Department of Neurology, University of Erlangen-Nuremberg, Germany Institute of Physiology and Experimental Pathophysiology, University of Erlangen-Nuremberg, Germany Department of Gynecology and Obstetrics, University of Erlangen-Nuremberg, Germany Department of Medicine, Division of Hematology and Oncology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA, USA.
Pain. 2011 Jun;152(6):1298-1303. doi: 10.1016/j.pain.2011.02.005. Epub 2011 Mar 4.
Sensory gain (i.e., hyperalgesia) and sensory loss (ie, hypoalgesia) are key features of neuropathic pain syndromes. Previously, we showed that conditioning electrical stimuli may provoke either sensory gain or decline in healthy subjects, depending on the stimulation frequencies applied. In the present study we sought to determine whether sensory decline induced by 20-Hz electrical stimulation preferentially of peptidergic C-nociceptors induces antihyperalgesic effects in a transdermal electrical pain model. Twelve healthy volunteers underwent 0.5-Hz noxious electrical stimulation of the right volar forearm for 35minutes, leading to secondary mechanical hyperalgesia. In 5 sessions the 0.5-Hz stimulus was applied either alone (Stim1) or with concurrent noxious 20-Hz stimulation at different sites (Stim2: ipsilateral 5 cm distance; Stim3: ipsilateral 10 cm distance; Stim4: contralateral arm; Stim5: contralateral dorsal foot). Close concurrent 20-Hz stimulation (Stim2) inhibited the development of hyperalgesia, as measured using the mechanical pain threshold, while remote and contralateral 20-Hz stimulation had no impact on mechanical pain threshold. However, after ipsilateral (stim2, stim3) and contralateral (stim4) forearm stimulation the area of hyperalgesia around the 0.5-Hz stimulation site was significantly reduced. Thus, antihyperalgesia was induced in a homotopic and in a heterotopic ipsisegmental manner. Underlying mechanisms may include neuroplastic changes of pro- and antinociceptive systems at the spinal or supraspinal level. We conclude that 20-Hz noxious electrical stimulation may represent a neurostimulatory paradigm with antihyperalgesic properties. These findings may thus be of relevance for the future therapy of neuropathic pain syndromes as well. Sensory decline induced by 20-Hz electrical stimulation of peptidergic C-nociceptors induces antihyperalgesic effects in a transdermal electrical pain model.
感觉增益（即痛觉过敏）和感觉损失（即痛觉减退）是神经病理性疼痛综合征的主要特征。此前，我们已经表明，根据施加的刺激频率，条件性电刺激可能会引起健康受试者的感觉增益或感觉减退。在本研究中，我们试图确定优先刺激肽能 C 伤害感受器的 20Hz 电刺激引起的感觉减退是否会在经皮电痛模型中引起抗痛觉过敏作用。12 名健康志愿者接受右侧掌屈前臂的 0.5Hz 伤害性电刺激 35 分钟，导致继发性机械性痛觉过敏。在 5 个疗程中，0.5Hz 刺激单独应用（Stim1）或同时在不同部位施加伤害性 20Hz 刺激（Stim2：同侧 5cm 距离；Stim3：同侧 10cm 距离；Stim4：对侧手臂；Stim5：对侧脚背）。密切同时的 20Hz 刺激（Stim2）抑制了机械痛阈的痛觉过敏发展，而远程和对侧的 20Hz 刺激对机械痛阈没有影响。然而，同侧（Stim2、Stim3）和对侧（Stim4）前臂刺激后，0.5Hz 刺激部位周围的痛觉过敏面积明显减小。因此，在同部位和异部位同侧段诱导了抗痛觉过敏。潜在的机制可能包括脊髓或脊髓上水平的促伤害和抗伤害系统的神经可塑性变化。我们得出结论，20Hz 伤害性电刺激可能代表一种具有抗痛觉过敏特性的神经刺激范式。这些发现可能对未来神经病理性疼痛综合征的治疗也具有重要意义。肽能 C 伤害感受器的 20Hz 电刺激引起的感觉减退在经皮电痛模型中诱导抗痛觉过敏作用。
