Keck P E, Caroff S N, McElroy S L
Department of Psychiatry, University of Cincinnati College of Medicine, OH 45267-0559, USA.
J Neuropsychiatry Clin Neurosci. 1995 Spring;7(2):135-44. doi: 10.1176/jnp.7.2.135.
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.
为解释抗精神病药恶性综合征（NMS）的病理生理学，已提出两种主要假说：1）NMS是由抗精神病药突然且广泛地阻断中枢多巴胺受体所致，尤其是在黑质纹状体和下丘脑通路；2）NMS与恶性高热（MH）一样，是由骨骼肌代谢预先存在的缺陷引起，这种缺陷在接触抗精神病药后被暴露或激发。为评估这些模型，作者回顾了自1980年以来发表的关于NMS和MH的临床特征、流行病学、危险因素、实验室评估及相关动物模型的研究。这些研究数据表明，尽管NMS和MH在临床上相似，但它们在药理学上是不同的，这意味着触发药物之间不太可能发生交叉反应。
