Chronic pain as a symptom or a disease: the IASP Classification of Chronic Pain for the International Classification of Diseases (ICD-11)

Treede, R.‐D.; Rief, Winfried; Barke, Antonia; Aziz, Qasim; Bennett, Mike; Benoliel, Rafael; Cohen, Milton; Evers, Stefan; Finnerup, Nanna Brix; First, Michael B.; Giamberardino, Maria Adele; Kaasa, Stein; Korwisi, Beatrice; Kosek, Eva; Lavand’homme, Patricia; Nicholas, Michael K.; Perrot, Serge; Scholz, Joachim; Schug, Stephan A.; Smith, Blair H.; Svensson, Peter; Vlaeyen, Johan W.S.; Wang, Shuu Jiun

doi:10.1097/j.pain.0000000000001384

Cited by 1,651 publications

(983 citation statements)

References 42 publications

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“…However, when pain occurs outside the window of usefulness it is termed pathological. It is considered chronic when it lasts 3 months or greater (1). Chronic pain is a global problem affecting more than 1.5 billion people, and in 2015 was the leading cause of disability in most countries (2,3).…”

Section: Introductionmentioning

confidence: 99%

Cytokines in Pain: Harnessing Endogenous Anti-Inflammatory Signaling for Improved Pain Management

2019

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Current pain therapeutics offer inadequate relief to patients with chronic pain. A growing literature supports that pro-inflammatory cytokine signaling between immune, glial, and neural cells is integral to the development of pathological pain. Modulation of these communications may hold the key to improved pain management. In this review we first offer an overview of the relationships between pro-inflammatory cytokine and chemokine signaling and pathological pain, with a focus on the actions of cytokines and chemokines in communication between glia (astrocytes and microglia), immune cells (macrophages and T cells), and neurons. These interactions will be discussed in relation to both peripheral and central nervous system locations. Several novel non-neuronal drug targets for controlling pain are emerging as highly promising, including non-viral IL-10 gene therapy, which offer the potential for substantial pain relief through localized modulation of targeted cytokine pathways. Preclinical investigation of the mechanisms underlying the success of IL-10 gene therapy revealed the unexpected discovery of the powerful anti-nociceptive anti-inflammatory properties of D-mannose, an adjuvant in the non-viral gene therapeutic formulation. This review will include gene therapeutic approaches showing the most promise in controlling pro-inflammatory signaling via increased expression of anti-inflammatory cytokines like interleukin-10 (IL-10) or IL-4, or by directly limiting the bioavailability of specific pro-inflammatory cytokines, as with tumor necrosis factor (TNF) by the TNF soluble receptor (TNFSR). Approaches that increase endogenous anti-inflammatory signaling may offer additional opportunities for pain therapeutic development in patients not candidates for gene therapy. Promising novel avenues discussed here include the disruption of lymphocyte function-associated antigen (LFA-1) activity, antagonism at the cannabinoid 2 receptor (CB2R), and toll-like receptor 4 (TLR4) antagonism. Given the partial efficacy of current drugs, new strategies to manipulate neuroimmune and cytokine interactions hold considerable promise.

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Section: Introductionmentioning

confidence: 99%

Cytokines in Pain: Harnessing Endogenous Anti-Inflammatory Signaling for Improved Pain Management

2019

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“…Yet, in its chronic form, it can become uncoupled from underlying disease, causing independent nervous system dysfunction which requires bespoke treatment approaches. In recognition of this, chronic pain syndromes have just been added to the World Health Organisation's International Classification of Diseases (ICD-11) 3 .…”

