Wagner R L, Jeste D V, Phelps B H, Wyatt R D
J Clin Psychopharmacol. 1982 Oct;2(5):312-4.
Over a 1-year period we followed 12 female in-patients with and 13 without persistent tardive dyskinesia. Clinical signs of tardive dyskinesia as well as plasma dopamine-beta-hydroxylase and platelet monoamine oxidase activities remained stable over time in spite of medication changes. Tardive dyskinesia was associated with higher plasma dopamine-beta-hydroxylase and lower monoamine oxidase activities, both initially and at follow-up. In two patients, an apparent elevation in dopamine-beta-hydroxylase activity preceded the onset of clinical dyskinesia, suggesting that elevated plasma dopamine-beta-hydroxylase activity might be a potential risk marker for the development of tardive dyskinesia.
在为期1年的时间里,我们对12名患有持续性迟发性运动障碍的女性住院患者和13名未患该疾病的女性住院患者进行了跟踪研究。尽管药物治疗有所改变,但迟发性运动障碍的临床体征以及血浆多巴胺-β-羟化酶和血小板单胺氧化酶活性随时间保持稳定。无论是在初始阶段还是随访阶段,迟发性运动障碍都与较高的血浆多巴胺-β-羟化酶和较低的单胺氧化酶活性相关。在两名患者中,多巴胺-β-羟化酶活性的明显升高先于临床运动障碍的发作,这表明血浆多巴胺-β-羟化酶活性升高可能是迟发性运动障碍发生的一个潜在风险标志物。