reaction to dopamine-receptor blockade or abrupt withdrawal of dopaminergic treatment, producing altered mental state, generalised rigidity, hyperthermia and autonomic instability.
- High-potency antipsychotics, rapid dose escalation, parenteral or depot administration, agitation, dehydration and previous NMS increase risk, but any dopamine antagonist can be implicated.
- Symptoms usually evolve over one to three days rather than within hours: anxiety or confusion and rigidity may precede the peak fever and laboratory injury.
- Rigidity is typically severe and generalised with reduced or normal reflexes, contrasting with the clonus and hyperreflexia that favour serotonin syndrome.
- Creatine kinase is often markedly raised from muscle injury, but diagnosis is clinical and an early normal CK does not safely exclude evolving disease.
- Leucocytosis, transaminase elevation, metabolic acidosis, myoglobinuria and renal injury support severity but are neither specific nor all required.
- Immediately stop the culprit and other non-essential psychoactive medicines, provide active external cooling, intravenous fluids, thrombosis prevention and organ support.
- Benzodiazepines reduce agitation and may help overlapping catatonic features; avoid physical restraint where possible because struggle increases heat and rhabdomyolysis.
- Bromocriptine, amantadine, dantrolene and electroconvulsive therapy have selected roles in severe or refractory cases, but evidence is limited and specialist advice is essential.
- Restarting antipsychotic therapy should wait until full recovery and use a lower-risk medicine, low dose, slow titration, hydration and close monitoring through psychiatry.
Key red flags
Temperature rise with dysrhythmia, hypoxia, acidosis, oliguria, coagulopathy or reduced consciousness requires immediate intensive-care escalation.
Investigation priorities
Identify dopamine blockade, depot exposure, interaction or dopaminergic withdrawal.
Management branches
Hyperthermia, rigidity and mental-state change follows dopamine blockade or withdrawal.
- Stop the suspected culprit and non-essential psychoactive medicines, restore omitted dopaminergic therapy only through specialist advice and contact critical care and poisons information.
- Use ABCDE assessment, active external cooling, intravenous fluids, cardiac monitoring and rapid treatment of hypoxia, hyperkalaemia, seizure and aspiration.
- Minimise struggling and restraint, use benzodiazepine for severe agitation when safe, and record temperature, rigidity, urine output and neurological state repeatedly.
Key medicines
LorazepamUse small titrated intravenous or oral doses from the current BNF with airway and respiratory monitoring, especially when agitation or catatonic features are prominent.Sedation, aspiration and respiratory depression can obscure deterioration; reduce for frailty and never use it as a substitute for cooling and organ support.
BromocriptineSpecialists may use an enteral dopamine-agonist regimen titrated over several days from toxicology guidance; there is no routine unsupervised ward dose.Hypotension, nausea, confusion, psychosis and drug interactions require monitored use; evidence is observational and abrupt withdrawal after longer use is avoided.