Understanding pain in psoriatic disease

Why is pain so important to understand?

Chronic pain is a major global health issue which is associated with increased levels of disability, reduced quality of life and increased mortality.¹⁰ This ‘paindemic’ is evident in the general population whereby chronic pain is the main reason people seek medical care,¹¹ accounts for between 22 and 50% of consultations with a General Practitioner¹² and has been shown to have a prevalence of between 11 and 40% of the general adult population.^12,13 Furthermore, the global impact of musculoskeletal pain is highlighted by findings from The Global Burden of Diseases, Injuries, and Risk Factors Study 2017, which showed that lower back pain was the leading cause of years lived with disability worldwide.¹⁴

When we consider the cohort of people attending rheumatology clinics due to a variety of rheumatic conditions, pain is the most common symptom experienced by patients.¹⁵ More specifically, it is also the main reason that patients with inflammatory arthritis seek input from a rheumatologist and is the single most important factor influencing patient global assessment of disease activity.¹⁶ Previous work has shown that amongst the treatment priorities identified by patients living with PsA, control of pain emerges as a dominant treatment goal, particularly due to its link with improved overall quality of life.¹⁷

There is increasing recognition that cutaneous pain is also prevalent in PSO, affecting over 40% of patients, with an average pain severity of 4.4 out of 10 on the numerical rating scale.⁸ The focus of investigation in PSO has typically been on symptoms such as the appearance of plaques, pruritus, fatigue, and joint pain, but reduction of burning and pain sensations in the skin were also identified as important treatment goals, in 70.6% and 60.6% of patients, respectively.⁸ Like PsA, the underlying mechanisms driving pain are likely to be multifactorial. This hypothesis is supported by the range of descriptors used to describe the qualities of skin pain which include neuropathic characteristics like burning, stinging, sensitivity and tingling as well as aching and tenderness which are more typically associated with both nociceptive and nociplastic pain.⁸ The presence of neuropathic pain is further supported by the identification of a neuropathic component, using the Douleur Neuropathique (DN4) Questionnaire, in the majority of PSO patients with skin pain.⁴ Neurogenic inflammation, resulting in upregulation of pain-inducing neuropeptides, including substance P and nerve growth factor, may be driving some of the neuropathic pain mechanisms in PSO.⁸ In parallel, the known effects of PSO on sleep, activity and mood may be risk factors for the development of nociplastic pain.^6,8 Given that sleep disorders can elevate cytokine secretion such as tumour necrosis factor (TNF)-α and interleukin (IL)-6 in PsA, another possibility is that centrally-driven circadian mechanisms may also contribute to skin inflammation in PSO,^18,19 but these hypotheses require further investigation and validation.

Taken together, a better understanding of the underlying pain mechanisms in both PSO and PsA is urgently needed to address patient concerns and help them achieve the improved quality of life that they seek.

Where is the pain coming from?

Traditionally, it has been assumed that pain in inflammatory arthritis is either due to joint inflammation or, later in the disease course, structural damage affecting the joints. An MRI-based study in patients with early rheumatoid arthritis (RA) suggested that inflammation was a stronger driver of pain than structural changes.²⁰ Whilst treatment of inflammation results in improved pain, the correlation between inflammation and pain intensity is not perfect and many patients continue to suffer from moderate pain, despite adequate treatment with DMARDs or biological agents such as TNFi.^16,21 For example, data from an observational, cross-sectional study of patients registered in DANBIO, the Danish nationwide rheumatologic registry, showed that despite treatment with DMARDS and/or Biologics, over 50% of patients with a diagnosis of inflammatory arthritis continued to experience clinically significant residual pain which was greater than 30 out of 100mm in severity on a visual analogue scale.²² Furthermore, data from the South Swedish Arthritis Treatment Group register have also shown that 40% of patients with PsA still reported unacceptable pain 12 months after starting anti-TNF therapy.²³ This study also distinguished between persistent pain due to ongoing inflammation versus refractory pain occurring in the absence of joint swelling or an elevated CRP. This non-inflammatory pain accounted for almost two-thirds of persistent, unacceptable pain experienced 1 year after starting anti-TNF therapy.²³

