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      Review of complex regional pain syndrome and the role of the neuroimmune axis

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          Abstract

          Background

          Complex regional pain syndrome (CRPS) is a progressive and painful disease of the extremities that is characterized by continuous pain inconsistent with the initial trauma. CRPS is caused by a multi-mechanism process that involves both the peripheral and central nervous system, with a prominent role of inflammation in CRPS pathophysiology. This review examines what is currently known about the CRPS inflammatory and pain mechanisms, as well as the possible impact of neurostimulation therapies on the neuroimmune axis of CRPS.

          Study design

          A narrative review of preclinical and clinical studies provided an overview of the pain and inflammatory mechanisms in CRPS and addressed the effect of neurostimulation on immunomodulation.

          Methods

          A systematic literature search was conducted based on the PRISMA guidelines between September 2015 to September 2020. Data sources included relevant literature identified through searches of PubMed, Embase and the Cochrane Database of Systematic Reviews.

          Results

          Sixteen preclinical and eight clinical studies were reviewed. Preclinical studies identified different mechanisms of pain development in the acute and chronic CRPS phases. Several preclinical and clinical studies investigating inflammatory mechanisms, autoimmunity, and genetic profiles in CRPS, supported a role of neuroinflammation in the pathophysiology of CRPS. The immunomodulatory effects of neurostimulation therapy is still unclear, despite clinical improvement in the CRPS patients.

          Conclusions

          Increasing evidence supports a role for inflammation and neuroinflammation in CRPS pathophysiology. Preliminary neurostimulation findings, together with the role of (neuro)inflammation in CRPS, seems to provide a compelling rationale for its use in CRPS pain treatment. The possible immunomodulatory effects of neurostimulation opens new therapeutic possibilities, however further research is needed to gain a better understanding of the working mechanisms.

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          Most cited references83

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          The PRISMA statement for reporting systematic reviews and meta-analyses of studies that evaluate healthcare interventions: explanation and elaboration

          Alessandro Liberati, Douglas G. Altman, Jennifer Tetzlaff … (2010)
          Systematic reviews and meta-analyses are essential to summarise evidence relating to efficacy and safety of healthcare interventions accurately and reliably. The clarity and transparency of these reports, however, are not optimal. Poor reporting of systematic reviews diminishes their value to clinicians, policy makers, and other users. Since the development of the QUOROM (quality of reporting of meta-analysis) statement—a reporting guideline published in 1999—there have been several conceptual, methodological, and practical advances regarding the conduct and reporting of systematic reviews and meta-analyses. Also, reviews of published systematic reviews have found that key information about these studies is often poorly reported. Realising these issues, an international group that included experienced authors and methodologists developed PRISMA (preferred reporting items for systematic reviews and meta-analyses) as an evolution of the original QUOROM guideline for systematic reviews and meta-analyses of evaluations of health care interventions. The PRISMA statement consists of a 27-item checklist and a four-phase flow diagram. The checklist includes items deemed essential for transparent reporting of a systematic review. In this explanation and elaboration document, we explain the meaning and rationale for each checklist item. For each item, we include an example of good reporting and, where possible, references to relevant empirical studies and methodological literature. The PRISMA statement, this document, and the associated website (www.prisma-statement.org/) should be helpful resources to improve reporting of systematic reviews and meta-analyses.
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            Neuroinflammation and Central Sensitization in Chronic and Widespread Pain.

            Ru-Rong Ji, Andrea Nackley, Yul Huh … (2018)
            Chronic pain is maintained in part by central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is also driven by neuroinflammation in the peripheral and central nervous system. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines. Recent studies suggest that central cytokines and chemokines are powerful neuromodulators and play a sufficient role in inducing hyperalgesia and allodynia after central nervous system administration. Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites. Thus, neuroinflammation drives widespread chronic pain via central sensitization. We also discuss sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain.
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              Validation of proposed diagnostic criteria (the "Budapest Criteria") for Complex Regional Pain Syndrome.

              Norman R. Harden, Stephen Bruehl, Roberto Perez … (2010)
              Current IASP diagnostic criteria for CRPS have low specificity, potentially leading to overdiagnosis. This validation study compared current IASP diagnostic criteria for CRPS to proposed new diagnostic criteria (the "Budapest Criteria") regarding diagnostic accuracy. Structured evaluations of CRPS-related signs and symptoms were conducted in 113 CRPS-I and 47 non-CRPS neuropathic pain patients. Discriminating between diagnostic groups based on presence of signs or symptoms meeting IASP criteria showed high diagnostic sensitivity (1.00), but poor specificity (0.41), replicating prior work. In comparison, the Budapest clinical criteria retained the exceptional sensitivity of the IASP criteria (0.99), but greatly improved upon the specificity (0.68). As designed, the Budapest research criteria resulted in the highest specificity (0.79), again replicating prior work. Analyses indicated that inclusion of four distinct CRPS components in the Budapest Criteria contributed to enhanced specificity. Overall, results corroborate the validity of the Budapest Criteria and suggest they improve upon existing IASP diagnostic criteria for CRPS. Copyright (c) 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Pain
                Journal ID (iso-abbrev): Mol Pain
                Journal ID (publisher-id): MPX
                Journal ID (hwp): spmpx
                Title: Molecular Pain
                Publisher: SAGE Publications (Sage CA: Los Angeles, CA )
                ISSN (Electronic): 1744-8069
                Publication date (Electronic): 31 March 2021
                Publication date Collection: 2021
                Volume: 17
                Electronic Location Identifier: 17448069211006617
                Affiliations
                [1 ]Axxon Pain, Brisbane Private Hospital, 259 Wickham Terrace, Brisbane, Queensland 4000, Australia
                [2 ]Division of Pain Medicine, Department of Anesthesiology, University of California San Diego, La Jolla, CA, USA
                [3 ]Department of Anesthesiology and Pain Medicine, VA San Diego Health Care, San Diego, CA, USA
                Author notes
                [*]Amrita Prasad MD, Axxon Pain, Brisbane Private Hospital, 259 Wickham Terrace, Brisbane, Queensland 4000, Australia. Email: a.prasad@ 123456live.com.au
                Author information
                https://orcid.org/0000-0003-2595-1286
                Article
                Publisher ID: 10.1177_17448069211006617
                DOI: 10.1177/17448069211006617
                PMC ID: 8020088
                PubMed ID: 33788654
                SO-VID: ab55b123-da64-4368-9c51-94f3df3b7fc1
                Copyright © © The Author(s) 2021
                License:

                Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 1 March 2021
                Date revision received : 1 March 2021
                Date accepted : 9 March 2021
                Categories
                Subject: Review
                Custom metadata
                cover-date January-December 2021
                typesetter ts2

                ScienceOpen disciplines: Molecular medicine
                Keywords: complex regional pain syndrome,pathophysiology,inflammation,neuromodulation,neuroimmunity,dorsal root ganglion stimulation
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: complex regional pain syndrome, pathophysiology, inflammation, neuromodulation, neuroimmunity, dorsal root ganglion stimulation

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