The treatment of fibromyalgia can be difficult. Recommendations often include getting enough sleep, exercising regularly, and eating a healthy diet.Cognitive behavioral therapy (CBT) may also be helpful. The medications duloxetine, milnacipran or pregabalin may be used. Use of opioid pain medication is controversial, with some stating their usefulness is poorly supported by evidence and others saying that weak opioids may be reasonable if other medications are not effective.Dietary supplements lack evidence to support their use. While fibromyalgia can last a long time, it does not result in death or tissue damage.
Fibromyalgia is estimated to affect 2-8% of the population. Women are affected about twice as often as men. Rates appear similar in different areas of the world and among different cultures. Fibromyalgia was first defined in 1990, with updated criteria in 2011. There is controversy about the classification, diagnosis and treatment of fibromyalgia. While some feel the diagnosis of fibromyalgia may negatively affect a person, other research finds it to be beneficial. The term "fibromyalgia" is from New Latinfibro-, meaning "fibrous tissues", Greekmyo-, "muscle", and Greek algos, "pain"; thus, the term literally means "muscle and fibrous connective tissue pain".
Differences in psychological and autonomic nervous system profiles among affected individuals may indicate the existence of fibromyalgia subtypes. A 2007 review divides individuals with fibromyalgia into four groups as well as "mixed types":
"extreme sensitivity to pain but no associated psychiatric conditions" (may respond to medications that block the 5-HT3 receptor)
"fibromyalgia and comorbid, pain-related depression" (may respond to antidepressants)
"depression with concomitant fibromyalgia syndrome" (may respond to antidepressants)
"fibromyalgia due to somatization" (may respond to psychotherapy)
The cause of fibromyalgia is unknown. However, several hypotheses have been developed including "central sensitization". This theory proposes that people with fibromyalgia have a lower threshold for pain because of increased reactivity of pain-sensitive nerve cells in the spinal cord or brain. Neuropathic pain and major depressive disorder often co-occur with fibromyalgia - the reason for this comorbidity appears to be due to shared genetic abnormalities, which leads to impairments in monoaminergic, glutamatergic, neurotrophic, opioid and proinflammatory cytokine signaling. In these vulnerable individuals, psychological stress or illness can cause abnormalities in inflammatory and stress pathways that regulate mood and pain. Eventually, a sensitization and kindling effect occur in certain neurons leading to the establishment of fibromyalgia and sometimes a mood disorder. The evidence suggests that the pain in fibromyalgia results primarily from pain-processing pathways functioning abnormally. In simple terms, it can be described as the volume of the neurons being set too high and this hyper-excitability of pain-processing pathways and under-activity of inhibitory pain pathways in the brain results in the affected individual experiencing pain. Some neurochemical abnormalities that occur in fibromyalgia also regulate mood, sleep, and energy, thus explaining why mood, sleep, and fatigue problems are commonly co-morbid with fibromyalgia.
Stress may be an important precipitating factor in the development of fibromyalgia. Fibromyalgia is frequently comorbid with stress-related disorders such as chronic fatigue syndrome, posttraumatic stress disorder, irritable bowel syndrome and depression. A systematic review found significant association between fibromyalgia and physical and sexual abuse in both childhood and adulthood, although the quality of studies was poor. Poor lifestyles including being a smoker, obesity and lack of physical activity may increase the risk of an individual developing fibromyalgia. A meta analysis found psychological trauma to be associated with FM, although not as strongly as in chronic fatigue syndrome.
Some authors have proposed that, because exposure to stressful conditions can alter the function of the hypothalamic-pituitary-adrenal (HPA) axis, the development of fibromyalgia may stem from stress-induced disruption of the HPA axis.
Poor sleep is a risk factor for fibromyalgia. In 1975, Moldofsky and colleagues reported the presence of anomalous alpha wave activity (typically associated with arousal states) measured by electroencephalogram (EEG) during non-rapid eye movement sleep of "fibrositis syndrome". By disrupting stage IV sleep consistently in young, healthy subjects, the researchers reproduced a significant increase in muscle tenderness similar to that experienced in "neurasthenic musculoskeletal pain syndrome" but which resolved when the subjects were able to resume their normal sleep patterns. Mork and Nielsen used prospective data and identified a dose-dependent association between sleep problems and risk of FM.