This presence of persistent pain despite the use of immunomodulatory therapy, raises the possibility of pain mechanisms which are independent of inflammation within the joints. Pre-clinical studies have demonstrated that pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6 and IL-17 may also mediate pain by acting directly on nociceptive sensory neurons.²⁴ By inducing sensitization of peripheral sensory neurons to mechanical stimuli, these cytokines can drive persistent joint hyperalgesia in the absence of synovitis.²⁴ Furthermore, the release of cytokines in the spinal cord is also able to trigger central sensitization which is also likely to contribute to the persistent pain state in inflammatory arthritis.²⁴

With advances in neuroimaging techniques, including multi-modal scanning, the link between peripheral joint inflammation levels and changes in connectivity between brain regions can be further investigated. Initial analyses, conducted in patients with RA, have demonstrated greater connections to the left inferior parietal lobe and bilateral medial prefrontal cortex in patients with higher levels of inflammation, measured by venous blood erythrocyte sedimentation rate.²⁵ In addition, the subgroup of RA patients, who also have more prominent features of coexisting fibromyalgia, showed changes in functional brain connectivity which are typically seen in patients with primary fibromyalgia.²⁶ Furthermore, these pronociceptive patterns of brain connectivity were linked to the levels of inflammation seen in the periphery, suggesting that the response to peripheral inflammation in the brain may be contributing to the concomitant fibromyalgia seen in some patients with RA.²⁷ A more recent study has confirmed that a similar neurobiological process is likely to be present in patients with PsA as well.⁹ In this study, increased functional brain connectivity was observed between the mid-posterior insular cortex and brain areas involved in sensory (thalamus), learning/affective (parahippocampal gyrus), and cognitive (prefrontal cortex) aspects of pain modulation.⁹

Taken together, pain in PsA should be thought of as multifactorial in nature, similar to fibromyalgia where a variety of environmental, genetic, biological and psychological factors are thought to influence pain processing in both the peripheral and central nervous system (Figure 1).²⁸ In an ideal world, it would be possible to disambiguate the different mechanisms which may be causing pain at an individual level, to guide the optimal treatment approach.

Figure 1. Summary of the various factors which may influence the pathogenesis of chronic pain²⁸

How can we categorize pain in the clinical setting?

As highlighted above, multiple mechanisms for pain may be present among individuals living with PsA. The International Association for the Study of Pain (IASP) has provided an infrastructure for considering these mechanistic groups by defining three classes of pain: nociceptive, neuropathic and nociplastic pain.^29,30 Nociceptive pain is defined as “pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors” and so is appropriate when synovitis is thought to be driving joint pain in PsA. Neuropathic pain describes “pain caused by a lesion or disease of the somatosensory nervous system” which is likely to be rare in PsA. Nociplastic pain refers to “pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain”. Whilst it is not yet clear how best to identify this more recently introduced category of nociplastic pain in clinical practice, for practical purposes it can be considered to be similar to older terms such as central sensitization, or centralized pain with fibromyalgia being the prototypical nociplastic pain condition.^29,31

