Section of Clinical Neurophysiology, Department of Neurology, Oslo University Hospital, Rikshospitalet, Oslo, Norway Department of Physiology and Experimental Pathophysiology, University of Erlangen/Nürnberg, Erlangen, Germany Department of Clinical Neurophysiology, University Hospital, Uppsala, Sweden Department of Anesthesiology and Operative Intensive Care, Mannheim, Heidelberg University, Germany.
Pain. 2012 Oct;153(10):2040-2047. doi: 10.1016/j.pain.2012.05.017.
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.
多发性神经病可与慢性疼痛相关，也可与疼痛敏感性降低相关。我们研究了有疼痛和无痛多发性神经病患者的周围 C 伤害感受器，以确定疼痛特异性变化。通过常规临床方法研究了 11 例持续性自发性疼痛的多发性神经病患者和 8 例无自发性疼痛的多发性神经病患者。为了专门检查伤害感受器功能，通过微神经记录法记录了包括 214 个 C 伤害感受器在内的单个 C 纤维的动作电位。通过 C 伤害感受器自发性活动和机械敏感性来区分有痛和无痛患者。有疼痛的患者中自发活动或机械敏感性的 C 伤害感受器的平均百分比明显更高（分别为 40.5%和 14.6%，P=.02）。差异主要是由于疼痛患者中有更多自发性活动的机械不敏感 C 伤害感受器（通过其机械不敏感性和轴突特征来操作定义）（56 个中有 19 个，43 个中有 6 个；P=.02）。致敏的机械不敏感 C 伤害感受器的百分比与自发性活动的机械不敏感 C 伤害感受器的百分比相关（Kendall 的 tau=.55，P=.004）。此外，机械不敏感 C 伤害感受器的自发性活动与传导的明显活动依赖性减慢相关（Kendall 的 tau=-.48，P=.009），表明轴突被包括在敏化过程中。与无痛多发性神经病患者相比，有疼痛的多发性神经病患者的机械不敏感 C 伤害感受器的过度兴奋明显更高，而在机械敏感（多模式）C 伤害感受器中，这种差异则不那么明显。这种过度兴奋可能是有疼痛的周围神经病患者疼痛的主要潜在机制。