There is strong evidence that major depression is associated with fibromyalgia as with other chronic pain conditions (1999), although the direction of the causal relationship is unclear. A comprehensive review into the relationship between fibromyalgia and major depressive disorder (MDD) found substantial similarities in neuroendocrine abnormalities, psychological characteristics, physical symptoms and treatments between fibromyalgia and MDD, but currently available findings do not support the assumption that MDD and fibromyalgia refer to the same underlying construct or can be seen as subsidiaries of one disease concept. Indeed, the sensation of pain has at least two dimensions: a sensory dimension which processes the magnitude and location of the pain, and an affective-motivational dimension which processes the unpleasantness. Accordingly, a study that employed functional magnetic resonance imaging to evaluate brain responses to experimental pain among people with fibromyalgia found that depressive symptoms were associated with the magnitude of clinically induced pain response specifically in areas of the brain that participate in affective pain processing, but not in areas involved in sensory processing which indicates that the amplification of the sensory dimension of pain in fibromyalgia occurs independently of mood or emotional processes. Fibromyalgia has also been linked with bipolar disorder, particularly the hypomania component.
Abnormalities in the ascending and descending pathways involved in processing pain have been observed in fibromyalgia. Fifty percent less stimulus is needed to evoke pain in those with fibromyalgia. A proposed mechanism for chronic pain is sensitization of secondary pain neurons mediated by increased release of proinflammatory cytokines and nitric oxide by glial cells. Inconsistent reports of decreased serum and CSF values of serotonin have been observed. There is also some data that suggests altered dopaminergic and noradrenergic signaling in fibromyalgia. Supporting the monoamine related theories is the efficacy of monoaminergic antidepressants in fibromyalgia.
Studies on the neuroendocrine system and HPA axis in fibromyalgia have been inconsistent. One study found fibromyalgia patients exhibited higher plasma cortisol, more extreme peaks and troughs, and higher rates of dexamethasone non suppression. However, other studies have only found correlations between a higher cortisol awakening response and pain, and not any other abnormalities in cortisol. Increased baseline ACTH and increase in response to stress have been observed, hypothesized to be a result of decreased negative feedback.
Autonomic nervous system
Autonomic nervous system abnormalities have been observed in fibromyalgia, including decreased vasoconstriction response, increased drop in blood pressure and worsening of symptoms in response to tilt table test, and decreased heart rate variability. Heart rate variabilities observed were different in males and females.
Disrupted sleep, insomnia, and poor-quality sleep occur frequently in FM, and may contribute to pain by decreased release of IGF-1 and human growth hormone, leading to decreased tissue repair. Restorative sleep was correlated with improvement in pain related symptoms.
Neuroimaging studies have observed decreased levels of N-acetylaspartic acid (NAA) in the hippocampus of people with fibromyalgia, indicating decreased neuron functionality in this region. Altered connectivity and decreased grey matter of the default mode network, the insula, and executive attention network have been found in fibromyalgia. Increased levels of glutamate and glutamine have been observed in the amygdala, parts of the prefrontal cortex, the posterior cingulate cortex, and the insula, correlating with pain levels in FM. Decreased GABA has been observed in the anterior insular in fibromyalgia. However, neuroimaging studies, in particular neurochemical imaging studies, are limited by methodology and interpretation. Increased cerebral blood flow in response to pain was found in one fMRI study. Findings of decreased blood flow in the thalamus and other regions of the basal ganglia correlating with treatment have been relatively consistent over three studies. Decreased binding of ?-opioid receptor have been observed; however, it is unknown if this is a result of increased endogenous binding in response to pain, or down regulation.
