探索一个完善的妇女条件疼痛调节范式的价值:盆腔疼痛(TRiPP)研究的转化研究。

IF 2.5 Q2 CLINICAL NEUROLOGY
Frontiers in pain research (Lausanne, Switzerland) Pub Date : 2025-03-12 eCollection Date: 2025-01-01 DOI:10.3389/fpain.2025.1439563
Lysia Demetriou, Danielle Perro, Lydia Coxon, Michal Krassowski, Claire E Lunde, Joana Ferreira-Gomes, Ana Charrua, Pedro Abreu-Mendes, Lars Arendt-Nielsen, Qasim Aziz, Judy Birch, Kurtis Garbutt, Andrew Horne, Anja Hoffman, Lone Hummelshoj, Jane Meijlink, Maik Obendorf, Esther Pogatzki-Zahn, Naoko Sasamoto, Kathryn Terry, Rolf-Detlef Treede, Allison Vitonis, Jan Vollert, Nilufer Rahmioglu, Christian M Becker, Francisco Cruz, Stacey A Missmer, Krina Zondervan, Christine B Sieberg, Jens Nagel, Katy Vincent
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引用次数: 0

摘要

背景:条件疼痛调节(CPM)被认为是人类下行抑制性疼痛通路的代理。然而,文献中描述的CPM反应存在很大差异,关于其效用的争论正在进行中。方法:我们对慢性盆腔疼痛(CPP)患者(n = 59)和非慢性盆腔疼痛患者(n = 26)的CPM进行了研究,旨在确定CPM反应的影响程度和影响变异性的因素。结果:使用压力疼痛阈值测试刺激和缺血压力袖带调节刺激(CS),我们发现CPP和对照组之间的平均CPM效应无显著差异。采用稳健统计方法(+/-2测量标准误差)进一步调查CPM,对照组和CPP参与者表现出抑制的比例无显著差异(X2 = 0.003, p = 0.96)。值得注意的是,只有23.1%的健康对照显示出“真正的”CPM效应(n = 4抑制,n = 2促进)。尽管有丰富的数据集,但我们无法确定任何单一的问卷,临床或心理物理协变量与CPM效应相关。结论:尽管使用了推荐的CPM范式之一,我们只能在23.1%的对照参与者中证明“真实”的CPM。因此,有和没有慢性盆腔疼痛的女性之间没有差异必须谨慎解释。未来使用不同CPM范式或更大样本量的研究可能会发现不同的结果。尽管慢性疼痛人群的CPM具有重要的理论机制意义,但缺乏既定的评估标准导致我们质疑其在当前临床研究中的附加价值。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exploring the value of a well-established conditioned pain modulation paradigm in women: a Translational Research in Pelvic Pain (TRiPP) study.

Background: Conditioned pain modulation (CPM) is considered a human proxy for descending inhibitory pain pathways. However, there is wide variation in the CPM response described in the literature and ongoing debate about its utility.

Methods: Here we explored CPM in women with (n = 59) and without (n = 26) chronic pelvic pain (CPP), aiming to determine the magnitude of effect and factors influencing variability in the CPM response.

Results: Using a pressure pain threshold test stimulus and ischaemic pressure cuff conditioning stimulus (CS), we found no significant difference in the mean CPM effect between CPP and control participants. Using a robust statistical method (+/-2 standard error of measurement) to further investigate CPM, there was no significant difference in the proportion exhibiting inhibition between controls and CPP participants (X2  = 0.003, p = 0.96). Notably, only 23.1% of our healthy controls demonstrated a "true" CPM effect (n = 4 inhibitory, n = 2 facilitatory). Despite a rich data set, we were unable to identify any single questionnaire, clinical or psychophysical covariate correlating with the CPM effect.

Conclusions: Despite using one of the recommended CPM paradigms we were only able to demonstrate "true" CPM in 23.1% of control participants. Thus, the absence of differences between women with and without chronic pelvic pain must be interpreted with caution. Future studies using different CPM paradigms or larger sample sizes may find different results. Although CPM in chronic pain populations is of major theoretical mechanistic interest, the lack of an established assessment standard led us to question its added value in current clinical research.

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CiteScore
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