Etiopathogenetic mechanisms of fibromyalgia syndrome

Stisi, S.; Cazzola, M.; Buskila, Dan; Späth, M.; Giamberardino, M. A.; Sarzi-Puttini, Piercarlo; Arioli, G.; Alciati, Alessandra; Leardini, G.; Gorla, Roberto; Marsico, A.; Ceccherelli, Francesco; Bazzichi, Laura; Carignola, R.; Gracely, R.; Salaffi, Fausto; Marinangeli, Franco; Torta, Riccardo; M, Di Franco; Biasi, Giovanni; Cassisi, G.; Casale, Roberto; Altomonte, L; Atzeni, Fabiola

doi:10.4081/reumatismo.2008.1s.25

Cited by 26 publications

(29 citation statements)

References 75 publications

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“…Immunological cascades may play a role in maintaining central sensitivity and chronic pain, which is increased when CNS glial cells release pro-inflammatory cytokines; the traditional dichotomy of inflammatory vs non-inflammatory pain may therefore be less appropriate than previously thought (6). One of the simplest means of identifying subjects whose chronic pain has become centralised is to look for the symptoms of co-morbidities (1,8). The occurrence of multifocal pain in conjunction with other centrally mediated symptoms is frequently observed in patients developing centralised pain (8,9).…”

Section: N the Role Of Centralised Pain In Classic Rheumatic Diseasesmentioning

confidence: 99%

“…low levels of norepinephrine, GABA or serotonin, and high levels of glutamate or substance P) are also involved in controlling sleep, mood and alertness (8). The best support for this hypothesis is that when centrally acting analgesics such as selective serotonin and norepinephrine re-uptake inhibitors (SSNRIs), gabapentinoids, tricyclic antidepressant or g-hydroxybutyrate are effective in relieving chronic pain, this is frequently accompanied by improvements in other symptom domains (1,(10)(11)(12).…”

Section: N the Role Of Centralised Pain In Classic Rheumatic Diseasesmentioning

confidence: 99%

“…Similarly, there are other somatic symptoms that cannot be explained on the basis of a purely peripheral condition: studies have found that fatigue is a major problem in patients with knee OA as many of them find it a more functionally limiting symptom than pain (5,8). Peripherally based theories of the pathogenesis of OA, systemic lupsu erythematosus (SLE), and inflammatory arthritis simply do not explain why these other symptoms are so common and often refractory to standard therapies (1,5).…”

Section: N the Role Of Centralised Pain In Classic Rheumatic Diseasesmentioning

confidence: 99%

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Pain in rheumatic diseases: how relevant is it?

2014

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summary Pain, a complex phenomenon influenced by a series of genetic, biological, psychological and social factors, is a major component of many rheumatological conditions and the result of physiological interactions between central and peripheral nervous system signalling (1, 2). It may be acute or chronic (generally defined as lasting ≥ three months): acute pain is often primarily attributable to inflammation and/or damage to peripheral structures (i.e. nociceptive input), whereas chronic pain is more likely to be due to input from the central nervous system (CNS) (2, 3). The many different aspects of pain mean that rheumatologists and other clinicians need to have enough expertise to diagnose the type of pain correctly and treat it appropriately (3, 4). However, most rheumatologists receive little formal training concerning contemporary theories of pain processing or management, and this may affect the clinical results of any specific target therapy.

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Section: N the Role Of Centralised Pain In Classic Rheumatic Diseasesmentioning

confidence: 99%

Section: N the Role Of Centralised Pain In Classic Rheumatic Diseasesmentioning

confidence: 99%

Section: N the Role Of Centralised Pain In Classic Rheumatic Diseasesmentioning

confidence: 99%

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Pain in rheumatic diseases: how relevant is it?