The presence and clinical relevance of nociplastic pain in patients with established inflammatory arthritis has been previously investigated using symptom-based assessments,^32-35 clinical diagnosis of co-existing fibromyalgia,^36-38 quantitative sensory testing^39-43 and neuroimaging.^{9,25-27,44,45} The prevalence of comorbid fibromyalgia amongst patients with inflammatory arthritis is much higher than amongst the general population, with an estimated pooled prevalence of 18% in patients with PsA.³⁸ In addition, a recent study identified widespread pain in 20.6% of over 1800 patients with PsA in the CorEvitas US registry.⁴⁶ Symptom-based evaluation has demonstrated that around 40% of patients with established PsA have features suggestive of pain sensitivity.³⁵ Furthermore, studies utilizing quantitative sensory testing have shown that patients with inflammatory arthritis have a reduced pressure pain threshold, consistent with allodynia, in painful joints as well as at extra-articular sites, which suggests the presence of more generalized pain sensitivity which is likely to mediated by central sensitization.⁴⁷ Advances in neuroimaging have facilitated the further understanding of the neurobiology underpinning the experience of pain in humans.⁴⁸ In particular, it has enabled us to investigate the role of the descending pain modulatory system, a well-characterized anatomical network in the central nervous system which enables us to exert top-down regulation of nociceptive processing resulting in either pronociception or antinociception.⁴⁸ Since the introduction of the term nociplastic pain, it has been recognized that screening tools for neuropathic pain may be used to identify components of centrally mediated pain.⁴⁹ The painDETECT questionnaire has been commonly applied in this context and a study of inflammatory arthritis showed that the prevalence of centrally mediated pain is significantly higher amongst patients with PsA compared to either RA or SpA.²² The presence of pain arising from skin lesions several years prior to the onset of musculoskeletal symptoms may be one explanation for this higher prevalence of pain sensitization in patients with PsA. An alternative hypothesis is that the development of multisite enthesitis in PsA creates an additional and more widespread burden of pain, which drives this phenomenon. Using the same screening tool, areas in the brainstem including the periaqueductal gray and rostral ventromedial medulla, which contribute to this descending modulation, have also been shown to be linked to the presence of neuropathic-like symptoms in musculoskeletal pain associated with osteoarthritis.^50,51 Preliminary evidence suggests that the presence of centrally mediated pain also has a negative impact on outcomes following arthroplasty.⁵¹ Similarly, a study using conditioned pain modulation (CPM) as a clinical measure of descending inhibition in patients with RA showed that low CPM was significantly associated with lower odds of achieving a good EULAR response after commencing DMARD therapy.⁴⁰ In PsA, the presence of co-existing fibromyalgia is also associated with higher disease activity coupled with a lower chance of experiencing an adequate response to standard immunomodulatory therapy.⁴⁶

The increasing recognition that different pain mechanisms can be present amongst individuals with inflammatory arthritis^31,52 is also addressed by the introduction of a new classification system for chronic pain, implemented in 2019 in ICD-11, proposed by IASP.⁵³ Using this approach, chronic pain is subdivided into chronic primary pain and chronic secondary pain syndromes (Figure 2). Whilst chronic primary pain conditions include a collection of syndromes, such as fibromyalgia, which are considered health conditions in their own right, chronic secondary pain is reserved for pain which initially manifested as the result of another condition, such as PsA. In the latter example, the diagnostic label of chronic secondary pain highlights the stage at which the pain occurs independently of any evidence of active PsA and could in turn inform subsequent treatment selection. However, this can be challenging to implement in clinical practice and Figure 3 summarizes the known factors which should prompt clinicians to suspect the presence of a chronic primary pain condition, which may also be relevant to chronic secondary pain, when pain becomes the principal problem in PsA.

Figure 2. Overview of the features of chronic primary or secondary painFigure 3. Summary of the known factors which may indicate the presence of chronic primary or secondary pain

What strategies can we use to help our patients manage their pain?

The first hurdle is to identify which mechanism or mechanisms are contributing to the current pain experience. As highlighted above, this can be difficult, but the main consideration is whether the pain is likely to be due to a consequence of active inflammation within the joints, and/or centrally mediated pain. Here we will focus on the evidence available to support treatment approaches in the context of centrally mediated pain.

Ideally, treatment strategies should be personalized to the needs of the individual patient, as highlighted by guidance issued by EULAR for the management of pain in inflammatory arthritis and osteoarthritis in 2018.⁵⁴ A similar theme emerged from subsequent recommendations, including those produced by The National Institute for Health and Care Excellence (NICE) for the management of chronic primary pain.⁵⁵

Acknowledging the fact that the symptoms the patient is experiencing are real, despite the presence of normal test results, such as normal inflammatory markers or imaging, has also been recognized as a key component of sharing the diagnosis of chronic pain in order to create a productive therapeutic relationship,^56-58 and as a foundation for other management strategies including supported self-management.⁵⁹

The core principles which are consistent across the various guidelines which are currently available include the use of non-pharmacological treatments as first line, including promoting physical activity and the use of psychological therapies such as cognitive behavioural therapy or acceptance and commitment therapy.^54-56,58 Pharmacological treatment recommendations are somewhat controversial, but overall there is a preference for considering tricyclic antidepressant agents, such as amitriptyline or minocycline, and serotonin–noradrenaline reuptake inhibitors, such as duloxetine and milnacipran, whilst also recognizing that long term efficacy and safety data for the use of these drugs in patients with chronic pain are lacking.^55,56,58,60 Other treatment options, with less robust evidence base, have been suggested including acupuncture and integrative therapies such as yoga and tai chi.^55,56,58 Future treatment options including cognitive behavioural therapy for insomnia⁶¹, neuromodulation, such as transcranial and deep brain stimulation, and newer pharmacological agents such as cannabinoids require further investigation.⁵⁸

Conflict of interest

The authors report there are no competing interests to declare.

