Temperature-dependent double spikes in C-nociceptors of neuropathic pain patients
Temperature-dependent double spikes in C-nociceptors of neuropathic pain patients
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DOI：
10.1093/brain/awh552
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发表时间：
2005-09-01
期刊：
影响因子：
14.5
通讯作者：
Ochoa, JL
中科院分区：
文献类型：
--
作者：
Bostock, H;Campero, M;Ochoa, JL
5例小纤维神经病变的特点是温度依赖性自发性疼痛，痛觉过敏/异常性疼痛和神经源性炎症的迹象进行了研究，临床和热成像，并通过显微神经摄影。热成像显示高热局限于疼痛和痛觉过敏的皮肤远端四肢，在没有交感神经血管去神经支配。定量感觉测试记录了热痛的阈值降低或阈值上幅度增加。神经电描记法确定了13个初级皮肤C-伤害感受器产生异常脉冲响应电刺激，在一个病人，伤害感受器自发放电。所有五名患者都表现出双尖峰的例子，其中一个短暂的电刺激偶尔或定期引起两个脉冲。在一种情况下，第二个脉冲发生在三个不同延迟中的一个。在所有五名患者中，皮肤变暖增加了第二次冲动发生的可能性。冲动倍增以前曾报道在正常受试者中很少发生，并且可归因于分支点处的单向传导失败导致的多个顺向冲动未过滤。神经性疼痛患者中双放电的发生率较高可能是由于其C-伤害感受器末端分支传导的安全系数降低。这些观察结果表明，单向传导阻滞提供了一种外周机制的温度依赖性伤害性感受器过度活跃的小纤维神经病变，可能有助于痛觉过敏。
Five patients with small-fibre neuropathy characterized by temperature-dependent spontaneous pain, hyperalgesia/allodynia and signs of neurogenic inflammation were studied clinically and thermographically, and by microneurography. Thermography revealed hyperthermia confined to painful and hyperalgesic skin of distal extremities, in absence of sympathetic vasomotor denervation. Quantitative sensory testing documented either reduced thresholds or increased suprathreshold magnitude for heat pain. Microneurography identified 13 primary cutaneous C-nociceptors generating abnormal impulses in response to electrical stimuli and, in one patient, nociceptors firing spontaneously. All five patients showed examples of double spikes, in which a single brief electrical stimulus occasionally or regularly evoked two impulses. In one case, a second impulse occurred at one of three different delays. In all five patients, warming of the skin increased the probability of a second impulse occurring. Impulse doubling has previously been reported as occurring rarely in normal subjects and is attributable to unfiltering of multiple orthodromic impulses due to unidirectional conduction failure at branch points. A higher incidence of double firing in neuropathic pain patients is probably due to a reduced safety factor for conduction in the terminal arborizations of their C-nociceptors. These observations show that unidirectional conduction block provides a peripheral mechanism of temperature-dependent nociceptor hyperactivity in small-fibre neuropathy that may contribute to hyperalgesia.