Overlaps have been drawn between chronic fatigue syndrome and fibromyalgia. One study found increased levels of pro-inflammatory cytokines in fibromyalgia, which may increase sensitivity to pain, and contribute to mood problems. Increased levels of IL-1RA, Interleukin 6 and Interleukin 8 have been found. Neurogenic inflammation has been proposed as a contributing factor to fibromyalgia. A systematic review found most cytokines levels were similar in patients and controls, except for IL-1 receptor antagonist, IL-6 and IL-8.
There is no single test that can fully diagnose fibromyalgia and there is debate over what should be considered essential diagnostic criteria and whether an objective diagnosis is possible. In most cases, people with fibromyalgia symptoms may also have laboratory test results that appear normal and many of their symptoms may mimic those of other rheumatic conditions such as arthritis or osteoporosis. The most widely accepted set of classification criteria for research purposes was elaborated in 1990 by the Multicenter Criteria Committee of the American College of Rheumatology. These criteria, which are known informally as "the ACR 1990", define fibromyalgia according to the presence of the following criteria:
A history of widespread pain lasting more than three months - affecting all four quadrants of the body, i.e., both sides, and above and below the waist.
Tender points - there are 18 designated possible tender points (although a person with the disorder may feel pain in other areas as well). Diagnosis is no longer based on the number of tender points.
The ACR criteria for the classification of patients were originally established as inclusion criteria for research purposes and were not intended for clinical diagnosis but have now become the de facto diagnostic criteria in the clinical setting. The number of tender points that may be active at any one time may vary with time and circumstance. A controversial study was done by a legal team looking to prove their client's disability based primarily on tender points and their widespread presence in non-litigious communities prompted the lead author of the ACR criteria to question now the useful validity of tender points in diagnosis. Use of control points has been used to cast doubt on whether a person has fibromyalgia, and to claim the person is malingering; however, no research has been done for the use of control points to diagnose fibromyalgia, and such diagnostic tests have been advised against, and people complaining of pain all over should still have fibromyalgia considered as a diagnosis.
2010 provisional criteria
Widespread pain index (WPI) areas
In 2010, the American College of Rheumatology approved provisional revised diagnostic criteria for fibromyalgia that eliminated the 1990 criteria's reliance on tender point testing. The revised criteria use a widespread pain index (WPI) and symptom severity scale (SS) in place of tender point testing under the 1990 criteria. The WPI counts up to 19 general body areas[a] in which the person has experienced pain in the preceding two weeks. The SS rates the severity of the person's fatigue, unrefreshed waking, cognitive symptoms, and general somatic symptoms,[b] each on a scale from 0 to 3, for a composite score ranging from 0 to 12. The revised criteria for diagnosis are:
WPI >= 7 and SS >= 5 OR WPI 3-6 and SS >= 9,
Symptoms have been present at a similar level for at least three months, and
No other diagnosable disorder otherwise explains the pain.:607
Some research has suggested not to categorise fibromyalgia as a somatic disease or a mental disorder, but to use a multidimensional approach taking into consideration somatic symptoms, psychological factors, psychosocial stressors and subjective belief regarding fibromyalgia. A review has looked at self-report questionnaires assessing fibromyalgia on multiple dimensions, including:
As with many other medically unexplained syndromes, there is no universally accepted treatment or cure for fibromyalgia, and treatment typically consists of symptom management. Developments in the understanding of the pathophysiology of the disorder have led to improvements in treatment, which include prescription medication, behavioral intervention, and exercise. Indeed, integrated treatment plans that incorporate medication, patient education, aerobic exercise, and cognitive behavioral therapy have been shown to be effective in alleviating pain and other fibromyalgia-related symptoms.
Antidepressants are "associated with improvements in pain, depression, fatigue, sleep disturbances, and health-related quality of life in people with FMS." The goal of antidepressants should be symptom reduction and if used long term, their effects should be evaluated against side effects. A small number of people benefit significantly from the SNRIs duloxetine and milnacipran and the tricyclic antidepressants (TCAs), such as amitriptyline. However, many people experience more adverse effects than benefits. While amitriptyline has been used as a first line treatment, the quality of evidence to support this use is poor.
