The fibromyalgia problem. A Latin American point of view

C. V. Caballero-Uribe

Unidad de Reumatología, Hospital Universidad del Norte, Barranquilla, Calle 30, Vía al aeropuerto, Al lado del Parque Mundi, Colombia, Sur América

Correspondence to: C. V. Caballero-Uribe. E-mail: carvica{at}etb.net.co

SIR, I read with interest the article by Hazemeijer and Rasker on fibromyalgia and the therapeutic domain [1] and the recent editorial comments by Harth and Nielson [2] and Wolfe [3]. Controversy about fibromyalgia as a ‘real’ or ‘false’ disease is frequent. Recently, an article on fibromyalgia in an Amish community by White and Thompson [4] had four accompanying editorials and points of views from Gordon, Ehrlich, Hadler, and again Wolfe [5–8]. I have also had the opportunity to read the recent articles by Gracely et al. [9] and Paiva et al. [10] and the editorial by Crofford and Clauw in a recent journal [11].

After a more than a decade of ACR criteria, controversies remain. Is fibromyalgia syndrome (FMS) really a disease? If it is, is it a rheumatological disease or a psychiatric or psychological disease? Are the current criteria useful? Moreover, is there something useful for these patients?

FMS is a costly disease, which represents an economic problem for health care systems. Although chronic pain has always existed, since we started labeling it as FMS using the ACR criteria, work disability payments have grown up to 25.3% in developed countries [12, 13]. From my Latin American point of view, economic matters is one of the main reasons why, in developed countries, the rheumatological community is looking desperately for a cause and a marker for chronic widespread pain. Doctors need to justify diagnosis and disability in patients to the health care system and insurance companies in order for them to cover the costs of the disease. The Amish community is known for their absence of economic influences. High prevalence of FMS (7%) in this population attempts to ‘prove’ that the disease develops independently from economic matters [4]. However, the controversy is still open. Current candidates for disease markers could be the substance P level in the cerebrospinal fluid [14], neurohormonal alterations [15], dysautonomic dysfunctions [16], altered alpha sleep characteristics [17] and functional magnetic resonance imaging [18], which offers interesting data but incomplete or circumstantial explanations for disease.

Furthermore, there is strong evidence that previous features of somatization contribute to the development of chronic widespread pain, and persons with FMS exhibit functional impairment, high levels of some lifetime and current psychiatric disorders, and significant psychological distress [18] labelling FMS as a ‘mind disease’ with rheumatic complaints, as Hazemeijer and Rasker point out in their philosophical study [1].

Current criteria take into account only the expression (tender points) and not the causes of pain. It is well known that pain can arise from the involvement of peripheral nerve fibres but also can arise from central nerve fibres. In the 1960s, Ronald Melzac proposed a gate theory whereby physical conditions (damage extension or an inappropriate level of activity), emotional conditions (anxiety or depression) and mental conditions (boredom or subjects who are focused in pain) can open the pain gate. On the other hand, medicines or physical therapy (heat or cold), positive emotions or relaxation, an adequate level of mental concentration, extreme distraction or interest in daily activities can close the gate that modulates pain. This model posits that the brain possesses a neural network that consists of pathways linking the thalamus, cortex and limbic system, termed the ‘neuromatrix’, which integrates multiple inputs to generate patterns of neural activity. These inputs include multiple sources of afferent input, pathological input (injured nerves), endocrine, immune and autonomic system activity, medullary descending activity, CNS plasticity, attention, and psychosocial and health status factors. Therefore, any factor that alters the function of pain transmission or pain modulation pathways in the neuromatrix will influence pain perception and pain behaviour [19]. It is clear that there are several pathways of pain in rheumatic diseases, and FMS could be a natural model to explain centrally mediated pain in these diseases; neuromatrix is a conceptual framework, in addition to the therapeutic domain. In research on FMS, it would be therefore be reasonable to include patients with the different subtypes or the entire spectrum of disease rather than just those with the ACR criteria.

In the mestizo patients of Columbia, FMS is a highly recognizable disease with clinical and psychological outcomes as reported worldwide [20, 21]. In our country it is very infrequent to have a conflict of interest or legal issues because of an FMS diagnosis. FMS is still poorly recognized by the health care system and by professionals other than rheumatologists. In our setting, disability benefits paid by the healthcare system or insurance companies are as yet infrequent. Until now, we have found useful the label of FMS, since it doesn't represent an economic connotation or secondary gain and can help the patients to understand the disease.

In our experience, and according to the current evidence-based treatment of FMS [22]; FMS is a difficult clinical problem with lack of adequate treatments. Our approach to the management of patients includes an analogy of the algorithm treatment of rheumatoid arthritis proposed by the American College of Rheumatology [23]. In this analogy the initial evaluation must include a clinical examination (tender point count) and an assessment of the patient's functional and psychological status with an assessment questionnaire (Fibromyalgia Impact Questionnaire) [24]. Patient education is very important as well as indicating physical and occupational therapy and asking questions about sleep patterns before medications. Follow up management should be done. Further referrals will be done according status and response. Most drugs with acceptable evidence to treat FMS act by blocking central pain mechanisms and psychological or psychiatric evaluation is very important in some stages of disease. We find, as in RA ‘refractory patients’ or ‘resistant fibromyalgia’ and, of course, real psychiatric patients but, according to Crofford and Clauw [11], most patients will find quicker, better answers and hope from interested rheumatologists than other specialists.

