Pain Catastrophising Amplifies Parietal Responses to Painful Laser Stimulation in Healthy Controls

IF 3.4 2区医学 Q1 ANESTHESIOLOGY

European Journal of Pain Pub Date : 2025-09-05 DOI:10.1002/ejp.70117

Dan Wang, Xiaohan Zhang, Shuqi Ye, Patrick Realyvasquez, Patrick Finan, Mark Quigg, Shayan Moosa, W. Jeffrey Elias, Chang-Chia Liu

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引用次数: 0

Abstract

Background

Pain catastrophising is a maladaptive cognitive–emotional trait linked to greater pain severity and poorer outcomes, yet its neurophysiological correlates remain unclear.

Objectives

We tested whether pain catastrophising amplifies cortical responses to nociceptive input, independent of subjective pain intensity.

Methods

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.

Results

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.

Conclusions

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.

Significance Statement

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.

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疼痛灾变放大健康对照对疼痛激光刺激的顶叶反应

疼痛灾难化是一种不适应的认知情绪特征，与更严重的疼痛和更差的结果有关，但其神经生理学相关性尚不清楚。目的：我们测试疼痛灾难化是否会放大皮层对伤害性输入的反应，而不受主观疼痛强度的影响。方法52例健康成人在疼痛性激光刺激（n = 29，平均年龄24.3±10.9岁，女性占55.2%）或非疼痛性电刺激（n = 23，平均年龄23.3±8.5岁，女性占56.5%）下行脑电图检查。每个试验包括三组刺激（S1、S2、S3），刺激间隔为1.5 s；每种模式接生30个三胞胎。疼痛灾难量表（PCS）评分与激光诱发电位（LEP-N2P2）和躯体感觉诱发电位（SEP-N1P2）振幅之间的关联使用混合效应模型进行了测试，试验水平的疼痛评分作为协变量。结果疼痛状态下，第一次刺激（S1）的PCS评分越高，顶叶中线电极（Pz）的LEP-N2P2振幅越大，与疼痛评分无关。在非疼痛状态下，PCS和SEP- n1p2之间没有关联，在LEP或SEP的早期N1组分之间也没有关联。结论疼痛突变选择性地放大了后期皮层对疼痛刺激的反应，在首次呈现（S1）时最强，并局限于顶叶Pz通道，而在非疼痛对照刺激模式下没有影响。这些发现支持LEPs作为巨灾相关脆弱性的机制生物标志物。结合心理评估，这些标记可以改善早期筛查，风险分层，针对疼痛的适应不良突出和注意力过程的个性化干预。在健康成人中，疼痛灾变与疼痛而非非疼痛刺激时激光诱发电位（LEP-N2P2）反应的放大有关。这种影响只局限于顶叶中线，在连续的第一次刺激时最强烈，随着重复而减弱。这些发现提示了模式依赖的皮质调节，并强调了LEP-N2P2是不适应疼痛处理的潜在神经标志物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

European Journal of Pain 医学-临床神经学

CiteScore

7.50

自引率

5.60%

发文量

163

审稿时长

4-8 weeks

期刊介绍： European Journal of Pain (EJP) publishes clinical and basic science research papers relevant to all aspects of pain and its management, including specialties such as anaesthesia, dentistry, neurology and neurosurgery, orthopaedics, palliative care, pharmacology, physiology, psychiatry, psychology and rehabilitation; socio-economic aspects of pain are also covered. Regular sections in the journal are as follows: • Editorials and Commentaries • Position Papers and Guidelines • Reviews • Original Articles • Letters • Bookshelf The journal particularly welcomes clinical trials, which are published on an occasional basis. Research articles are published under the following subject headings: • Neurobiology • Neurology • Experimental Pharmacology • Clinical Pharmacology • Psychology • Behavioural Therapy • Epidemiology • Cancer Pain • Acute Pain • Clinical Trials.