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首页> 外文期刊>Drugs of today: Medicamentos de actualidad >Pathophysiology and drug therapy of tardive dyskinesia: current concepts and future perspectives.
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Pathophysiology and drug therapy of tardive dyskinesia: current concepts and future perspectives.

机译：迟发性运动障碍的病理生理学和药物治疗：当前概念和未来观点。

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Nearly 1% of the world population suffers from schizophrenia, and neuroleptics are the major class of drugs used to treat this disorder. Neuroleptics are associated with wide variety of extrapyramidal side effects, such as akathesia, dystonia, neuroleptic malignant syndrome, Parkinson-ism and tardive dyskinesia. Despite the awareness that neuroleptics could cause extrapyramidal side effects, these drugs remain the most effective means of treating schizophrenia and Tourette's syndrome, as well as for the management of behavioral disorders in developmentally disabled individuals. Tardive dyskinesia is a complex hyperkinetic syndrome consisting of choriform, athetoid or rhythmically abnormal involuntary movements. Estimates of the prevalence rate of tardive dyskinesia in patients receiving neuroleptics range from 0.5-70%, with an average prevalence rate of 24%. Despite much research, the pathogenesis of tardive dyskinesia remains elusive. So far, various neurochemical hypotheses have been proposed for thedevelopment of tardive dyskinesia. These include dopaminergic hypersensitivity, disturbed balance between dopamine and cholinergic systems, dysfunctions of striatonigral GABAergic neurons and excitotoxicity. Similarly, different suppressive agents have been tried with limited success. Recently, the role of oxidative stress and structural abnormality in the pathophysiology of tardive dyskinesia has gained much impetus. Induction of free radicals by neuroleptic drugs leading to the oxidative stress and resultant structural abnormality could be the key factor in the pathogenesis of tardive dyskinesia. This hypothesis has been supported by numerous reports that chronic neuroleptic treatment increases free radical production and causes structural damage. More recently, the genetic vulnerability for the predisposition for the development of tardive dyskinesia, i.e., pharmacogenetic aspect of tardive dyskinesia, is also gaining impetus as a research area, and is discussed in detail in this article.
机译：世界人口中有将近1％患有精神分裂症，而抗精神病药是治疗这种疾病的主要药物。抗精神病药与多种锥体束外副作用相关，例如感觉异常，肌张力障碍，抗精神病药恶性综合征，帕金森氏病和迟发性运动障碍。尽管认识到抗精神病药可能会引起锥体束外副作用，但这些药物仍然是治疗精神分裂症和图雷特氏综合症以及发展性残疾个体行为障碍的最有效手段。迟发性运动障碍是一种复杂的运动亢进综合症，由脉络膜状，动脉粥样硬化或有节律的不自主运动组成。接受抗精神病药治疗的患者迟发性运动障碍的患病率估计为0.5-70％，平均患病率为24％。尽管进行了大量研究，但迟发性运动障碍的发病机制仍然难以捉摸。迄今为止，已经提出了各种神经化学假说来发展迟发性运动障碍。这些包括多巴胺能超敏反应，多巴胺与胆碱能系统之间的平衡紊乱，纹状体的GABA能神经元功能异常和兴奋性毒性。类似地，已经尝试了不同的抑制剂，但效果有限。近来，氧化应激和结构异常在迟发性运动障碍的病理生理中的作用得到了很大的推动。抗精神病药诱导自由基导致氧​​化应激和由此引起的结构异常可能是迟发性运动障碍发病的关键因素。长期的精神安定治疗会增加自由基的产生并引起结构性损伤的大量报道支持了这一假设。最近，迟发性运动障碍易感性的遗传易感性，即迟发性运动障碍的药理遗传学方面，也得到了研究领域的推动，并在本文中进行了详细讨论。

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