Brain moderators supporting the relationship between depressive mood and pain
Brain moderators supporting the relationship between depressive mood and pain
复制标题
DOI：
10.1097/j.pain.0000000000001595
复制
发表时间：
2019-09-01
期刊：
影响因子：
7.4
通讯作者：
Zeidan, Fadel
中科院分区：
文献类型：
--
作者：
Adler-Neal, Adrienne L.;Emerson, Nichole M.;Zeidan, Fadel
疼痛和抑郁情绪通常表现出一种共病关系。然而，缓和烦躁情绪和疼痛之间关系的大脑机制仍不清楚。从以前的一项研究中收集了76名健康、无抑郁和无疼痛的个体的功能性磁共振成像、行为和心理物理数据的探索性分析。参与者完成了Beck Depression Inventory-II(BDI)，这是一种衡量负面情绪/抑郁症状的指标，并在基于灌注的动脉自旋标记功能磁共振成像期间提供疼痛强度和疼痛不适评级，以响应有害的高温(49摄氏度)。适度分析被用来确定促进抑郁情绪和疼痛敏感性之间假设关系的神经机制。BDI-II评分越高，疼痛强度(R2=0.1；P=0.006)和疼痛不适(R2=0.12；P=0.003)评分越高。疼痛强度和不愉快等级之间有很高的相关性(r=0.94P<；0.001)；因此，大脑调节分析集中在疼痛强度等级上。抑郁情绪水平较高的个体对实验性疼痛表现出高度的敏感性。支持疼痛评估的区域(腹外侧额叶皮质；前脑岛)和感觉辨别(次级躯体感觉皮质；后脑岛)的激活程度较高，缓和了BDI-II评分较高与疼痛强度等级之间的关系。这项研究表明，执行水平和感觉辨别的大脑机制在促进负面情绪和疼痛之间的双向关系中发挥着多模式的作用。
Pain and depressive mood commonly exhibit a comorbid relationship. Yet, the brain mechanisms that moderate the relationship between dysphoric mood and pain remain unknown. An exploratory analysis of functional magnetic resonance imaging, behavioral, and psychophysical data was collected from a previous study in 76 healthy, nondepressed, and pain-free individuals. Participants completed the Beck Depression Inventory-II (BDI), a measure of negative mood/depressive symptomology, and provided pain intensity and pain unpleasantness ratings in response to noxious heat (49 degrees C) during perfusion-based, arterial spin-labeled functional magnetic resonance imaging. Moderation analyses were conducted to determine neural mechanisms involved in facilitating the hypothesized relationship between depressive mood and pain sensitivity. Higher BDI-II scores were positively associated with pain intensity (R-2 = 0.10; P = 0.006) and pain unpleasantness (R-2 = 0.12; P = 0.003) ratings. There was a high correlation between pain intensity and unpleasantness ratings (r = 0.94; P < 0.001); thus, brain moderation analyses were focused on pain intensity ratings. Individuals with higher levels of depressive mood exhibited heightened sensitivity to experimental pain. Greater activation in regions supporting the evaluation of pain (ventrolateral prefrontal cortex; anterior insula) and sensory-discrimination (secondary somatosensory cortex; posterior insula) moderated the relationship between higher BDI-II scores and pain intensity ratings. This study demonstrates that executive-level and sensory-discriminative brain mechanisms play a multimodal role in facilitating the bidirectional relationship between negative mood and pain.