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Commentary Sympathetic blockade for complex regional pain syndrome In the 1990s, the dogma that sympathetic blockade was a first- line treatme nt for compl ex regional pain synd rome (CRPS) was shattered by accusations that benefits were due to placebo effects and that this treatment approach was ‘‘entrepreneurially inspired’’ [7]. Since then, systematic examination of the literature base has provided little support for the use of local anesthetic sympathetic blockade for CRPS, and has highlighted the scarcity of high-quality doubl e-bli nd place bo-controlled trial s with an adeq uate sampl e size and follow-up period [1,9]. However, as sympathetic blockade continues to be used therapeutically for CRPS in clinical practice [10], further examination of its efficacy is imperative. In this issue of PAIN , Rocha et al. [8] report that thoracic sym- pathetic blockade, as an adjunct to pharmacological and physical thera py for patients with uppe r-limb CRPS, resulte d in posit ive effects on mood and reductions in pain detectable 12 months later. During the blockade, 1 mL of contrast media, followed by 5 mL of local anesthetic agent and another 5 mL of corticosteroid solution, were injected under fluoroscopic guidance around the second tho- rac ic gan gli on of the sympat het ic cha in. In the control gro up, 10 mL of local anesthetic agent and corticosteroid solution were injected subcutaneously at the T2 level to cover the possibility that placebo effects or systemic absorption of these agents might provide thera- peutic benefits. Scores on the McGill Pain Questionnaire and the ave rag e evo ked pai n score on the Neu ropath ic Pai n Symptom Inventoryweresig nifi can tly lower in thetreat ed tha n con trol gro up at 1 and 12 months, and average pain and depression scores were significantly lower in the treated than control group at 12 months. What might account for such persistent treatment gains after just one sympathetic block? It seems quite unlikely that a placebo response to sympathetic blockade would be detected 12 months later. Subst anti al incre ases in hand temperatu re indicated that sympa theti c block ade was succ essfu l. Howe ver, patie nts appa r- ent ly remain ed bli nd to the typ e of tre atment the y rec eiv ed, des pit e the inc rea se in han d temper ature and the occ asi ona l presen ce of Hor ner ’s sig n. Alt hou gh a cas e mig ht be made for tempor ary treatment gai ns in pat ien ts wit h a compon ent of ‘‘sympathetical ly maintained’’ pain [3], it seems inconceivable that transient blockade of gang lia in the thora cic sympa theti c chain would inhibit pain and lift mood 12 months later. Might the infusion of corticosteroid solution around the sympa- thetic chain have mediated long-term benefits? Adding steroids to loc al ane sth eti c agents for sympat hetic ner ve blocks is bas ed on the premise that suppressing inflammation in the sympathetic chain inhibits pain. There is some support for this. For example, when administered repetitively over the course of a week to the sympa- the tic chain wit h local ane stheti c age nt, ste roi ds seemed to pro vid e thera peuti c bene fits for patie nts with acute herp es zoster and reduced the rate of progression to postherpetic neuralgia [4] . However, one might question whether the sympathetic chain was the only target of the local anesthetic agent and corticosteroid solution in Rocha’s study, because contrast media in 11 mL of fluid (the volume injected by Rocha et al.) can disperse a considerable distance from the site of injection. For example, local anesthetic agent in volumes as low as 2 mL spreads across approximately 5 spinal segments and produces physiological signs of sympathetic blockade [5]. In an animal model of low back pain, steroids applied locally to inflamed dorsal root ganglia inhibited mechanical sensi- tivity and reduced abnormal spontaneous activity in myelinated sensory neurons [11]. Furthermore, after spinal nerve ligation in rats, corticosteroids infused around the involved dorsal root gan- glia inhib ited mech anic al sens itivi ty and symp athet ic sprou ting into the ganglia [6]. Potentially, then, absorption of the corticoste- roid solution into nearby dorsal root ganglia of patients in Rocha’s study might have contributed to treatment gains. Perhaps this or some other effect of the steroids, loc al anesthetic agent, or blocking procedure augmented the efficacy of physical treatments or phar- macotherapy, resulting in progressive reductions in pain and posi- tive effects on mood over the 12 months of follow-up. Although this study casts little light on the role, if any, of local anesthetic sympathetic blockade in the management of CRPS, ther- apeutic effects were promising and warrant further investigation. And we should not lose si ght of the bi gger pi cture. A cl ear dis tin ction needs to be mad e bet wee n the use of sympat het ic nerve blocks to identify sympathetically maintained pain (when compa red agai nst an activ e plac ebo proce dure ) and the thera peut ic application of sympathetic blockade for CRPS. Indeed, we may be asking the wrong question by querying the therapeu tic role of local anes theti c symp athe tic block ade for CRPS [1,9]—it