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Changes in D 2 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 D 2 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 [ 11 C]raclopride ([ 11 C]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 [ 11 C]Rac binding potential (BP) in the basal ganglia of OCD patients (7.575.2, 6.976.9, and 9.979.3% in dorsal caudate, dorsal putamen, and ventral basal ganglia, respectively; po0.01) to values closer to those observed in the group of normal subjects. Chronic treatment with fluvoxamine induces a slight but significant increase in striatal [ 11 C]Rac BP of previously drug-naïve OCD patients. The modifications in D 2 receptor availability might be secondary to fluvoxamine effects on serotoninergic activity.

Delayed event-related desynchronization in OCD is consistent with involvement of structures related to motor programming, such as basal ganglia. Lower levels of postmovement beta synchronization suggest impairment of the inhibitory system in OCD.

In several reports, the acute oral administration of the partial serotonergic agonist meta-chlorophenylpiperazine (mCPP)

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