Neuroleptic malignant syndrome and malignant hyperthermia: end of a controversy?
Two primary hypotheses have been proposed to explain the pathophysiology of the neuroleptic malignant syndrome (NMS): 1) that NMS is produced by abrupt and extensive central dopamine receptor blockade by neuroleptics, particularly in nigrostriatal and hypothalamic pathways; and 2) that NMS, like malignant hyperthermia (MH), results from a preexisting defect in skeletal muscle metabolism that is unmasked or provoked by neuroleptic exposure. To evaluate these models, the authors review studies published since 1980 of the clinical features, epidemiology, risk factors, laboratory assessment, and relevant animal models of NMS and MH. Data from these studies suggest that although NMS and MH are clinically similar, they are pharmacologically distinct, implying that cross-reactivity between triggering agents is unlikely to occur.
Keck
P E
PE
Department of Psychiatry, University of Cincinnati College of Medicine, OH 45267-0559, USA.
Caroff
S N
SN
McElroy
S L
SL
D000818:Animals; D014150:Antipsychotic Agents / Q000008:administration & dosage / Q000009:adverse effects*; D003342:Corpus Striatum / Q000187:drug effects / Q000503:physiopathology; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007031:Hypothalamus / Q000187:drug effects / Q000503:physiopathology; D008305:Malignant Hyperthermia / Q000175:diagnosis / Q000503:physiopathology*; D018482:Muscle, Skeletal / Q000187:drug effects / Q000503:physiopathology; D009434:Neural Pathways / Q000187:drug effects / Q000503:physiopathology; D009459:Neuroleptic Malignant Syndrome / Q000175:diagnosis / Q000503:physiopathology*; D011954:Receptors, Dopamine / Q000187:drug effects / Q000502:physiology; D012307:Risk Factors; D013378:Substantia Nigra / Q000187:drug effects / Q000503:physiopathology
D014150:Antipsychotic Agents; D011954:Receptors, Dopamine