Tardive dyskinesia: pathophysiology and animal models.
Tardive dyskinesia: pathophysiology and animal models.
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发表时间：
2000-04
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通讯作者：
D. Casey
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作者：
D. Casey
迟发性运动障碍刺激了对抗精神病药物作用机制的广泛研究。已经开发了广泛的同源、类似和相关的动物模型来探索典型的抗精神病药物和非典型的抗精神病药物似乎不会引起迟发性运动障碍。迟发性运动障碍的潜在病理生理学的主要假设包括多巴胺受体超敏反应、GABA不足和/或结构异常。所有这些假设都有支持和反对它们的数据。在对迟发性运动障碍的任何解释中，也必须考虑精神病和衰老的作用。如何准确地将这些因素中的每一个的相对贡献归因于迟发性运动障碍的发病机制和病理生理学仍然是一个挑战。幸运的是，非典型抗精神病药物似乎大大降低了发展迟发性运动障碍的可能性，但这是如何发生的仍然是一个开放和迷人的调查路线。
Tardive dyskinesia stimulated extensive research into the mechanisms of antipsychotic drug action. A wide range of homologous, analogous, and correlational animal models have been developed to explore how typical neuroleptic drugs do and atypical antipsychotic agents do not seem to cause tardive dyskinesia. The leading hypotheses of the underlying pathophysiology of tardive dyskinesia include dopamine receptor hypersensitivity, GABA insufficiency, and/or structural abnormalities. All these hypotheses have data both for and against them. The roles of psychosis and aging must also be considered in any explanation of tardive dyskinesia. The challenge still remains of how to accurately attribute the relative contributions of each of these factors to the pathogenesis and pathophysiology of tardive dyskinesia. Fortunately, the atypical antipsychotic agents appear to greatly decrease the liability of developing tardive dyskinesia, but how this occurs remains an open and fascinating line of inquiry.