Imaging results showed increased task-associated activation in controls compared with OCD patients in several regions previously found to be involved in planning, particularly DLPFC, basal ganglia, and parietal cortex. Task load–correlated activity was found in left DLPFC in control subjects compared with OCD patients. In contrast, OCD patients showed increased activation, correlated with increased task load, in bilateral cingulate, ventrolateral prefrontal, and parahippocampal cortices, in left anterior temporal cortex, and in dorsal brainstem. Our finding of decreased responsiveness of dorsal prefrontal-striatal circuits during planning in OCD patients is in accord with previous findings with regard to basal ganglia dysfunction in OCD in implicit learning.28,29 However, in the study by Rauch et al,28 OCD subjects showed impaired performance during motor skill acquisition, suggesting basal ganglia–motor cortical rather than dorsal prefrontal-striatal dysfunction, as found in the present study. In addition, several functional imaging studies36- 40 using symptom provocation designs have reported abnormalities in orbitofrontal-striatal function in OCD, thought to reflect its role in ritualistic behavior. Most of these studies,36,37,40 however, lacked adequate control groups or failed to find significant group-by-task interactions in subcortical areas. Increased prefrontal-subcortical glucose uptake in OCD patients relative to controls, resolving after successful therapy, has also been reported in several resting-state imaging studies.41- 45 Although dorsal prefrontal abnormalities were apparently found in 1 study,43 most of these studies reported increased orbitofrontal-striatal metabolism. Moreover, although dorsal PFC and ventral PFC are known to project to dorsal and ventral parts of the striatum, spatial resolution of positron emission tomography with [18F]fluorodeoxyglucose may have been insufficient to detect differences based on topographical organization within the basal ganglia. Therefore, the evidence for pathologically increased baseline activity in dorsal prefrontal-striatal, as opposed to ventral prefrontal-striatal, loops in OCD is still inconclusive. However, although the present fMRI data do not allow baseline comparisons, our finding of decreased or absent prefrontal-striatal responsiveness is compatible with existing pathophysiological models of OCD hypothesizing basal ganglia disinhibition due to an altered balance between indirect, inhibitory, and direct excitatory cortico-striatal-thalamico-cortical circuits.46,47 Whether the failure of OCD patients to recruit dorsal prefrontal-striatal regions compared with controls, as found in the present study, is specific for planning tasks is also not yet clear. In a recent fMRI study, van der Wee et al48 found decreased performance only at the highest task level in OCD patients compared with controls during performance of a spatial n-back task. Imaging results showed similar activity in bilateral DLPFC and parietal cortex in both groups, from which the authors concluded that (spatial) working memory in OCD was not abnormal. The findings of the present study provide support for this conclusion. Whereas it might be argued that in our paradigm not only planning complexity but also working memory load was (linearly) increased, our results reveal impaired planning at all levels, which is difficult to explain by differences in working memory capacity.