FUNDING

None

Acknowledgements

None

REFERENCES

1. Ballegaard C, Skougaard M, Guldberg-Moller J, et al. Comorbidities, pain and fatigue in psoriatic arthritis, psoriasis and healthy controls: a clinical cohort study. Rheumatology (Oxford). 2021;60(7):3289-3300. 10.1093/rheumatology/keaa780
2. Ljosaa TM, Rustoen T, Mork C, et al. Skin pain and discomfort in psoriasis: an exploratory study of symptom prevalence and characteristics. Acta Derm Venereol. 2010;90(1):39-45. 10.2340/00015555-0764
3. Martin ML, Gordon K, Pinto L, Bushnell DM, Chau D, Viswanathan HN. The experience of pain and redness in patients with moderate to severe plaque psoriasis. J Dermatolog Treat. 2015;26(5):401-5. 10.3109/09546634.2014.996514
4. Misery L, Shourick J, Taieb C. Skin pain and psoriasis. J Am Acad Dermatol. 2020;83(1):245-246. 10.1016/j.jaad.2019.12.066
5. Sanader Vucemilovic A, Krnic Martinic M, Lazic Mosler E, Puljak L. Pain associated with psoriasis: a qualitative study. Pain Med. 2023;24(10):1189-1196. 10.1093/pm/pnad067
6. Kodumudi V, Rajput K. Pain Management in Painful Psoriasis and Psoriatic Arthropathy: Challenging and Intricately Intertwined Issues Involving Several Systems. Curr Pain Headache Rep. 2021;25(6):36. 10.1007/s11916-021-00952-5
7. Ljosaa TM, Mork C, Stubhaug A, Moum T, Wahl AK. Skin pain and skin discomfort is associated with quality of life in patients with psoriasis. J Eur Acad Dermatol Venereol. 2012;26(1):29-35. 10.1111/j.1468-3083.2011.04000.x
8. Pithadia DJ, Reynolds KA, Lee EB, Wu JJ. Psoriasis-associated cutaneous pain: etiology, assessment, impact, and management. J Dermatolog Treat. 2019;30(5):435-440. 10.1080/09546634.2018.1528330
9. Sunzini F SK, Al-Wasity S, Harte S, Harris R, Clauw D, Siebert S, Goodyear C, Waiter G, Basu N. Increased Brain Functional Connectivity to the Insula Is Associated with Nociplastic Pain in Psoriatic Arthritis. Arthritis Rheumatol. 2022;74(suppl 9): abstract 2256.
10. Mills SEE, Nicolson KP, Smith BH. Chronic pain: a review of its epidemiology and associated factors in population-based studies. Br J Anaesth. 2019;123(2):e273-e283. 10.1016/j.bja.2019.03.023
11. St Sauver JL, Warner DO, Yawn BP, et al. Why patients visit their doctors: assessing the most prevalent conditions in a defined American population. Mayo Clin Proc. 2013;88(1):56-67. 10.1016/j.mayocp.2012.08.020
12. Smith BH, Fors EA, Korwisi B, et al. The IASP classification of chronic pain for ICD-11: applicability in primary care. Pain. 2019;160(1):83-87. 10.1097/j.pain.0000000000001360
13. Eoin Kelleher, Xin You Tai, Trishna Rathod Mistry, Thomas Nichols, Irene Tracey, Anushka Soni. Multi-site chronic pain and cognitive function: a cross-sectional study of UK Biobank. British Journal of Pain. 2023;17(1_suppl): abstract PP030.
14. GBD 2017 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 354 diseases and injuries for 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2018;392(10159):1789-1858. 10.1016/S0140-6736(18)32279-7
15. American College of Rheumatology Pain Management Task Force. Report of the American College of Rheumatology Pain Management Task Force. Arthritis Care Res (Hoboken). 2010;62(5):590-9. 10.1002/acr.20005
16. Lee YC. Effect and treatment of chronic pain in inflammatory arthritis. Curr Rheumatol Rep. 2013;15(1):300. 10.1007/s11926-012-0300-4
