Drummond Peter D, Vo Lechi, Carabetta Matthew
School of Psychology and Centre for Healthy Ageing, College of Health and Education, Murdoch University, 90 South Street, Murdoch, Western Australia 6150, Australia.
Pain Res Manag. 2025 Jul 16;2025:6601529. doi: 10.1155/prm/6601529. eCollection 2025.
Exposing the skin to high levels of ultraviolet B (UVB) radiation induces an inflammatory response that upregulates local nociceptive processing; this, in turn, facilitates protective responses to limit further injury. In this study, the UVB model was used to explore additional effects of inflammation on supraspinal nociceptive processing. Thirty-one healthy participants attended two sessions approximately 24 h apart. In each session, pressure-pain thresholds and sensitivity to sharp stimulation and heat were assessed in both forearms, and pressure-pain thresholds and sensitivity to sharp stimulation were assessed on each side of the forehead. In a novel paradigm, supraspinal nociceptive processing was explored by assessing pain and blink reflexes to electrical stimulation of the forehead, paired with acoustic startle stimuli. At the end of the first session, UVB radiation at a dose sufficient to induce erythema at the most exposed site was administered to one forearm. Consistent with local sensitization, sensitivity to heat and sharp stimulation had increased at the maximally exposed site 24 h later. This local response was accompanied by changes in supraspinal nociceptive processing-pressure-pain thresholds were lower on the ipsilateral than contralateral side of the forehead, and acoustic startle stimuli augmented electrically evoked pain. Blink reflexes weakened from the first to the second session, but decreases were smaller on the UVB-treated than contralateral side. Together, these findings suggest that acoustic startle stimuli facilitated activity in sensitized supraspinal nociceptive pathways. Potentially, this supraspinal mechanism adds to the burden of chronic nociplastic pain during states of heightened arousal and stress.
将皮肤暴露于高水平的紫外线B(UVB)辐射会引发炎症反应,从而上调局部伤害性处理过程;反过来,这又有助于产生保护性反应以限制进一步的损伤。在本研究中,采用UVB模型来探究炎症对脊髓上伤害性处理的额外影响。31名健康参与者参加了两场相隔约24小时的实验。在每场实验中,对双侧前臂评估压力痛阈值以及对锐刺激和热刺激的敏感性,并对额头两侧评估压力痛阈值和对锐刺激的敏感性。在一个新的范式中,通过评估对额头电刺激的疼痛和眨眼反射,并结合听觉惊吓刺激,来探究脊髓上伤害性处理过程。在第一场实验结束时,对一侧前臂给予足以在最暴露部位诱发红斑的剂量的UVB辐射。与局部敏化一致,24小时后在最大暴露部位对热刺激和锐刺激的敏感性增加。这种局部反应伴随着脊髓上伤害性处理的变化——额头同侧的压力痛阈值低于对侧,并且听觉惊吓刺激增强了电诱发的疼痛。眨眼反射从第一场实验到第二场实验减弱,但UVB处理侧的减弱程度小于对侧。这些发现共同表明,听觉惊吓刺激促进了致敏的脊髓上伤害性通路的活动。这种脊髓上的机制可能会在觉醒和压力增加的状态下加重慢性伤害感受性疼痛的负担。