Nissen Thomas Dahl, Mørch Carsten Dahl, Arendt-Nielsen Lars, Drewes Asbjørn Mohr, Olesen Anne Estrup
Mech-Sense, Department of Gastroenterology and Hepatology, Aalborg University Hospital, Aalborg, Denmark.
Center for Sensory-Motor Interaction (SMI), Department of Health Science and Technology, School of Medicine, Aalborg University, Aalborg, Denmark.
Scand J Pain. 2018 Oct 25;18(4):695-701. doi: 10.1515/sjpain-2018-0082.
Background and aims Offset analgesia (OA) is a pain modulating mechanism described as a disproportionately large decrease in pain intensity evoked by a minor decrease in stimulus intensity. Precise mechanisms of OA are still not elucidated and studies are needed to evaluate factors modulating OA. The aim of this study was to investigate OA before and during tonic cold pain (thought to induce descending inhibition), in a group of healthy volunteers. Methods A randomized, crossover study was performed in 17 healthy participants (8 males and 9 females). The OA paradigm lasted 35 s and was induced by the traditional method using thermal stimulation applied to the forearm. A constant control heat stimulus (CTL) paradigm was used as control to assess adaptation. Pain intensity was assessed continuously. For induction of tonic cold pain, the participants immersed their hand into 2°C water for 2 min. After 1 min and 25 s, the heat stimulation (OA or CTL paradigm) was repeated to assess the modulatory effect of the cold pressor test. Results It was possible to induce OA both before and during the cold pressor test. Tonic cold pain modulated the peak pain reported during both the OA (p=0.015) and CTL paradigms (p=0.001) reflecting endogenous pain modulation. However, the magnitude of OA was not modulated by tonic cold pain (p>0.05). Conclusions The offset analgesia magnitude was not modulated by simultaneously tonic cold pain, thought to reflect another endogenous pain modulation mechanism. Implications Neither offset analgesia magnitude nor adaptation were modulated by cold pressor induced endogenous analgesia. This could be explained by the fact, that offset analgesia was already at maximum in healthy participants. Hence, offset analgesia may not be a suitable assessment tool to investigate modulation induced by experimental methods or pharmacology in healthy participants.
背景与目的
抵消性镇痛（OA）是一种疼痛调节机制，其描述为刺激强度的微小降低会引起疼痛强度不成比例的大幅下降。OA的确切机制仍未阐明，需要开展研究以评估调节OA的因素。本研究的目的是在一组健康志愿者中，调查紧张性冷痛（被认为可诱发下行抑制）之前及期间的OA情况。
方法
对17名健康参与者（8名男性和9名女性）进行了一项随机交叉研究。OA范式持续35秒，采用传统方法通过对前臂施加热刺激来诱发。使用恒定的对照热刺激（CTL）范式作为对照来评估适应性。持续评估疼痛强度。为诱发紧张性冷痛，参与者将手浸入2°C的水中2分钟。在1分25秒后，重复热刺激（OA或CTL范式）以评估冷加压试验的调节作用。
结果
在冷加压试验之前和期间均有可能诱发OA。紧张性冷痛调节了OA（p = 0.015）和CTL范式（p = 0.001）期间报告的峰值疼痛，反映了内源性疼痛调节。然而，OA的幅度未受紧张性冷痛调节（p>0.05）。
结论
抵消性镇痛幅度未受同时存在的紧张性冷痛调节，紧张性冷痛被认为反映了另一种内源性疼痛调节机制。
启示
冷加压诱导的内源性镇痛既未调节抵消性镇痛幅度，也未调节适应性。这可能是因为抵消性镇痛在健康参与者中已达到最大值。因此，抵消性镇痛可能不是研究健康参与者中实验方法或药理学诱导调节的合适评估工具。
