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暴露外周神经的有害热刺激所致的预计疼痛——病例报告

Projected pain from noxious heat stimulation of an exposed peripheral nerve--a case report.

作者信息

Hoffmann T, Sauer S K, Horch R E, Reeh P W

机构信息

Institute for Physiology and Pathophysiology, University of Erlangen-Nuremberg Universitaetsstrasse 17, D-91054 Erlangen, Germany.

出版信息

Eur J Pain. 2009 Jan;13(1):35-7. doi: 10.1016/j.ejpain.2008.09.014. Epub 2008 Nov 6.

Abstract

Distinct sensory properties of unmyelinated axons in the isolated rat sciatic nerve have previously been revealed by measuring stimulated neuropeptide (CGRP) release in response to noxious stimuli. Axonal sensitization to heat by inflammatory mediators has been demonstrated and shown to depend on the heat- and proton-activated ion channel TRPV1. Recently, we have demonstrated in vitro that heat stimulation of nociceptive axons generates ectopic action potential discharge which resembles the heat response of the corresponding cutaneous nerve endings. It remained however, to be established whether adequate axonal stimulation could also generate projected sensations in a conscious human subject. In a singular human trial, the superficial radial nerve (SR) was exposed and stimulated mechanically as well as with noxious cold (3 degrees C). These stimuli were unable to induce any conscious local or projected sensations. However, controlled radiant heat applied to the nerve resulted in intense slowly adapting burning pain sensations projected into the center of the SR innervation area. No local sensation was reported. Thus, presumably activated nervi nevorum in the sheath of a healthy nerve do not cause conscious sensations, while axons of passage in mid-nerve exhibit a sensory transduction capacity for noxious heat though not for mechanical and cold stimulation. Axonal heat transduction may therefore become a source of ectopic discharge and neuropathic pain when heat threshold drops to body temperature as is the case with peripheral nerve endings in inflamed skin.

摘要

先前通过测量对伤害性刺激作出反应时受刺激的神经肽(降钙素基因相关肽,CGRP)释放,已揭示了分离的大鼠坐骨神经中无髓鞘轴突独特的感觉特性。炎症介质对轴突热敏感性已得到证实,并表明其依赖于热和质子激活的离子通道TRPV1。最近,我们在体外证明,伤害性轴突的热刺激会产生异位动作电位发放,这类似于相应皮肤神经末梢的热反应。然而,充分的轴突刺激是否也能在清醒的人类受试者中产生投射性感觉仍有待确定。在一项独特的人体试验中,桡神经浅支(SR)被暴露,并受到机械刺激以及有害冷刺激(3摄氏度)。这些刺激未能诱发任何有意识的局部或投射性感觉。然而,对神经施加可控的辐射热会导致强烈的、缓慢适应的灼痛感觉投射到SR神经支配区域的中心。未报告有局部感觉。因此,健康神经鞘中可能被激活的神经内膜神经不会引起有意识的感觉,而神经中部的过路轴突对有害热具有感觉转导能力,但对机械和冷刺激则没有。因此,当热阈值降至体温时,如炎症皮肤中的周围神经末梢那样,轴突热转导可能会成为异位放电和神经性疼痛的一个来源。

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