Is there a difference between heat-capsaicin induced low back pain and placebo for neural oscillations and inflammatory blood markers? An experimental randomized crossover study.

IF 2.5 Q2 CLINICAL NEUROLOGY
Frontiers in pain research (Lausanne, Switzerland) Pub Date : 2025-09-11 eCollection Date: 2025-01-01 DOI:10.3389/fpain.2025.1621810
Mona Frey, Allyson Summers, Sarah D Power, Felipe C K Duarte, Diana E De Carvalho
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Abstract

Purpose: Low back pain is difficult to study due to its heterogeneity. Inducing back pain experimentally, with an established model such as heat-capsaicin, would beneficially control for some variability. How heat-capsaicin affects neurophysiological factors relevant to back pain is currently unknown, therefore, this study used a randomized crossover design with the aim to explore the differences between heat-capsaicin and placebo on brain activity and blood markers.

Methods: 18 healthy participants completed two sessions: heat-capsaicin (45°C heat + capsaicin) and placebo (reduced heat + placebo). Pre- and post-pain-induction/placebo, electroencephalogram and blood draws were taken, and perceived pain was rated with a 100 m visual analog scale. Band power was calculated for theta (4-8 Hz), alpha (8-13 Hz), beta (13-30 Hz), gamma1 (30-58 Hz), and gamma2 (62-100 Hz) for six brain regions. An immune assay was run on plasma in duplicate for cytokines IL-1β, IL-6, IL-10, and TNFα. A repeated measures ANCOVA was run for all variables comparing between conditions (heat-capsaicin, placebo) with baseline measures as covariates. A Pearson's correlation was used to determine the relationship between perceived pain ratings and brain wave and blood biomarkers.

Results: The heat-capsaicin model induced transient mild to moderate pain which was significantly higher than placebo (24.50 vs. 0.39; p < 0.001). Brain wave and blood biomarkers were not significantly different between heat-capsaicin and placebo (p ≥ 0.05) or correlated to perceived pain ratings (p ≥ 0.15).

Conclusion: Levels of perceived pain did not relate to neurophysiological changes that may occur immediately after heat-capsaicin exposure. Although changes have been found with other pain models and clinical low back pain, a statistically significant systematic response was not measurable using blood cytokine markers immediately after pain induction and may take longer to develop.

辣椒素引起的腰痛和安慰剂在神经振荡和炎症血液标志物方面有区别吗?一项实验性随机交叉研究。
目的:腰痛因其异质性而难以研究。用辣椒素等已建立的模型实验性地诱导背部疼痛,将有利于控制一些可变性。热辣椒素如何影响与背部疼痛相关的神经生理因素目前尚不清楚,因此,本研究采用随机交叉设计,旨在探讨热辣椒素和安慰剂在脑活动和血液标志物方面的差异。方法:18名健康参与者完成了两个疗程:热辣椒素(45°C热+辣椒素)和安慰剂(减热+安慰剂)。疼痛诱导/安慰剂前后分别进行脑电图和抽血,并以100米视觉模拟量表对感知疼痛进行评分。计算了6个脑区的theta (4-8 Hz)、alpha (8-13 Hz)、beta (13-30 Hz)、gamma1 (30-58 Hz)和gamma2 (62-100 Hz)的波段功率。在血浆中重复进行细胞因子IL-1β、IL-6、IL-10和tnf - α的免疫测定。以基线测量作为协变量,对所有变量(热辣椒素、安慰剂)进行重复测量ANCOVA比较。皮尔逊相关性被用来确定感知疼痛等级与脑电波和血液生物标志物之间的关系。结果:辣椒素模型引起的一过性轻至中度疼痛显著高于安慰剂(24.50 vs. 0.39; p p≥0.05)或与感知疼痛评分相关(p≥0.15)。结论:感知疼痛的水平与热辣椒素暴露后可能立即发生的神经生理变化无关。虽然在其他疼痛模型和临床腰痛中也发现了变化,但在疼痛诱导后,使用血液细胞因子标志物不能立即测量具有统计学意义的系统反应,并且可能需要更长的时间才能发展。
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
CiteScore
2.10
自引率
0.00%
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审稿时长
13 weeks
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