It can take up to three months to derive benefit from the antidepressant amitriptyline and between three and six months to gain the maximal response from duloxetine, milnacipran, and pregabalin. Some medications have the potential to cause withdrawal symptoms when stopping so gradual discontinuation may be warranted particularly for antidepressants and pregabalin.
Tentative evidence suggests that monoamine oxidase inhibitors (MAOIs) such as pirlindole and moclobemide are moderately effective for reducing pain. Very low-quality evidence suggests pirlindole as more effective at treating pain than moclobemide. Side effects of MAOIs may include nausea and vomiting.
The anti-convulsant medications gabapentin and pregabalin may be used to reduce pain. There is tentative evidence that gabapentin may be of benefit for pain in about 18% of people with fibromyalgia. It is not possible to predict who will benefit, and a short trial may be recommended to test the effectiveness of this type of medication. Approximately 6/10 people who take gabapentin to treat pain related to fibromyalgia experience unpleasant side effects such as dizziness, abnormal walking, or swelling from fluid accumulation. Pregabalin demonstrates a benefit in about 9% of people. Pregabalin reduced time off work by 0.2 days per week.
The use of opioids is controversial. As of 2015, no opioid is approved for use in this condition by the FDA. The National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) in 2014 stated that there was a lack of evidence for opioids for most people. The Association of the Scientific Medical Societies in Germany in 2012 made no recommendation either for or against the use of weak opioids because of the limited amount of scientific research addressing their use in the treatment of FM. They strongly advise against using strong opioids. The Canadian Pain Society in 2012 said that opioids, starting with a weak opioid like tramadol, can be tried but only for people with moderate to severe pain that is not well-controlled by non-opioid painkillers. They discourage the use of strong opioids and only recommend using them while they continue to provide improved pain and functioning. Healthcare providers should monitor people on opioids for ongoing effectiveness, side effects and possible unwanted drug behaviors.
The European League Against Rheumatism in 2008 recommends tramadol and other weak opioids may be used for pain but not strong opioids. A 2015 review found fair evidence to support tramadol use if other medications do not work. A 2018 review found little evidence to support the combination of paracetamol (acetaminophen) and tramadol over a single medication. Goldenberg et al suggest that tramadol works via its serotonin and norepinephrine reuptake inhibition, rather than via its action as a weak opioid receptor agonist.
A large study of US people with fibromyalgia found that between 2005 and 2007 37.4% were prescribed short-acting opioids and 8.3% were prescribed long-acting opioids, with around 10% of those prescribed short-acting opioids using tramadol; and a 2011 Canadian study of 457 people with FM found 32% used opioids and two thirds of those used strong opioids.
A 2007 review concluded that a period of nine months of growth hormone was required to reduce fibromyalgia symptoms and normalize IGF-1. A 2014 study also found some evidence supporting its use.Sodium oxybate increases growth hormone production levels through increased slow-wave sleep patterns. However, this medication was not approved by the FDA for the indication for use in people with fibromyalgia due to the concern for abuse.
The muscle relaxants cyclobenzaprine, carisoprodol with acetaminophen and caffeine and tizanidine are sometimes used to treat fibromyalgia; however as of 2015 they are not approved for this use in the United States. The use of NSAIDs is not recommended as first line therapy. Moreover, NSAIDs cannot be considered as useful in the management of fibromyalgia.
Dopamine agonists (e.g. pramipexole and ropinirole) resulted in some improvement in a minority of people, but side effects, including the onset of impulse control disorders like compulsive gambling and shopping, might be a concern for some people.
Very low-quality evidence suggests quetiapine may be effective in fibromyalgia.
No high-quality evidence exists that suggests synthetic THC (nabilone) helps with fibromyalgia.
Intravenous Iloprost may be effective in reducing frequency and severity of attacks for people with fibromyalgia secondary to scleroderma.
Due to the uncertainty about the pathogenesis of FM, current treatment approaches focus on management of symptoms to improve quality of life, using integrated pharmacological and non-pharmacological approaches. There is no single intervention shown to be effective for all patients  and no gold treatment standard exists for FM. Multimodal/multidisciplinary therapy is recommended to target multiple underlying factors of FM. A meta-analysis of 1,119 subjects found "strong evidence that multicomponent treatment has beneficial short-term effects on key symptoms of FMS."  There is weak evidence to support the use of multidisciplinary rehabilitation programs.
