Gerlach J, Thorsen K
Int Pharmacopsychiatry. 1976;11(1):1-7. doi: 10.1159/000468206.
24 hospitalized psychiatric patients with neuroleptic-induced tardive dyskinesia were treated with alpha-methyl-para-tyrosine (AMPT), 4 g daily for 3 days, and biperiden, 12 mg daily for 3 weeks. The results were evaluated blindly by means of videotape technique. The frequency of tardive dyskinesia was significantly reduced by AMPT and significantly increased by biperiden. The amplitude was reduced by AMPT in ten cases, unchanged in 12 cases and increased in two cases. Biperiden significantly increased the amplitude. The duration of each separate tongue protrusion and/or mouth opening was significantly increased by AMPT and reduced or unchanged by biperiden. It is concluded that a reduced dopaminergic activity (pharmacological or organic) may constitute the primary pathogenetic background for tardive dyskinesia, but that dopaminergic hypersensitivity and/or cholinergic hypofunction is necessary before the hyperkinetic element of the movement disturbances can minifest itself.
24例因使用抗精神病药物导致迟发性运动障碍的住院精神病患者，接受了α-甲基对酪氨酸（AMPT）治疗，每日4克，持续3天，以及安克痉治疗，每日12毫克，持续3周。通过录像技术对结果进行了盲法评估。AMPT可显著降低迟发性运动障碍的频率，而安克痉则使其显著增加。AMPT使10例患者的运动障碍幅度减小，12例不变，2例增加。安克痉显著增加了运动障碍幅度。AMPT使每次单独伸舌和/或张口的持续时间显著增加，而安克痉则使其减少或不变。结论是，多巴胺能活性降低（药理学或器质性）可能是迟发性运动障碍的主要发病机制背景，但在运动障碍的多动成分表现出来之前，多巴胺能超敏和/或胆碱能功能减退是必要的。
