Anxiety disorders have been linked to a hyperactivated cortico-amygdalar circuitry, but the amygdala's role in the pathophysiology of obsessive-compulsive disorder (OCD) remains unclear. This fMRI study examined the cortico-limbic correlates of individually tailored symptom provocation in 14 unmedicated OCD patients and 14 controls. In addition to OCD-relevant pictures, aversive and neutral control stimuli were included. Patients showed increased fronto-striatal activation to OCD-relevant stimuli contrasted with both control categories. Briefly presented symptom-related triggers elicited stronger amygdala engagement in patients than in controls. This effect, however, did also occur to aversive stimuli and was not symptom specific. Augmented amygdala involvement in patients reflects general emotional hyperarousal. Symptom-specific frontal activation points towards a sustained endeavor to suppress exaggerated emotional responses to OCD triggers.

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Obsessive-compulsive disorder (OCD) patients show deficits in tasks of executive functioning like the antisaccade (AS) task. These deficits suggest problems in response inhibition or volitional saccade generation. Thirty patients (15 nonmedicated) and 30 healthy subjects performed antisaccades and simple volitional saccades (SVS), that is, centrally cued saccades. In SVS, two aspects of volitional saccade generation were disentangled: response selection and initiation. Latencies of OCD patients were increased in volitional saccades independent of response selection demands. AS performance did not differ. Across groups, latencies in AS were faster than in SVS. Medicated patients did not differ from nonmedicated patients. In sum, response initiation is deficient in OCD patients, which may reflect a general problem in volitional action generation. This deficit did not affect antisaccade performance, possibly due to a lower volitional demand in that task.

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