Abstract
Fibromyalgia is a disorder characterized by chronic widespread pain and non-pain symptoms, such as fatigue, dysautonomia, and cognitive and sleep disturbances. Its pathogenesis and treatment continue to be the subject of debate. We highlight the role of three mechanisms—autoimmunity, neuroinflammation, and small fiber neuropathy—in the pathogenesis of the disease. These mechanisms are shown to be closely interlinked (also on a molecular level), and the review considers the implementation of this relationship in the search for therapeutic options. We also pay attention to chronic fatigue syndrome, which overlaps with fibromyalgia, and propose a concept of “autoimmune hypothalamopathy” for its pathogenesis. Finally, we analyze the molecular mechanisms underlying the neuroinflammatory background in the development of adverse events following HPV vaccination and suggesting neuroinflammation, which could exacerbate the development of symptoms following HPV vaccination (though this is hotly debated), as a model for fibromyalgia pathogenesis.
Highlights
Fibromyalgia (FM) is recognized by the World Health Organization under ICD-10 code M79.7 and defined as a chronic widespread pain condition associated with fatigue, sleep and cognitive disturbances, and a variety of somatic symptoms [1,2]
The American College of Rheumatology (ACR)-2010 criteria established a widespread pain index, which replaced the assessment of tender points and required numerical assessment of 41 possible somatic symptoms with individual assessment the severity of 3 major extra-pain symptoms of fatigue, sleep disturbance and cognitive impairments
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) (ICD-10-CM R53.82 or G93.3 if postviral) is a heterogeneous disease that presents with pronounced disabling fatigue without relief after rest, sleep disturbances, and cognitive impairment [1,68]
Summary
Fibromyalgia (FM) is recognized by the World Health Organization under ICD-10 code M79.7 and defined as a chronic widespread pain condition associated with fatigue, sleep and cognitive disturbances, and a variety of somatic symptoms [1,2]. The Canadian guidelines for the diagnosis and management of FM syndrome (2012) acknowledge that the criteria for the diagnosis of FM, as developed by the ACR, were primarily intended for research purposes [9] These guidelines define FM as “a condition that can wax and wane over time and should be diagnosed in an individual with diffuse body pain that has been present for at least three months, and who may have symptoms of fatigue, sleep disturbance, cognitive changes, mood disorder, and other somatic symptoms to variable degree, and when symptoms cannot be explained by some other illness” [9]. The newest ACTTION-APS taxonomy (AATP) diagnostic criteria for FM (2016) are similar to the Canadian guidelines (2012) with respect to the ease of use in clinical practice 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 health care professional without any score [10]. A lack of specific biomarkers for FM diagnosis is a well-known weakness [4], and the elimination of the tender point examination from the modern criteria makes the diagnosis of FM even more subjective
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