Individuals who experience military combat obviously endure extreme stress, and this exposure leaves many diagnosed with the psychiatric condition of post-traumatic stress disorder, or PTSD. PTSD is associated with several abnormalities in brain structure and function. However, as researcher Roger Pitman explains, “Although it is tempting to conclude that these abnormalities were caused by the traumatic event, it is also possible that they were pre-existing risk factors that increased the risk of developing PTSD upon the traumatic event’s occurrence.” Drs. Kasai and Yamasue along with their colleagues sought to examine this association in a new study published in the March 15th issue of Biological Psychiatry.

The authors measured the gray matter density of the brains of combat-exposed Vietnam veterans, some with and some without PTSD, and their combat-unexposed identical twins using a technology called magnetic resonance imaging (MRI). The detailed images provided by the MRI scans then allowed the investigators to compare specific brain regions of the siblings. They found that the gray matter density of the pregenual anterior cingulate cortex, an area of the brain involved in emotional functioning, was reduced in veterans with PTSD, but not in their twins who had not experienced combat. According to Dr. Pitman, “this finding supports the conclusion that the psychological stress resulting from the traumatic stressor may damage this brain region, with deleterious emotional consequences.”

John H. Krystal, M.D., Editor of Biological Psychiatry and affiliated with both Yale University School of Medicine and the VA Connecticut Healthcare System, discusses the need for this kind of research because of two separate sets of prior findings: “On the one hand, compelling data from animal research indicates that stress can cause brain atrophy and even neural death in some brain regions. On the other hand, the volume of several brain regions are highly heritable and small brain volumes, presumably related to reduced function, in the hippocampus may increase stress reactivity or impair the capacity for resilience.” He adds that findings from this study “suggest that volume reductions in [the anterior cingulate cortex] associated with PTSD arise as a consequence of stress exposure rather than emerging as a heritable trait,” leaving one to conclude that “the extent to which particular genes and environmental exposures interact to shape the development of the brain thus appears to be complex and region-specific.”

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Notes to Editors:

The article is “Evidence for Acquired Pregenual Anterior Cingulate Gray Matter Loss from a Twin Study of Combat-Related Posttraumatic Stress Disorder” by Kiyoto Kasai, Hidenori Yamasue, Mark W. Gilbertson, Martha E. Shenton, Scott L. Rauch and Roger K. Pitman. Drs. Kasai and Yamasue are affiliated with the Department of Neuropsychiatry, Graduate School of Medicine, University of Tokyo in Tokyo, Japan. Drs. Gilbertson, Shenton, Rauch and Pitman are with the Department of Psychiatry, Harvard Medical School, Boston, Massachusetts. Dr. Gilbertson is also from the Research Service, VA Medical Center, Manchester, New Hampshire. Dr. Shenton is also affiliated with the Psychiatry Neuroimaging Laboratory, Department of Psychiatry, and the Surgical Planning Laboratory, MRI Division, Department of Radiology, Brigham & Women’s Hospital in Boston, Massachusetts. Dr. Rauch is also with McLean Hospital in Belmont, Massachusetts. Dr. Pitman is also from the Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts. The article appears in Biological Psychiatry, Volume 63, Issue 6 (March 15, 2008), published by Elsevier.

Full text of the article mentioned above is available upon request. Contact Jayne M. Dawkins at (215) 239-3674 or .(JavaScript must be enabled to view this email address) to obtain a copy or to schedule an interview.

About Biological Psychiatry

This international rapid-publication journal is the official journal of the Society of Biological Psychiatry. It covers a broad range of topics in psychiatric neuroscience and therapeutics. Both basic and clinical contributions are encouraged from all disciplines and research areas relevant to the pathophysiology and treatment of major neuropsychiatric disorders. Full-length and Brief Reports of novel results, Commentaries, Case Studies of unusual significance, and Correspondence and Comments judged to be of high impact to the field are published, particularly those addressing genetic and environmental risk factors, neural circuitry and neurochemistry, and important new therapeutic approaches. Concise Reviews and Editorials that focus on topics of current research and interest are also published rapidly.

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