17. Garrido-Cumbrera M, Hillmann O, Mahapatra R, et al. Improving the Management of Psoriatic Arthritis and Axial Spondyloarthritis: Roundtable Discussions with Healthcare Professionals and Patients. Rheumatol Ther. 2017;4(2):219-231. 10.1007/s40744-017-0066-2
18. Halioua B, Chelli C, Misery L, Taieb J, Taieb C. Sleep Disorders and Psoriasis: An Update. Acta Derm Venereol. 2022;102:adv00699. 10.2340/actadv.v102.1991
19. Skougaard M, Stisen ZR, Jorgensen TS, et al. Increased prevalence of sleep disturbance in psoriatic arthritis is associated with inflammatory and non-inflammatory measures. Scand J Rheumatol. 2023;52(3):259-267. 10.1080/03009742.2022.2044116
20. Glinatsi D, Baker JF, Hetland ML, et al. Magnetic resonance imaging assessed inflammation in the wrist is associated with patient-reported physical impairment, global assessment of disease activity and pain in early rheumatoid arthritis: longitudinal results from two randomised controlled trials. Ann Rheum Dis. 2017;76(10):1707-1715. 10.1136/annrheumdis-2017-211315
21. Conaghan PG, Alten R, Deodhar A, et al. Relationship of pain and fatigue with health-related quality of life and work in patients with psoriatic arthritis on TNFi: results of a multi-national real-world study. RMD Open. 2020;6(2)10.1136/rmdopen-2020-001240
22. Rifbjerg-Madsen S, Christensen AW, Christensen R, et al. Pain and pain mechanisms in patients with inflammatory arthritis: A Danish nationwide cross-sectional DANBIO registry survey. PLoS One. 2017;12(7):e0180014. 10.1371/journal.pone.0180014
23. Roseman C, Wallman JK, Joud A, et al. Persistent pain and its predictors after starting anti-tumour necrosis factor therapy in psoriatic arthritis: what is the role of inflammation control? Scand J Rheumatol. 2024;53(2):94-103. 10.1080/03009742.2023.2258644
24. Schaible HG. Nociceptive neurons detect cytokines in arthritis. Arthritis Res Ther. 2014;16(5):470. 10.1186/s13075-014-0470-8
25. Schrepf A, Kaplan CM, Ichesco E, et al. A multi-modal MRI study of the central response to inflammation in rheumatoid arthritis. Nat Commun. 2018;9(1):2243. 10.1038/s41467-018-04648-0
26. Basu N, Kaplan CM, Ichesco E, et al. Neurobiologic Features of Fibromyalgia Are Also Present Among Rheumatoid Arthritis Patients. Arthritis Rheumatol. 2018;70(7):1000-1007. 10.1002/art.40451
27. Kaplan CM, Schrepf A, Ichesco E, et al. Association of Inflammation With Pronociceptive Brain Connections in Rheumatoid Arthritis Patients With Concomitant Fibromyalgia. Arthritis Rheumatol. 2020;72(1):41-46. 10.1002/art.41069
28. Gyorfi M, Rupp A, Abd-Elsayed A. Fibromyalgia Pathophysiology. Biomedicines. 2022;10(12)10.3390/biomedicines10123070
29. Kosek E, Clauw D, Nijs J, et al. Chronic nociplastic pain affecting the musculoskeletal system: clinical criteria and grading system. Pain. 2021;162(11):2629-2634. 10.1097/j.pain.0000000000002324
30. Kosek E, Cohen M, Baron R, et al. Do we need a third mechanistic descriptor for chronic pain states? Pain. 2016;157(7):1382-6. 10.1097/j.pain.0000000000000507
31. Murphy AE, Minhas D, Clauw DJ, Lee YC. Identifying and Managing Nociplastic Pain in Individuals With Rheumatic Diseases: A Narrative Review. Arthritis Care Res (Hoboken). 2023;10.1002/acr.25104