would seem more perti nent to determi ne wheth er and how to interrup t symp a- thetic activity in patients with sympathetically maintained CRPS rather than in CRPS patients overall. To avoid a tautology, new appro ache s may be requi red to iden tify symp athe tica lly main - tained pain (eg, placebo-controlled electrical or pharmacological stimulation of the sympathetic chain or sympathetic nerve termi- nals), and to distinguish between central and peripheral forms of this disorder [2]. We might then be better placed to determine wheth er thera pies that targe t the symp athe tic nerv ous syst em provide benefits for an identifiable subgroup of patients with CRPS. http://dx.doi.org/10.1016/j.pain.2014.09.005 0304-3959/ 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. DOI of original article: http://dx.doi.org/10 .1016/j.pain.2014.08.015 www.elsevier.com/locate/pain PAIN 155 (2014) 2218–2219
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Transcript of 1-s2.0-S0304395914004254-main
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alater. Substantial increases in hand temperature indicated thatsympathetic blockade was successful. However, patients appar-ently remained blind to the type of treatment they received,
would inhibit pain and lift mood 12 months later.Might the infusion of corticosteroid solution around the sympa-
thetic chain have mediated long-term benets? Adding steroids tolocal anesthetic agents for sympathetic nerve blocks is based on thepremise that suppressing inammation in the sympathetic chain
nerve blocks to identify sympathetically maintained pain (whencompared against an active placebo procedure) and the therapeuticapplication of sympathetic blockade for CRPS. Indeed, we may be
]it woulinterrupt
approaches may be required to identify sympathetically main-tained pain (eg, placebo-controlled electrical or pharmacologicalstimulation of the sympathetic chain or sympathetic nerve termi-nals), and to distinguish between central and peripheral forms ofthis disorder [2]. We might then be better placed to determinewhether therapies that target the sympathetic nervous systemprovide benets for an identiable subgroup of patients with CRPS.
DOI of original article: http://dx.doi.org/10.1016/j.pain.2014.08.015
21sympathetically maintained pain [3], it seems inconceivable thattransient blockade of ganglia in the thoracic sympathetic chain
thetic activity in patients with sympathetically maintained CRPSrather than in CRPS patients overall. To avoid a tautology, newpresence of Horners sign. Although a case might be made fortemporary treatment gains in patients with a component of
anesthetic sympathetic blockade for CRPS [1,9more pertinent to determine whether and how tohttp://dx.doi.org/10.1016/j.pain.2014.09.0050304-3959/ 2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.of locald seemsympa-despite the increase in hand temperature and the occasional asking the wrong question by querying the therapeutic roleCommentary
Sympathetic blockade for complex region
In the 1990s, the dogma that sympathetic blockade was a rst-line treatment for complex regional pain syndrome (CRPS) wasshattered by accusations that benets were due to placebo effectsand that this treatment approach was entrepreneurially inspired[7]. Since then, systematic examination of the literature base hasprovided little support for the use of local anesthetic sympatheticblockade for CRPS, and has highlighted the scarcity of high-qualitydouble-blind placebo-controlled trials with an adequate samplesize and follow-up period [1,9]. However, as sympathetic blockadecontinues to be used therapeutically for CRPS in clinical practice[10], further examination of its efcacy is imperative.
In this issue of PAIN, Rocha et al. [8] report that thoracic sym-pathetic blockade, as an adjunct to pharmacological and physicaltherapy for patients with upper-limb CRPS, resulted in positiveeffects on mood and reductions in pain detectable 12 months later.During the blockade, 1 mL of contrast media, followed by 5 mL oflocal anesthetic agent and another 5 mL of corticosteroid solution,were injected under uoroscopic guidance around the second tho-racic ganglion of the sympathetic chain. In the control group, 10 mLof local anesthetic agent and corticosteroid solution were injectedsubcutaneously at the T2 level to cover the possibility that placeboeffects or systemic absorption of these agents might provide thera-peutic benets. Scores on the McGill Pain Questionnaire and theaverage evoked pain score on the Neuropathic Pain SymptomInventorywere signicantly lower in the treated than control groupat 1 and 12 months, and average pain and depression scores weresignicantly lower in the treated than control group at 12 months.
What might account for such persistent treatment gains afterjust one sympathetic block? It seems quite unlikely that a placeboresponse to sympathetic blockade would be detected 12 months
PAIN155 (2014) 2l pain syndrome
inhibits pain. There is some support for this. For example, whenadministered repetitively over the course of a week to the sympa-thetic chain with local anesthetic agent, steroids seemed to providetherapeutic benets for patients with acute herpes zoster andreduced the rate of progression to postherpetic neuralgia [4].
