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Prog Neuropsychopharmacol Biol Psychiatry. 2013 Jan 10;40:340-6. doi: 10.1016/j.pnpbp.2012.11.001. Epub 2012 Nov 9.

Neural correlates of altered response inhibition and dysfunctional connectivity at rest in obsessive-compulsive disorder.

Author information

1
Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea.

Abstract

OBJECTIVE:

Functional imaging studies of obsessive-compulsive disorder (OCD) have reported altered fronto-striatal activity during executive tasks. Additionally, altered connectivity of these regions during resting state was found. However, the relationship between brain activity during tasks and resting state remains poorly understood. The present study investigated neural correlates associated with abnormal response inhibition in OCD and to examine how resting state functional connectivity relates to task-related activity.

METHOD:

Eighteen unmedicated adult OCD patients and 18 age- and sex-matched control subjects underwent functional magnetic resonance imaging scans during both resting state and a response inhibition task. Brain activation during response inhibition was compared between groups. Fronto-striatal regions showing altered task-related activity were used as seeds for connectivity analyses during resting state.

RESULTS:

During the response inhibition task, OCD patients had lower activation in areas including the cingulate cortex and basal ganglia regions. Compared with control subjects, patients with OCD showed increased functional connectivity of the caudate nucleus with the middle cingulate cortex and precentral gyrus during rest, suggesting hyperactive striatal-cortical connections.

CONCLUSION:

This study found altered function in fronto-striatal regions during response inhibition and its relation to resting state functional connectivity in OCD. Our results suggest that dysfunctional striatal-cortical connections even during rest may result in the failure of response inhibition and error monitoring observed in OCD patients.

PMID:
23146681
DOI:
10.1016/j.pnpbp.2012.11.001
[Indexed for MEDLINE]

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