32. Moore MN, Wallace BI, Song J, et al. Correlation of Fibromyalgia Survey Questionnaire and Quantitative Sensory Testing Among Patients With Active Rheumatoid Arthritis. J Rheumatol. 2022;49(9):1052-1057. 10.3899/jrheum.220046
33. Ahmed S, Magan T, Vargas M, Harrison A, Sofat N. Use of the painDETECT tool in rheumatoid arthritis suggests neuropathic and sensitization components in pain reporting. J Pain Res. 2014;7:579-88. 10.2147/JPR.S69011
34. Koop SM, ten Klooster PM, Vonkeman HE, Steunebrink LM, van de Laar MA. Neuropathic-like pain features and cross-sectional associations in rheumatoid arthritis. Arthritis Res Ther. 2015;17:237. 10.1186/s13075-015-0761-8
35. Rutter-Locher Z, Arumalla N, Norton S, Taams LS, Kirkham BW, Bannister K. A systematic review and meta-analysis of questionnaires to screen for pain sensitisation and neuropathic like pain in inflammatory arthritis. Semin Arthritis Rheum. 2023;61:152207. 10.1016/j.semarthrit.2023.152207
36. Kim H, Cui J, Frits M, et al. Fibromyalgia and the Prediction of Two-Year Changes in Functional Status in Rheumatoid Arthritis Patients. Arthritis Care Res (Hoboken). 2017;69(12):1871-1877. 10.1002/acr.23216
37. Lee YC, Lu B, Boire G, et al. Incidence and predictors of secondary fibromyalgia in an early arthritis cohort. Ann Rheum Dis. 2013;72(6):949-54. 10.1136/annrheumdis-2012-201506
38. Zhao SS, Duffield SJ, Goodson NJ. The prevalence and impact of comorbid fibromyalgia in inflammatory arthritis. Best Pract Res Clin Rheumatol. 2019;33(3):101423. 10.1016/j.berh.2019.06.005
39. Heisler AC, Song J, Dunlop DD, et al. Association of Pain Centralization and Patient-Reported Pain in Active Rheumatoid Arthritis. Arthritis Care Res (Hoboken). 2020;72(8):1122-1129. 10.1002/acr.23994
40. Heisler AC, Song J, Muhammad LN, et al. Association of Dysregulated Central Pain Processing and Response to Disease-Modifying Antirheumatic Drug Therapy in Rheumatoid Arthritis. Arthritis Rheumatol. 2020;72(12):2017-2024. 10.1002/art.41440
41. Lee YC, Bingham CO, 3rd, Edwards RR, et al. Association Between Pain Sensitization and Disease Activity in Patients With Rheumatoid Arthritis: A Cross-Sectional Study. Arthritis Care Res (Hoboken). 2018;70(2):197-204. 10.1002/acr.23266
42. Song J, Muhammad LN, Neogi T, et al. Pain Sensitization as a Potential Mediator of the Relationship Between Sleep Disturbance and Subsequent Pain in Rheumatoid Arthritis. Arthritis Care Res (Hoboken). 2023;75(4):778-784. 10.1002/acr.24888
43. Wohlfahrt A, Muhammad LN, Song J, et al. Pain Mechanisms Associated With Disease Activity in Patients With Rheumatoid Arthritis Treated With Disease-Modifying Antirheumatic Drugs: A Regression Tree Analysis. J Rheumatol. 2023;50(6):741-747. 10.3899/jrheum.220500
44. Sandstrom A, Ellerbrock I, Jensen KB, et al. Altered cerebral pain processing of noxious stimuli from inflamed joints in rheumatoid arthritis: An event-related fMRI study. Brain Behav Immun. 2019;81:272-279. 10.1016/j.bbi.2019.06.024
45. Sandstrom A, Ellerbrock I, Lofgren M, et al. Distinct aberrations in cerebral pain processing differentiating patients with fibromyalgia from patients with rheumatoid arthritis. Pain. 2022;163(3):538-547. 10.1097/j.pain.0000000000002387
46. Mease P, Reed G, Ogdie A, Pappas DA, Kremer JM. Prevalence of Fibromyalgia and Widespread Pain in Psoriatic Arthritis: Association With Disease Severity Assessment in a Large US Registry. Arthritis Care Res (Hoboken). 2024;76(9):1313-1321. 10.1002/acr.25358
