High spontaneous activity of C-nociceptors in painful polyneuropathy
High spontaneous activity of C-nociceptors in painful polyneuropathy
复制标题
DOI：
10.1016/j.pain.2012.05.017
复制
发表时间：
2012-10-01
期刊：
影响因子：
7.4
通讯作者：
Jorum, Ellen
中科院分区：
文献类型：
--
作者：
Kleggetveit, Inge Petter;Namer, Barbara;Jorum, Ellen
多发性神经病可能与慢性疼痛有关，但也与疼痛敏感性降低有关。我们研究了疼痛和无痛性多发性神经病患者的外周C-伤害感受器，以确定疼痛特异性变化。对11例持续性自发痛的多发性神经病患者和8例无自发痛的多发性神经病患者进行常规临床检查。对于伤害感受器功能的特定检查，通过显微神经摄影术记录来自包括214个C-伤害感受器的单个C-纤维的动作电位。通过C-伤害感受器自发活动和机械致敏的发生来区分有疼痛和无疼痛的患者。疼痛患者C-伤害感受器自发活动或机械致敏的平均百分比显著较高（分别为40.5%和14.6%，P = 0.02）。这种差异主要是由于疼痛患者中有更多自发活动的机械不敏感性C-伤害感受器（操作上由其机械不敏感性和轴突特征定义）（56例中的19例vs 43例中的6例; P = 0.02）。致敏的机械不敏感的C-伤害感受器的百分比与自发活性的机械不敏感的C-伤害感受器的百分比相关（Kendall τ = .55，P = .004）。此外，机械不敏感的C-伤害感受器的自发活动与不太明显的活动依赖性传导减慢相关（Kendall τ =-0.48，P = 0.009），表明轴突包括在敏化过程中。与无疼痛的多发性神经病患者相比，患有多发性神经病和疼痛的患者中机械不敏感性C伤害性感受器的超兴奋性显着更高，而机械敏感性（多模态）C伤害性感受器的差异则不太明显。这种过度兴奋可能是疼痛性周围神经病变患者疼痛的主要潜在机制。(C)2012年国际疼痛研究协会。由Elsevier B. V.出版，版权所有。
Polyneuropathy can be linked to chronic pain but also to reduced pain sensitivity. We investigated peripheral C-nociceptors in painful and painless polyneuropathy patients to identify pain-specific changes. Eleven polyneuropathy patients with persistent spontaneous pain and 8 polyneuropathy patients without spontaneous pain were investigated by routine clinical methods. For a specific examination of nociceptor function, action potentials from single C-fibres including 214 C-nociceptors were recorded by microneurography. Patients with and without pain were distinguished by the occurrence of spontaneous activity and mechanical sensitization in C-nociceptors. The mean percentage of C-nociceptors being spontaneously active or mechanically sensitized was significantly higher in patients with pain (mean 40.5% and 14.6%, respectively, P = .02). The difference was mainly due to more spontaneously active mechanoinsensitive C-nociceptors (operationally defined by their mechanical insensitivity and their axonal characteristics) in the pain patients (19 of 56 vs 6 of 43; P = .02). The percentage of sensitized mechanoinsensitive C-nociceptors correlated to the percentage of spontaneously active mechanoinsensitive C-nociceptors (Kendall's tau = .55, P = .004). Moreover, spontaneous activity of mechanoinsensitive C-nociceptors correlated to less pronounced activity-dependent slowing of conduction (Kendall's tau = -.48, P = .009), suggesting that axons were included in the sensitization process. Hyperexcitability in mechanoinsensitive C-nociceptors was significantly higher in patients with polyneuropathy and pain compared to patients with polyneuropathy without pain, while the difference was much less prominent in mechanosensitive (polymodal) C-nociceptors. This hyperexcitability may be a major underlying mechanism for the pain experienced by patients with painful peripheral neuropathy. (C) 2012 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.