Birmes P, Escande M, Gourdy P, Schmitt L
Service Universitaire de Psychiatrie et Psychologie Médicale, Hôpital Purpan-Casselardit, Centre Hospitalier Universitaire de Toulouse, place Baylac, F-31059 Toulouse.
Encephale. 2000 Nov-Dec;26(6):55-61.
The core symptoms of post-traumatic stress disorder (PTSD) include persistent reexperiencing of the traumatic event, avoidance of stimuli associated with the trauma, and autonomic hyperarousal. Many neurotransmitter systems and neurobiologic mechanisms may account for these primary symptoms of PTSD. Severe psychological trauma results in the parallel activation of these systems, producing an array of adaptive behavioral and physiologic responses necessary for survival. The pathophysiology of PTSD may involve dysfunction of several brain structures, particularly the amygdala, locus coeruleus, and hippocampus, as well as noradrenergic system and hypothalamic-pituitary-adrenal (HPA) axis. The neuroendocrinology of PTSD, and specifically hypothalamic-pituitary-adrenal axis alterations, are ways of examining biologic heterogeneity following trauma and its possible clinical implications. The decreased levels of cortisol, the increased responsiveness of glucocorticoid receptors, the increased sensitivity of the HPA negative feedback inhibition and its progressive sensitization are the neuroendocrine alterations specifically associated with the development of PTSD.
创伤后应激障碍（PTSD）的核心症状包括创伤事件的持续重现、对与创伤相关刺激的回避以及自主神经高度兴奋。许多神经递质系统和神经生物学机制可能导致PTSD的这些主要症状。严重的心理创伤会导致这些系统同时被激活，产生一系列生存所需的适应性行为和生理反应。PTSD的病理生理学可能涉及多个脑结构功能失调，特别是杏仁核、蓝斑和海马体，以及去甲肾上腺素能系统和下丘脑-垂体-肾上腺（HPA）轴。PTSD的神经内分泌学，特别是下丘脑-垂体-肾上腺轴的改变，是研究创伤后生物异质性及其可能临床意义的方法。皮质醇水平降低、糖皮质激素受体反应性增加、HPA负反馈抑制敏感性增加及其逐渐敏感化是与PTSD发展特别相关的神经内分泌改变。
