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Research Article| Volume 30, ISSUE 10, P1031-1048, November 15, 1991

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Hypothalamic-pituitary-adrenal dysfunction in posttraumatic stress disorder

  • Rachel Yehuda
    Correspondence
    Address reprint requests to Rachel Yehuda, Ph.D., Psychiatry Department, Mount Sinai School of Medicine, Bronx VAMC 116A, 130 West Kingsbridge Rd., Bronx, NY 10468
    Affiliations
    Psychiatry Department, Mt. Sinai School of Medicine, New York, N.Y., USA

    Clinical Neuroscience Division, National Center for Posttraumatic Stress Disorder, West Haven Veterans' Administration Medical Center, West Haven, CT, 06516, USA
    Search for articles by this author
  • Earl L. Giller
    Affiliations
    Psychiatry Department, University of Connecticut Health Center, Farmington, CT 06030, USA
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  • Steven M. Southwick
    Affiliations
    Clinical Neuroscience Division, National Center for Posttraumatic Stress Disorder, West Haven Veterans' Administration Medical Center, West Haven, CT, 06516, USA

    Psychiatry Department, Yale University School of Medicine, New Haven, CT 06510, USA
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  • Martin T. Lowy
    Affiliations
    Psychiatry Department. Case Western Reserve University Medical School, Cleveland, OH 44116, USA
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  • John W. Mason
    Affiliations
    Clinical Neuroscience Division, National Center for Posttraumatic Stress Disorder, West Haven Veterans' Administration Medical Center, West Haven, CT, 06516, USA

    Psychiatry Department, Yale University School of Medicine, New Haven, CT 06510, USA
    Search for articles by this author
DOI:https://doi.org/10.1016/0006-3223(91)90123-4
Hypothalamic-pituitary-adrenal dysfunction in posttraumatic stress disorder
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      Abstract

      Neuroendocrine studies examining the hypothalamic-pituitary-adrenal (HPA) axis under baseline conditions and in response to neuroendocrine challenges have supported the hypothesis of altered HPA functioning in posttraumatic stress disorder (PTSD). However, to date, there is much debate concerning the nature of HPA changes in PTSD. Furthermore, in studies showing parallel findings in PTSD and major depressive disorder there is controversy regarding whether the HPA alterations suggest a specific pathophysiology of PTSD, or, rather, reflect comorbid major depressive disorder. This review summarizes findings of HPA axis dysfunction in both PTSD and major depressive disorder, and shows distinct patterns of HPA changes, which are probably due to different mechanisms of action for cortisol and its regulatory factors.
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      Article info

      Publication history

      Received in revised form: June 23, 1991
      Received: April 20, 1991

      Identification

      DOI: https://doi.org/10.1016/0006-3223(91)90123-4

      Copyright

      © 1991 Published by Elsevier Inc.

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