1. ¹Institute of Molecular Bioimaging and Physiology – National Research Council, Milan, Italy
2. ²Department of Nuclear Medicine, University of Milan-Bicocca, Milan, Italy
3. ³Department of Nuclear Medicine, Scientific Institute H San Raffaele, Milan, Italy
4. ⁴Department of Psychiatry, Scientific Institute H San Raffaele, Milan, Italy
5. ⁵Universita(c) Vita – Salute San Raffaele, Milan, Italy

Correspondence: Dr RM Moresco, Department of Nuclear Medicine, San Raffaele Hospital, Via Olgettina 60, 20132 Milan, Italy. Tel: +39 0226433817, Fax: +39 0226415202; E-mail: moresco.rosamaria@hsr.it

Received 2 December 2005; Revised 16 June 2006; Accepted 19 July 2006; Published online 4 October 2006.

Abstract

Changes in D₂ receptors during antidepressant therapy have been reported in patients with major depressive disorder using PET/SPET. The aim of this study was to evaluate modifications in D₂ receptors that might occur in patients affected by obsessive-compulsive disorder (OCD) during serotonin reuptake sites inhibitors (SSRIs). To this purpose, we measured the in vivo binding of [¹¹C]raclopride ([¹¹C]Rac)in the brain of a group of OCD naïve patients before and after the repeated administration of the inhibitor SSRI fluvoxamine. Eight patients with a Diagnostic and Statistical Manual of Mental Disorders IVth edition diagnosis of OCD completed the study undergoing a PET scan and a complete clinical evaluation before and during treatment with fluvoxamine. Patients have been compared also with a group of nine age-matched normal volunteers. Fluvoxamine treatment significantly improved clinical symptoms and increased [¹¹C]Rac binding potential (BP) in the basal ganglia of OCD patients (7.55.2, 6.96.9, and 9.99.3% in dorsal caudate, dorsal putamen, and ventral basal ganglia, respectively; p<0.01) to values closer to those observed in the group of normal subjects. Chronic treatment with fluvoxamine induces a slight but significant increase in striatal [¹¹C]Rac BP of previously drug-naïve OCD patients. The modifications in D₂ receptor availability might be secondary to fluvoxamine effects on serotoninergic activity.