Commentary| Volume 63, ISSUE 6, P542-543, March 15, 2008

Targeting Brain Regions and Symptoms: Neuronal Single-Unit Recordings and Deep Brain Stimulation in Obsessive-Compulsive Disorder

  • Igor Nenadic
    Address reprint requests to Igor Nenadic, M.D., Department of Psychiatry and Psychotherapy, Friedrich-Schiller-University of Jena, Philosophenweg 3, D-07743 Jena, Germany
    Department of Psychiatry and Psychotherapy, Friedrich-Schiller-University of Jena, Philosophenweg 3, D-07743 Jena, Germany.
    Search for articles by this author
      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 (
      • Graybiel A.M.
      • Rauch S.L.
      Toward a neurobiology of obsessive-compulsive disorder.
      ). 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.
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