Fibromyalgia …

Rinie Geenen PhD

Headache & Pain

Updated 02.16.2026
Released 12.03.2014
Expires For CME 02.16.2029

Fibromyalgia

Author: Rinie Geenen PhD

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Editor: Federica Provini MD

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Fibromyalgia

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Introduction

Overview

Fibromyalgia is characterized by chronic widespread pain and other symptoms, such as fatigue, waking unrefreshed, and cognitive problems. It is regarded as a primary and nociplastic pain condition. Central sensitization is considered the core pathophysiological mechanism in fibromyalgia, but its cause is unclear. Optimal management requires prompt diagnosis and patient education. Initially, nonpharmacological therapies are recommended, especially exercise. Further therapies should be tailored to the individual and may involve psychological therapies, pharmacotherapy, or multimodal rehabilitation.

Key points

	• Fibromyalgia is a chronic generalized primary pain disorder.
	• Central sensitization is considered core to fibromyalgia.
	• Fibromyalgia is a clinical diagnosis based on patients’ self-reports of widespread, functionally limiting pain and frequently occurring other symptoms.
	• Fibromyalgia can be a comorbid condition of inflammatory rheumatic diseases.
	• Psychoeducation and treatment tailored to the individual should aim to increase functioning, well-being, and ways of dealing with adversities in addition to improving pain and fatigue.

Historical note and terminology

Fibromyalgia originates from the Latin word for “fibrous tissue” (fibro) and the Greek words for “muscle” (myo) and “pain” (algia). The descriptive term refers to generalized pain in the soft tissues (not joints, ligaments, or bone) of the body. Previously, multiple names were given to this condition, eg, muscular rheumatism, neuralgia, neurasthenia, fibrositis, and psychogenic rheumatism (26). Several of the older labels already reflected that the pain might not be driven by peripheral (eg, muscle) damage or inflammation. In the 1970s, Smythe laid the foundation for fibromyalgia as it is seen now by describing it exclusively as a generalized pain syndrome, along with fatigue, poor sleep, morning stiffness, aggravating and relieving factors, emotional distress, and multiple tender points (26). In 1990, Wolfe emphasized the importance of widespread pain as a diagnostic criterion for fibromyalgia (07). From the end of the previous century, Yunus emphasized the importance of conceiving of fibromyalgia as a central sensitivity syndrome, which is broadly accepted nowadays (50).

Clinical manifestations

Presentation and course

	• Fibromyalgia is a chronic condition characterized by widespread pain, predominantly in muscles and tendons.
	• Symptoms also include fatigue and sleep problems, among many others.
	• ICD-11 classifies fibromyalgia as a chronic widespread pain disorder.
	• Several sets of diagnostic criteria for fibromyalgia exist. The most commonly used are the 2016 Fibromyalgia Diagnostic Criteria (49).

The International Classification of Diseases, version 11 (ICD-11), classifies fibromyalgia as chronic widespread pain in the category of chronic primary pain disorders. Chronic primary pain is pain that has persisted for more than 3 months and is associated with significant emotional distress or functional disability; the pain is not better accounted for by another condition (39). A biopsychosocial framework is suggested for understanding chronic primary pain, ie, all subtypes of the diagnosis are considered to be multifactorial in nature, with biological, psychological, and social factors contributing to each (39).

Fibromyalgia among central sensitization syndromes and ICD-11

(Contributed by Dr. J W G Jacobs.)

Patients describe deep aching muscle pain and generalized burning, throbbing, or tingling throughout the body. The pain is diffuse or multifocal and often migratory. Patients may note discomfort when touched and exhibit signs of global sensory hyperresponsiveness (06). The pain is typically of gradual onset. The course is usually not progressive. Patients generally also report fatigue, unrefreshed sleep, and impaired cognition and may report several other symptoms, including headaches, pain or cramps in the lower abdomen, and depression. Stigma and low social support are frequently reported (09). Comorbid diagnoses may be observed, including mood disorders, restless legs syndrome, chronic headache, and sleep disorder. Assignment of patients with fibromyalgia into four clusters based on the severity of pain, fatigue, sleep disturbance, function, stiffness, dyscognition, depression, and anxiety has shown moderate stability over a 2-year follow-up, with little reassignment from one group to another (25). The heterogeneity of fibromyalgia was also shown with respect to modifiable factors comprising objective functional, cognitive, and psychological measures. Five subgroups were identified: adapted (16%), fit (18%), poor performer (20%), positive (20%), and maladapted (26%) (16).

Diagnostic criteria. Several sets of classification and diagnostic criteria for fibromyalgia exist. The most commonly used is the 2016 fibromyalgia diagnostic criteria, which stem from the field of rheumatology (49). Another set that is often used is the AAPT Diagnostic Criteria for Fibromyalgia, which originates from the field of pain medicine (01).

2016 fibromyalgia diagnostic criteria. A patient satisfies these criteria if the following three conditions are met:

(1) Widespread pain index (WPI) ≥ 7 and symptom severity scale (SSS) score ≥ 5 OR WPI of 4–6 and SSS score ≥ 9.

