Mario Campero1, Hugh Bostock, Thomas K Baumann, José L Ochoa. 1. Departamento de Neurología, Clínica Alemana-Universidad del Desarrollo, Santiago, Chile. Av. Manquehue Norte 1410, piso 10, Vitacura, Santiago, Chile. mcampero@med.uchile.cl
Abstract
OBJECTIVE: Although the term 'reflex sympathetic dystrophy' has been replaced by 'complex regional pain syndrome' (CRPS) type I, there remains a widespread presumption that the sympathetic nervous system is actively involved in mediating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 six CRPS II patients exhibited unrelated spontaneous pathological nerve impulse activity. CONCLUSIONS: 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 exception. Copyright 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
OBJECTIVE: Although the term 'reflex sympathetic dystrophy' has been replaced by 'complex regional pain syndrome' (CRPS) type I, there remains a widespread presumption that the sympathetic nervous system is actively involved in mediating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 IIpatients (28 nociceptors). No evidence of activation of nociceptors related to sympathetic discharge was found, although nociceptors in six CRPS IIpatients exhibited unrelated spontaneous pathological nerve impulse activity. CONCLUSIONS: We conclude that activation of nociceptors by sympathetic efferent discharges is not a cardinal pathogenic event in either CRPS I or CRPS IIpatients. SIGNIFICANCE: This study shows that sympathetic-nociceptor interactions, if they exist in patients communicating chronic neuropathic pain, must be the exception. Copyright 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.
Authors: Ellen Jørum; Kristin Ørstavik; Roland Schmidt; Barbara Namer; Richard W Carr; Gunnvald Kvarstein; Marita Hilliges; Hermann Handwerker; Erik Torebjörk; Martin Schmelz Journal: Pain Date: 2006-09-25 Impact factor: 6.961
Authors: Ann T Farrell; Julie Panepinto; C Patrick Carroll; Deepika S Darbari; Ankit A Desai; Allison A King; Robert J Adams; Tabitha D Barber; Amanda M Brandow; Michael R DeBaun; Manus J Donahue; Kalpna Gupta; Jane S Hankins; Michelle Kameka; Fenella J Kirkham; Harvey Luksenburg; Shirley Miller; Patricia Ann Oneal; David C Rees; Rosanna Setse; Vivien A Sheehan; John Strouse; Cheryl L Stucky; Ellen M Werner; John C Wood; William T Zempsky Journal: Blood Adv Date: 2019-12-10