2014

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“…It has been postulated that it can be the consequence of a chronic stress mediated mainly through the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system [4][5][6], in fact FM seems a disorder of the central nervous system sensitization, but this definition seems too simple and reductive. Despite an increasingly impressive research effort, there are many aspects of fibromyalgia that need further clarification.…”

Section: Introductionmentioning

confidence: 99%

Thyroid autoimmunity may represent a predisposition for the development of fibromyalgia?

et al. 2010

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In our previous study, we observed that the presence of autoimmune thyroid disease worsens fibromyalgia (FM) symptoms. The aims of this study are to evaluate whether there is a predisposition for the development of FM in patients with Hashimoto's thyroiditis (HT) with or without subclinical hypothyroidism (SCH) and in patients with SCH alone and what is the weight of antithyroid antibody positivity and SCH on FM comorbidity. Fifty-two patients, 39 affected by HT with or without SCH and 13 by SCH, were matched with 37 patients affected by FM and 25 healthy subjects. Blood samples were collected from all study subjects for the determination of serum TSH, free triiodothyronine, free thyroxine, antithyroperoxidase antibody (TPOAb), antithyroglobulin antibody (TgAb) and non-organ-specific autoantibodies. Clinical assessment of patients and controls included the "Fibromyalgia Impact Questionnaire" (FIQ), while pain severity was evaluated using a visual analogue scale (VAS). Patients and controls were also characterized by the presence of diffuse pain, fatigue, paresthesiae, muscle spasms, non-restful sleep, tension headache and presence of mood disorders. FM comorbidity resulted in twelve HT subjects (31%) and none in SCH patient. In particular, FM comorbidity in HT patients without SCH was 33.3% and in HT patients with SCH was 28.5%. Based on our data, we speculate that maybe there is more than a hypothesis regarding the cause-effect relation between thyroid autoimmunity and the presence of FM, thus suggesting a hypothetical role of thyroid autoimmunity in FM pathogenesis.

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“…This interpretation is still supported by many rheumatologists despite the repeated clinical evidence of a discrepancy between the intensity and characteristics of the pain reported by patients and the extent of the anatomical alterations detectable at the sites of the perceived pain, as in the case of the radiological grading of osteoarthritis (OA) (6). Over the last 20 years, the greatest advances in interpreting musculoskeletal pain have been made in the ambit of the widespread extra-articular forms of rheumatism, particularly the protypical form of fibromyalgia (FM) (7)(8)(9)(10)(11)(12). Studies of fibromyalgic patients have made it possible to recognise multiple neurophysiological modifications in the perception, transmission and, above all, processing of nociceptive afferents at the level of the central nervous system CNS (13)(14)(15)(16)(17).…”

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confidence: 99%

Physiopathology of pain in rheumatology

et al. 2014

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summary Pain is the main manifestation of many rheumatic diseases (be they overtly inflammatory such as rheumatoid arthritis or dysfunctional such as fibromyalgia) but, at least initially, the mechanisms involved in the genesis, amplification and chronicisation of the persistent pain characterising the various conditions can be very different. The main peripheral mechanism underlying acute nociceptive pain is a change in the activity of the nociceptors located in the affected anatomical structures (joints, tendons and ligaments), which makes them more sensitive to normally painful stimuli (hyperalgesia) or normally non-painful stimuli (allodynia). This physiopathological mechanism of peripheral sensitisation plays a primary role in rheumatic diseases characterised by acute inflammation, such as the arthritides due to microcrystals. In the case of chronic rheumatic diseases that do not regress spontaneously, functional and structural central nervous system changes cause a generalised reduction in the pain threshold that is not limited to the anatomical structures involved, thus leading to the appearance of hyperalgesia and allodynia in many, if not all body districts. This is the physiopathological basis of chronic, widespread musculoskeletal pain.

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Etiopathogenetic mechanisms of fibromyalgia syndrome

Cited by 26 publications

References 75 publications

Pain in rheumatic diseases: how relevant is it?

Pain in rheumatic diseases: how relevant is it?

Thyroid autoimmunity may represent a predisposition for the development of fibromyalgia?

Physiopathology of pain in rheumatology

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