Stevens Jennifer S, Kim Ye Ji, Galatzer-Levy Isaac R, Reddy Renuka, Ely Timothy D, Nemeroff Charles B, Hudak Lauren A, Jovanovic Tanja, Rothbaum Barbara O, Ressler Kerry J
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia.
Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia.
Biol Psychiatry. 2017 Jun 15;81(12):1023-1029. doi: 10.1016/j.biopsych.2016.11.015. Epub 2016 Dec 23.
Studies suggest that exaggerated amygdala reactivity is a vulnerability factor for posttraumatic stress disorder (PTSD); however, our understanding is limited by a paucity of prospective, longitudinal studies. Recent studies in healthy samples indicate that, relative to reactivity, habituation is a more reliable biomarker of individual differences in amygdala function. We investigated reactivity of the amygdala and cortical areas to repeated threat presentations in a prospective study of PTSD.
Participants were recruited from the emergency department of a large level I trauma center within 24 hours of trauma. PTSD symptoms were assessed at baseline and approximately 1, 3, 6, and 12 months after trauma. Growth curve modeling was used to estimate symptom recovery trajectories. Thirty-one individuals participated in functional magnetic resonance imaging around the 1-month assessment, passively viewing fearful and neutral face stimuli. Reactivity (fearful > neutral) and habituation to fearful faces was examined.
Amygdala reactivity, but not habituation, 5 to 12 weeks after trauma was positively associated with the PTSD symptom intercept and predicted symptoms at 12 months after trauma. Habituation in the ventral anterior cingulate cortex was positively associated with the slope of PTSD symptoms, such that decreases in ventral anterior cingulate cortex activation over repeated presentations of fearful stimuli predicted increasing symptoms.
Findings point to neural signatures of risk for maintaining PTSD symptoms after trauma exposure. Specifically, chronic symptoms were predicted by amygdala hyperreactivity, and poor recovery was predicted by a failure to maintain ventral anterior cingulate cortex activation in response to fearful stimuli. The importance of identifying patients at risk after trauma exposure is discussed.
研究表明,杏仁核反应过度是创伤后应激障碍(PTSD)的一个易患因素;然而,我们的理解受到前瞻性纵向研究匮乏的限制。近期对健康样本的研究表明,相对于反应性,习惯化是杏仁核功能个体差异更可靠的生物标志物。我们在一项PTSD前瞻性研究中调查了杏仁核和皮质区域对重复威胁刺激的反应性。
参与者在创伤后24小时内从一家大型一级创伤中心的急诊科招募。在基线以及创伤后约1、3、6和12个月评估PTSD症状。使用生长曲线模型估计症状恢复轨迹。31名个体在1个月评估左右参与功能磁共振成像,被动观看恐惧和中性面部刺激。检查对恐惧面孔的反应性(恐惧>中性)和习惯化。
创伤后5至12周,杏仁核反应性而非习惯化与PTSD症状截距呈正相关,并预测创伤后12个月的症状。腹侧前扣带回皮质的习惯化与PTSD症状斜率呈正相关,即随着恐惧刺激的重复呈现,腹侧前扣带回皮质激活的减少预示着症状增加。
研究结果指出了创伤暴露后维持PTSD症状风险的神经特征。具体而言,杏仁核反应过度可预测慢性症状,而对恐惧刺激未能维持腹侧前扣带回皮质激活则可预测恢复不良。文中讨论了识别创伤暴露后高危患者的重要性。