Sympathetically maintained pain could either be mediated by ephaptic interactions between sympathetic efferent and afferent nociceptive fibers or by catecholamine-induced activation of nociceptive nerve endings. We report here single fiber recordings from C nociceptors in a patient with sympathetically maintained pain, in whom sympathetic blockade had repeatedly eliminated the ongoing pain in both legs. We classified eight C-fibers as mechano-responsive and six as mechano-insensitive nociceptors according to their mechanical responsiveness and activity-dependent slowing of conduction velocity (latency increase of 0.5+/-1.1 vs. 7.1+/-2.0 ms for 20 pulses at 0.125 Hz). Two C-fibers were activated with a delay of several seconds following strong endogenous sympathetic bursts; they were also excited for about 3 min following the injection of norepinephrine (10 microl, 0.05%) into their innervation territory. In these two fibers, a prolonged activation by injection of low pH solution (phosphate buffer, pH 6.0, 10 microl) and sensitization of their heat response following prostaglandin E2 injection were recorded, evidencing their afferent nature. Moreover, their activity-dependent slowing was typical for mechano-insensitive nociceptors. We conclude that sensitized mechano-insensitive nociceptors can be activated by endogenously released catecholamines and thereby may contribute to sympathetically maintained pain. No evidence for ephaptic interaction between sympathetic efferent and nociceptive afferent fibers was found.

译文

:交感神经维持的疼痛可能由交感传入和传入的伤害性纤维之间的神经元相互作用或儿茶酚胺诱导的伤害性神经末梢的激活介导。我们在这里报告了在交感神经痛患者中,C伤害感受器的单纤维记录,在该患者中,交感神经阻滞反复消除了双腿持续的疼痛。根据它们的机械响应性和依赖于传导速度的活动性减慢,我们将8根C纤维分类为机械响应伤害感受器,将6根C纤维分类为对机械响应不敏感的伤害感受器(在20脉冲下于0.125时,延迟时间为0.5 /-1.1与7.1 /-2.0 ms的增加)赫兹)。在强烈的内源性交感神经爆发后,几秒钟的延迟激活了两根C纤维。在将去甲肾上腺素(10微升,0.05%)注入其神经支配区域后,他们还兴奋了约3分钟。在这两种纤维中,记录了通过注射低pH溶液(磷酸盐缓冲液,pH 6.0、10微升)的长时间激活以及注射前列腺素E2后对其热响应的敏化,证明了它们的传入性质。此外,它们对机械不敏感的伤害感受器的活动依赖性减慢作用是典型的。我们得出结论,致敏的对机械不敏感的伤害感受器可以被内源性释放的儿茶酚胺激活,从而可能有助于交感神经维持性疼痛。没有发现交感传入纤维和伤害性传入纤维之间的神经元相互作用的证据。

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