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地塞米松抑制皮质醇可减少创伤后应激障碍中的过度恐惧反应。

Cortisol suppression by dexamethasone reduces exaggerated fear responses in posttraumatic stress disorder.

机构信息

Emory University School of Medicine, Department of Psychiatry and Behavioral Sciences, Atlanta, GA 30303, United States.

出版信息

Psychoneuroendocrinology. 2011 Nov;36(10):1540-52. doi: 10.1016/j.psyneuen.2011.04.008. Epub 2011 May 20.

Abstract

PTSD symptoms are associated with heightened fear responses in laboratory fear conditioning paradigms. This study examined the effects of dexamethasone administration on hypothalamic-pituitary-adrenal (HPA) function and fear-potentiated startle (FPS) in trauma-exposed individuals with and without PTSD. We used an established fear discrimination procedure, in which one visual stimulus (CS+, danger cue) was paired with aversive airblasts to the throat (unconditioned stimulus, US), and another stimulus (CS-, safety cue) was presented without airblasts. In addition to FPS, the dexamethasone suppression test (DST) was performed. The study sample (N=100) was recruited from a highly traumatized civilian population in Atlanta, GA. Half of the subjects (n=54, 16 PTSD, 38 controls) underwent conditioning at baseline and the other half (n=46, 17 PTSD, 29 controls) after DST, in a cross-sectional design. We found a significant interaction effect of diagnostic group and dexamethasone treatment. Under baseline conditions, subjects with PTSD showed more than twice as much fear-potentiated startle to the danger cue compared to traumatized controls, F(1,53)=8.08, p=0.006. However, there was no group difference in subjects tested after dexamethasone suppression. Furthermore, there was a significant treatment effect in PTSD subjects but not in controls, with dexamethasone reducing fear-potentiated startle to the CS+, F(1,32)=4.00, p=0.05. There was also a positive correlation between PTSD subjects' FPS and cortisol levels, r=0.46, p=0.01. These results suggest that transient suppression of HPA function via dexamethasone suppression may reduce exaggerated fear in patients with PTSD.

摘要

创伤后应激障碍症状与实验室恐惧条件反射范式中的恐惧反应增强有关。本研究探讨了地塞米松给药对下丘脑-垂体-肾上腺(HPA)功能和创伤后暴露个体的恐惧增强性惊吓(FPS)的影响,这些个体患有或未患有创伤后应激障碍。我们使用了一种既定的恐惧辨别程序,其中一个视觉刺激(CS+,危险线索)与喉部的厌恶性空气爆炸(无条件刺激,US)配对,另一个刺激(CS-,安全线索)在没有空气爆炸的情况下呈现。除了 FPS 外,还进行了地塞米松抑制试验(DST)。研究样本(N=100)是从佐治亚州亚特兰大的一个高度创伤化的平民人群中招募的。一半的受试者(n=54,16 例 PTSD,38 例对照组)在基线时进行了条件作用,另一半受试者(n=46,17 例 PTSD,29 例对照组)在 DST 后进行了交叉设计。我们发现诊断组和地塞米松治疗的交互作用有显著影响。在基线条件下,与创伤对照组相比,PTSD 患者对危险线索的恐惧增强性惊吓增加了两倍多,F(1,53)=8.08,p=0.006。然而,在接受地塞米松抑制后测试的受试者中,没有组间差异。此外,PTSD 受试者中有显著的治疗效果,但对照组没有,地塞米松降低了对 CS+的恐惧增强性惊吓,F(1,32)=4.00,p=0.05。PTSD 受试者的 FPS 和皮质醇水平之间也存在正相关,r=0.46,p=0.01。这些结果表明,通过地塞米松抑制短暂抑制 HPA 功能可能会降低 PTSD 患者的过度恐惧。

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