Gerlach J
Am J Psychiatry. 1977 Jul;134(7):781-4. doi: 10.1176/ajp.134.7.781.
The author analyzes parkinsonism and hyperkinesia in psychiatric patients with tardive dyskinesia before and during treatment with alpha-methyl-p-tyrosine (AMPT, a dopamine antagonist), biperiden (an acetylcholine antagonist), and baclofen (a GABA agonist); and in patients with paralysis agitans and L-dopa-induced hyperkinesia. AMPT and baclofen had similar influences on oral dyskinesia, resulting in reduced frequency, unchanged or slightly reduced amplitude, and increased duration of each movement. The author concludes that: 1) reduced dopaminergic activity may be the primary pathogenetic background for tardive dyskinesia; 2) dopaminergic hypersensitivity and/or cholinergic hypofunction is necessary before hyperkinesia breaks through; and 3) the neurotoxic effects of neuroleptics may be associated with age-dependent changes in nigrostriatal regions representing oral innervation.
作者分析了迟发性运动障碍的精神科患者在使用α-甲基-对-酪氨酸(AMPT,一种多巴胺拮抗剂)、安坦(一种乙酰胆碱拮抗剂)和巴氯芬(一种GABA激动剂)治疗前及治疗期间的帕金森综合征和运动亢进;以及帕金森病患者和左旋多巴诱发的运动亢进患者。AMPT和巴氯芬对口腔运动障碍有相似影响,导致频率降低、幅度不变或略有降低,且每次运动持续时间增加。作者得出结论:1)多巴胺能活性降低可能是迟发性运动障碍的主要发病机制背景;2)在运动亢进突破之前,多巴胺能超敏反应和/或胆碱能功能减退是必要的;3)抗精神病药物的神经毒性作用可能与代表口腔神经支配的黑质纹状体区域的年龄依赖性变化有关。