![]() Immediate cessation of the antipsychotic medication and supportive measures (volume resuscitation, physical cooling) are essential in management. It includes malignant hyperthermia of anesthesia, serotonin syndrome, parkinsonism hyperpyrexia syndrome, heat stroke, idiopathic malignant catatonia, infections (sepsis, meningitis, encephalitis), autoimmune disorders (limbic encephalitis with NMDA receptor antibodies, lupus cerebritis) delirium tremens, status epilepticus, salicylate poisoning, endocrinopathies, stroke, and brain trauma. The differential diagnosis is of prime importance. A total cut-off threshold score of ≥74 on the IEC criteria offers 69.6% sensitivity and 90.7% specificity in diagnosing NMS. The likelihood of an NMS diagnosis can be assessed using the International Expert Consensus (IEC) criteria which are based on priority scores assigned to major clinical features (antipsychotic exposure, hyperthermia, rigidity, mental status changes, CK elevation, etc.). Although elevated CK is a frequent correlate of muscle dysfunction in NMS, it is nonspecific. Diagnostic methodsÄiagnosis is based on clinical signs of the syndrome in the context of treatment with dopamine blocking agents, and the exclusion of alternative etiologies via thorough investigation with laboratory and imaging tests. Dopamine blocking agents used in non-psychiatric settings (metoclopramide, prochlorperazine, droperidol) and dopamine depleting agents (tetrabenazine) have also been implicated. All antipsychotic agents, typical or atypical, may trigger the syndrome, although potent antipsychotics (haloperidol, fluphenazine) are more frequently associated. The syndrome is thought to result from acute central dopamine receptor blockade. ![]() ![]() Risk factors include prior NMS episodes, physical exhaustion, agitation, dehydration, pre-existing catatonia, use of restraints, use of high doses, high potency drugs, acute parenteral forms of antipsychotics, and rapid antipsychotic dosage increase. Once symptoms develop, they last on average 7-10 days after discontinuation of oral triggering drugs, with peak intensity within the first 72 hours. Other signs may include profuse diaphoresis, tachycardia, tachypnea, labile blood pressure, acidosis, incontinence, and elevated serum creatine kinase (CK) and transaminases from rhabdomyolysis with risk of subsequent renal failure. ![]() Manifestations include hyperthermia, muscular rigidity and tremor, mental status alteration and autonomic dysfunction. In about 16% of patients, the syndrome occurs within 24 hours after the initiation of the antipsychotic treatment, 66% within the first week, and less commonly within or after 30 days on stable medication regimens. The incidence may be lower with newer less potent antipsychotics and with reduced severity of symptoms, particularly for clozapine. Neuroleptic malignant syndrome (NMS) occurs in 1/5,000 to 10,000 patients treated with antipsychotics or other central dopamine (D2) receptor antagonists (all age groups male:female ratio 2:1 in some studies higher incidence rates have been reported in the past).
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