Center for Neuroplasticity and Pain (CNAP), Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Aalborg, Denmark.
Institute of Neuroscience (IONS), Université catholique de Louvain, Brussels, Belgium.
Eur J Pain. 2023 Sep;27(8):995-1005. doi: 10.1002/ejp.2141. Epub 2023 May 31.
Alterations in the default mode network (DMN) connectivity across pain stages suggest a possible DMN involvement in the transition to persistent pain.
This study examined whether pain-free DMN connectivity at lower alpha oscillations (8-10 Hz) accounts for a unique variation in experimental peak pain intensity beyond the contribution of factors known to influence pain intensity.
Pain-free DMN connectivity was measured with electroencephalography prior to 1 h of capsaicin-evoked pain using a topical capsaicin patch on the right forearm. Pain intensity was assessed on a (0-10) numerical rating scale and the association between peak pain intensity and baseline measurements was examined using hierarchical multiple regression in 52 healthy volunteers (26 women). The baseline measurements consisted of catastrophizing (helplessness, rumination, magnification), vigilance, depression, negative and positive affect, sex, age, sleep, fatigue, thermal and mechanical pain thresholds and DMN connectivity (medial prefrontal cortex [mPFC]-posterior cingulate cortex [PCC], mPFC-right angular gyrus [rAG], mPFC-left Angular gyrus [lAG], rAG-mPFC and rAG-PCC).
Pain-free DMN connectivity increased the explained variance in peak pain intensity beyond the contribution of other factors (ΔR = 0.10, p = 0.003), with the final model explaining 66% of the variation (R = 0.66, ANOVA: p < 0.001). In this model, negative affect (β = 0.51, p < 0.001), helplessness (β = 0.49, p = 0.007), pain-free mPFC-lAG connectivity (β = 0.36, p = 0.003) and depression (β = -0.39, p = 0.009) correlated significantly with peak pain intensity. Interestingly, negative affect and depression, albeit both being negative mood indices, showed opposing relationships with peak pain intensity.
This work suggests that pain-free mPFC-lAG connectivity (at lower alpha) may contribute to individual variations in pain-related vulnerability.
These findings could potentially lead the way for investigations in which DMN connectivity is used in identifying individuals more likely to develop chronic pain.
在疼痛阶段，默认模式网络（DMN）连接的改变表明 DMN 可能参与到向持续性疼痛的转变。
本研究旨在探讨在已知影响疼痛强度的因素之外，无疼痛的 DMN 在较低的阿尔法振荡（8-10Hz）下的连接是否能解释实验性峰值疼痛强度的独特变化。
在右前臂使用辣椒素贴片诱发疼痛的 1 小时前，使用脑电图测量无疼痛的 DMN 连接。使用（0-10）数字评分量表评估疼痛强度，并在 52 名健康志愿者（26 名女性）中使用分层多元回归分析峰值疼痛强度与基线测量之间的关系。基线测量包括灾难化（无助、反刍、夸大）、警觉、抑郁、消极和积极情绪、性别、年龄、睡眠、疲劳、热觉和机械觉阈值以及 DMN 连接（内侧前额叶皮质 [mPFC]-后扣带回皮质 [PCC]、mPFC-右侧角回 [rAG]、mPFC-左侧角回 [lAG]、rAG-mPFC 和 rAG-PCC）。
无疼痛的 DMN 连接增加了峰值疼痛强度的可解释方差，超出了其他因素的贡献（ΔR=0.10，p=0.003），最终模型解释了 66%的变异（R=0.66，ANOVA：p<0.001）。在该模型中，消极情绪（β=0.51，p<0.001）、无助感（β=0.49，p=0.007）、无疼痛的 mPFC-lAG 连接（β=0.36，p=0.003）和抑郁（β=-0.39，p=0.009）与峰值疼痛强度显著相关。有趣的是，消极情绪和抑郁，尽管都是负性情绪指标，但与峰值疼痛强度呈相反的关系。
本研究表明，无疼痛的 mPFC-lAG 连接（在较低的阿尔法波）可能有助于个体对疼痛相关易感性的差异。
这些发现可能为使用 DMN 连接来识别更有可能发展为慢性疼痛的个体的研究开辟道路。