However, one might question whether the sympathetic chainwas the only target of the local anesthetic agent and corticosteroidsolution in Rochas study, because contrast media in 11 mL of uid(the volume injected by Rocha et al.) can disperse a considerabledistance from the site of injection. For example, local anestheticagent in volumes as low as 2 mL spreads across approximately 5spinal segments and produces physiological signs of sympatheticblockade [5]. In an animal model of low back pain, steroids appliedlocally to inamed dorsal root ganglia inhibited mechanical sensi-tivity and reduced abnormal spontaneous activity in myelinatedsensory neurons [11]. Furthermore, after spinal nerve ligation inrats, corticosteroids infused around the involved dorsal root gan-glia inhibited mechanical sensitivity and sympathetic sproutinginto the ganglia [6]. Potentially, then, absorption of the corticoste-roid solution into nearby dorsal root ganglia of patients in Rochasstudy might have contributed to treatment gains. Perhaps this orsome other effect of the steroids, local anesthetic agent, or blockingprocedure augmented the efcacy of physical treatments or phar-macotherapy, resulting in progressive reductions in pain and posi-tive effects on mood over the 12 months of follow-up.
Although this study casts little light on the role, if any, of localanesthetic sympathetic blockade in the management of CRPS, ther-apeutic effects were promising and warrant further investigation.And we should not lose sight of the bigger picture. A cleardistinction needs to be made between the use of sympathetic
www.e l sev ie r . com/ loca te /pa in
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Conict of interest
The authors declare no conict of interest.
Acknowledgements
Supported by grants from the National Health and MedicalResearch Council of Australia (grant APP1030379) and the Austra-lian and New Zealand College of Anaesthetists (grant 12/24).
References
[1] Cepeda MS, Carr DB, Lau J. Local anesthetic sympathetic blockade for complexregional pain syndrome. Cochrane Database Syst Rev 2005;4:CD004598.
[2] Drummond PD, Finch PM. Persistence of pain induced by startle and foreheadcooling after sympathetic blockade in patients with complex regional painsyndrome. J Neurol Neurosurg Psychiatry 2004;75:98102.
[3] Gibbs GF, Drummond PD, Finch PM, Phillips JK. Unravelling thepathophysiology of complex regional pain syndrome: focus onsympathetically maintained pain. Clin Exp Pharmacol Physiol 2008;35:71724.
[4] Ji G, Niu J, Shi Y, Hou L, Lu Y, Xiong L. The effectiveness of repetitiveparavertebral injections with local anesthetics and steroids for the preventionof postherpetic neuralgia in patients with acute herpes zoster. Anesth Analg2009;109:16515.
[5] Lee MH, Kim KY, Song JH, Jung HJ, Lim HK, Lee DI, Cha YD. Minimal volume oflocal anesthetic required for an ultrasound-guided SGB. Pain Med 2012;13:13818.
[6] Li JY, Xie W, Strong JA, Guo QL, Zhang JM. Mechanical hypersensitivity,sympathetic sprouting, and glial activation are attenuated by local injection ofcorticosteroid near the lumbar ganglion in a rat model of neuropathic pain. RegAnesth Pain Med 2011;36:5662.
[7] Ochoa JL. Truths, errors, and lies around reex sympathetic dystrophy andcomplex regional pain syndrome. J Neurol 1999;246:8759.
[8] Rocha RO, Teixeira MJ, Yeng LT, Cantara MG, Faria VG, Liggieri V, Loduce A,Mller BM, Souza ACMS, de Andrade DC. Thoracic sympathetic block for thetreatment of complex regional pain syndrome type I: A double-blindrandomized controlled study. PAIN 2014;155:227481.
[9] Stanton TR, Wand BM, Carr DB, Birklein F, Wasner GL, OConnell NE. Localanaesthetic sympathetic blockade for complex regional pain syndrome.Cochrane Database Syst Rev 2013;8:CD004598.
[10] van Eijs F, Geurts J, van Kleef M, Faber CG, Perez RS, Kessels AG, van Zundert J.Predictors of pain relieving response to sympathetic blockade in complexregional pain syndrome type 1. Anesthesiology 2012;116:11321.
[11] Ye L, Xie W, Strong JA, Zhang JM. Blocking the mineralocorticoid receptorimproves effectiveness of steroid treatment for low back pain in rats.Anesthesiology 2014;121:63243.
Peter D. DrummondPhilip M. Finch
Centre for Research on Chronic Pain and Inammatory Diseases, and theSchool of Psychology and Exercise Science, Murdoch University,
Perth 6150, Australia Tel.: +61 893602415; Fax: +61 893606492.
E-mail address: [email protected] (P.D. Drummond)
Commentary / PAIN155 (2014) 22182219 2219
Sympathetic blockade for complex regional pain syndromeConflict of interestAcknowledgementsReferences
