
J Neuropsychiatry Clin Neurosci 20:390-408, November 2008
doi: 10.1176/appi.neuropsych.20.4.390
© 2008 American Neuropsychiatric Association
A Psychological and Neuroanatomical Model of Obsessive-Compulsive Disorder
Edward D. Huey, M.D.,
Roland Zahn, M.D., Ph.D.,
Frank Krueger, Ph.D.,
Jorge Moll, M.D., Ph.D.,
Dimitrios Kapogiannis, M.D.,
Eric M. Wassermann, M.D. and
Jordan Grafman, Ph.D.
Received August 2, 2007; revised November 6, 2007; accepted November 12, 2007. The authors are affiliated with the Cognitive Neuroscience Section, National Institute of Neurological Disorders and Stroke, at NIH in Bethesda, M.D.; Dr. Huey is affiliated with the Litwin-Zucker Research Center for the Study of Alzheimers Disease and Memory Disorders in Great Neck, N.Y.; Dr. Moll is affiliated with the Cognitive and Behavioral Neuroscience Unit at LABS–DOr Hospital Network in Rio de Janeiro, Brazil; Dr. Wasserman is affiliated with the Brain Stimulation Unit at the National Institute of Neurological Disorders and Stroke, NIH, in Bethesda. Address correspondence to Jordan Grafman, Ph.D., The National Institute of Neurological Disorders and Stroke, Cognitive Neuroscience Section, Bldg. 10, Rm. 7D43; MSC 1440 NIH/NINDS, Bethesda, MD 20892-1440; grafmanj{at}ninds.nih.gov (e-mail).
Imaging, surgical, and lesion studies suggest that the prefrontal cortex (orbitofrontal and anterior cingulate cortexes), basal ganglia, and thalamus are involved in the pathogenesis of obsessive-compulsive disorder (OCD). On the basis of these findings several models of OCD have been developed, but have had difficulty fully integrating the psychological and neuroanatomical findings of OCD. Recent research in the field of cognitive neuroscience on the normal function of these brain areas demonstrates the role of the orbitofrontal cortex in reward, the anterior cingulate cortex in error detection, the basal ganglia in affecting the threshold for activation of motor and behavioral programs, and the prefrontal cortex in storing memories of behavioral sequences (called "structured event complexes" or SECs). The authors propose that the initiation of these SECs can be accompanied by anxiety that is relieved with completion of the SEC, and that a deficit in this process could be responsible for many of the symptoms of OCD. Specifically, the anxiety can form the basis of an obsession, and a compulsion can be an attempt to receive relief from the anxiety by repeating parts of, or an entire, SEC. The authors discuss empiric support for, and specific experimental predictions of, this model. The authors believe that this model explains the specific symptoms, and integrates the psychology and neuroanatomy of OCD better than previous models.
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