Response to Editorial on Albrecht et al. (2006)
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 postganglionic sympathetic 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 Ab 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) Agreeing with cautions raised by Janig and Baron, we explicitly noted in our publication, that our study was limited to two CRPS I patients who were very chronic and who went through many medical and interventional procedures. As such, we raised the concern that previously unknown effects of the various treatment regimens might also contribute to the observed pathologies. We quite agree with Janig and Baron that the manner in which peripheral and central changes interact is poorly understood, as well as the manner in which peripheral components interact with each other. As Janig and Baron suggest, with limited animal or human models to study CRPS type I, any insights gained from analyses of available materials (e.g. human tissue) may be critical for advancing the understanding and treatment of this devastating disease. We hope our study is such a contribution.
Pain