Section: Introductionmentioning

confidence: 99%

A transcriptional toolbox for exploring peripheral neuro-immune interactions

Liang

Hore

Harley

et al. 2019

Preprint

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Correct communication between immune cells and peripheral neurons is crucial for the protection of our bodies. Its breakdown is observed in many common, often painful conditions, including arthritis, neuropathies and inflammatory bowel or bladder disease. Here, we have characterised the immune response in a mouse model of neuropathic pain using flow cytometry and cell-type specific RNA sequencing (RNA-seq). We found few striking sex differences, but a very persistent inflammatory response, with increased numbers of monocytes and macrophages up to 3½ months after the initial injury. This raises the question of whether the commonly used categorisation of pain into "inflammatory" and "neuropathic" is one that is mechanistically appropriate. Finally, we collated our data with other published RNA-seq datasets on neurons, satellite glial cells, macrophages and Schwann cells in naïve and nerve injury states. The result is a practical web-based tool for the transcriptional data-mining of peripheral neuroimmune interactions. Figure 8: At one week post PSNL, MHCII+/Ly6C-myeloid cells from sciatic nerve upregulate functions relating to interactions with other immune cells, in favour of more generic pro-inflammatory and homeostatic activities.A) STRING network analysis reveals that 77 of 186 genes upregulated in ipsilateral MHCII+ macrophages at adj. p < 0.05 are likely to be functionally connected with overrepresented processes including antigen presentation, regulation of lymphocytes and myeloid cell activation. B) Conversely, 41 of 93 significantly downregulated genes formed a network that includes transcripts relating to pro-inflammatory function (TNF, complements), regulation of angiogenesis and canonical macrophage markers, like CD163 typically found in resident macrophages. See Suppl. Table 5 for differential expression tables.

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“…The World Health Organisation (WHO) recognises chronic pain as a long-term condition in its own right and as a secondary consequence of other long-term conditions [1]. It has been estimated that 28 million adults in the UK (43%) are affected by chronic pain and that the pain of 7.9 million of these adults is moderately or severely limiting [2].…”

Section: Introductionmentioning

confidence: 99%

Acupuncture for the Relief of Chronic Pain: A Synthesis of Systematic Reviews

Paley

Johnson

2019

Medicina

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Background and Objectives: It is estimated that 28 million people in the UK live with chronic pain. A biopsychosocial approach to chronic pain is recommended which combines pharmacological interventions with behavioural and non-pharmacological treatments. Acupuncture represents one of a number of non-pharmacological interventions for pain. In the current climate of difficult commissioning decisions and constantly changing national guidance, the quest for strong supporting evidence has never been more important. Although hundreds of systematic reviews (SRs) and meta-analyses have been conducted, most have been inconclusive, and this has created uncertainty in clinical policy and practice. There is a need to bring all the evidence together for different pain conditions. The aim of this review is to synthesise SRs of RCTs evaluating the clinical efficacy of acupuncture to alleviate chronic pain and to consider the quality and adequacy of the evidence, including RCT design. Materials and Methods: Electronic databases were searched for English language SRs and meta-analyses on acupuncture for chronic pain. The SRs were scrutinised for methodology, risk of bias and judgement of efficacy. Results: A total of 177 reviews of acupuncture from 1989 to 2019 met our eligibility criteria. The majority of SRs found that RCTs of acupuncture had methodological shortcomings, including inadequate statistical power with a high risk of bias. Heterogeneity between RCTs was such that meta-analysis was often inappropriate. Conclusions: The large quantity of RCTs on acupuncture for chronic pain contained within systematic reviews provide evidence that is conflicting and inconclusive, due in part to recurring methodological shortcomings of RCTs. We suggest that an enriched enrolment with randomised withdrawal design may overcome some of these methodological shortcomings. It is essential that the quality of evidence is improved so that healthcare providers and commissioners can make informed choices on the interventions which can legitimately be provided to patients living with chronic pain.

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Chronic pain as a symptom or a disease: the IASP Classification of Chronic Pain for the International Classification of Diseases (ICD-11)

Cited by 1,651 publications

References 42 publications

Cytokines in Pain: Harnessing Endogenous Anti-Inflammatory Signaling for Improved Pain Management

Cytokines in Pain: Harnessing Endogenous Anti-Inflammatory Signaling for Improved Pain Management

A transcriptional toolbox for exploring peripheral neuro-immune interactions

Acupuncture for the Relief of Chronic Pain: A Synthesis of Systematic Reviews

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