SMI®, Department of Health Science and Technology, Faculty of Medicine, Aalborg University, Denmark.
Eur J Pain. 2018 Oct;22(9):1678-1684. doi: 10.1002/ejp.1250. Epub 2018 Jun 14.
Offset analgesia (OA) is a disproportionally large decrease in the pain perception in response to a small decrease in the stimulation intensity. Traditionally, heat stimulation has been used to evoke OA. The aim of this study was to investigate whether OA could be evoked by electrical stimulation.
Healthy volunteers (N = 24) underwent two OA-experimental sessions consisting of heat stimuli intensities of 48-49-48 °C (traditional OA-paradigm) and electrical stimuli at 150%-180%-150% of the electrical pain perception (EPP) threshold. The three stimuli were delivered for 5 s (STIM1), 5 s (STIM2) and 20 s (STIM3), respectively. The sessions were randomized to the dominant or nondominant volar forearm. Two control sessions were performed with 30 s constantly heat (48 °C) and electrical stimuli (150% of the EPP) (CONTROL-STIM). In all sessions, the pain intensities were constantly rated on a Visual Analog Scale (VAS, 0-10).
Significantly reduced STIM3 VAS ratings as compared to the CONTROL-STIM were reported for heat (1.81 ± 0.54; p < 0.001) and electrical (2.12 ± 0.42; p < 0.001) stimuli. The degrees of OA produced by heat and electrical stimuli were similar. A significantly positive correlation was found between thermal and electrical OA-effects (r = 0.48, p < 0.02).
These findings demonstrate that electrical stimulation can elicit significant OA in humans indicating that the peripheral receptors can be bypassed and still evoke OA. Application of the electrical OA model may be of interest for further basic and clinical investigations as a potential new biomarker for central pain inhibition and provide the option to back-translate the technology to animals to understand the underlying neurobiology.
Electrical stimulation can elicit offset analgesia in humans, indicating that this perceptual modification can be obtained even bypassing peripheral receptors.
偏移镇痛（OA）是指对刺激强度的微小降低，产生不成比例的疼痛感知降低。传统上，热刺激已被用于引发 OA。本研究旨在探讨电刺激是否能引发 OA。
健康志愿者（N=24）接受了两个 OA 实验，包括 48-49-48°C 的热刺激强度（传统 OA 范式）和 150%-180%-150%的电痛感知（EPP）阈值的电刺激。三种刺激分别持续 5 秒（STIM1）、5 秒（STIM2）和 20 秒（STIM3）。这些会话是随机分配到优势或非优势掌侧前臂。还进行了两个对照会话，使用 30 秒恒定的热（48°C）和电刺激（EPP 的 150%）（CONTROL-STIM）。在所有会话中，疼痛强度都在视觉模拟量表（VAS，0-10）上进行了恒定评分。
与 CONTROL-STIM 相比，热（1.81±0.54；p<0.001）和电（2.12±0.42；p<0.001）刺激的 STIM3 VAS 评分显著降低。热刺激和电刺激引起的 OA 程度相似。发现热和电 OA 效应之间存在显著的正相关（r=0.48，p<0.02）。
这些发现表明，电刺激可以在人类中引起显著的 OA，表明可以绕过外周受体并仍然引发 OA。电 OA 模型的应用可能对进一步的基础和临床研究具有重要意义，作为中枢抑制疼痛的潜在新生物标志物，并提供将技术反向转化为动物以了解潜在神经生物学的选择。
电刺激可以在人类中引发偏移镇痛，表明即使绕过外周受体，也可以获得这种感知改变。
