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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。
Delayed dystonia (TDt) is one of the extrapyramidal symptoms caused by chronic antipsychotics. It is reported that the incidence was 2.7% ~ 5.3%. The main clinical manifestations of single or multiple voluntary muscle dyskinesia, or because of dyskinesia due to postural abnormalities. The pathogenesis is generally considered to be a prolonged inhibition of dopamine neurotransmitter caused by excessive hypersensitivity to postsynaptic dopamine receptors or anti-antipsychotic anti-norepinephrine effect. TDt should be with acute dystonia, tardive dyskinesia, idiopathic dystonia, secondary dystonia, familial dystonia, the conversion of symptoms such as differential diagnosis. TDt should be discontinued in the event of atypical antipsychotic or other drug treatment, or deep brain stimulation. After treatment, the symptoms may be improved.