Cognitive behavioural therapy
Non-pharmacological components include cognitive-behavioural therapy (CBT), exercise and psychoeducation (specifically, sleep hygiene). CBT and related psychological and behavioural therapies have a small to moderate effect in reducing symptoms of fibromyalgia. Effect sizes tend to be small when CBT is used as a stand-alone treatment for FM patients, but these improve significantly when CBT is part of a wider multidisciplinary treatment program. The greatest benefit occurs when CBT is used along with exercise.
A 2010 systematic review of 14 studies reported that CBT improves self-efficacy or coping with pain and reduces the number of physician visits at post-treatment, but has no significant effect on pain, fatigue, sleep or health-related quality of life at post-treatment or follow-up. Depressed mood was also improved but this could not be distinguished from some risks of bias.
Mind-body therapies focus on interactions among the brain, mind, body and behaviour. The National Centre for Complementary and Alternative Medicine defines the treatments under holistic principle that mind-body are interconnected and through treatment there is improvement in psychological and physical well-being, and allow patient to have an active role in their treatment. There are several therapies such as mindfulness, movement therapy (yoga, tai chi), psychological (including CBT) and biofeedback (use of technology to give audio/visual feedback on physiological processes like heart rate). There is only weak evidence that psychological intervention is effective in the treatment of fibromyalgia and no good evidence for the benefit of other mind-body therapies.
There is strong evidence indicating that exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia. In particular, there is strong evidence that cardiovascular exercise is effective for some people. Low-quality evidence suggests that high-intensity resistance training may improve pain and strength in women. Studies of different forms of aerobic exercise for adults with fibromyalgia indicate that aerobic exercise improves quality of life, decreases pain, slightly improves physical function and makes no difference in fatigue and stiffness. Long-term effects are uncertain. Combinations of different exercises such as flexibility and aerobic training may improve stiffness. However, the evidence is of low-quality. Tentative evidence suggests aquatic training can improve symptoms and wellness but, further research is required.
A recommended approach to a graded exercise program begins with small, frequent exercise periods and builds up from there. In children, fibromyalgia is often treated with an intense physical and occupational therapy program for musculoskeletal pain syndromes. These programs also employ counseling, art therapy, and music therapy. These programs are evidence-based and report long-term total pain resolution rates as high as 88%. Limited evidence suggests vibration training in combination with exercise may improve pain, fatigue and stiffness.
Although in itself neither degenerative nor fatal, the chronic pain of fibromyalgia is pervasive and persistent. Most people with fibromyalgia report that their symptoms do not improve over time. An evaluation of 332 consecutive new people with fibromyalgia found that disease-related factors such as pain and psychological factors such as work status, helplessness, education, and coping ability had an independent and significant relationship to FM symptom severity and function.
Fibromyalgia is estimated to affect 2-8% of the population. Females are affected about twice as often as males based on criteria as of 2014.
Fibromyalgia may not be diagnosed in up to 75% of affected people.
Chronic widespread pain had already been described in the literature in the 19th century but the term fibromyalgia was not used until 1976 when Dr P.K. Hench used it to describe these symptoms. Many names, including "muscular rheumatism", "fibrositis", "psychogenic rheumatism", and "neurasthenia" were applied historically to symptoms resembling those of fibromyalgia. The term fibromyalgia was coined by researcher Mohammed Yunus as a synonym for fibrositis and was first used in a scientific publication in 1981. Fibromyalgia is from the Latinfibra (fiber) and the Greek words myo (muscle) and algos (pain).
Historical perspectives on the development of the fibromyalgia concept note the "central importance" of a 1977 paper by Smythe and Moldofsky on fibrositis. The first clinical, controlled study of the characteristics of fibromyalgia syndrome was published in 1981, providing support for symptom associations. In 1984, an interconnection between fibromyalgia syndrome and other similar conditions was proposed, and in 1986, trials of the first proposed medications for fibromyalgia were published.
