抗精神病药物引起的迟发性肌张力障碍研究进展  

Progress in studies on tardive dystonia induced by antipsychotic drugs

作　　者：孙振晓[1] 于相芬[1] 

机构地区：[1]山东省临沂市精神卫生中心精神科,276005

出　　处：《药物不良反应杂志》2012年第1期34-38,共5页Adverse Drug Reactions Journal

摘　　要：迟发性肌张力障碍(TDt)是长期应用抗精神病药物引起的锥体外系症状之一。据报道,发生率为2.7%～5.3%。临床主要表现为单个或多个随意肌自主运动困难,或因自主运动困难所致姿势异常。发病机制一般认为是多巴胺神经递质的持久抑制引起突触后多巴胺受体敏感性过度增高所致或与抗精神病药的抗去甲肾上腺素能效应有关。TDt须与急性肌张力障碍、迟发性运动障碍、特发性肌张力障碍、继发性肌张力障碍,家族性肌张力障碍、转换症状等进行鉴别诊断。一旦发生TDt应停药,换用非典型抗精神病药或其他药物治疗,或进行脑深部电刺激治疗。经治疗后症状可能有所改善。Tardive dystonia （TDt） is one of extrapyramidal symptoms that starts after long-term use of antipsychotic drugs. It has been reported that the incidence of TDt ranged from 2.7% to 5.3%. Its main clinical feature is that voluntary movements of one or more voluntary muscles are difficult, or abnormal postures because of difficult voluntary movements. The mechanism of TDt is generally considered to be associated with postsynaptic dopamine receptor supersensitivity caused by sustained inhibition of the dopaminergic neurotransmission or anti-noradrenergie effect of antipsychoties. TDt should be distinguished from acute dystonia, tardive dyskinesia, idiopathic dystonia, secondary dystonia, familial dystonia and conversion symptoms. Once TDt developed, dopamine receptor antagonists should be stopped, atypical antipsychotic drugs or other drugs or deep brain stimulation could be used. Symptoms might improve after such treatment.

关 键 词：抗精神病药物 迟发性肌张力障碍 

分 类 号：R971[医药卫生—药品]