Rütgen Markus, Seidel Eva-Maria, Silani Giorgia, Riečanský Igor, Hummer Allan, Windischberger Christian, Petrovic Predrag, Lamm Claus
Social, Cognitive and Affective Neuroscience Unit, Department of Basic Psychological Research and Research Methods, Faculty of Psychology, University of Vienna, Vienna 1010, Austria;
Cognitive Neuroscience Sector, International School for Advanced Studies, Trieste 34136, Italy; Department of Applied Psychology: Health, Development, Enhancement and Intervention, Faculty of Psychology, University of Vienna, Vienna 1010, Austria;
Proc Natl Acad Sci U S A. 2015 Oct 13;112(41):E5638-46. doi: 10.1073/pnas.1511269112. Epub 2015 Sep 28.
Empathy for pain activates brain areas partially overlapping with those underpinning the first-hand experience of pain. It remains unclear, however, whether such shared activations imply that pain empathy engages similar neural functions as first-hand pain experiences. To overcome the limitations of previous neuroimaging research, we pursued a conceptually novel approach: we used the phenomenon of placebo analgesia to experimentally reduce the first-hand experience of pain, and assessed whether this results in a concomitant reduction of empathy for pain. We first carried out a functional MRI experiment (n = 102) that yielded results in the expected direction: participants experiencing placebo analgesia also reported decreased empathy for pain, and this was associated with reduced engagement of anterior insular and midcingulate cortex: that is, areas previously associated with shared activations in pain and empathy for pain. In a second step, we used a psychopharmacological manipulation (n = 50) to determine whether these effects can be blocked via an opioid antagonist. The administration of the opioid antagonist naltrexone blocked placebo analgesia and also resulted in a corresponding "normalization" of empathy for pain. Taken together, these findings suggest that pain empathy may be associated with neural responses and neurotransmitter activity engaged during first-hand pain, and thus might indeed be grounded in our own pain experiences.
对疼痛的共情会激活大脑中与亲身经历疼痛时部分重叠的区域。然而，目前尚不清楚这种共同激活是否意味着疼痛共情与亲身疼痛体验具有相似的神经功能。为了克服以往神经影像学研究的局限性，我们采用了一种概念上新颖的方法：利用安慰剂镇痛现象来实验性地减轻亲身疼痛体验，并评估这是否会导致对疼痛的共情同时减少。我们首先进行了一项功能性磁共振成像实验（n = 102），结果符合预期：经历安慰剂镇痛的参与者对疼痛的共情也有所降低，这与前岛叶和扣带中部皮质的活动减少有关，即这些区域之前与疼痛和对疼痛的共情中的共同激活有关。在第二步中，我们采用了一种心理药理学操作（n = 50）来确定这些效应是否可以通过阿片类拮抗剂来阻断。阿片类拮抗剂纳曲酮的给药阻断了安慰剂镇痛，并且还导致了对疼痛共情的相应“正常化”。综上所述，这些发现表明，疼痛共情可能与亲身疼痛时参与的神经反应和神经递质活动有关，因此可能确实基于我们自身的疼痛体验。