(2) Generalized pain, defined as pain in at least four of five regions, must be present. Jaw, chest, and abdominal pain are not included in the definition of generalized pain.

(3) Symptoms have generally been present for at least 3 months.

A diagnosis of fibromyalgia does not exclude the presence of other illnesses.

WPI. WPI is the sum of the number of areas in which the patient has had pain over the last week. The score will be between 0 and 19.

Four areas in the left upper body (Region 1)
	• Jaw, left • Shoulder girdle, left • Upper arm, left • Lower arm, left
Four areas in the right upper body (Region 2)
	• Jaw, right • Shoulder girdle, right • Upper arm, right • Lower arm, right
Three areas in the left lower body (Region 3)
	• Hip (buttock, trochanter), left • Upper leg, left • Lower leg, left
Three areas in the right lower body (Region 4)
	• Hip (buttock, trochanter), right • Upper leg, right • Lower leg, right
Five areas in the axial body region (Region 5)
	• Neck • Upper back • Lower back • Chest • Abdomen

SSS score. For each of the symptoms, a) fatigue, b) waking unrefreshed, and c) cognitive symptoms, the level of severity over the past week is indicated using the following scale:

0 = no problem
1 = slight or mild problems, generally mild, or intermittent
2 = moderate, considerable problems, often present and/or at a moderate level
3 = severe: pervasive, continuous, life-disturbing problems

The SSS score (range 0–12) is the sum of the symptom score above (range 0–9) plus the sum (0–3) of the number of the following symptoms that occurred during the previous 6 months: headaches (0–1), pain or cramps in lower abdomen (0–1), and depression (0–1).

The fibromyalgia severity scale, also known as the polysymptomatic distress scale, is the sum of the WPI and SSS scores.

AAPT Diagnostic Criteria for Fibromyalgia. The AAPT group developed a diagnostic system for fibromyalgia (01). The following are the core criteria:

(1) Multisite pain defined as six or more pain sites from a total of nine possible sites.

(2) Moderate to severe sleep problems OR fatigue.

(3) Multisite pain plus sleep problems or fatigue must have been present for at least 3 months.

The presence of another pain disorder or related symptoms does not rule out a diagnosis of fibromyalgia. However, a clinical assessment is recommended to evaluate for any conditions that could fully account for the patient’s symptoms or contribute to the severity of the symptoms.

Nine areas for self-assessment by patients with fibromyalgia

This figure shows the nine areas for self-assessment by patients. Patients are asked to check the areas in which they experience pain on the 2-view manikins. Alternatively, patients may use the checklist of body sites. The numb...

Other symptoms and overlapping syndromes

In addition to chronic pain, fatigue, and sleep problems, several other symptoms and comorbidities are often present in fibromyalgia. Yunus postulated that, similar to fibromyalgia, many overlapping conditions can be considered central sensitivity syndromes (50).

• Chronic fatigue syndrome / myalgic encephalomyelitis
• Female urethral syndrome
• Irritable bowel syndrome
• Migraine
• Multiple chemical sensitivity
• Myofascial pain syndrome / regional soft tissue pain syndrome
• Pelvic pain syndromes
• Periodic limb movements in sleep
• Posttraumatic stress disorder
• Primary dysmenorrhea
• Restless legs syndrome
• Temporo-mandibular disorders
• Tension-type headache

Although there are differences in etiology, structural pathology, and symptoms and signs of these conditions, they share features of central sensitivity. Several post-acute infectious syndromes (PAIS) could be added to this list, eg, post-treatment Lyme disease and post COVID.

ICD-11

In the 11th version of the International Classification of Diseases (ICD-11), the subdiagnosis for fibromyalgia is chronic widespread pain (MG30.01). The diagnosis of chronic primary pain should be assigned unless the symptoms are better accounted for by another diagnosis (eg, rheumatoid arthritis or neuropathic pain).

Similar to the definition of fibromyalgia, the definition of chronic primary pain is purely descriptive; this neither means that no somatic factors contribute to the diagnosis nor that psychosocial factors are the main contributors. The ICD-11 group postulates that the biopsychosocial model may be relevant for any type of chronic pain. The difference is that for chronic primary pain, significant distress or functional interference (or both) are required as part of the definition, whereas for chronic secondary pain, a clearly defined somatic factor as expressed in another ICD-11 diagnosis is required and should be co-diagnosed.

Nociplastic pain

In 2017, the term “nociplastic pain” was adopted by the International Association for the Study of Pain (30). Besides fibromyalgia, nociplastic pain is typically present in complex regional pain syndrome, temporomandibular disorders, certain chronic nonspecific neck and back pain conditions, disorders of brain–gut interaction, and bladder pain syndrome (29). The term connects Yunus’s description of central sensitivity and the chronic (primary) widespread pain description in ICD-11 (50; 39). Four conditions define nociplastic pain: (1) pain duration of more than 3 months; (2) regional, multifocal, or widespread rather than discrete distribution of pain; (3) pain cannot entirely be explained by nociceptive or neuropathic mechanisms; and (4) clinical signs of pain hypersensitivity present in the region of pain (29). The pathophysiology of nociplastic pain is heterogeneous. The descriptive construct can stimulate research in this field by emphasizing that the CNS plays a major role in causing and maintaining nociplastic pain and that CNS factors may, in some cases, be driven by ongoing peripheral nociceptive input (07).

