A prostaglandin theory of neuroleptic malignant syndrome.
A subgroup of patients with schizophrenia or other psychoses may have an increased PGE receptor sensitivity in the brain, which may be due to low levels of PGE. Some of these patients may develop a severe dopaminergic blockade when given neuroleptics which stimulate PGE synthesis. This may lead to the symptoms of neuroleptic malignant syndrome. Calcium channel blockers inhibit the prostaglandin output caused by norepinephrine and these agents may prove useful in the treatment of neuroleptic malignant syndrome.
D000818:Animals; D002375:Catalepsy / Q000503:physiopathology; D005334:Fever / Q000150:complications; D006359:Heat Exhaustion / Q000503:physiopathology; D006801:Humans; D008305:Malignant Hyperthermia / Q000503:physiopathology; D009459:Neuroleptic Malignant Syndrome / Q000378:metabolism* / Q000503:physiopathology; D011458:Prostaglandins E / Q000502:physiology*; D011618:Psychotic Disorders / Q000150:complications; D011982:Receptors, Prostaglandin / Q000502:physiology; D018078:Receptors, Prostaglandin E; D012559:Schizophrenia / Q000378:metabolism
D011458:Prostaglandins E; D011982:Receptors, Prostaglandin; D018078:Receptors, Prostaglandin E