Dept of Molecular Medicine and Surgery, Clinical Pain Research, Pain Center, Karolinska Institutet/University Hospital, Solna, S-171 76 Stockholm, Sweden.
Eur J Pain. 2011 May;15(5):498-503. doi: 10.1016/j.ejpain.2010.10.003. Epub 2010 Nov 20.
Eighteen patients with peripheral neuropathic pain (PNeP) and seven patients with central post-stroke pain (CPSP) all suffering from dynamic mechanical allodynia (DMA) in a limb were studied. From recent research it is reasonable to suggest that A-beta fibres constitute the peripheral substrate for DMA in patients with PNeP. The pathophysiological basis for DMA in patients with CPSP is unknown. It is clinically observed that some patients with neuropathic pain report variable intensity of DMA and volunteer that the phenomenon at times is only an unpleasant, i.e., dysesthetic sensation. The pathophysiological basis for dynamic mechanical dysesthesia (DMD) has never been addressed. Based on the aforementioned clinical observations we aimed at investigating if DMA is the hyperbole of DMD both mediated by A-beta fibres in the periphery. A compression/ischemia-induced (differential) nerve block in conjunction with repeated quantitative sensory testing of A-delta and C-fibre function using cold and warm stimuli was used to assess which nerve fibre population that contributes to DMA and DMD, respectively. During the nerve block there was a transition of DMA to DMD in all patients with PNeP and in 3/7 patients with CPSP. The rest of the patients lost DMA without transition to DMD. The transition or loss of DMA without transition occurred early and concurrently in time during the block and was paralleled by a continuous impairment of mainly A-beta fibre function. We therefore suggest DMA to be the hyperbole of DMD, the difference being the number of mechanoreceptive fibres having access to the nociceptive system.
研究了 18 例患有周围神经病理性疼痛（PNeP）和 7 例患有中风后中枢性疼痛（CPSP）的患者，他们在肢体中均患有动态机械性触诱发痛（DMA）。根据最近的研究，合理的假设是 A-β纤维构成了 PNeP 患者 DMA 的外周基础。CPSP 患者 DMA 的病理生理基础尚不清楚。临床上观察到，一些患有神经性疼痛的患者报告 DMA 的强度不同，并自愿表示这种现象有时只是一种不愉快的、即感觉异常的感觉。动态机械性感觉异常（DMD）的病理生理基础从未得到解决。基于上述临床观察，我们旨在研究 DMA 是否是由周围 A-β纤维介导的 DMD 的夸张形式。使用冷和热刺激的压缩/缺血诱导（差异）神经阻滞以及对 A-δ和 C-纤维功能的重复定量感觉测试，评估哪些神经纤维群体分别导致 DMA 和 DMD。在神经阻滞期间，所有 PNeP 患者和 7 例 CPSP 患者中的 3 例均从 DMA 转变为 DMD。其余患者失去了 DMA，而没有转变为 DMD。DMA 的转变或丧失发生在阻滞早期且同时发生，并且与主要 A-β纤维功能的持续损害平行。因此，我们建议将 DMA 视为 DMD 的夸张形式，区别在于进入伤害感受系统的机械感觉纤维的数量。
