A psychological and neuroanatomical model of obsessive-compulsive disorder

Edward D. Huey, Roland Zahn, Frank Krueger, Jorge Moll, Dimitrios Kapogiannis, Eric M. Wassermann, Jordan Grafman

    Research output: Contribution to journalArticlepeer-review


    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. © 2008 American Psychiatric Publishing, Inc.
    Original languageEnglish
    Pages (from-to)390-408
    Number of pages18
    JournalJournal of Neuropsychiatry and Clinical Neurosciences
    Issue number4
    Publication statusPublished - Nov 2008


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