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      Terminology, criteria, and definitions in complex regional pain syndrome: challenges and solutions

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          Abstract

          Complex regional pain syndrome has long been recognized as a severe and high impact chronic pain disorder. However, the condition has historically been difficult to define and classify and little attention has been given to where complex regional pain syndrome sits within other apparently similar chronic pain disorders, such as fibromyalgia and regional pain syndrome. In this review challenges in regard to nomenclature, definitions, and classification of complex regional pain syndrome are reviewed and suggestions are provided about future directions.

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          Most cited references 38

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          Inflammation in complex regional pain syndrome: a systematic review and meta-analysis.

          We conducted a systematic review of the literature with meta-analysis to determine whether complex regional pain syndrome (CRPS) is associated with a specific inflammatory profile and whether this is dependent on the duration of the condition. Comprehensive searches of the literature using MEDLINE, Embase, Scopus, Web of Science, and reference lists from published reviews identified articles that measured inflammatory factors in CRPS. Two independent investigators screened titles and abstracts, and performed data extraction and risk of bias assessments. Studies were subgrouped by medium (blood, blister fluid, and CSF) and duration (acute and chronic CRPS). Where possible, meta-analyses of inflammatory factor concentrations were performed and pooled effect sizes were calculated using random-effects models. Twenty-two studies were included in the systematic review and 15 in the meta-analysis. In acute CRPS, the concentrations of interleukin (IL)-8 and soluble tumor necrosis factor receptors I (sTNF-RI) and II (sTNF-RII) were significantly increased in blood. In chronic CRPS, significant increases were found in 1) TNFα, bradykinin, sIL-1RI, IL-1Ra, IL-2, sIL-2Ra, IL-4, IL-7, interferon-γ, monocyte chemoattractant protein-1 (MCP-1), and sRAGE (soluble receptor for advanced glycation end products) in blood; 2) IL-1Ra, MCP-1, MIP-1β, and IL-6 in blister fluid; and 3) IL-1β and IL-6 in CSF. Chronic CRPS was also associated with significantly decreased 1) substance P, sE-selectin, sL-selectin, sP-selectin, and sGP130 in blood; and 2) soluble intercellular adhesion molecule-1 (sICAM-1) in CSF. Most studies failed to meet 3 or more of our quality criteria. CRPS is associated with the presence of a proinflammatory state in the blood, blister fluid, and CSF. Different inflammatory profiles were found for acute and chronic cases.
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            Signs and symptoms of reflex sympathetic dystrophy: prospective study of 829 patients.

            The pathogenesis of reflex sympathetic dystrophy--variously known as Sudeck's atrophy, causalgia, algodystrophy, and peripheral trophoneurosis--is not yet understood, and diagnosing and treating patients is difficult. We have prospectively studied 829 patients, paying particular attention to early signs and symptoms. In its early phase, reflex sympathetic dystrophy is characterised by regional inflammation, which increases after muscular exercise. Pain was present in 93% of patients, and hypoaesthesia and hyperpathy were present in 69% and 75% respectively. With time, tissue atrophy may occur as well as involuntary movements, muscle spasms, or pseudoparalysis. Tremor was found in 49% and muscular incoordination in 54% of patients. Sympathetic signs such as hyperhidrosis are infrequent and therefore have no diagnostic value. We found no evidence consistent with the presence of three consecutive phases of the disease. Early symptoms are those of an inflammatory reaction and not of a disturbance of the sympathetic nervous system. These data support the concept of an exaggerated regional inflammatory response to injury or operation in reflex sympathetic dystrophy.
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              Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy).

              CRPS-I consists of post-traumatic limb pain and autonomic abnormalities that continue despite apparent healing of inciting injuries. The cause of symptoms is unknown and objective findings are few, making diagnosis and treatment controversial, and research difficult. We tested the hypotheses that CRPS-I is caused by persistent minimal distal nerve injury (MDNI), specifically distal degeneration of small-diameter axons. These subserve pain and autonomic function. We studied 18 adults with IASP-defined CRPS-I affecting their arms or legs. We studied three sites on subjects' CRPS-affected and matching contralateral limb; the CRPS-affected site, and nearby unaffected ipsilateral and matching contralateral control sites. We performed quantitative mechanical and thermal sensory testing (QST) followed by quantitation of epidermal neurite densities within PGP9.5-immunolabeled skin biopsies. Seven adults with chronic leg pain, edema, disuse, and prior surgeries from trauma or osteoarthritis provided symptom-matched controls. CRPS-I subjects had representative histories and symptoms. Medical procedures were unexpectedly frequently associated with CRPS onset. QST revealed mechanical allodynia (P<0.03) and heat-pain hyperalgesia (P<0.04) at the CRPS-affected site. Axonal densities were highly correlated between subjects' ipsilateral and contralateral control sites (r=0.97), but were diminished at the CRPS-affected sites of 17/18 subjects, on average by 29% (P<0.001). Overall, control subjects had no painful-site neurite reductions (P=1.00), suggesting that pain, disuse, or prior surgeries alone do not explain CRPS-associated neurite losses. These results support the hypothesis that CRPS-I is specifically associated with post-traumatic focal MDNI affecting nociceptive small-fibers. This type of nerve injury will remain undetected in most clinical settings.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2015
                11 December 2015
                : 8
                : 871-877
                Affiliations
                [1 ]Department of Rheumatology, Townsville Hospital, Douglas, QLD, Australia
                [2 ]Department of Medicine, Monash University, Melbourne, VIC, Australia
                Author notes
                Correspondence: Geoffrey Littlejohn, Suite H, Monash Medical Centre, 246 Clayton Road, Clayton, Melbourne, VIC, Australia, Email geoff.littlejohn@ 123456monash.edu
                Article
                jpr-8-871
                10.2147/JPR.S53113
                4686318
                © 2015 Dutton and Littlejohn. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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