Miedl Stephan F, Franke Laila K, Danböck Sarah K, Martini Michael, Hettegger Sabrina, Kronbichler Martin, Flor Herta, Wilhelm Frank H
Clinical Stress and Emotion Laboratory, Division of Clinical Psychology and Psychopathology, Department of Psychology, Paris-Lodron University Salzburg, Salzburg, Austria.
Department of Psychology, School of Social Sciences, University of Mannheim, Mannheim, Germany.
Eur J Psychotraumatol. 2024;15(1):2388429. doi: 10.1080/20008066.2024.2388429. Epub 2024 Sep 16.
Posttraumatic stress disorder and medically unexplained pain frequently co-occur. While pain is common during traumatic events, the processing of pain during trauma and its relation to audiovisual and pain intrusions is poorly understood. Here we investigate neural activations during painful analogue trauma, focusing on areas that have been related to threat and pain processing, and how they predict intrusion formation. We also examine the moderating role of cumulative lifetime adversity. Sixty-five healthy women were assessed using functional magnetic resonance imaging. An analogue trauma was induced by an adaptation of the trauma-film paradigm extended by painful electrical stimulation in a 2 (film: aversive, neutral) x 2 (pain: pain, no-pain) design, followed by 7-day audiovisual and pain intrusion assessment using event-based ecological momentary assessment. Intrusions were fitted with Bayesian multilevel regression and a hurdle lognormal distribution. Conjunction analysis confirmed a wide network including anterior insula (AI) and dorsal anterior cingulate cortex (dACC) being active both, during aversive films and pain. Pain resulted in activation in areas amongst posterior insula and deactivation in a network around ventromedial prefrontal cortex (VMPFC). Higher AI and dACC activity during aversive>neutral film predicted greater audiovisual intrusion probability over time and predicted greater audiovisual intrusion frequency particularly for participants with high lifetime adversity. Lower AI, dACC, hippocampus, and VMPFC activity during pain>no-pain predicted greater pain intrusion probability particularly for participants with high lifetime adversity. Weak regulatory VMPFC activation was associated with both increased audiovisual and pain intrusion frequency. Enhanced AI and dACC processing during aversive films, poor pain vs. no-pain discrimination in AI and dACC, as well as weak regulatory VMPFC processing may be driving factors for intrusion formation, particularly in combination with high lifetime adversity. Results shed light on a potential path for the etiology of PTSD and medically unexplained pain.
创伤后应激障碍与医学上无法解释的疼痛经常同时出现。虽然疼痛在创伤事件中很常见，但创伤期间疼痛的处理及其与视听和疼痛侵入的关系却知之甚少。在这里，我们研究了模拟创伤疼痛期间的神经激活情况，重点关注与威胁和疼痛处理相关的区域，以及它们如何预测侵入的形成。我们还研究了累积终生逆境的调节作用。使用功能磁共振成像对65名健康女性进行了评估。采用2（电影：厌恶、中性）×2（疼痛：疼痛、无疼痛）设计，通过在创伤电影范式中加入疼痛电刺激来诱发模拟创伤，随后使用基于事件的生态瞬时评估对视听和疼痛侵入进行为期7天的评估。侵入情况采用贝叶斯多级回归和障碍对数正态分布进行拟合。联合分析证实，包括前岛叶（AI）和背侧前扣带回皮质（dACC）在内的广泛网络在观看厌恶电影和疼痛期间均处于活跃状态。疼痛导致后岛叶区域激活以及腹内侧前额叶皮质（VMPFC）周围网络失活。在厌恶电影期间，与中性电影相比，AI和dACC活动较高预示着随着时间推移视听侵入的可能性更大，尤其对于终生逆境较高的参与者，预示着视听侵入频率更高。与无疼痛相比，疼痛期间AI、dACC、海马体和VMPFC活动较低预示着疼痛侵入的可能性更大，尤其对于终生逆境较高的参与者。VMPFC调节性激活较弱与视听和疼痛侵入频率增加均相关。在厌恶电影期间AI和dACC处理增强、AI和dACC中疼痛与无疼痛辨别能力较差以及VMPFC调节性处理较弱可能是侵入形成的驱动因素，尤其是与高终生逆境相结合时。研究结果揭示了创伤后应激障碍和医学上无法解释的疼痛病因的潜在途径。
