Institute Guttmann, Neurorehabilitation Hospital, Camí Can Ruti s/n, Badalona, 08916, Barcelona, Spain.
Department of Psychological and Brain Sciences, Texas A&M University, College Station, TX, 77843, USA.
Exp Brain Res. 2019 Jul;237(7):1735-1744. doi: 10.1007/s00221-019-05545-8. Epub 2019 Apr 27.
Pain is a complex experience involving both nociceptive and affective-cognitive mechanisms. The present study evaluated whether modulation of pain perception, employing a conditioned pain modulation (CPM) paradigm, is paralleled by changes in contact heat-evoked potentials (CHEPs), a brain response to nociceptive stimuli.
Participants were 25 healthy, pain-free, college students (12 males, 13 females, mean age 19.24 ± 0.97 years). Twenty computer-controlled heat stimuli were delivered to the non-dominant forearm and CHEPs were recorded at Cz using a 32-channel EEG system. After each stimulus, participants rated the intensity of the heat pain using the 0-100 numerical rating scale. The latency and amplitude of N2, P2 components as well as single-sweep spectral analysis of individual CHEPs were measured offline. For CPM, participants had to submerge their dominant foot into a neutral (32 °C) or noxious (0 °C) water bath. CHEPs and heat pain ratings were recorded in 3 different conditions: without CPM, after neutral CPM (32 °C) and after noxious CPM (0 °C).
The noxious CPM induced a facilitatory pain response (p = 0.001) with an increase in heat pain following noxious CPM compared to neutral CPM (p = 0.001) and no CPM (p = 0.001). Changes in CHEPs did not differ between conditions when measured as N2-P2 peak-to-peak amplitude (p = 0.33) but the CPM significantly suppressed the CHEPs-related delta power (p = 0.03). Changes in heat pain in the noxious CPM were predicted by trait catastrophizing variables (p = 0.04).
The current study revealed that pain facilitatory CPM is related to suppression of CHEPs delta power which could be related to dissociation between brain responses to noxious heat and pain perception.
疼痛是一种复杂的体验,涉及伤害性和情感认知机制。本研究评估了使用条件性疼痛调制(CPM)范式调节疼痛感知是否与接触热诱发电位(CHEPs)的变化相关,后者是对伤害性刺激的大脑反应。
参与者为 25 名健康、无痛、大学生(12 名男性,13 名女性,平均年龄 19.24±0.97 岁)。使用 32 通道 EEG 系统在非优势前臂上施加 20 个计算机控制的热刺激,并在 Cz 记录 CHEPs。在每次刺激后,参与者使用 0-100 数字评分量表对热痛强度进行评分。离线测量 N2、P2 成分的潜伏期和振幅以及个体 CHEPs 的单次扫描谱分析。对于 CPM,参与者必须将其优势脚浸入中性(32°C)或有害(0°C)水浴中。在 3 种不同条件下记录 CHEPs 和热痛评分:无 CPM、中性 CPM(32°C)后和有害 CPM(0°C)后。
有害 CPM 诱导了促痛反应(p=0.001),与中性 CPM(p=0.001)和无 CPM(p=0.001)相比,有害 CPM 后热痛增加。当以 N2-P2 峰峰值幅度测量时,CHEPS 变化在条件之间没有差异(p=0.33),但 CPM 显著抑制了 CHEPs 相关的 delta 功率(p=0.03)。有害 CPM 中的热痛变化可由特质灾难化变量预测(p=0.04)。
本研究表明,疼痛促通 CPM 与 CHEPs delta 功率的抑制有关,这可能与伤害性热刺激和疼痛感知之间的大脑反应分离有关。