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Neuroimage. 2005 Feb 15;24(4):1180-91. Epub 2004 Dec 28.

Increased MEG activation in OCD reflects a compensatory mechanism specific to the phase of a visual working memory task.

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MGH/MIT/HMS Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital/Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA.


We examined spatio-temporal patterns of evoked magnetoencephalographic signals (MEG) in patients with obsessive-compulsive disorder (OCD) during the Encoding, Retention, and Retrieval phases of a Delayed Matching-to-Sample working memory task (DMST). The question was whether the mechanisms of abnormally increased cortical excitability, frequently reported in OCD, relate to a global cortical disinhibition and unselective over-processing of stimuli or, alternatively, to a compensatory mechanism of effortful enhanced inhibitory control. The DMST-related network of activation in OCD was found similar to that of Controls, and to that reported in other neuroimaging studies. The pattern of increased MEG activation in OCD patients was phase specific. During the Encoding phase, the activation was enhanced in the region of anterior insula and reduced in the posterior-inferior parietal cortex. During Retention, the activation was reduced in the occipital, parietal, superior temporal sulcus, and dorsolateral prefrontal cortex (BA 6/8/9). During Retrieval, a significant increase of activation was found in the right anterior insula extending towards the orbital region and right superior temporal sulcus, along with reduced activation in the left parietal cortex. The performance accuracy was high in OCD and comparable to Controls, although the RTs were prolonged. The results are discussed as being consistent with the hypothesis of a compensatory mechanism of effortful inhibitory control. This mechanism may be a major contributor to the increased cortical activation during Encoding and, in particular, Retrieval of the DMST task in patients suffering OCD. The findings do not support the concept of a faulty working memory mechanism per se in OCD.

[Indexed for MEDLINE]

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