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Editorial |

Augmenting Obsessive-Compulsive Disorder Treatment From Brain to Mind

Kerry J. Ressler, MD, PhD1,2; Barbara O. Rothbaum, PhD1
[+] Author Affiliations
1Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia
2Howard Hughes Medical Institute, Chevy Chase, Maryland
JAMA Psychiatry. 2013;70(11):1129-1131. doi:10.1001/jamapsychiatry.2013.2116.
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The article “Cognitive-Behavioral Therapy vs Risperidone for Augmenting Serotonin Reuptake Inhibitors in Obsessive-Compulsive Disorder: A Randomized Clinical Trial” by Simpson et al1 in this issue reports that exposure/ritual prevention (EX/RP) is without question more effective than risperidone or placebo in augmenting serotonin reuptake inhibitor (SRI) response in an 8-week randomized clinical trial with 100 participants. Simpson et al call for a change in practice, because augmentation for SRI nonresponders with atypical antipsychotics is recommended in the American Psychiatric Association guidelines.2 This is a well-controlled randomized clinical trial worthy of strong conclusions. Simpson et al have a track record of well-controlled combination studies in obsessive-compulsive disorder (OCD), and the conclusion that EX/RP should be considered first for SRI treatment augmentation is supported by the current data.

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Neural Circuitry Associated With Obsessive-Compulsive Disorder (OCD)

For more than 20 years, cortical-striatal-thalamic-cortical (yellow arrows) dysfunction has been associated with OCD symptoms, with the orbitofrontal cortex (OFC) being most directly implicated. Multiple regions within this behavioral circuit, in particular the striatum and OFC, are heavily innervated and modulated by the amygdala in response to emotional stimuli (red arrows). Functional imaging studies have suggested dysfunction within these pathways and abnormal circuit regulation correlating with OCD symptoms. These cortical and subcortical regions are regulated by the 3 monoamine systems that are targeted by current psychiatric medications, serotonin from the raphe nuclei, dopamine from the ventral tegmental area (VTA) and substantia nigra, and norepinephrine from the locus coeruleus (LC). Selective serotonin reuptake inhibitors and antipsychotics are thought to act primarily by altering serotonin and dopamine synapse functioning, respectively, thus altering monoaminergic regulation as their mechanism of symptom reduction. In contrast, exposure and ritual prevention is thought to directly alter the connectivity in the cortical-striatal-thalamic-cortical–amygdala circuits via emotional learning processes.

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