Neuroleptic Malignant Syndrome: A Review

Abstract

Virtually all neuroleptics are capable of inducing the syndrome, including the newer atypical antipsychotics. The standard of care for the recognition of neuroleptic malignant syndrome has shifted considerably over the past 15 years. Neuroleptic malignant syndrome belongs in the differential diagnosis of any patient receiving a neuroleptic who develops a high fever or severe rigidity. In addition to measurement of creatinine phosphokinase and white blood cell count, important tests to rule out other etiologies include urinalysis to measure electrolytes, including calcium and magnesium; kidney, liver, and thyroid function tests; lumbar puncture; an electroencephalogram; and a computed tomography or magnetic resonance imaging scan of the head. Although specific treatment remains controversial, supportive treatment such as antipyretics, a cooling blanket, and intravenous fluids to correct dehydration and electrolyte abnormalities is critical and widely supported by consensus. Most patients recover from neuroleptic malignant syndrome in two to 14 days without any cognitive impairment, and new dysfunction usually is attributable to very high fever, hypoxia, or other complications, rather than neuroleptic malignant syndrome per se.

Neuroleptic malignant syndrome

“…NMS is classically associated with the use of high-potency antipsychotics (AP), such as butyrophenones and phenothiazines, but has also been described with newer agents, commonly described as "atypical" AP (risperidone, olanzapine, quetiapine), other D2-receptor antagonists (metoclopramide) and following withdrawal of anti dopaminergic agents [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] . Although the precise pathophysiologic mechanism underlying NMS remains unknown, a reduction in dopaminergic activity in the brain probably by dopamine D2 receptor blockade in the striatum and hypothal-amus is generally assumed as a potential cause 4,20 .…”

“…Although the precise pathophysiologic mechanism underlying NMS remains unknown, a reduction in dopaminergic activity in the brain probably by dopamine D2 receptor blockade in the striatum and hypothal-amus is generally assumed as a potential cause 4,20 . NMS is characterized by a distinctive clinical tetrad of mental status changes, motor abnormalities (bradykinesia and muscle rigidity), autonomic dysfunction (blood pressure instability, diaphoresis and tachycardia), and hyperthermia [2][3][4][5] . Laboratory findings include elevation of serum creatine phosphokinase (CK), liver enzymes, and leukocitosis [2][3][4][5][6][7]21 .…”

“…NMS is characterized by a distinctive clinical tetrad of mental status changes, motor abnormalities (bradykinesia and muscle rigidity), autonomic dysfunction (blood pressure instability, diaphoresis and tachycardia), and hyperthermia [2][3][4][5] . Laboratory findings include elevation of serum creatine phosphokinase (CK), liver enzymes, and leukocitosis [2][3][4][5][6][7]21 . Estimates of the incidence of this syndrome ranges from 0.01 to 3.23 accordingly to diagnostic criteria and drug prescription practices 3,4,6,22 .…”

“…Laboratory findings include elevation of serum creatine phosphokinase (CK), liver enzymes, and leukocitosis [2][3][4][5][6][7]21 . Estimates of the incidence of this syndrome ranges from 0.01 to 3.23 accordingly to diagnostic criteria and drug prescription practices 3,4,6,22 . Mortality is estimated at about 10% 3,4,23,24 .…”

“…Estimates of the incidence of this syndrome ranges from 0.01 to 3.23 accordingly to diagnostic criteria and drug prescription practices 3,4,6,22 . Mortality is estimated at about 10% 3,4,23,24 . Treatment is mainly supportive and includes withdrawal of the AP or other causative agent, and occasional use of drugs such as dopaminergic agonist (bromocriptine) and dantrolene [2][3][4][25][26][27][28] .…”