Wang Dan, Zhang Xiaohan, Ye Shuqi, Realyvasquez Patrick, Finan Patrick, Quigg Mark, Moosa Shayan, Elias W Jeffrey, Liu Chang-Chia
Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Department of Anesthesiology, University of Virginia School of Medicine, Charlottesville, Virginia, USA.
Eur J Pain. 2025 Oct;29(9):e70117. doi: 10.1002/ejp.70117.
Pain catastrophising is a maladaptive cognitive-emotional trait linked to greater pain severity and poorer outcomes, yet its neurophysiological correlates remain unclear.
We tested whether pain catastrophising amplifies cortical responses to nociceptive input, independent of subjective pain intensity.
Fifty-two healthy adults underwent EEG during painful laser stimulation (n = 29; mean age 24.3 ± 10.9 years; 55.2% female) or non-painful electrical stimulation (n = 23; mean age 23.3 ± 8.5 years; 56.5% female). Each trial comprised a triplet of stimuli (S1, S2, S3) with a 1.5-s interstimulus interval; 30 triplets were delivered per modality. Associations between Pain Catastrophising Scale (PCS) scores and amplitudes of laser-evoked potentials (LEP-N2P2) and somatosensory-evoked potentials (SEP-N1P2) were tested using mixed-effects models, with trial-level pain ratings as a covariate.
Higher PCS scores were associated with greater LEP-N2P2 amplitude for the first stimulus (S1) in the painful condition, independent of pain ratings, at the parietal midline electrode (Pz). No associations were observed between PCS and SEP-N1P2 in the non-painful condition, or between PCS and early N1 components of LEP or SEP.
Pain catastrophising selectively amplifies later-stage cortical responses to painful stimuli, strongest at first presentation (S1) and localised to parietal Pz channel, with no effects in non-painful controls stimulation modality. These findings support LEPs as mechanistic biomarkers of catastrophising-related vulnerability. Combined with psychological assessment, such markers could improve early screening, risk stratification, and personalised interventions targeting maladaptive salience and attentional processes in pain.
Pain catastrophising was associated with amplified laser-evoked potential (LEP-N2P2) responses during painful, but not non-painful, stimulation in healthy adults. The effect was localised to the parietal midline, strongest for the first stimulus in a sequence, and diminished with repetition. These findings suggest modality-dependent cortical modulation and highlight LEP-N2P2 as a potential neural marker of maladaptive pain processing.
疼痛灾难化是一种适应不良的认知-情绪特质，与更高的疼痛严重程度和更差的预后相关，但其神经生理相关性仍不清楚。
我们测试了疼痛灾难化是否会增强皮层对伤害性输入的反应，而与主观疼痛强度无关。
52名健康成年人在接受疼痛性激光刺激（n = 29；平均年龄24.3±10.9岁；55.2%为女性）或非疼痛性电刺激（n = 23；平均年龄23.3±8.5岁；56.5%为女性）时进行脑电图检查。每次试验包括一组三联刺激（S1、S2、S3），刺激间隔为1.5秒；每种刺激方式发放30组三联刺激。使用混合效应模型测试疼痛灾难化量表（PCS）评分与激光诱发电位（LEP-N2P2）和体感诱发电位（SEP-N1P2）振幅之间的关联，并将试验水平的疼痛评分作为协变量。
在疼痛状态下，较高的PCS评分与顶叶中线电极（Pz）处第一个刺激（S1）的LEP-N2P2振幅增大相关，与疼痛评分无关。在非疼痛状态下，未观察到PCS与SEP-N1P2之间的关联，也未观察到PCS与LEP或SEP的早期N1成分之间的关联。
疼痛灾难化选择性地增强了皮层对疼痛刺激的后期反应，在首次呈现（S1）时最强，且定位于顶叶Pz通道，在非疼痛对照刺激方式中无影响。这些发现支持将LEP作为与灾难化相关易感性的机制性生物标志物。结合心理评估，此类标志物可改善针对疼痛中适应不良的显著性和注意力过程的早期筛查、风险分层及个性化干预。
在健康成年人中，疼痛灾难化与疼痛刺激而非非疼痛刺激期间激光诱发电位（LEP-N2P2）反应增强相关。该效应定位于顶叶中线，对序列中的第一个刺激最强，且随重复而减弱。这些发现提示了刺激方式依赖的皮层调制，并突出了LEP-N2P2作为适应不良疼痛处理的潜在神经标志物。