Prognosis and complications

Complications of fibromyalgia are psychological distress and physical deconditioning with resulting disability, loss of paid jobs, and limitations in leisure activities. The rate of mortality is increased in patients with fibromyalgia, but it appears comorbidity rather than fibromyalgia per se is associated with mortality (48).

Publications about the prognosis of fibromyalgia are limited. Some studies observed that psychosocial factors are associated with symptoms, psychological distress, and functioning, eg, catastrophizing (fatalism), pain avoidance, and lack of social support, but it is not clear whether these are causes or consequences of fibromyalgia.

There is no known cure for fibromyalgia. The main challenge for patients is to manage this condition. The majority (greater than 80%) of patients with juvenile fibromyalgia continue to experience fibromyalgia symptoms into early adulthood, whereas 51% meet diagnostic criteria for adult fibromyalgia (28).

Biological basis

Etiology and pathogenesis

	• The etiology of fibromyalgia is largely unknown.
	• Multiple factors are considered to be involved in the pathophysiology of fibromyalgia, including genetic, biological, and psychosocial.
	• The multiple factors involved in fibromyalgia are potential etiologic, moderating, or mediating mechanisms; a consequence of the condition; or both cause and consequence. The importance of pathophysiologic and etiologic factors varies between individual patients with fibromyalgia.
	• There is evidence for dysregulation of pain processing in the central nervous system of patients with fibromyalgia: central sensitization.
	• Multiple biological factors may play a role as an instantiating or maintaining factor in fibromyalgia or may be a consequence of fibromyalgia and its associated features.

Fibromyalgia is considered a primary and nociplastic pain condition: central sensitization is reflected in widespread pain. The precise causes of central sensitivity are unclear and may be multimodal. Various biological and psychosocial factors may affect hypersensitivity for pain and other stimuli. However, it is unclear whether the biological and psychosocial deviations that are observed are a cause or consequence of fibromyalgia. Many findings could be secondary to core features of fibromyalgia, eg, the stress from pain, reduced physical activity, sleep disturbance, and obesity. Moreover, the studies showing significant differences between fibromyalgia and control samples reflect mean levels in the investigated samples instead of biomarkers or diagnostic features that hold for the larger part of the population of people with fibromyalgia. A search of the published literature will reveal many seemingly associated findings that likely reflect publication bias. Associations are often falsely interpreted as causal mechanisms. In all, no valid laboratory test for fibromyalgia exists (18). Some of the many biological factors that have been examined are described in this section.

Neurotransmitters. Findings in neurotransmitters have been summarized (44). In agreement with the assumed hypoactivity of the descending analgesic pathways during fibromyalgia, the levels of noradrenergic and serotoninergic neurotransmitters in the biological fluid of patients with fibromyalgia are lower than in healthy individuals, and brain dopaminergic activity during painful stimulation is attenuated. Moreover, hypersensitivity might be mirrored by an excess of excitatory neurotransmitters in brain areas important for pain modulation. Compared to healthy controls, increased levels of substance P (a neurotransmitter that affects pain), lower μ-opioid receptor availability in regions of the brain involved in pain modulation, and higher levels of opioids in the cerebrospinal fluid have been observed.

Glial cells. Positron emission tomography investigations support a role for glial activation in the pathophysiology of fibromyalgia. Several types of glial cells exist both in the central and peripheral nervous systems. They support nerve cells and aid in the maintenance of homeostasis by helping them work properly. It has been suggested that satellite glial cells in the dorsal root ganglia transform emotional, physical, infectious, or autoimmune stressors into biochemical signals that can activate primary pain-sensing neurons in fibromyalgia (36). Another study suggested that patients with fibromyalgia had elevated levels of immunoglobulin G (IgG) antibodies against satellite glia cells, which may be clinically relevant for spontaneous, non-evoked pain (17).

Neuroendocrine levels. Some studies suggested that patients with fibromyalgia have lower levels of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol (42). Group findings may be inconsistent due to reduced hypothalamic-pituitary-adrenal axis activity in fibromyalgia being partly masked by comorbid depressive and anxiety disorders (20).

Autonomic nervous system. It has been suggested that fibromyalgia is a stress-evoked sympathetically maintained pain syndrome (35). There is indeed evidence for a persistent overactive sympathetic nervous system, especially at night, and some evidence for high serum levels of neuropeptide Y and reduced autonomic nervous system responses to applied stressors.

Inflammation. C-reactive protein, a biomarker of systemic inflammation, is significantly but modestly elevated in groups of patients with fibromyalgia, which may be explained by body mass index and comorbidities (19).

Autoimmune disorder. There is ongoing discussion about whether fibromyalgia is an autoimmune disorder (07). Supportive evidence shows that anti-G protein-coupled receptor antibodies directed against the autonomic nervous system receptors have been detected in the serum of patients with fibromyalgia; additionally, their titers correlated with clinical symptoms. However, due to the complexity of the condition, it is not possible to identify a single etiological factor, whether autoimmune or nonautoimmune.

