Yehuda R, Giller E L, Southwick S M, Lowy M T, Mason J W
Psychiatry Department, Mt. Sinai School of Medicine, New York, N.Y.
Biol Psychiatry. 1991 Nov 15;30(10):1031-48. doi: 10.1016/0006-3223(91)90123-4.
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.
神经内分泌学研究在基线条件下以及应对神经内分泌刺激时对下丘脑 - 垂体 - 肾上腺(HPA)轴进行了检测,这些研究支持了创伤后应激障碍(PTSD)中HPA功能改变的假说。然而,迄今为止,关于PTSD中HPA变化的性质存在诸多争议。此外,在显示PTSD和重度抑郁症有相似发现的研究中,关于HPA改变是表明PTSD的特定病理生理学,还是相反,反映了共病的重度抑郁症,存在争议。本综述总结了PTSD和重度抑郁症中HPA轴功能障碍的研究结果,并显示出HPA变化的不同模式,这可能是由于皮质醇及其调节因子的不同作用机制所致。