Müller N, Putz A, Klages U, Hofschuster E, Straube A, Ackenheil M
Psychiatric Hospital, Klinikum Innenstadt, University of Munich, Germany.
Psychoneuroendocrinology. 1994;19(4):335-41. doi: 10.1016/0306-4530(94)90014-0.
Noradrenergic mechanisms have been involved in the pathogenesis of Gilles de la Tourette Syndrome (GTS). Since the central alpha 2 adrenergic agonist clonidine is widely used as a therapeutic agent in GTS, the present study aimed at assessing whether GH release after clonidine, representing central alpha 2-adrenergic receptor sensitivity, was altered in GTS. After administration of 2 micrograms/kg body weight clonidine, the GH response was examined in nine drug-free, alcohol-abstinent GTS patients (eight men, one woman) and in nine age- and sex-matched abstinent healthy controls. A blunted response of GH release (< 5 ng/ml) was observed in seven patients and the area under the curve (AUC) of the GH-release was significantly reduced (p < .01) compared to controls. This finding indicates an involvement of the noradrenergic system in GTS.
去甲肾上腺素能机制与抽动秽语综合征(GTS)的发病机制有关。由于中枢α2肾上腺素能激动剂可乐定被广泛用作GTS的治疗药物,本研究旨在评估可乐定给药后代表中枢α2 - 肾上腺素能受体敏感性的生长激素(GH)释放是否在GTS中发生改变。在给予2微克/千克体重的可乐定后,对9名未服用药物、戒酒的GTS患者(8名男性,1名女性)和9名年龄和性别匹配的戒酒健康对照者的GH反应进行了检测。7名患者观察到GH释放反应减弱(<5纳克/毫升),与对照组相比,GH释放的曲线下面积(AUC)显著降低(p < 0.01)。这一发现表明去甲肾上腺素能系统参与了GTS的发病过程。