Enhanced avoidance learning was found in OCD patients that points to exaggerated anticipation and avoidance of aversive outcomes. Further studies are required to investigate whether neurobiological mechanisms, such as dopaminergic signaling or outcome processing, in the orbitofrontal cortex relate to enhanced negative learning in OCD.

Recent research suggests that patients with obsessive-compulsive disorder (OCD) have deficits in the volitional control of saccades. Specific evidence comes from increased latencies of saccadic eye movements when they were volitionally executed but not when they were visually guided. The present study sought to test whether this deviance represents a cognitive endophenotype. To this end, first-degree relatives of OCD patients as genetic risk carriers were compared with OCD patients and healthy controls without a family history of OCD. Furthermore, as volitional response generation comprises selection and initiation of the required response, the study also sought to specify the cognitive mechanisms underlying impaired volitional response generation. Twenty-two unaffected first-degree relatives of OCD patients, 22 unmedicated OCD patients, and 22 healthy comparison subjects performed two types of volitional saccade tasks measuring response selection or only response initiation, respectively. Visually guided saccades were used as a control condition. Our results showed that unaffected first-degree relatives and OCD patients were significantly slowed compared to healthy comparison subjects in volitional response selection. Patients and relatives did not differ from each other. There was no group difference in the visually guided control condition. Taken together, the study provides first evidence that dysfunctional volitional response selection is a candidate endophenotype for OCD.

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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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