[Psychobiology of compulsive disease]

Area of Science:

• Psychoneurobiology
• Neuroscience
• Pharmacology

Context:

• Current understanding links obsessive-compulsive disorder (OCD) pathophysiology to basal ganglia dysfunction and central serotonin (5-HT) system dysregulation.
• Basal ganglia, including the striatum and pallidum, play complex perceptual and cognitive roles beyond motor functions.
• Obsessive-compulsive symptoms in related disorders like Tourette syndrome suggest shared neurobiological underpinnings.

Purpose:

• To review and evaluate recent psychoneurobiological findings concerning the serotonin and basal ganglia hypotheses of OCD.
• To explore the role of specific serotonin receptor subtypes (5-HT1D and 5-HT1A) in OCD pathophysiology and treatment.
• To integrate evidence from neuroanatomical, pharmacological, ethological, and brain imaging studies.

Summary:

• Evidence from neuroimaging (PET), pharmacological studies, and clinical observations supports a frontal cortex/basal ganglia dysfunction in OCD.
• Serotonin reuptake inhibitors and 5-HT1A receptor partial agonists (azapirones) demonstrate therapeutic efficacy in OCD.
• The 5-HT1D and 5-HT1A receptor-effector system complex is implicated as central to OCD symptoms and the action of antiobsessional drugs.

Impact:

• Findings enhance the therapeutic perspective for OCD by identifying key neurobiological targets.
• The study provides insights into the complex aetiopathogenesis of OCD, linking neurotransmitter systems and brain circuitry.
• This review integrates diverse research, strengthening the serotonin and basal ganglia hypotheses of OCD.