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Response to Editorial on Albrecht et al. (2006)

机译:对Albrecht等人社论的回应。 (2006年)

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We would like to thank Janig and Baron (2006) for providing an Editorial on our article, and wish to clarify and extend what we did and did not say in our study (Albrecht et al., 2006).In their editorial, Janig and Baron state that we had hypothesized that the primary underlying mechanism of CRPS I "involves widespread changes of the cutaneous innervation by small-diameter afferent and postganglionicsympathetic efferent fibers". In addition to the small-fiber epidermal ending loss also observed by Oaklander et al. (2006), our study documents extensive peripheral neuropathologies involving virtually all components of the cutaneous innervation, which included not just small fibers, but also Abeta-fiber innervation such as that to hair follicles. However, we specifically did not hypothesize that the observed peripheral neuropathologies were the mechanism of initiation or maintenance of the affliction, nor did we hypothesize that they were a unitary mechanism for CRPS I. We did conclude that CRPS I may include a true neuropathic component because the neuropathologies we observed: (1) are consistent with the peripheral symptoms diagnostic for CRPS I and (2) did include pathologies such as alterations in the structure and chemistry of remaining epidermal endings like those seen in neuropathic conditions such as postherpetic neuralgia and diabetic neuropathy (Petersen et al., 2002; Kennedy, 2004).
机译:我们要感谢Janig和Baron(2006)对我们的文章提供社论,并希望澄清和扩展我们在研究中没有说过的内容(Albrecht et al。,2006)。 Baron指出,我们已经假设CRPS I的主要潜在机制“涉及小直径传入神经节后交感神经传出纤维对皮肤神经支配的广泛变化”。除小纤维表皮末梢损失外,Oaklander等人也观察到。 (2006),我们的研究记录了广泛的周围神经病变,涉及皮肤神经支配的几乎所有组成部分,不仅包括小纤维,还包括Abeta纤维神经支配,例如毛囊。但是,我们没有明确地假设观察到的周围神经病变是引发或维持疼痛的机制,也没有假设它们是CRPS I的单一机制。我们的结论是,CRPS I可能包括真正的神经病变成分,因为我们观察到的神经病理学:(1)与诊断CRPS I的周围症状一致,(2)确实包括诸如表皮末梢残留结构和化学变化的病理学,例如在带疱疹后神经痛和糖尿病性神经病等神经病变中所见(Petersen等,2002; Kennedy,2004)。

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