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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.
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