People with fibromyalgia generally have higher health-care costs and utilization rates. A study of almost 20,000 Humana members enrolled in Medicare Advantage and commercial plans compared costs and medical utilizations and found that people with fibromyalgia used twice as much pain-related medication as those without fibromyalgia. Furthermore, the use of medications and medical necessities increased markedly across many measures once diagnosis was made.
Fibromyalgia was defined relatively recently. It continues to be a disputed diagnosis. Dr. Frederick Wolfe, lead author of the 1990 paper that first defined the diagnostic guidelines for fibromyalgia, stated in 2008 that he believed it "clearly" not to be a disease but instead a physical response to depression and stress. In 2013 Wolfe added that its causes "are controversial in a sense" and "there are many factors that produce these symptoms - some are psychological and some are physical and it does exist on a continuum".
Some members of the medical community do not consider fibromyalgia a disease because of a lack of abnormalities on physical examination and the absence of objective diagnostic tests.
Neurologists and pain specialists tend to view fibromyalgia as a pathology due to dysfunction of muscles and connective tissue as well as functional abnormalities in the central nervous system. Rheumatologists define the syndrome in the context of "central sensitization" - heightened brain response to normal stimuli in the absence of disorders of the muscles, joints, or connective tissues. On the other hand, psychiatrists often view fibromyalgia as a type of affective disorder, whereas specialists in psychosomatic medicine tend to view fibromyalgia as being a somatic symptom disorder. These controversies do not engage healthcare specialists alone; some patients object to fibromyalgia being described in purely somatic terms. There is extensive research evidence to support the view that the central symptom of fibromyalgia, namely pain, has a neurogenic origin, though this is consistent in both views.
The validity of fibromyalgia as a unique clinical entity is a matter of contention because "no discrete boundary separates syndromes such as FMS, chronic fatigue syndrome, irritable bowel syndrome, or chronic muscular headaches". Because of this symptomatic overlap, some researchers have proposed that fibromyalgia and other analogous syndromes be classified together as functional somatic syndromes for some purposes.
A small 2018 study found some neuroinflammation in people with fibromyalgia.
^Shoulder girdle (left & right), upper arm (left & right), lower arm (left & right), hip/buttock/trochanter (left & right), upper leg (left & right), lower leg (left & right), jaw (left & right), chest, abdomen, back (upper & lower), and neck.:607
^Somatic symptoms include, but are not limited to: muscle pain, irritable bowel syndrome, fatigue or tiredness, problems thinking or remembering, muscle weakness, headache, pain or cramps in the abdomen, numbness or tingling, dizziness, insomnia, depression, constipation, pain in the upper abdomen, nausea, nervousness, chest pain, blurred vision, fever, diarrhea, dry mouth, itching, wheezing, Raynaud's phenomenon, hives or welts, ringing in the ears, vomiting, heartburn, oral ulcers, loss of or changes in taste, seizures, dry eyes, shortness of breath, loss of appetite, rash, sun sensitivity, hearing difficulties, easy bruising, hair loss, frequent or painful urination, and bladder spasms.:607
^Ferri, Fred F. (2010). Ferri's differential diagnosis : a practical guide to the differential diagnosis of symptoms, signs, and clinical disorders (2nd ed.). Philadelphia, PA: Elsevier/Mosby. p. Chapter F. ISBN978-0323076999.
^Glass JM (December 2006). "Cognitive dysfunction in fibromyalgia and chronic fatigue syndrome: new trends and future directions". Curr Rheumatol Rep. 8 (6): 425-9. doi:10.1007/s11926-006-0036-0. PMID17092441.
^Yunus MB (June 2007). "Role of central sensitization in symptoms beyond muscle pain, and the evaluation of a patient with widespread pain". Best Pract Res Clin Rheumatol. 21 (3): 481-97. doi:10.1016/j.berh.2007.03.006. PMID17602995.
^Maletic V, Raison CL (2009). "Neurobiology of depression, fibromyalgia and neuropathic pain". Front Biosci. 14: 5291-338. doi:10.2741/3598. PMID19482616.
