Goetz C G, Klawans H L
Neurol Clin. 1984 Aug;2(3):605-14.
The basic pathogenesis of tardive dyskinesia appears to relate to chronic pharmacologic denervation of specific dopaminergic receptor sites in the striatum. The pathophysiology of the disorder relates to the resultant denervation hypersensitivity. The mainstay of treatment includes withdrawal of neuroleptics where feasible and the use of dopamine-depleting agents. Enhancement of the striatal cholinergic input offers potential ancillary benefit to the alleviation of abnormal movements. The benefit of manipulating other neurotransmitters remains experimental. Treatment of tardive dyskinesia with neuroleptics themselves is clearly treatment with the presumed offending agent, and should be avoided. This shortsighted therapy may temporarily abate the pathophysiology of the condition but serves to aggravate its pathogenesis.
迟发性运动障碍的基本发病机制似乎与纹状体中特定多巴胺能受体部位的慢性药物去神经支配有关。该疾病的病理生理学与由此产生的去神经超敏反应有关。治疗的主要方法包括在可行的情况下停用抗精神病药物以及使用耗竭多巴胺的药物。增强纹状体胆碱能输入可能有助于缓解异常运动。调节其他神经递质的益处仍处于实验阶段。使用抗精神病药物本身治疗迟发性运动障碍显然是用假定的致病药物进行治疗，应予以避免。这种短视的治疗方法可能会暂时减轻病情的病理生理学，但会加剧其发病机制。
