Campero, MarioBostock, HughBaumann, ThomasOchoa, José2021-10-072021-10-072010Clin Neurophysiol. 2010 July ; 121(7): 1072–1079. doi:10.1016/j.clinph.2009.12.038.http://hdl.handle.net/11447/4800Objective—Although the term ‘reflex sympathetic dystrophy’ has been replaced by ‘complex regional pain syndrome’ (CRPS) type I, there remains a widespread presumption that the sympathetic nervous system is actively involved in mediating chronic neuropathic pain [“sympathetically maintained pain” (SMP)], even in the absence of detectable neuropathophysiology. Methods—We have used microneurography to evaluate possible electrophysiological interactions in 24 patients diagnosed with CRPS I (n=13), or CRPS II (n=11) by simultaneously recording from single identified sympathetic efferent fibers and C nociceptors, while provoking sympathetic neural discharges in cutaneous nerves. Results—We assessed potential effects of sympathetic activity upon 35 polymodal nociceptors and 19 mechano-insensitive nociceptors, recorded in CRPS I (26 nociceptors) and CRPS II patients (28 nociceptors). No evidence of activation of nociceptors related to sympathetic discharge was found, although nociceptors in 6 CRPS II patients exhibited unrelated spontaneous pathological nerve impulse activity. Conclusion—We conclude that activation of nociceptors by sympathetic efferent discharges is not a cardinal pathogenic event in either CRPS I or CRPS II patients. Significance—This study shows that sympathetic-nociceptor interactions, if they exist in patients communicating chronic neuropathic pain, must be the exceptionenCRPSsympathetically maintained painnociceptorsympathetic efferentsympathetic-sensory interactionArticle