^Cohen H, Buskila D, Neumann L, Ebstein RP (March 2002). "Confirmation of an association between fibromyalgia and serotonin transporter promoter region (5- HTTLPR) polymorphism, and relationship to anxiety-related personality traits". Arthritis Rheum. 46 (3): 845-7. doi:10.1002/art.10103. PMID11920428.
^Buskila D, Dan B, Cohen H, Hagit C, Neumann L, Lily N, Ebstein RP (August 2004). "An association between fibromyalgia and the dopamine D4 receptor exon III repeat polymorphism and relationship to novelty seeking personality traits". Mol. Psychiatry. 9 (8): 730-1. doi:10.1038/sj.mp.4001506. PMID15052273.
^Zubieta JK, Heitzeg MM, Smith YR, Bueller JA, Xu K, Xu Y, Koeppe RA, Stohler CS, Goldman D (February 2003). "COMT val158met genotype affects mu-opioid neurotransmitter responses to a pain stressor". Science. 299 (5610): 1240-3. doi:10.1126/science.1078546. PMID12595695.
^Narita M, Nishigami N, Narita N, Yamaguti K, Okado N, Watanabe Y, Kuratsune H (November 2003). "Association between serotonin transporter gene polymorphism and chronic fatigue syndrome". Biochem. Biophys. Res. Commun. 311 (2): 264-6. doi:10.1016/j.bbrc.2003.09.207. PMID14592408.
^Camilleri M, Atanasova E, Carlson PJ, Ahmad U, Kim HJ, Viramontes BE, McKinzie S, Urrutia R (August 2002). "Serotonin-transporter polymorphism pharmacogenetics in diarrhea-predominant irritable bowel syndrome". Gastroenterology. 123 (2): 425-32. doi:10.1053/gast.2002.34780. PMID12145795.
^Hudson JI, Mangweth B, Pope HG, De Col C, Hausmann A, Gutweniger S, Laird NM, Biebl W, Tsuang MT (February 2003). "Family study of affective spectrum disorder". Arch. Gen. Psychiatry. 60 (2): 170-7. doi:10.1001/archpsyc.60.2.170. PMID12578434.
^Lee YH, Choi SJ, Ji JD, Song GG (February 2012). "Candidate gene studies of fibromyalgia: a systematic review and meta-analysis". Rheumatol. Int. 32 (2): 417-26. doi:10.1007/s00296-010-1678-9. PMID21120487.
^Anderberg UM, Marteinsdottir I, Theorell T, von Knorring L (August 2000). "The impact of life events in female patients with fibromyalgia and in female healthy controls". Eur Psychiatry. 15 (5): 33-41. doi:10.1016/S0924-9338(00)00397-7. PMID10954873.
^Häuser W, Kosseva M, Üceyler N, Klose P, Sommer C (2011). "Emotional, physical, and sexual abuse in fibromyalgia syndrome: A systematic review with meta-analysis". Arthritis Care & Research. 63 (6): 808-820. doi:10.1002/acr.20328. PMID20722042.
^Sommer C, Häuser W, Burgmer M, Engelhardt R, Gerhold K, Petzke F, Schmidt-Wilcke T, Späth M, Tölle T, Uçeyler N, Wang H, Winkelmann A, Thieme K (June 2012). "[Etiology and pathophysiology of fibromyalgia syndrome]". Schmerz. 26 (3): 259-67. doi:10.1007/s00482-012-1174-0. PMID22760458.
^Pae CU, Luyten P, Marks DM, Han C, Park SH, Patkar AA, Masand PS, Van Houdenhove B (August 2008). "The relationship between fibromyalgia and major depressive disorder: a comprehensive review". Curr Med Res Opin. 24 (8): 2359-71. doi:10.1185/03007990802288338. PMID18606054.
^Alciati A, Sarzi-Puttini P, Batticiotto A, Torta R, Gesuele F, Atzeni F, Angst J (2012). "Overactive lifestyle in patients with fibromyalgia as a core feature of bipolar spectrum disorder". Clinical and Experimental Rheumatology. 30 (6): 122-128. PMID23261011.
