Obsessive-compulsive disorder (OCD) has become one of the clearest examples of how
biological psychiatry has successfully identified neural underpinnings of a mental
disorder. Our current understanding of OCD, although still far from complete, heavily
relies on studies of dysfunction in discrete neuronal circuits as well as abnormalities
of neurotransmission. The most established circuitry model of OCD assumes dysfunction
of specific frontostriatal loops, that is, segregated circuits connecting the prefrontal
cortices with the striatum and specific thalamic nuclei. At the core of this model
is a disturbed interaction between the orbitofrontal cortex (OFC) and the caudate
nucleus/ventral striatum (
1
). This loop is thought to integrate affective aspects of behavior and is modulated
by adjacent brain structures such as the anterior cingulate cortex (ACC) and possibly
the subgenual cingulate cortex (Brodmann area 25). In fact, there is a wealth of data
to support this model. For example, elevated glucose metabolism in the OFC has repeatedly
been shown in OCD, both at rest and during symptom provocation.To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
January 25,
2008
Received in revised form:
January 25,
2008
Received:
January 2,
2008
Identification
Copyright
© 2008 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