Proteins. It has been suggested that proteins may play a role in the pathophysiology and might be potential biomarkers for the diagnosis and evaluation of fibromyalgia (22). Several proteomic biomarkers are correlated with the levels of pain, depression, and dysautonomia in patients with fibromyalgia. Some studies indicated a potential biomarker of fibromyalgia; however, this could be nonspecific findings, secondary to fibromyalgia. A retrospective study suggested that insulin resistance is the cause of fibromyalgia and that metformin caused a marked improvement. However, this study was retracted because of severe methodological issues. Any publication that claims to present a valid laboratory test should be critically read.

Small fiber pathology. Both skin biopsy and corneal confocal microscopy have consistently demonstrated that about 50% of people with fibromyalgia have small fiber pathology (21). However, the significance of its role in fibromyalgia remains unclear. Small fiber pathology could contribute to pain, but it could also be a byproduct of physical deconditioning, associated symptoms, or comorbidities (34).

Gut microbiome. The gut-brain axis attracts continuing interest given its bidirectional crosstalk, regulatory effect on the body’s processes, and involvement in many disorders. Research has revealed differences in the gut microbiome of patients with fibromyalgia compared to controls as well as an association with symptom severity. Experiments suggest that altering gut microbiota is a potential target for therapeutic interventions (05).

Genetic factors. Genetic findings in fibromyalgia have been summarized (41). Approximately 50% of individual variation in the risk of developing fibromyalgia has been ascribed to genetic factors, most likely a polygenic inherited dysregulation of neurotransmitters. Several genetic polymorphisms involving serotoninergic, catecholaminergic, dopaminergic, glutamatergic, cannabinoidergic, and adrenergic pathways have been associated with a higher risk of developing and a greater severity of fibromyalgia.

Psychosocial factors. Patients with fibromyalgia are more likely to have heightened psychological distress and psychiatric comorbidities, including depression, anxiety, and posttraumatic stress disorder. This may be a consequence of fibromyalgia and associated features or the result of common predisposing factors, such as early-life stress or trauma. It has been suggested that an imbalance of two neuropsychological systems may affect the severity of fibromyalgia. An overactive threat system and underactive soothing system may keep the midcingulo-insular network (also known as the “salience network”) in continuous alert mode (40).

Individual biopsychosocial models. Many factors could worsen pain and other symptoms, eg, physical inactivity, obesity, mental distress, sleep disturbance, or comorbidities. All these factors can also be a consequence of fibromyalgia. Group findings may not hold for individuals. Information from interviews and experience sampling methods can give insight into the dynamic interplay and influences between biological and psychosocial factors that are found in individuals with fibromyalgia.

Differential diagnosis

Confusing conditions

Fibromyalgia is a clinical diagnosis based on self-report of the patient, history, and physical examination. There are no laboratory tests or imaging that can be performed to diagnose fibromyalgia. Fibromyalgia is not a diagnosis of exclusion. It often exists alongside other conditions (04). Patients should be examined for treatable comorbid conditions. Clinicians should look for and exclude discriminatory signs and symptoms of arthritis (swelling of joints), Sjögren disease (dry eyes and mouth), polymyalgia rheumatica (more acute onset, weight loss), inflammatory myositis (muscle weakness), metabolic myopathies, hypothyroidism (bradycardia, myxedema), peripheral neuropathies, and cancer (weight loss). In the absence of signs or symptoms of a specific disease, clinicians are advised against performing laboratory studies, such as testing for antinuclear antibody (ANA), neutrophil anticytoplasmic antibody, rheumatoid factor, SSA, or double-stranded DNA, given the risk of false positive test results in that setting. Similarly, no screening test for a disease can be recommended without clinical indication (history or physical exam) of the disease; this includes laboratory studies (eg, thyroid studies, vitamin D level, and creatine kinase) as well as x-ray studies (eg, electromyography).

For clinical management, fibromyalgia should be differentiated from similar conditions, such as generalized myofascial pain or widespread pain syndrome not fulfilling the diagnostic criteria of fibromyalgia, only if doing so would have clinical implications for the patient. The Royal College of Physicians states that “diagnostic uncertainty should not preclude agreeing [on] a shared plan using the best evidence for the management of chronic widespread pain and any associated symptoms” (04). The following table differentiates key medical disorders from fibromyalgia (01).