47. Trouvin AP, Attal N, Perrot S. Assessing central sensitization with quantitative sensory testing in inflammatory rheumatic diseases: A systematic review. Joint Bone Spine. 2022;89(5):105399. 10.1016/j.jbspin.2022.105399
48. Tracey I, Mantyh PW. The cerebral signature for pain perception and its modulation. Neuron. 2007;55(3):377-91. 10.1016/j.neuron.2007.07.012
49. Bailly F, Cantagrel A, Bertin P, et al. Part of pain labelled neuropathic in rheumatic disease might be rather nociplastic. RMD Open. 2020;6(2)10.1136/rmdopen-2020-001326
50. Gwilym SE, Keltner JR, Warnaby CE, et al. Psychophysical and functional imaging evidence supporting the presence of central sensitization in a cohort of osteoarthritis patients. Arthritis Rheum. 2009;61(9):1226-34. 10.1002/art.24837
51. Soni A, Wanigasekera V, Mezue M, et al. Central Sensitization in Knee Osteoarthritis: Relating Presurgical Brainstem Neuroimaging and PainDETECT-Based Patient Stratification to Arthroplasty Outcome. Arthritis Rheumatol. 2019;71(4):550-560. 10.1002/art.40749
52. Sunzini F, Schrepf A, Clauw DJ, Basu N. The Biology of Pain: Through the Rheumatology Lens. Arthritis Rheumatol. 2023;75(5):650-660. 10.1002/art.42429
53. Nicholas M, Vlaeyen JWS, Rief W, et al. The IASP classification of chronic pain for ICD-11: chronic primary pain. Pain. 2019;160(1):28-37. 10.1097/j.pain.0000000000001390
54. Geenen R, Overman CL, Christensen R, et al. EULAR recommendations for the health professional's approach to pain management in inflammatory arthritis and osteoarthritis. Ann Rheum Dis. 2018;77(6):797-807. 10.1136/annrheumdis-2017-212662
55. Chronic pain (primary and secondary) in over 16s: assessment of all chronic pain and management of chronic primary pain. 2021. National Institute for Health and Care Excellence: Guidelines.
56. Fitzcharles MA, Cohen SP, Clauw DJ, Littlejohn G, Usui C, Hauser W. Nociplastic pain: towards an understanding of prevalent pain conditions. Lancet. 2021;397(10289):2098-2110. 10.1016/S0140-6736(21)00392-5
57. Kang Y, Trewern L, Jackman J, McCartney D, Soni A. Chronic pain: definitions and diagnosis. BMJ. 2023;381:e076036. 10.1136/bmj-2023-076036
58. Kaplan CM, Kelleher E, Irani A, Schrepf A, Clauw DJ, Harte SE. Deciphering nociplastic pain: clinical features, risk factors and potential mechanisms. Nat Rev Neurol. 2024;20(6):347-363. 10.1038/s41582-024-00966-8
59. Kang Y, Trewern L, Jackman J, Irani Nee Soni A, McCartney D. Chronic pain: supported self-management. BMJ. 2024;384:e072362. 10.1136/bmj-2022-072362
60. Birkinshaw H, Friedrich CM, Cole P, et al. Antidepressants for pain management in adults with chronic pain: a network meta-analysis. Cochrane Database Syst Rev. 2023;5(5):CD014682. 10.1002/14651858.CD014682.pub2
61. Latocha KM, Loppenthin KB, Ostergaard M, et al. The effect of group-based cognitive behavioural therapy for insomnia in patients with rheumatoid arthritis: a randomized controlled trial. Rheumatology (Oxford). 2023;62(3):1097-1107. 10.1093/rheumatology/keac44

 

©2024 the author(s). Published with license by Medicom Medical Publishers.
This an Open Access article distributed under the terms of the Creative Commons attribution-non Commercial license (http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Posted on 11 November 202425 November 2024