Douglas Katie M, Groves Samantha, Porter Richard J, Jordan Jenny, Wilson Lynere, Melzer Tracy R, Wise Richard G, Bisson Jonathan I, Bell Caroline J
Department of Psychological Medicine, University of Otago, Christchurch, Christchurch, New Zealand.
New Zealand Brain Research Institute, Christchurch, New Zealand.
Aust N Z J Psychiatry. 2019 Dec;53(12):1167-1178. doi: 10.1177/0004867419851860. Epub 2019 May 31.
Post-traumatic stress disorder involves excessive retrieval of traumatic memories. Glucocorticoids impair declarative memory retrieval. This preliminary study examined the effect of acute hydrocortisone administration on brain activation in individuals with earthquake-related post-traumatic stress disorder compared with earthquake-exposed healthy individuals, during retrieval of traumatic memories.
Participants exposed to earthquakes with ( = 11) and without post-traumatic stress disorder ( = 11) underwent two functional magnetic resonance imaging scans, 1-week apart, in a double-blind, placebo-controlled, counter-balanced design. On one occasion, they received oral hydrocortisone (20 mg), and on the other, placebo, 1 hour before scanning. Symptom provocation involved script-driven imagery (traumatic and neutral scripts) and measures of self-reported anxiety.
Arterial spin labelling showed that both post-traumatic stress disorder and trauma-exposed controls had significantly reduced cerebral blood flow in response to retrieval of traumatic versus neutral memories in the right hippocampus, parahippocampal gyrus, calcarine sulcus, middle and superior temporal gyrus, posterior cingulate, Heschl's gyrus, inferior parietal lobule, angular gyrus, middle occipital gyrus, supramarginal gyrus, lingual gyrus and cuneus, and the left prefrontal cortex. Hydrocortisone resulted in non-significant trends of increasing subjective distress and reduced regional cerebral blood flow in the left inferior frontal gyrus, left anterior cingulate gyrus, middle temporal gyrus, cerebellum, postcentral gyrus and right frontal pole, during the trauma script.
Findings do not fit with some aspects of the accepted neurocircuitry model of post-traumatic stress disorder, i.e., failure of the medial prefrontal cortex to quieten hyperresponsive amygdala activity, and the potential therapeutic benefits of hydrocortisone. They do, however, provide further evidence that exposure to earthquake trauma, regardless of whether post-traumatic stress disorder eventuates, impacts brain activity and highlights the importance of inclusion of trauma-exposed comparisons in studies of post-traumatic stress disorder.
创伤后应激障碍涉及创伤性记忆的过度提取。糖皮质激素会损害陈述性记忆提取。本初步研究考察了与经历地震但无创伤后应激障碍的健康个体相比,急性给予氢化可的松对地震相关创伤后应激障碍个体在提取创伤性记忆时脑激活的影响。
有(n = 11)和无创伤后应激障碍(n = 11)的地震暴露参与者在双盲、安慰剂对照、平衡设计下,相隔1周接受两次功能磁共振成像扫描。一次扫描前1小时,他们口服氢化可的松(20毫克),另一次口服安慰剂。症状激发包括脚本驱动的意象(创伤性和中性脚本)以及自我报告焦虑的测量。
动脉自旋标记显示,创伤后应激障碍患者和经历创伤的对照组在提取创伤性记忆与中性记忆时,右侧海马体、海马旁回、距状沟、颞中回和颞上回、后扣带回、颞横回、顶下小叶、角回、枕中回、缘上回、舌回和楔叶以及左侧前额叶皮质的脑血流量均显著减少。在创伤脚本过程中,氢化可的松导致主观痛苦增加和左侧额下回、左侧前扣带回、颞中回、小脑、中央后回和右侧额极区域脑血流量减少的趋势,但不显著。
研究结果与创伤后应激障碍公认的神经回路模型的某些方面不符,即内侧前额叶皮质无法抑制杏仁核的过度反应活动以及氢化可的松的潜在治疗益处。然而,它们确实提供了进一步的证据,表明接触地震创伤,无论是否发生创伤后应激障碍,都会影响大脑活动,并突出了在创伤后应激障碍研究中纳入经历创伤对照的重要性。