Medical disorder		Differentiating signs and symptoms
Endocrine
	• Addison disease	Postural hypotension, nausea, vomiting, skin pigmentation, weight loss
	• Cushing syndrome	Hypertension, diabetes, hirsutism, moon facies, weight gain
	• Hyperparathyroidism	Increased thirst and urination, kidney stones, nausea/vomiting, decreased appetite, thinning bones, constipation
	• Hypothyroidism	Cold intolerance, mental slowing, constipation, weight gain, hair loss
Infectious
	• Hepatitis	Right upper quadrant pain, nausea, decreased appetite
	• Lyme disease	Rash, arthritis, or arthralgia; occurs in areas of endemic disease
Neurologic
	• Multiple sclerosis	Visual changes (unilateral partial or complete loss, double vision); ascending numbness in a leg or bandlike, truncal numbness; slurred speech (dysarthria)
	• Neuropathy	Shooting or burning pain, tingling, numbness, weakness
Rheumatologic
	• Osteomalacia	Diffuse bone pain, fractures, proximal myopathy with muscle weakness
	• Polyarticular osteoarthritis	Joint stiffness, crepitus, multiple painful joints
	• Polymyalgia rheumatica	Proximal shoulder and hip girdle pain, weakness, stiffness, more common in the elderly
	• Polymyositis, other myopathies	Symmetric, proximal muscle weakness and pain
	• Rheumatoid arthritis	Predominant joint pain, symmetric joint swelling, joint line tenderness, morning stiffness for more than 1 hour
	• Spondyloarthropathy	Localization of spinal pain to specific sites in the neck, mid-thoracic, anterior chest wall, or lumbar regions; objective limitation of spinal mobility due to pain and stiffness
	• Systemic lupus erythematosus	Multisystem involvement, joint or muscle pain, rash, photosensitivity, fever

Associated or underlying disorders

Major depressive disorder and obstructive sleep apnea with daytime sleepiness are prevalent in fibromyalgia. Patients with fibromyalgia are also likely to have symptoms that also exist as solitary conditions, mostly central sensitivity syndromes other chronic pain conditions.

There is discussion about whether fibromyalgia could be differentiated from somatic symptom disorder. However, the excessive and disproportionate psychological reaction that is needed to get a somatic symptom disorder diagnosis may hold for part of the fibromyalgia population, but it is not a diagnostic feature of fibromyalgia. The criteria for fibromyalgia hardly include psychological variables and are more specific regarding widespread pain than those for somatic symptom disorder.

Diagnostic workup

	• Careful history and general physical examination are paramount to check the differential diagnosis.
	• Fibromyalgia is a clinical diagnosis that is not solely based on diagnostic criteria, but diagnostic criteria are helpful.
	• Routine laboratory tests as screening tools, including erythrocyte sedimentation rate, C-reactive protein, complete blood count, and tests for rheumatic conditions and thyroid, are not recommended.
	• Laboratory tests may be used in the differential diagnosis if there is a clinical indication in an individual to perform a laboratory test.
	• The diagnosis of a rheumatic condition, eg, rheumatoid arthritis, does not rule out concomitant fibromyalgia.
	• There is no valid biomarker-based test that can be recommended for diagnosing fibromyalgia.

Fibromyalgia is a clinical diagnosis, and diagnostic workup should begin—and often ends—with careful history taking and a general physical examination. Typically, the physical exam is unremarkable in patients with fibromyalgia, with the exception of diffuse tenderness and hyperalgesia to touch or palpation. If tenderness is localized to joints or additional features are noted, such as joint swelling or skin changes, systemic autoimmune conditions should be considered. Similarly, other symptoms and signs could raise clinical suspicion of other diagnoses. It is unwise to limit the history taking and general physical examination to assessment of diagnostic criteria of fibromyalgia due to the risk of missing clinically relevant diagnoses in situations in which fibromyalgia is a false diagnosis or fibromyalgia is a comorbid diagnosis.

The FM/a^® blood test, based on a cytokine assay of in vitro stimulated peripheral blood mononuclear cells, was developed to diagnose fibromyalgia, but this test cannot be recommended. The research used to develop this test has severe methodological flaws (45). No research has been completed on its validity to differentiate fibromyalgia from another disorder, and the clinical relevance of the test results for patients has not been assessed.

Several laboratory tests may be useful for ruling out conditions in the differential diagnosis if there is clinical suspicion based on the history and physical examination. It is important to draft the differential diagnosis after, and on the basis of, the specifics of the individual’s history and physical exam and not to apply a generic differential diagnosis list from, for instance, a textbook. Lab studies as a pure screening tool, without clinical indication in an individual, might give a false feeling of diagnostic comprehensiveness but are, in fact, a sign of diagnostic incompetence.

Routine neuroimaging and, in fact, any routine workup are not used in the diagnostic workup of fibromyalgia. On a group level, imaging research has demonstrated differences between fibromyalgia and control groups. The conundrum of whether these changes are primary and etiologic or secondary and a consequence of fibromyalgia has yet to be resolved. These findings do not have any diagnostic or management consequences for the individual with fibromyalgia.

Management

	• Management of fibromyalgia and its consequences requires a biopsychosocial approach, including comprehensive assessment of pain, function, and psychosocial context.
	• The first step in managing fibromyalgia requires a prompt diagnosis and providing information about fibromyalgia and its management.
	• Because of the heterogeneity in terms of symptoms, features, maintaining factors, and psychosocial characteristics of the group, it is important to tailor interventions to the needs and priorities of the individual.
	• Psychoeducation and treatment should aim to increase function, well-being, and ways of dealing with adversities, not only to improve pain and fatigue, because the potential to improve these symptoms is limited.
	• Initial management should focus on nonpharmacological therapies. In case of non-response, further therapies are recommended tailored to the specific needs of the individual.
	• Based on evidence from meta-analyses and expert opinion, physical exercise is the only “strong for” recommendation. Further therapies are considered “weak for” recommendations.

