from Section III - Anxiety Disorders
Published online by Cambridge University Press: 10 January 2011
Functional magnetic resonance imaging (fMRI) research in obsessive–compulsive disorder (OCD) has explored a broad range of cognitive functions, in addition to the neural correlates of symptom provocation and symptom improvement after treatment. Additionally, given the heterogeneity of patients with OCD, some fMRI research has examined symptom-specific neural correlates or comparisons of different symptom dimensions in these patients. fMRI research on OCD has also included family members of patients with OCD, and have suggested trait-dependent neural patterns of cognitive dysfunction and genetic susceptibility to OCD.
The current model of OCD pathophysiology involves cortico basal ganglia–thalamo-cortical loop dysfunction, especially including dysfunction in the orbitofrontal cortex (OFC), caudate nucleus, and anterior cingulate cortex (ACC). The major findings in neuroimaging research in OCD suggest hyperactivation in the ventral frontal–striatal areas, such as the OFC, insula, ACC, and caudate head, during symptom provocation or resting states, and generally show normalized activation after symptom improvement. Additionally, various cognitive paradigms have been applied to fMRI research in OCD, and have provided evidence of neural correlates of specific cognitive dysfunction. The overall results of fMRI research in cognitive paradigms indicate reduced brain activation in the dorsolateral prefrontal cortex (dlPFC) or parietal lobes, related to executive function or cognitive flexibility, increased hippocampus activation, as compensation for dysfunction in the basal ganglia during implicit sequence learning, and hyperactivation in ACC, related to error processing.
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