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首页> 外文期刊>The journal of clinical psychiatry >Pathophysiology of antipsychotic drug-induced movement disorders.
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Pathophysiology of antipsychotic drug-induced movement disorders.

机译：抗精神病药诱发的运动障碍的病理生理学。

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摘要

Explaining the underlying mechanisms of antipsychotic drug-induced movement disorders remains a substantial challenge. The association of atypical antipsychotic agents with fewer drug-induced movement disorders than conventional agents has engendered several pathophysiologic hypotheses: (1) the hypothesis that, unlike conventional antipsychotic agents, atypical antipsychotics have greater activity in blocking serotonin-2A (5-HT(2A)) receptors than dopamine-2 (D(2)) receptors, which mitigates extrapyramidal symptoms; (2) the hypothesis that atypical antipsychotics block D(2) receptors only long enough to cause an antipsychotic action, but not as long as conventional agents; (3) the hypothesis that, in tardive dyskinesia, the nigrostriatal dopamine receptor system might develop increased sensitivity to dopamine as a result of treatment with conventional antipsychotic drugs, but this may not occur with atypical antipsychotics; and (4) the hypothesis that there might be a genetic association in tardive dystonia relating to the dopamine D(3) allele. A number of factors contribute to the difficult task of gaining insight into the pathophysiologic processes of antipsychotic agents and why these agents may lead to drug-induced movement disorders.
机译：解释抗精神病药诱发的运动障碍的潜在机制仍然是一项重大挑战。与常规药物相比，非典型抗精神病药与药物引起的运动障碍较少相关，从而产生了几种病理生理学假设：（1）与常规抗精神病药不同，非典型抗精神病药在阻断5-羟色胺2A（5-HT（2A ））受体比多巴胺2（D（2））受体强，可减轻锥体束外症状; （2）假设非典型抗精神病药仅阻断D（2）受体的时间足以引起抗精神病作用，但不像常规药物那样长。 （3）假说，在迟发性运动障碍中，黑质纹状体多巴胺受体系统可能会因使用常规抗精神病药治疗而增加对多巴胺的敏感性，但非典型抗精神病药可能不会发生这种情况; （4）假设迟发性肌张力障碍可能与多巴胺D（3）等位基因相关。许多因素导致难以完成对抗精神病药的病理生理过程的了解以及为什么这些药可能导致药物引起的运动障碍。

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