^ abRossi A, Di Lollo AC, Guzzo MP, Giacomelli C, Atzeni F, Bazzichi L, Di Franco M (2015). "Fibromyalgia and nutrition: what news?". Clin Exp Rheumatol. 33 (1 Suppl 88): S117-25. PMID25786053.
^San Mauro Martín I, Garicano Vilar E, Collado Yurrutia L, Ciudad Cabañas MJ (December 2014). "[Is gluten the great etiopathogenic agent of disease in the XXI century?] [Article in Spanish]". Nutr Hosp. 30 (6): 1203-10. doi:10.3305/nh.2014.30.6.7866. PMID25433099.
^Dadabhoy, Dina; Clauw, Daniel J. (1 July 2006). "Therapy Insight: fibromyalgia--a different type of pain needing a different type of treatment". Nature Clinical Practice Rheumatology. 2 (7): 364-372. doi:10.1038/ncprheum0221. ISSN1745-8382. PMID16932722.
^Wolfe, Frederick; Clauw, Daniel J.; Fitzcharles, Mary-Ann; Goldenberg, Don L.; Katz, Robert S.; Mease, Philip; Russell, Anthony S.; Russell, I. Jon; Winfield, John B. (1 May 2010). "The American College of Rheumatology Preliminary Diagnostic Criteria for Fibromyalgia and Measurement of Symptom Severity". Arthritis Care & Research. 62 (5): 600-610. doi:10.1002/acr.20140. hdl:2027.42/75772. ISSN2151-4658. PMID20461783.
^Seidenberg, Michael; Haltiner, Alan; Taylor, Michael; Hermann, Bruce; Wyler, Allen (2008). "Development and validation of a multiple ability self-report questionnaire". Journal of Clinical and Experimental Neuropsychology. 16 (1): 93-104. doi:10.1080/01688639408402620. PMID8150893.
^Häuser W, Bernardy K, Uçeyler N, Sommer C (January 2009). "Treatment of fibromyalgia syndrome with antidepressants: a meta-analysis". JAMA. 301 (2): 198-209. doi:10.1001/jama.2008.944. PMID19141768.
^Häuser W, Wolfe F, Tölle T, Uçeyler N, Sommer C (April 2012). "The role of antidepressants in the management of fibromyalgia syndrome: a systematic review and meta-analysis". CNS Drugs. 26 (4): 297-307. doi:10.2165/11598970-000000000-00000. PMID22452526.
^Cuatrecasas, G.; Alegre, C.; Casanueva, FF. (June 2014). "GH/IGF1 axis disturbances in the fibromyalgia syndrome: is there a rationale for GH treatment?". Pituitary. 17 (3): 277-83. doi:10.1007/s11102-013-0486-0. PMID23568565.
^Karjalainen, Kaija A; Malmivaara, Antti; van Tulder, Maurits W; Roine, Risto; Jauhiainen, Merja; Hurri, Heikki; Koes, Bart W (26 July 1999). "Multidisciplinary rehabilitation for fibromyalgia and musculoskeletal pain in working age adults". Cochrane Database of Systematic Reviews (2): CD001984. doi:10.1002/14651858.cd001984. ISSN1465-1858. PMID10796458.
^Yunus M, Masi AT, Calabro JJ, Miller KA, Feigenbaum SL (August 1981). "Primary fibromyalgia (fibrositis): clinical study of 50 patients with matched normal controls". Seminars in Arthritis and Rheumatism. 11 (1): 151-171. doi:10.1016/0049-0172(81)90096-2. ISSN0049-0172. PMID6944796.
^"Fibro-". Dictionary.com. Archived from the original on 13 December 2009. Retrieved 2008.
^Wolfe F, Smythe HA, Yunus MB, Bennett RM, Bombardier C, Goldenberg DL, Tugwell P, Campbell SM, Abeles M, Clark P (February 1990). "The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee". Arthritis Rheum. 33 (2): 160-72. doi:10.1002/art.1780330203. PMID2306288.