Dopaminergic activity in Tourette syndrome and obsessive-compulsive disorder

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• 作者：Damiaan Denys ; Froukje de Vries ; Danielle Cath ; Martijn Figee ; Nienke Vulink ; Dick J. Veltman ; Thalia F. van der Doef ; Ronald Boellaard ; Herman Westenberg ; Anton van Balkom ; Adriaan A. Lammertsma ; Bart N.M. van Berckel
• 关键词：Tourette syndrome ; Obsessive-compulsive disorder ; Dopamine ; Amphetamine ; Positron emission tomography ; [11C]raclopride
• 刊名：European Neuropsychopharmacology
• 出版年：November, 2013
• 年：2013
• 卷：23
• 期：11
• 页码：1423-1431
• 全文大小：2654 K

文摘

Tourette syndrome (TS) and obsessive-compulsive disorder (OCD) both are neuropsychiatric disorders associated with abnormalities in dopamine neurotransmission. Aims of this study were to quantify striatal D_2/3 receptor availability in TS and OCD, and to examine dopamine release and symptom severity changes in both disorders following amphetamine challenge.<p>Changes in [p>11p>C]raclopride binding potential (BP_ND) were assessed using positron emission tomography before and after administration of d-amphetamine (0.3 mg kgp>鈭?p>) in 12 TS patients without comorbid OCD, 12 OCD patients without comorbid tics, and 12 healthy controls. Main outcome measures were baseline striatal D_2/3 receptor BP_ND and change in BP_ND following amphetamine as a measure of dopamine release.<p>Voxel-based analysis revealed significantly decreased baseline [p>11p>C]raclopride BP_ND in bilateral putamen of both patient groups vs. healthy controls, differences being more pronounced in the TS than in the OCD group. Changes in BP_ND following amphetamine were not significantly different between groups. Following amphetamine administration, tic severity increased in the TS group, which correlated with BP_ND changes in right ventral striatum. Symptom severity in the OCD group did not change significantly following amphetamine challenge and was not associated with changes in BP_ND.<p>This study provides evidence for decreased striatal D_2/3 receptor availability in TS and OCD, presumably reflecting higher endogenous dopamine levels in both disorders. In addition, it provides the first direct evidence that ventral striatal dopamine release is related to the pathophysiology of tics.