NEUROLEPTIC MALIGNANT SYNDROME AND MALIGNANT HYPERTHERMIA - END OF A CONTROVERSY

Two primary hypotheses have been proposed to explain the pathophysiolo gy of the neuroleptic malignant syndrome (NMS): 1) that NMS is produce d by abrupt and extensive central dopamine receptor blockade by neurol eptics, particularly in nigrostriatal and hypothalamic pathways; and 2 ) that NMS, like malignant hyperthermia (MH), results fi om a preexist ing 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, r isk factors, laboratory assessment, and relevant animal models of NMS and MH. Data from these studies suggest that although NMS and MH are c linically similar, they are pharmacologically distinct, implying that cross-reactivity between triggering agents is unlikely to occur.