Functional neuroimaging and the neuroanatomy of obsessive-compulsive disorder

Advances in neuroimaging have led to a greater understanding of the neurobiology of obsessive-compulsive disorder, providing strong evidence that its pathophysiology involves abnormal functioning along specific frontal-subcortical brain circuits. An updated review and analysis of the functional neuroimaging studies, including single photon emission computed tomography, positron emission tomography, magnetic resonance spectroscopy, and functional magnetic resonance imaging, is provided. Also reviewed is the basic science literature on the functional neuroanatomy of corticobasal gangliathalamocortical circuits, and this information is integrated with neuroimaging data in obsessive-compulsive disorder to present a theoretic model of brain mediation of obsessive-compulsive disorder symptoms and response to treatment. Functional neuroimaging studies indicate that obsessive-compulsive disorder symptoms are mediated by hyperactivity in orbitofrontal-subcortical circuits that may be caused by an imbalance of tone between direct and indirect striatopallidal pathways. Serotonergic drugs may ameliorate obsessive-compulsive disorder symptoms by changing the relative balance of tone through the indirect versus direct orbitofrontal-subcortical pathways, with therapy decreasing activity in the overall circuit that exists in the symptomatic state.