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Central sensitization in rheumatoid arthritis

PainSci » bibliography » Meeus et al 2012
Tags: pain, arthritis, sensitization, aging, pain problems, neurology, sensation

Two pages on PainSci cite Meeus 2012: 1. Sensitization in Chronic Pain2. Rheumatoid arthritis and central sensitization

PainSci notes on Meeus 2012:

Sometimes the central nervous system changes so that we feel more pain with less provocation (sensitization). How much does this phenomenon complicate chronic pain problems? For instance, rheumatoid arthritis (RA) is a nasty source of chronic pain, but could some of the pain be caused by central sensitization instead of the disease itself?

Meeus et al. concluded that there are signs of this, from analyzing 24 scientific papers (although “more research is needed,” of course). RA mainly attacks joints, but patients often experience pain elsewhere, and in response to a variety of stimuli, and symmetrically — all of which are a good fit for central sensitization. Also, as with many other chronic pain conditions, in RA there’s often more (or less) pain than detectable tissue trouble (e.g. see Younes), indicating that the progress of the disease is probably not the only driver of pain. Sensitization may be the best way to explain this.

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

OBJECTIVE: The goal of the present study is to systematically review the scientific literature addressing central sensitization and central nociceptive processing in patients with rheumatoid arthritis (RA).

METHODS: To identify relevant articles, we searched PubMed and Web of Science. The search strategy was a combination of terms of the following groups: "Rheumatoid arthritis," inflammatory joint pain, or arthritis; AND (central) sensitization, (central) hypersensitivity, central hyperexcitability, pain modulation, pain processing, neural inhibition, or pain physiopathology; AND pain, nociception, hyperalgesia, pain threshold, or algometry. Articles fulfilling the inclusion criteria were screened for methodologic quality with specific checklists to evaluate different study designs (2 independent raters).

RESULTS: Twenty-four full-text articles were included, of which the majority were case-control studies, followed by nonsystematic reviews, cross-sectional studies, and case reports. Methodologic quality was very heterogeneous. Preliminary evidence for generalized hyperalgesia in RA is available. In addition, the mechanism behind impaired central nociceptive processing remains rather obscure. The role of cytokines and neuropeptides especially remains to be elucidated. Windup appears to develop more easily in RA, but evidence in support of impaired nociceptive inhibition and cognitive emotional sensitization (sensitization due to cognitive bias) is scarce.

CONCLUSIONS: The symmetrical manifestation of the disease, the poor relation between disease activity and symptoms, and the generalized hyperalgesia at both articular and nonarticular sites for different kinds of stimuli are indicative of the presence of central sensitization in RA patients. Further research is required to provide firm evidence in support of various aspects of central sensitization in humans with RA.

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