In 2017, an expert group of professionals and patients from the European Alliance of Associations for Rheumatology (EULAR) published recommendations for the management of fibromyalgia based on scientific evidence and the expert opinion of patients and professionals (32). This section generally follows these recommendations, with recent literature added.

General principles of management. Optimal management requires prompt diagnosis. A full understanding of fibromyalgia requires comprehensive assessment of pain, function, and psychosocial context. Fibromyalgia should be recognized as a complex and heterogeneous condition in which there is abnormal pain processing and other secondary features. In general, management should take the form of a graduated approach. Individual tailoring of the treatment can be achieved by discussing realistic goals of management in shared decision-making. While taking account of patient preferences, management should aim to improve health-related quality of life, balancing benefit and risk of treatment. The multiple factors involved in the maintenance of the condition often require a multidisciplinary approach with a combination of treatment modalities tailored according to pain intensity, function, associated features (such as depression), fatigue, sleep disturbance, and comorbidities. Initial management should involve patient education and focus on nonpharmacological therapies. In case of non-response, further therapies are recommended tailored to the specific needs of the individual.

Patient education. Education should include information regarding the nature of the condition, that symptoms are real, and that graded exercise, sleep hygiene, and management of stress are important.

Strength of recommendations. Based on meta-analyses, exercise was the only “strong for” therapy-based recommendation in the EULAR recommendations. Further therapies (all of which were evaluated as “weak for” based on meta-analyses) may involve psychological therapies (for mood disorders and unhelpful coping strategies), pharmacotherapy (for severe pain or sleep disturbance), or a multimodal rehabilitation program (for severe disability).

Physical exercise. In the EULAR recommendations, up to 34 trials and over 47 different interventions were used to evaluate aerobic and strengthening exercise. No main differences in effect were observed between aerobic versus strengthening exercise or land versus aquatic exercise. Although patients may initially notice a deterioration in symptoms, exercise is generally considered safe, especially when practiced under supervision. Aerobic and strengthening exercise was the only intervention for fibromyalgia receiving a “strong for” recommendation by EULAR. Six reviews that evaluated meditative exercise (tai chi, yoga, qigong) showed moderate improvements in sleep and fatigue, some of which were maintained in the longer term. EULAR gave a “weak for” recommendation for meditative exercise. A systematic review and meta-analysis indicated that aerobic and strengthening exercise was most effective for lowering fatigue, whereas meditative exercise was most effective for enhancing sleep quality (15).

Psychological therapies. In the EULAR recommendations, five reviews of cognitive behavioral therapy included up to 30 trials with, in general, poor-quality designs. Cognitive behavioral therapy was effective in reducing pain and disability (small effect sizes) and results were sustained long term. Six reviews of up to 13 trials of mindfulness-based stress were not robust against bias and showed improvement in pain immediately post treatment compared with usual care and compared with active control interventions (small effect sizes). A “weak for” recommendation was given for both types of psychological interventions. It appears that this also holds for acceptance and commitment therapy (ACT). This therapy is growing in popularity. ACT enhances psychological flexibility by helping patients to accept their thoughts and feelings while being committed to living their lives according to their own values. A meta-analysis of six randomized controlled trials of 384 mostly female participants with fibromyalgia showed that ACT was superior to control conditions in improving scores on the fibromyalgia impact questionnaire (FIQ) at postintervention and follow-up as well as chronic pain acceptance at follow-up (large effect sizes) (13). Effect sizes for pain and disability were moderate. In a recent meta-analysis, it was concluded that both CBT and ACT are efficient for decreasing depression and anxiety in fibromyalgia (10).

Aids and adaptations. These were not evaluated in the EULAR recommendations. Aids could positively affect physical deconditioning and quality of life and might enable patients to have or keep a paid job. From the viewpoint of the importance of enhancing physical activity, adaptations (eg, to homes) and medical devices should only be given if they enable patients to engage in activities that would otherwise not have been possible.

Pharmacologic treatment. Pharmacologic treatment is most often used in conjunction with other interventions. It is recommended to start medications at low doses and titrate slowly because many patients with fibromyalgia are sensitive to medications. Effective therapies may work by altering neurotransmission involved in pain transmission. Several classes of drugs have been used for treating fibromyalgia with variable evidence of efficacy. Often only short-term effects were evaluated.