Finally, it is important for the rheumatological community to recognize what our patients need. In a quality of life assessment [13] patients reported to need more support (52.3%), better-educated health professionals (50%), and people to believe that this disease does exist (30%). Surprisingly, issues such as better medications (15.2%), more funding for research (13.6%) or better diagnostic tools (7.6%) scored low [25].

After more than 10 yr of the ACR criteria, the current conclusion seems to be that we still lack conclusive empirical and biological evidence and we need to know more about central pain in FMS, as well as in other rheumatic diseases, and about our patients. Independently of the causes of psychological or physical widespread pain and of subsets of patients, the fibromyalgia problem may be that persistent rheumatic complaints put this syndrome for ever in the rheumatologist's agenda, and—like it or not—we need a better understanding of chronic pain mechanisms if we are to face it.

The author has declared no conflicts of interest.

References

  1. Hazemeijer I, Rasker JJ. Fibromyalgia and the therapeutic domain. A philosophical study on the origins of fibromyalgia in a specific social setting. Rheumatology 2003;42:507.[Abstract/Free Full Text]
  2. Harth M, Nielson W. Comment on ‘Fibromyalgia and the therapeutic domain. A philosophical study on the origins of fibromyalgia in a specific social setting.’ by Hazemeijer and Rasker. Rheumatology 2004;43:257.[Free Full Text]
  3. Wolfe F. From the outside of Plato's cave. Rheumatology 2004;43:112–3.[Free Full Text]
  4. White K, Thompson J. Fibromyalgia syndrome in an Amish community: a controlled study to determine disease and symptom prevalence. J Rheumatol 2003;30:1835–40.[ISI][Medline]
  5. Gordon D. Fibromyalgia—real or imagined? [comment]. J Rheumatol 2003;30:1665.
  6. Ehrlich G. Pain is real: fibromyalgia isn’t. J Rheumatol 2003;30:1666–7.[ISI][Medline]
  7. Hadler N. ‘Fibromyalgia’ and the medicalization of misery. [Editorial]. J Rheumatol 2003;30:1668–70.[ISI][Medline]
  8. Wolfe F. Stop using the American College of Rheumatology criteria in the clinic. J Rheumatol 2003;30:1671–3.[ISI][Medline]
  9. Gracely R, Petzke F, Wolfe J, Clauw D. Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum 2002;46:1333–43.[CrossRef][ISI][Medline]
  10. Paiva E, Deoddhar A, Jones K, Bennet R. Impaired growth hormone secretion in fibromyalgia patients. Evidence for augmented hypothalamic somatostatin tone. Arthritis Rheum 2002;46:1344–50.[CrossRef][ISI][Medline]
  11. Crofford L, Clauw D. Fibromyalgia: where are we a decade after the American College criteria were developed? Arthritis Rheum 2002;46:1136–8.[CrossRef][ISI][Medline]
  12. Wolfe F. The fibromyalgia problem. J Rheumatol 1997;24:1247–9.[ISI][Medline]
  13. White K, Harth M, Teasell R. Work disability evaluation and the fibromyalgia syndrome. Semin Arthritis Rheum 1995;24:371–81.[ISI][Medline]
  14. Russell IJ, Orr MD, Litman B et al. Elevated cerebrospinal fluid levels of substance P in patients with fibromyalgia syndrome. Arthritis Rheum 1994;37:593–601.
  15. Neeck G, Crofford LJ. Neuroendocrine perturbations in fibromyalgia and chronic fatigue syndrome. Rheum Dis Clin North Am 2000;26:989–1002.[ISI][Medline]
  16. Martínez-Lavin M, Hermosillo AG, Mendoza C et al. Circadian studies of autonomic nervous balance in patients with fibromyalgia: a heart rate variability analysis. Arthritis Rheum 1998;41:1966–71.[CrossRef][ISI][Medline]
  17. Roizenblatt S, Moldofsky H, Benedito-Silva AA, Tufik S. Alpha sleep characteristics in fibromyalgia. Arthritis Rheum 2001;44:222–30.[CrossRef][ISI][Medline]
  18. McBeth J, MacFarlane G, Benjamin S, Silman A. Features of somatization predict the onset of chronic widespread pain. Results of a large population based study. Arthritis Rheum 2001;44:940–6.[CrossRef][ISI][Medline]
  19. Melzack R. From the gate to the neuromatrix. Pain 1999;82(Suppl. 6):S121–6.[CrossRef]
  20. Caballero-Uribe C, Muvdi J, Navarro E et al. Fibromyalgia, stress related diseases and hyperprolactinemia. Arthritis Rheum 1996;39:S275 [abstract 1486].
  21. Caballero-Uribe Carlo, Abuchaibe I, Abuchaibe S. Treatment of tender points in patients with fibromyalgia syndrome (FMS) with therapeutic infrared laser ray [abstract]. Arthritis Rheum 1997;40:S44.
  22. Rao S, Bennet R. Pharmacological therapies in fibromyalgia. Best Pract Res Rheumatol 2003;17:611–27.[CrossRef][ISI]
  23. American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management of rheumatoid arthritis. Arthritis Rheum 2002;46:328–46.[CrossRef][ISI][Medline]
  24. Garcia R, Guarin C, Caballero CV et al. Validación de la versión en español del Fibromyalgia Impact Questionnarie (FIQ). Rev Colomb Reumatol 2003;10:218–25.
  25. Bernard A, Prince A, Edsall P. Quality of life issues for fibromyalgia patients. Arthritis Care Res 2000;13:42–50.[ISI][Medline]
Accepted 19 May 2004





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