Torta Diana M, De Laurentis Martina, Eichin Katharina Naomi, von Leupoldt Andreas, van den Broeke Emanuel N, Vlaeyen Johan W S
Health Psychology, KU Leuven, Leuven, Belgium.
Institute of Neuroscience, UCLouvain, Brussels, Belgium.
Pain. 2020 Jul;161(7):1459-1469. doi: 10.1097/j.pain.0000000000001841.
Whether, how, and which cognitive factors modulate the development of secondary hypersensitivity/hyperalgesia after central sensitization is not fully understood. Here, we tested, in 3 subsequent experiments, whether being engaged in non-pain-related cognitive demanding tasks: (1) lessens the amount of hypersensitivity developed after an experimental procedure sensitizing nociceptive pathways; and (2) modulates cortical responses to somatosensory stimuli (measured by electroencephalography, EEG). In the first experiment, we validated a novel model in humans using low-frequency stimulation of the skin and demonstrated that it was able to successfully induce hypersensitivity to mechanical pinprick stimuli in the area surrounding the sensitized site. In the second and third experiments, we engaged participants in tasks of increasing difficulty (the Eriksen Flanker Task in experiment 2, and a modified N-back task in experiment 3). We observed that hypersensitivity to mechanical stimuli still developed in experiment 2, that is, the pinprick stimuli applied on the sensitized arm were perceived as more intense after low-frequency stimulation. By contrast, no statistically significant enhancement of mechanical hypersensitivity was observed in experiment 3, indicating that, at the group level, being engaged in a difficult N-back task may interfere with the development of mechanical hypersensitivity. Contrary to previous studies, which have used different methods to induce sensitization, we did not observe any increase in the cortical response to somatosensory stimuli applied on the sensitized arm. We conclude that (1) the development of pinprick hypersensitivity is modulated by the concomitant execution of a difficult N-back task, and (2) the enhancement of cortical responses to somatosensory stimuli is related to the method used to induce central sensitization.
中枢敏化后,认知因素是否、如何以及哪些认知因素调节继发性超敏反应/痛觉过敏的发展尚未完全明确。在此,我们在3个后续实验中测试了参与非疼痛相关的认知要求较高的任务是否:(1)减少在使伤害性通路致敏的实验程序后产生的超敏反应量;以及(2)调节皮质对体感刺激的反应(通过脑电图,EEG测量)。在第一个实验中,我们使用皮肤低频刺激在人体中验证了一种新模型,并证明它能够成功诱导致敏部位周围区域对机械针刺刺激的超敏反应。在第二个和第三个实验中,我们让参与者参与难度逐渐增加的任务(实验2中的埃里克森侧翼任务和实验3中的改良N-back任务)。我们观察到,在实验2中对机械刺激的超敏反应仍然出现,即在低频刺激后,施加在致敏手臂上的针刺刺激被感知为更强烈。相比之下,在实验3中未观察到机械性超敏反应有统计学上的显著增强,这表明,在群体水平上,参与困难的N-back任务可能会干扰机械性超敏反应的发展。与以往使用不同方法诱导致敏的研究相反,我们未观察到对施加在致敏手臂上的体感刺激的皮质反应有任何增加。我们得出结论:(1)针刺超敏反应的发展受到困难的N-back任务同时执行的调节;以及(2)皮质对体感刺激反应的增强与诱导中枢敏化所使用的方法有关。