Response to "A new definition of neuropathic pain".
Response to "A new definition of neuropathic pain".
复制标题
对“神经性疼痛的新定义”的回应。
DOI：
10.1016/j.pain.2012.01.012
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发表时间：
2012
期刊：
影响因子：
7.4
通讯作者：
Bennett,GaryJ
中科院分区：
文献类型：
--
作者：
Oaklander,AnneLouise;Wilson,PeterR;Moskovitz,PeterA;Manning,DonaldC;Lubenow,Timothy;Levine,JonD;Harden,NormanR;Galer,BradleyS;Cooper,MarkS;Bruehl,Stephen;Broatch,James;Berde,Charles;Bennett,GaryJ
A recent commentary in PAIN® entitled ‘‘A new definition of neuropathic pain’’[4] contains inaccuracies concerning the complex regional pain syndrome (CRPS). The Scientific Advisory Committee of the Reflex Sympathetic Dystrophy Syndrome Association (RSDSA; http://www. rsds. org) would like to correct these in the interest of CRPS patients and to make the ongoing debate on the IASP definition of neuropathic pain factual. The commentary states that the new definition would exclude CRPS from among neuropathic pain syndromes because of ‘‘the lack of structural abnormalities in so-called dysfunctional states (fibromyalgia, CRPS, vulvodynia, interstitial cystitis, etc.)’’. In actuality, CRPS has a strong and clear link to nerve injury that keeps it squarely among neuropathic pain syndromes, even according to the new proposed definition that requires ‘‘a lesion or disease affecting the somatosensory system’’[4]. The location of CRPS-inducing lesions was first characterized after the US Civil War by pioneering neurologist S. Weir Mitchell in two books that meticulously localized multiple soldiers’ CRPS-inducing injuries to their peripheral nerves and nerve plexi [6, 7]. Mitchell first called the syndrome ‘‘causalgia,’’which the IASP Task Force on Taxonomy revised in 1994 to CRPS type II and defined as ‘‘burning pain, allodynia, and hyperpathia usually in the hand or foot after partial injury of a nerve or one of its major branches’’[5]. Almost all peripheral nerves are mixed and contain abundant sensory axons; the small fibers particularly linked to neuropathic pain and CRPS comprise the vast majority throughout mammalian nerves [10]. Hence peripheral nerves are universally considered part of the somatosensory nervous system, and indeed, peripheral nerves lesions are the most common cause of neuropathic pain [2]. Causalgia/CRPS II is a complex endophenotype of post-traumatic neuralgia, but its neurological origins are clear. The IASP labeled patients with similar phenotype but no known nerve injury as CRPS type I and localized this to the ‘‘peripheral nervous system, possibly the central nervous system’’[5]. During the next 2 decades, multiple independent research groups have identified smaller partial nerve injuries in patients with CRPS I—not surprising, because patients with CRPS I and CRPS II have identical symptoms and respond to the same therapies [8]. The initial discovery involved painstaking morphometric analyses of suralnerve biopsy samples taken from legs amputated from CRPS I patients [11]. More recent pathological confirmations of somatosensory axon injuries in CRPS I patients used skin or muscle [1, 3, 9]. There is still much we do not understand about CRPS—most notably why some people develop it after injuries that leave most without long-term harm. However, it would be a step backward to obscure the well-established facts about CRPS, specifically its identity as a neuropathic pain syndrome.
