Commentary| Volume 63, ISSUE 6, P539-541, March 15, 2008

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Regional Specificity of Traumatic Stress-Related Cortical Reduction: Further Evidence from a Twin Study of Post-Traumatic Stress Disorder

  • Kelly N. Botteron
    Address reprint requests to Kelly N. Botteron, M.D., 660 South Euclid, Campus Box 8134, St. Louis, MO 63110-1093
    Departments of Child Psychiatry and Radiology, Washington University School of Medicine, St. Louis, Missouri.
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      The physiologic response to stress and its effect on the structure and function of specific stress-related neural circuits has been an important topic of recent interest across a number of psychiatric disorders. This has been especially pertinent to the investigation of post-traumatic stress disorder (PTSD), which has also served as a model to further advance our understanding of the effects of traumatic stress on the brain. Much of this work has focused on stress-associated hypothalamic-pituitary-adrenocortical (HPA) axis dysregulation and its impact on several specific regions, such as the hippocampus and amygdala. A great deal of attention has focused on the HPA stress response and the regulatory role and susceptibility of the hippocampus to hypercortisolemic excitotoxic damage (
      • Vermetten E.
      • Vythilingam M.
      • Southwick S.M.
      • Charney D.S.
      • Bremner J.D.
      Long-term treatment with paroxetine increases verbal declarative memory and hippocampal volume in posttraumatic stress disorder.
      ). Few studies have focused on cortical structural changes associated with PTSD or traumatic stress exposure. The magnetic resonance imaging study of twins discordant for PTSD reported by Kasai et al. in this issue (pages 550–556) provides unique information about cortical change associated with PTSD and provides further insight related to the specificity of cortical regions involved in stress response and the cortical regions that are vulnerable to stress-related damage.
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