Orbital Frontal and Amygdala Volume Reductions in Obsessive-compulsive Disorder

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Abstract
CURRENT HYPOTHESES regarding the pathophysiology of obsessive-compulsive disorder (OCD) have emphasized abnormalities in cortical-striatal-thalamic-cortical circuits,1-4 and within these circuits the frontal lobes have been regarded as an important area for investigation. In particular, orbital frontal and anterior cingulate regions have been hypothesized to play an important role in producing the symptoms associated with the disorder.3,5-9 Neuropsychological studies have supported the hypothesis of abnormal orbital frontal10,11 and anterior cingulate12 functioning in OCD. The strongest evidence for dysfunction of these brain regions, however, comes from functional imaging studies, which have identified hypermetabolism during baseline conditions13-16 and symptom provocation9,17,18 as well as reduced metabolic activity with treatment.19-21 In contrast to orbital frontal and anterior cingulate regions, the evidence for abnormalities in other parts of the frontal lobes has been much less compelling, although some functional imaging studies have also implicated dysfunction of lateral (including superior, middle, and/or inferior) frontal gyri.17,22,23