Noradrenergic mechanisms have been involved in the pathogenesis of Gil
les de Ia Tourette Syndrome (GTS). Since the central alpha(2) adrenerg
ic 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 alt
ered in GTS. After administration of 2 mu g/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 absti
nent healthy controls. A blunted response of GH release ( < 5 ng/ml) w
as observed in seven patients and the area under the curve (AUC) of th
e GH-release was significantly reduced (p < .01) compared to controls.
This finding indicates an involvement of the noradrenergic system in
GTS.