Chadwick D, Jenner P, Harris R, Reynolds E H, Marsden C D
Lancet. 1975 Sep 6;2(7932):434-5. doi: 10.1016/s0140-6736(75)90846-6.
The response of myoclonus to oral and intravenous L-5-hydroxytryptophan (5-H.T.P.) in combination with a peripheral decarboxylase inhibitor (carbidopa) and to clonazepam has been examined in 9 patients. Moderate improvement or complete cessation of myoclonus followed treatment with one or both of these regimens in 5 patients, 1 of whom also responded to the concurrent administration of L-tryptophan and a monoamineoxidase inhibitor. The remaining 4 patients were at best only slightly improved by either 5-H.T.P. or clonazepam. The responsive group consisted of 3 patients with a history of anoxia, 1 patient with non-history of severe head injury, and 1 patient with non-progressive focal myoclonus and epilepsy. This group had low levels of 5-hydroxyindole acetic acid in the lumbar cerebrospinal fluid. It is suggested that 5-H.T.P. plus carbidopa, L-tryptophan plus a monoamine-oxidase inhibitor, and clonazepam may all act by elevating brain levels of serotonin (5-H.T.) and that some human myoclonic syndromes may be specifically related to a cerebral deficiency of 5-H.T.
我们对9例患者的肌阵挛对口服及静脉注射L-5-羟色氨酸（5-H.T.P.）联合外周脱羧酶抑制剂（卡比多巴）以及氯硝西泮的反应进行了研究。5例患者接受其中一种或两种治疗方案后，肌阵挛得到中度改善或完全停止，其中1例患者同时服用L-色氨酸和单胺氧化酶抑制剂也有反应。其余4例患者使用5-H.T.P.或氯硝西泮治疗后改善甚微。有反应的一组包括3例有缺氧病史的患者、1例无严重头部外伤史的患者以及1例患有非进行性局灶性肌阵挛和癫痫的患者。该组患者腰椎脑脊液中5-羟吲哚乙酸水平较低。提示5-H.T.P.加卡比多巴、L-色氨酸加单胺氧化酶抑制剂以及氯硝西泮可能均通过提高脑内5-羟色胺（5-H.T.）水平发挥作用，且某些人类肌阵挛综合征可能与脑内5-H.T.缺乏有特定关系。
