Patients with rheumatoid arthritis adapt differently to repetitive painful stimuli compared to healthy controls

Wendler, Jörg; Hummel, Thomas; Reissinger, M.; Manger, Bernhard; Pauli, E.; Kalden, Joachim R.; Kobal, Gerd

doi:10.1054/jocn.1999.0775

Cited by 36 publications

(20 citation statements)

References 35 publications

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“…They have been used successfully in studies of patients with peripheral neuropathies [38], trigeminal neuralgia [39], post herpetic neuralgia [40], and syringomyelia [41]. Laser evoked potential suppression helps diagnose neuropathic pain states [39,42,43], while laser evoked potential facilitation is described in fibromyalgic and chronic inflammatory pain [44,45]. The similarity between contact heat evoked and laser evoked potentials has already been described [5].…”

Section: Discussionmentioning

confidence: 99%

Use of the novel contact heat evoked potential stimulator (CHEPS) for the assessment of small fibre neuropathy: correlations with skin flare responses and intra-epidermal nerve fibre counts

et al. 2007

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Background: The Contact Heat Evoked Potential Stimulator (CHEPS) rapidly stimulates cutaneous small nerve fibres, and resulting evoked potentials can be recorded from the scalp. We have studied patients with symptoms of sensory neuropathy and controls using CHEPS, and validated the findings using other objective measures of small nerve fibres i.e. the histamine-induced skin flare response and intra-epidermal fibres (IEF), and also quantitative sensory testing (QST), a subjective measure.

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Section: Discussionmentioning

confidence: 99%

Use of the novel contact heat evoked potential stimulator (CHEPS) for the assessment of small fibre neuropathy: correlations with skin flare responses and intra-epidermal nerve fibre counts

et al. 2007

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“…Wendler and colleagues demonstrated using electroencephalography that, compared with age-matched and sex-matched controls, RA patients had enhanced cortical responses to repeated noxious stimulation, suggesting changes in CNS modulation of pain [60]. Morris and colleagues showed that capsaicin induces a larger area of hyperalgesia among RA patients compared with healthy controls [61].…”

Section: Rheumatoid Arthritismentioning

confidence: 99%

The role of the central nervous system in the generation and maintenance of chronic pain in rheumatoid arthritis, osteoarthritis and fibromyalgia

2011

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Pain is a key component of most rheumatologic diseases. In fibromyalgia, the importance of central nervous system pain mechanisms (for example, loss of descending analgesic activity and central sensitization) is well documented. A few studies have also noted alterations in central pain processing in osteoarthritis, and some data, including the observation of widespread pain sensitivity, suggest that central pain-processing defects may alter the pain response in rheumatoid arthritis patients. When central pain is identified, different classes of analgesics (for example, serotonin-norepinephrine reuptake inhibitors, α2δ ligands) may be more effective than drugs that treat peripheral or nociceptive pain (for example, nonsteroidal anti-inflammatory drugs and opioids).

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“…Central sensitization and changes in nociceptive processing in response to repeated stimulation by chemo-somatosensory event-related potentials (CSSERP) have been demonstrated encephalographically in RA patients (Wendler et al, 2001). Although increases in alpha 1 and beta 1 range are thought to be secondary to a chronic pain state it may be that these changes are in fact a result of direct neuroinflammation secondary to the arthritis itself.…”

Section: Neuro-immune Interaction In Rheumatoid Arthritismentioning

confidence: 99%

New insights into the impact of neuro-inflammation in rheumatoid arthritis

et al. 2014

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Rheumatoid arthritis (RA) is considered to be, in many respects, an archetypal autoimmune disease that causes activation of pro-inflammatory pathways resulting in joint and systemic inflammation. RA remains a major clinical problem with the development of several new therapies targeted at cytokine inhibition in recent years. In RA, biologic therapies targeted at inhibition of tumor necrosis factor alpha (TNFα) have been shown to reduce joint inflammation, limit erosive change, reduce disability and improve quality of life. The cytokine TNFα has a central role in systemic RA inflammation and has also been shown to have pro-inflammatory effects in the brain. Emerging data suggests there is an important bidirectional communication between the brain and immune system in inflammatory conditions like RA. Recent work has shown how TNF inhibitor therapy in people with RA is protective for Alzheimer's disease. Functional MRI studies to measure brain activation in people with RA to stimulus by finger joint compression, have also shown that those who responded to TNF inhibition showed a significantly greater activation volume in thalamic, limbic, and associative areas of the brain than non-responders. Infections are the main risk of therapies with biologic drugs and infections have been shown to be related to disease flares in RA. Recent basic science data has also emerged suggesting that bacterial components including lipopolysaccharide induce pain by directly activating sensory neurons that modulate inflammation, a previously unsuspected role for the nervous system in host-pathogen interactions. In this review, we discuss the current evidence for neuro-inflammation as an important factor that impacts on disease persistence and pain in RA.

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Patients with rheumatoid arthritis adapt differently to repetitive painful stimuli compared to healthy controls

Cited by 36 publications

References 35 publications

Use of the novel contact heat evoked potential stimulator (CHEPS) for the assessment of small fibre neuropathy: correlations with skin flare responses and intra-epidermal nerve fibre counts

Use of the novel contact heat evoked potential stimulator (CHEPS) for the assessment of small fibre neuropathy: correlations with skin flare responses and intra-epidermal nerve fibre counts

The role of the central nervous system in the generation and maintenance of chronic pain in rheumatoid arthritis, osteoarthritis and fibromyalgia

New insights into the impact of neuro-inflammation in rheumatoid arthritis

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