The official diagnostic criteria for fibromyalgia has changed and evolved since the condition was first recognized in 1976. With this has come a broader understanding for what the condition involves. And how to help it.
Though fibromyalgia (FM) has been with us a long time, our collective understanding of the condition has greatly changed. Just within the last few decades, it has gone from a condition where patients are often marginalized and not taken seriously, to having supportive evidence and underpinnings in multiple areas, including cerebrospinal fluid imbalances and genetic predispositions. (1)
Chronic Widespread Pain with 11 of 18 Tender Points
'Rheumatism' or 'muscular rheumatism' are terms that have been used for centuries to describe muscular pain. The term 'fibrositis' was coined by Sir William Gowers in 1904 and was not changed to 'fibromyalgia' (FM) until 1976.(2) Several researchers including Smythe, Moldofsky and Yunus laid the foundation of modern FM in the 1970s by describing widespread pain and tender points.(3) And in the early 1990s, a different team of researchers formulated diagnostic criteria for for 'generalized tenomyopathy', which was thought to be synonymous with FM.(4)
It was in 1990 when the American College of Rheumatology (ACR) published a definition and classification criteria for FM which required the existence of chronic, widespread pain for more than months, as well as the presence of at least 11 out of 18 specified tender points upon physical exam.(5) This definition was intended for advancing research studies, which it did; however, it was not intended for use in clinical practice. Yet many clinicians took the tender point examination and would use that to confirm or deny a diagnosis with patients. Furthermore, not only was this exam impractical for use clinically, the definition itself also omitted acknowledgement of the commonly associated subjective symptoms. In the coming years, this kind of hyper-focusing on pain would prove to be a limitation to defining FM, and give way to a broader multi-symptom disorder approach.
Shift from Chronic Widespread Pain and Tender Points to Multi-Symptom Disorder
In 2010, the definition was revised by the ACR to re-prioritize some of the more systemic features of FM, which had become marginalized when pain became the over-riding emphasis. This was followed by another revision in 2016, since several criticisms resulted including that criteria had become too ill-defined, completely symptom focused, and that a limitation of the WPI was the fact that it counted the number of painful areas without considering their distribution in the body. Hence patients with regional pain disorders could fulfill the 2010 ACR preliminary diagnostic criteria.
Collectively, this shift moved FM from a pain-specific disease to more of systemic symptom-based illness. The change in diagnostic criteria initially served to establish a 'Widespread Pain Index' (WPI) and eliminate the tender point exam as a requirement for diagnosis, replacing it with a numerical assessment of 41 possible body symptoms, each being individually scored and assessed. But when the 41 body symptom assessment itself became cumbersome in practice, this itself was replaced by a simple summation of six self-reported symptoms. These include:
fatigue
trouble thinking or remembering
waking up unrefreshed
pain or cramps in the lower abdomen
depression
headache
Multi-Site Pain and Sleep Problems OR Fatigue
These newest revisions, published in 2016, were by the Analgesic, Anesthetic, and Addiction Clinical Trial Translations Innovations Opportunities and Networks (ACTTION) (whew!) and took a multidimensional approach to diagnostic frameworks, really trying to improve recognition of FM in clinical practice. They focused on core diagnostic criteria, common features, common medical co-morbidities, as well as neurobiological and functional consequences.
These criteria require only multisite pain (6/9 body areas, present at least three months) and sleep problems OR fatigue, assessed as moderate to severe by the scoring health care practitioner. This diagnostic criteria is noticeably simplified and streamlined. This has made the diagnosis heavily subjective. All the more so because of the continued lack of specific biomarkers and laboratory values for diagnosis.
But it also means that the patient is more likely to be diagnosed 'correctly' because so many of the criteria are subjective. Instead of not being adequately heard or trivialized, this approach more fully puts the patient in the driver seat for recognition and hopefully for treatment.
Facing Future: Pathophysiology Updates in Fibromyalgia
In the past FM was thought to be a primary muscle disease. However, controlled studies found no evidence of significant pathologic or biochemical muscle abnormalities that can be the cause of chronic widespread pain and tenderness. Current research suggests that altered central nervous system (CNS) physiology might underlie the symptoms of FM, with abnormal central sensory processing of pain signals seemingly playing a significant role in the pathogenesis of this condition. This includes findings such as the higher amount of substance P located in the cerebrospinal fluid (CSF) of patients with FM compared to controls without the condition.(1)
Dysregulation of the sensory and nociceptive system can arise from a combination of interactions between neurotransmitters, neuropeptides, cytokines, hormones, the autonomic nervous system, behavioral constructs and external stressors. It is also currently well established that FM tends to go down family lines, with first degree relatives of FM patients are 8.5 times more likely to have it than relatives of patients with rheumatoid arthritis.(8) Ultimately, these imbalances align to point a pathogenesis for FM to be attributable to either one or a combination of autoimmunity, neuroinflammation, or abnormality of small nerve fibers with the degeneration of terminal nerve endings.
Though the debate continues about origins best diagnostic criteria for FM, it is comforting that strides have been made for acknowledging the patient experience for this highly subjective and problematic condition. It may not always seem it, but we have come a long way.
References:
Inanici, Fatma, and Muhammad B Yunus. “History of fibromyalgia: past to present.” Current pain and headache reports vol. 8,5 (2004): 369-78. doi:10.1007/s11916-996-0010-6.
Häuser, Winfried et al. “Fibromyalgia syndrome: classification, diagnosis, and treatment.” Deutsches Arzteblatt international vol. 106,23 (2009): 383-91. doi:10.3238/arztebl.2009.0383.
Müller, W, and J Lautenschläger. “Die generalisierte Tendomyopathie (GTM). Teil I: Klinik, Verlauf und Differentialdiagnose” [Generalized tendomyopathy. I: Clinical aspects, follow-up and differential diagnosis]. Zeitschrift fur Rheumatologie vol. 49,1 (1990): 11-21.
Wolfe, F et al. “The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee.” Arthritis and rheumatism vol. 33,2 (1990): 160-72. doi:10.1002/art.1780330203.
Arnold, Lesley M et al. “AAPT Diagnostic Criteria for Fibromyalgia.” The journal of pain vol. 20,6 (2019): 611-628. doi:10.1016/j.jpain.2018.10.008.
Ryabkova, Varvara A et al. “Neuroimmunology: What Role for Autoimmunity, Neuroinflammation, and Small Fiber Neuropathy in Fibromyalgia, Chronic Fatigue Syndrome, and Adverse Events after Human Papillomavirus Vaccination?.” International journal of molecular sciences vol. 20,20 5164. 18 Oct. 2019, doi:10.3390/ijms20205164.
Arnold, Lesley M et al. “Family study of fibromyalgia.” Arthritis and rheumatism vol. 50,3 (2004): 944-52. doi:10.1002/art.20042.
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