Table 1. EULAR Recommendations for The Pharmacological Management of Fibromyalgia

Treatment	Trial quality	Recommendation and comments
Amitriptyline	Low	Weak for, at low dose. Might be considered in case of sleep disturbance if nonpharmacological treatments are not effective. No analysis of safety. Discontinuation was similar with patients on placebo.
Selective serotonin reuptake inhibitors (SSRIs)	Moderate to high	Weak against. Acceptability and tolerability similar to placebo. Dropout rates higher compared with placebo, but no difference in serious adverse events.
Serotonin and noradrenaline reuptake inhibitors (SNRIs)	Moderate (duloxetine) to high (milnacipran)	Weak for. Duloxetine might be considered in case of severe pain.
Monoamine oxidase inhibitors (MAOIs)	Low	Weak against. Serious harm in interaction with specific foods and medications (including SSRIs, tricyclic antidepressants, and tramadol).
Anticonvulsants	Pregabalin: high	Pregabalin: Weak for in case of severe pain or sleep disturbance. Increased likelihood of withdrawal due to adverse events.
Anticonvulsants	Gabapentin: too few studies	Gabapentin: Use only in research.
Analgesics	Non-steroidal anti-inflammatory drugs (NSAIDs): low	Weak against NSAIDs. Adverse events are well established for NSAIDs. The National Institute for Health and Care Excellence advises not to prescribe NSAIDs or paracetamol (38).
Analgesics	Paracetamol: not evaluated
Opioids	Tramadol: high	Weak for tramadol in case of severe pain. Discontinuation due to adverse events was similar with patients on placebo. This recommendation is in contrast with recommendations against the use of tramadol based on more recent trials (11; 38).
Opioids	Strong opioids: not evaluated	Strong against strong opioids because of lack of evidence and high risk of side effects (other reviews report a similar conclusion).
Cyclobenzaprine	Moderate	Weak for in case of sleep disturbance. Many dropouts due to side effects.
Antipsychotics Corticosteroids Growth hormone Sodium oxybate	Not evaluated	Hardly studied and high risk of side effects, addiction, or safety concerns reported in individual trials. No approval of the European Medicines Agency and the U.S. Food and Drug Administration.
(32)

A summary and evaluation of Cochrane reviews of pharmacological therapies for adults with fibromyalgia roughly reached the same conclusions (37). No evidence was found for carbamazepine, clonazepam, lamotrigine, phenytoin, oxycodone, topiramate, and valproate. Limited and inadequate data were observed for antipsychotics, cannabinoids, combination therapy, gabapentin, lacosamide, monoamine oxidase inhibitors, and NSAIDs. Publications about amitriptyline and SSRIs were considered to be subject to publication bias. Mirtazapine had moderate evidence of no effect. Duloxetine, milnacipran, and pregabalin had moderate to good evidence that about 1 person in 10 with moderate or severe pain might experience a pain intensity reduction by at least 50%. A randomized controlled trial observed significantly more responders to cyclobenzaprine than to placebo medication: 24% versus 8% (31). A systematic review showed that there has not been a breakthrough in novel pharmacotherapies for fibromyalgia (46).

Overall, there is a discordance between evidence-based recommendations encouraging pharmacological treatment only if nonpharmacological treatment fails versus the high frequency of medication use in fibromyalgia (12).

Multicomponent therapy. There is enormous variation in the contents of multicomponent strategies. The most included combinations were of (land or water based) exercise, education, relaxation, or some other specific therapeutic component (eg, tai chi or massage). In a meta-analysis of nine trials and 1119 patients, combined therapies were effective in reducing pain and fatigue immediately post treatment, compared with waiting list, relaxation, treatment as usual, and education, but effects were short-lived (23). The EULAR recommendation was “weak for.”

Other therapies. Given the unclear and pathophysiological substrate and the heterogeneous influencing factors, multiple other therapies have been tried in fibromyalgia. Often the evidence is too low to recommend other therapies for fibromyalgia, but these therapies may bring some relief to some patients. The therapies discussed here are transcranial direct current stimulation, heat lamps and saunas, hyperbaric oxygen therapy, acupuncture, nutrient supplements (vitamin D, ferritin, vitamin B12), diet, and several non-mainstream, complementary, and alternative therapies.

Transcranial direct current stimulation (tDCS). tDCS is a noninvasive neurostimulation technique that modulates cortical excitability by using a constant low current delivered to the brain area of interest via electrodes placed on the scalp. It is not recommended in the EULAR recommendations due to low evidence to support the therapy and an unacceptably high rate of adverse events and discontinuation. Recent reviews are more positive about effects and safeness but conclude that effects depend on the site and intensity of stimulation. The National Institute for Health and Care Excellence decided not to recommend against this intervention but also decided not to make a research recommendation because other areas reviewed across the guideline showed more promising results for future research to be warranted (38).

Heat lamps and saunas. Far infrared radiation (FIR) has a wavelength of 0.7 to 1.4 μm and transfers energy in the form of heat, which can be perceived by the thermoreceptors in human skin. FIR-emitting heat lamps and FIR saunas have been used to relieve pain in fibromyalgia. Garments made of fibers impregnated with FIR-emitting nanoparticles are being used to deliver thermal radiation effects. There is some evidence for this therapy in reducing pain and the impact of fibromyalgia (43).

Hyperbaric oxygen therapy. Hyperbaric oxygen therapy increases delivery of oxygen to the body by providing pure oxygen in an enclosed space with higher-than-normal air pressure. One randomized controlled trial indicated that this intervention may improve the symptoms and quality of life of patients with fibromyalgia (14).

