Hayashi Y, Ohyagi Y, Inoue I, Arakawa K, Taniwaki T, Nakagawa M, Kuwabara Y, Yamada T, Kira J
Department of Neurology, Kyushu University, Fukuoka.
Rinsho Shinkeigaku. 2000 Apr;40(4):367-71.
We report a 63-year-old man who presented with amoxapine-induced tardive dystonia. At 49 years of age, he developed depression and was administrated 50 mg amoxapine, 4 mg cloxazoram and 3 mg biperiden per day. The daily dose of amoxapine was gradually increased up to 150 mg at 58 years of age. At 61 years of age and after having been taking amoxapine for twelve years, he noticed a rotating left arm and muscle pain in his left shoulder and arm while walking. At 62 years of age, he stopped taking these three drugs. However, the dystonic movements and pain both continued to get worse. Neurological findings revealed no abnormality except for a dystonic posture and movements in the neck and bilateral arms while sitting, standing and walking. Positron emission tomography with C-11 raclopride revealed a mild decrease in the dopamine D 2 receptor numbers in the bilateral striatum. However, two dopamine agonists, pergolide and bromocriptine, worsened his dystonia. In contrast, the daily administration of 2 mg of trihexyphenidyl, an anti-cholinergic agent, markedly ameliorated the dystonia symptoms. As a result, the long-term co-administration of biperiden, an anti-cholinergic agent, may mask the toxicity of amoxapine, which may induce tardive dystonia.
我们报告了一名63岁男性，他患有阿莫沙平引起的迟发性肌张力障碍。49岁时，他患上抑郁症，开始每天服用50毫克阿莫沙平、4毫克氯氮卓和3毫克安坦。在58岁时，阿莫沙平的每日剂量逐渐增加至150毫克。61岁时，在服用阿莫沙平12年后，他注意到走路时左臂旋转以及左肩和手臂肌肉疼痛。62岁时，他停止服用这三种药物。然而，肌张力障碍性运动和疼痛都继续恶化。神经系统检查结果显示，除了坐着、站立和行走时颈部和双侧手臂出现肌张力障碍姿势和运动外，没有其他异常。用C-11雷氯必利进行正电子发射断层扫描显示双侧纹状体中多巴胺D2受体数量略有减少。然而，两种多巴胺激动剂培高利特和溴隐亭使他的肌张力障碍恶化。相比之下，每天服用2毫克抗胆碱能药物苯海索可明显改善肌张力障碍症状。因此，长期联合使用抗胆碱能药物安坦可能会掩盖阿莫沙平的毒性，而阿莫沙平可能会诱发迟发性肌张力障碍。
