Recent brain-imaging studies have examined the neuroanatomy and pathophysiology of obsessive-compulsive disorder (OCD). Researchers have used computed tomography and magnetic resonance imaging to look at brain structure and single-photon emission computed tomography and positron emission tomography scanning to look at brain function in OCD subjects. In this article, we review these studies and discuss their methodology. We then present a theoretical model derived from these studies for how the brain mediates OCD symptomatology.
Functional neuroimaging studies have pointed to hyperactivity of orbitofrontal-basal ganglionic–thalamic circuitry in patients with OCD. Our model posits an imbalance between the classical “direct” and “indirect” orbitofrontal–basal ganglionic–thalamic pathways in OCD subjects. The direct circuit appears to function as a positive feedback loop and may “capture” or “lock in” symptomatic OCD subjects. The indirect circuit, which usually provides tonic inhibition to the direct circuit, may be relatively weak.
Finally, we discuss how frontal-subcortical brain circuitry may be involved in other neuropsychiatric illnesses, and we describe how monoamines, such as serotonin and dopamine, may be involved in regulating these circuits in OCD and other illnesses.