Last update:
08-Mar-2007

Obsessive-compulsive disorder (OCD) is a common and disabling psychiatric disorder. Significant progress has been made in the investigation of its neurobiological and neuropsychological substrate. From a neuroanatomical perspective, neuroimaging data associate OCD with dysfunction in the neuronal circuits connecting thalamus and cortex via the basal ganglia (metabolic changes in the orbitofrontal-striatal loop). On the neurochemical level, OCD has been associated mainly with serotonergic dysfunction, although the contribution of other neurotransmitter systems, the dopaminergic system in particular, is also under investigation. The hypothesis of a serotonin-dopamine interaction in the basal ganglia is particularly interesting, as it is congruent with the neuroimaging data and can accommodate the high comorbidity noted between OCD and the Tourette syndrome. A significant body of data supports neuroimmunological and genetic contributions to OCD pathophysiology. Neuropsychological findings in OCD patients indicate mild or no deficits in the areas of visuospatial function, attention and information processing speed, provided that pharmacological influences are excluded. The memory deficits reported appear to be secondary to executive dysfunction, specifically inefficient use of coding strategies. Data on executive functions such as coding, set shifting, planning and problem solving, although somewhat controversial, suggest deficits in OCD patients. Such deficits are compatible with the neuroimaging findings which associate OCD with dysfunction in the orbitofrontal-striatal loop. In conclusion, in spite of significant recent advances, OCD pathophysiology needs further clarification, which appears forthcoming mainly from the areas of neuroimaging and animal modeling.

Key words: Animal models, Dopamine, Neuroanatomy, Neuropsychology, Obsessive-compulsive disorder, Review, Serotonin.