Acupuncture. There is little understanding of the active component of acupuncture, and the evidence supporting the use of real versus sham acupuncture was less consistent. A “weak for” recommendation was given for acupuncture in the EULAR recommendations.

Nutrient supplements. In a meta-analysis, it was concluded that groups of patients with fibromyalgia generally had lower vitamin D and ferritin levels compared with healthy controls, whereas vitamin B12 showed no difference between the two groups (27). However, the effects of vitamin D in patients with fibromyalgia without a vitamin deficiency are not clear. This should be known before prescribing vitamin D to manage fibromyalgia. Also, further studies are needed to examine whether lower ferritin and vitamin B12 levels contribute to fibromyalgia (27).

Diet. A systematic review examined dietary effects on pain in fibromyalgia (33). Nine studies indicated beneficial effects of their respective diets, but the small sample sizes and short intervention do not warrant the recommendation of any specific diet to patients with fibromyalgia.

Non-mainstream, complementary, and alternative therapies. Disappointment about the effect of mainstream therapies on pain may be a reason to seek non-mainstream, complementary, or alternative care. Engaging in these therapies can provide some benefit and allow individual patients to feel that they have more control. The EULAR expert group gave a “strong against” recommendation for guided imagery, homeopathy, and chiropractic interventions. A “weak against” recommendation was given for biofeedback, capsaicin, hypnotherapy, massage, and S-adenosyl methionine. A “weak for” recommendation was given for hydrotherapy/spa therapy. Several reviews were identified that did not offer enough evidence or reported an unacceptably high rate of adverse events or discontinuation due to headache: electrothermal and phototherapeutic therapy, phytothermotherapy, music therapy, journaling/storytelling, and static magnet therapy. Some therapies may become mainstream when evidence of acceptable effect sizes is given in sound experimental studies. Points for the individual patient to consider before engaging in a specific complementary therapy are whether it might be harmful and the financial costs. When contemplating the start of such therapy, the patient should discuss what the level of improvement would and could be with the therapist, as well as how many sessions would be required and the risks. The patient could then decide whether this therapy would be worthwhile.

Outcomes

To assess the outcome of treatment, the FIQ and the revised version of the Fibromyalgia Impact Questionnaire (FIQR) appear to be the most often used instruments (03). These instruments mostly reveal small or moderate but statistically significant improvements in symptoms, well-being, and functioning after treatment. It is also possible to use the scale that is also used to diagnose fibromyalgia: the fibromyalgia severity scale or polysymptomatic distress scale (49). Perhaps effect sizes of interventions could be observed to be larger if generic outcome measures, such as the FIQR total score and polysymptomatic distress scale, are not used but instead more specific outcome measures that are the target in an intervention for a specific patient. Virtually all patients report pain and fatigue, but other variables differ between patients, eg, sleep problems, physical deconditioning, cognitive dysfunction, and psychological distress. Outcomes depend on associated disorders as well. To the extent that recommendations and guidelines encourage that therapies are tailored to the individual, it makes sense to tailor the outcome measures as well.

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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Rinie Geenen PhD

Dr. Geenen of Utrecht University has no relevant financial relationships to disclose.
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Editor

Federica Provini MD

Dr. Provini of the University of Bologna and IRCCS Institute of Neurological Sciences of Bologna received speakers' fees from Idorsia and Italfarmaco.
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Former Authors

Nicole Reams MD
K K Jain MD†
J W G Jacobs MD PhD
Peter J Koehler MD PhD

Patient Profile

Age range of presentation: Fibromyalgia can present at any age, and juvenile fibromyalgia is well described. Men reach peak prevalence at middle age. The prevalence in women increases steadily with age.
Sex preponderance: Fibromyalgia is more common in women.
Heredity: Hereditary factors probably play a (minor) role.
Population groups selectively affected: Polygenic inherited dysregulation of neurotransmitters has been indicated as a risk factor for fibromyalgia.

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Fibromyalgia

Associated Disorders

major depressive disorder
obstructive sleep apnea with daytime sleepiness
central sensitivity syndromes
chronic overlapping pain conditions

Differential Diagnosis

rheumatoid arthritis
systemic lupus erythematosus
ankylosing spondylitis
Sjogren disease
polymyalgia rheumatica
- inflammatory myositis
- metabolic myopathies
- hypothyroidism
- peripheral neuropathies
- cancer
- generalized myofascial pain
- widespread pain syndrome not fulfilling the diagnostic criteria of fibromyalgia

	• The prevalence of fibromyalgia in the general population is about 2%.
	• The prevalence is about six times higher in women than in men.

	• There are no clear methods for primary prevention of development of fibromyalgia.
	• Secondary prevention, ie, prevention of full-blown fibromyalgia in patients showing some signs and symptoms of the disorder, might be possible.

Fibromyalgia

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Other symptoms and overlapping syndromes

ICD-11

Nociplastic pain

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

Table 1. EULAR Recommendations for The Pharmacological Management of Fibromyalgia

Outcomes

Special considerations

Pregnancy

Anesthesia

Surgery

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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