Subjects with MDD had regional brain metabolic abnormalities at baseline that tended to normalize with treatment. Regional metabolic changes appeared similar with the 2 forms of treatment. These results should be interpreted with caution because of study limitations (small sample size, lack of random assignment to treatment groups, and differential treatment response between treatment subgroups).

Previous positron emission tomography (PET) studies of patients with obsessive-compulsive disorder (OCD) have found elevated glucose metabolic rates in the orbitofrontalPrevious positron emission tomography (PET) studies of obsessive-compulsive disorder (OCD) have found elevated glucose metabolic rates in the orbitofrontal cortex (OFC), anterior cingulate gyrus (AC), caudate nuclei, and thalamus (Baxter et al. 1987(Baxter et al. , 1988Nordahl et al. 1989;Swerdlow 1995; see Saxena et al. 1998 for review) or cognitive-behavioral treatment (Baxter et al. 1992;Schwartz et al. 1996) NO . 6 that provoke OCD symptoms have been found to increase blood flow to similar brain regions (McGuire et al. 1994;Rauch et al. 1994;Breiter et al. 1996). These and other findings have led to the theory that the symptomatic expression of OCD is mediated by hyperactivity along specific, frontal-subcortical circuits (Alexander et al. 1986) connecting the OFC, ventromedial caudate, globus pallidus, and the medial dorsal nucleus of the thalamus (Modell et al. 1989;Baxter et al. 1992;Baxter 1995;Insel 1992). Some studies have also suggested that hyperactivity in the AC, which is also linked to basal ganglia structures and thalamus along a parallel circuit, may be involved in mediating some OCD symptoms (Rapaport and Wise 1988;Perani et al. 1995).The OFC is a cytoarchitecturally heterogeneous structure that changes from agranular cortical tissue in its posteromedial region to more granular cortical tissue in its anterolateral region. These subregions have distinct patterns of connectivity and seem to serve different functions (see Zald and Kim 1996a; 1996b for detailed review). Previous PET studies of OCD treatment and symptom provocation suggest that different subregions of the OFC may be differentially involved in the pathophysiology of OCD. Benkelfat et al. (1990) found that the OFC subregion with the largest metabolic change with clomipramine treatment of OCD was right anterior OFC. McGuire et al. (1994) reported that OCD symptom intensity correlated with increased blood flow to right lateral OFC during symptom provocation. Rauch et al. (1994) found two centroids of OFC activation with symptomatic treatment-left anterior and right posterior OFC. Of these, only activation in left anterior OFC was positively correlated with the intensity of OCD symptoms; whereas, activation of right posterior OFC was negatively correlated with symptom intensity, suggesting that the two regions might play opposing roles in mediating and suppressing OCD symptoms, respectively. We sought to determine the role of specific subregions of the OFC and associated basal ganglia structures in mediating OCD symptoms, by determining how glucose metabolic rates in these structures changed with treatment of OCD patients. We sought to confirm and extend earlier findings using paroxetine hydrochloride, an OCD treatment that differs from those used in previous PET studies. Based on the previous findings noted above, we hypothesized that glucose metabolism in anterolate...

OCD patients with the compulsive hoarding syndrome had a different pattern of cerebral glucose metabolism than nonhoarding OCD patients and comparison subjects. Obsessive-compulsive hoarding may be a neurobiologically distinct subgroup or variant of OCD whose symptoms and poor response to anti-obsessional treatment are mediated by lower activity in the cingulate cortex.

These findings suggest that, although both OCD and major depressive disorder respond to SRIs, the two syndromes have different neurobiological substrates for response. Elevated activity in the right caudate may be a marker of responsiveness to antiobsessional treatment, while lower right amygdala activity and higher midline prefrontal activity may be required for response of depressive symptoms to treatment.

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