Obsessive compulsive disorder (OCD) affects 2-3% of the general population. The neurobiology of OCD has been linked to dysfunction of cortico-striatal circuits connecting the orbitofrontal (OFC) to the striatum. Recently, this loop has become an approved target for non-invasive neuromodulatory treatment of OCD.

To explore structural and functional connectivity of the OFC in OCD subjects and healthy controls.

14 OCD patients and 12 age/sex-matched controls underwent magnetic resonance imaging (MRI) (3T-Philips scanner) for diffusion tensor imaging (DTI) and resting state functional connectivity (rsFC). DTI images were brain extracted and corrected for movement and eddy currents. A diffusion tensor model was fitted to each voxel and used to generate Fractional Anisotropy (FA) maps. Voxel-wise statistical analysis of FA was performed using Tract-Based Spatial Statistics. RsFC images were preprocessed and seed-based correlation (SBC) analysis was performed using Data Processing Assistant for Resting-State fMRI.

We found decreased values of FA in the body of the Corpus Callosum bilaterally (MNI_coordinates: x= 16, y= -16, z= 33 and x= -19, y= -16, z= 42) and left superior longitudinal fasciculus in OCD patients (fig 1, left), as well as decreased rsFC of the right superior orbitofrontal seed with the left inferior frontal gyrus and left middle occipital gyrus (fig 2, right).

Using an exploratory multimodal approach we found evidence of abnormal structural and functional long-range connectivity of the OFC in OCD. If confirmed in a larger sample these connectivity abnormalities could be explored as potential predictors of response to OFC-targeted non-invasive neuromodulatory interventions.

No significant relationships.

Neuropsychological testing reveals a pattern of impairment among patients with obsessive-compulsive disorder (OCD) which implicates the orbitofrontal region. Studies of neuropsychological function in OCD differ regarding performance deficits on classical tests of frontal executive function. In some studies, OCD patients did not demonstrate impaired performance on tests of executive function. However, other researchers have documented performance deficits among OCD patients on measures of executive function. Patients with OCD also exhibit performance deficits on tests of visual/spatial memory and verbal memory. Again, in some studies, OCD patients did not demonstrate impaired performance on tests of memory function. How can we account for the conflicting findings? One possibility is that performance deficits on tests of cognitive function are associated with comorbid conditions. In prior work, we observed that OCD patients who did poorly on executive function tasks obtained high scores on a measure of schizotypal personality. A second possibility is that executive function deficits among patients with OCD are associated with comorbid depressive symptoms.

In the present study, a comprehensive neuropsychological test battery was administered to patients with OCD and matched healthy control subjects. We also administered dimensional measures of schizotypal personality and depression to patients with OCD and controls. We conducted analyses of covariance (ANCOVA), with scores on measures of schizotypal personality and depression used as covariates.

OCD patients demonstrated performance deficits on measures of delayed memory, response inhibition, alternation learning, and obtained significantly higher scores on measures of disinhibition, impulsivity, and temporolimbic symptoms; however, OCD patients did not exhibit impaired performance on tests of executive function and verbal fluency, and did not report a significantly greater number of dysexecutive symptoms, when coexistent depressive and schizotypal symptoms were taken into account.

Findings are consistent with the contention that dysfunction of an orbitofrontal-limbic network underlies OCD.