What pharmacology teaches us about the pathophysiology of obsessive-compulsive disorder

Abstract

Once considered rare and resistant to treatments, obsessive-compulsive disorders (OCD) has now emerged as one the most common psychiatric conditions, with a lifetime prevalence of about 2.5 %, and as a major cause of long-term disability to patients and their families. The treatment of OCD has changed dramatically over the last decade following the introduction of selective serotonin (5-HT) reuptake inhibitors (SSRIs), such as fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, which provide symptom remission in about 60% of the patients. OCD is unique in the response to serotonergic agents and it has been clearly demonstrated that non-serotonergic antidepressants such as desipramine have no effect. The specific response of OCD patients to SSRIs has emphasized the possible role of the main target of these drugs, namely the 5-HT system, in the pathophysiology of the disorder. If the role of 5-HT in OCD is not questionable, future studies should be directed towards the elucidation of the 5-HT receptor subtypes involved, of the second messengers transducing the signal, as well as of the interactions between 5-HT and the other neurotransmitters.