出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/05/01 19:32:33」(JST)
| Fibromyalgia | |
|---|---|
| Classification and external resources | |
The location of the nine paired tender points that comprise the 1990 American College of Rheumatology criteria for fibromyalgia.
|
|
| ICD-10 | M79.7 |
| ICD-9 | 729.1 |
| MedlinePlus | 000427 |
| eMedicine | med/790 med/2934 ped/777 pmr/47 |
| MeSH | D005356 |
Fibromyalgia (FM or FMS) is characterised by chronic widespread pain and allodynia (a heightened and painful response to pressure).[1] Fibromyalgia symptoms are not restricted to pain, leading to the use of the alternative term fibromyalgia syndrome for the condition. Other symptoms include debilitating fatigue, sleep disturbance, and joint stiffness. Some people[2] also report difficulty with swallowing,[3] bowel and bladder abnormalities,[4] numbness and tingling,[5] and cognitive dysfunction.[6] Fibromyalgia is frequently associated with psychiatric conditions such as depression and anxiety and stress-related disorders such as posttraumatic stress disorder.[7][8] Not all people with fibromyalgia experience all associated symptoms.[9]
Its exact cause is unknown but is believed to involve psychological, genetic, neurobiological and environmental factors.[10][11][12] There is evidence that environmental factors and certain genes increase the risk of developing fibromyalgia – these same genes are also associated with other functional somatic syndromes and major depressive disorder.[13] The central symptom of fibromyalgia, namely widespread pain, appears to result from neuro-chemical imbalances including activation of inflammatory pathways in the brain which results in abnormalities in pain processing.[14] The brains of fibromyalgia patients show functional and structural differences from those of healthy individuals, but it is unclear whether the brain anomalies cause fibromyalgia symptoms or are the product of an unknown underlying common cause. Some research suggests that these brain anomalies may be the result of childhood stress, or prolonged or severe stress.[8]
Fibromyalgia has been recognized as a diagnosable disorder by the US National Institutes of Health and the American College of Rheumatology.[15][16] On the other hand, Dr. Frederick Wolfe, the researcher credited with its discovery, has stated he believes that it is "clearly" not a disease but instead a physical response to depression and stress.[17] Fibromyalgia, a central nervous system disorder, is described as a "central sensitization syndrome" caused by neurobiological abnormalities which act to produce physiological pain and cognitive impairments as well as neuro-psychological symptomatology.[1] Despite this, there is controversy as to the cause and nature of fibromyalgia, as well as how patients are described by those in the medical community.[14][18]
Fibromyalgia is estimated to affect 2–8% of the population,[19] with a female to male incidence ratio of approximately 9:1.[20] The term "fibromyalgia" derives from New Latin, fibro-, meaning "fibrous tissues", Greek myo-, "muscle", and Greek algos, "pain"; thus the term literally means "muscle and connective tissue pain".
Fibromyalgia is classed as a disorder of pain processing due to abnormalities in how pain signals are processed in the central nervous system.[14] The American College of Rheumatology classify fibromyalgia as being a functional somatic syndrome.[18] The expert committee the European League Against Rheumatism classify fibromyalgia as a neurobiological disorder and as a result exclusively give pharmacotherapy their highest level of support.[18] The International Classification of Diseases (ICD-10) lists fibromyalgia as a diagnosable disease under "Diseases of the musculoskeletal system and connective tissue" and states that fibromyalgia syndrome should be classified as a functional somatic syndrome rather than a mental disorder. Although mental disorders and some physical disorders commonly are co-morbid with fibromyalgia — especially anxiety, depression and irritable bowel syndrome and chronic fatigue syndrome — the ICD states that these should be diagnosed separately.[18]
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":[21]
The defining symptoms of fibromyalgia are chronic widespread pain, fatigue, sleep disturbance, and heightened pain in response to tactile pressure (allodynia).[22] Other symptoms may include tingling of the skin (paresthesias),[22] prolonged muscle spasms, weakness in the limbs, nerve pain, muscle twitching, palpitations,[23] and functional bowel disturbances.[3][24]
Many patients experience cognitive dysfunction[6][22] (known as "fibrofog"), which may be characterized by impaired concentration,[25] problems with short[7][25] and long-term memory, short-term memory consolidation,[7] impaired speed of performance,[7][25] inability to multi-task, cognitive overload,[7][25] and diminished attention span. Fibromyalgia is often associated with anxiety and depressive symptoms.[7]
Other symptoms often attributed to fibromyalgia that may possibly be due to a comorbid disorder include myofascial pain syndrome, also referred to as chronic myofascial pain, diffuse non-dermatomal paresthesias, functional bowel disturbances and irritable bowel syndrome, genitourinary symptoms and interstitial cystitis, dermatological disorders, headaches, myoclonic twitches, and symptomatic hypoglycemia. Although fibromyalgia is classified based on the presence of chronic widespread pain, pain may also be localized in areas such as the shoulders, neck, low back, hips, or other areas. Many sufferers also experience varying degrees of myofascial pain and have high rates of comorbid temporomandibular joint dysfunction. 20–30% of patients with rheumatoid arthritis and systemic lupus erythematosus may also have fibromyalgia.[26]
The cause of fibromyalgia is unknown. However, several hypotheses have been developed including "central sensitization".[22] This theory proposes that fibromyalgia patients have a lower threshold for pain because of increased reactivity of pain-sensitive nerve cells in the spinal cord or brain.[1] 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 which regulate mood and pain. Eventually a sensitisation and kindling effect occurs in certain neurones leading to the establishment of fibromyalgia and sometimes a mood disorder.[10] 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 neurones 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 of the 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.[14]
There is evidence that genetic factors may play a role in the development of fibromyalgia. For example, there is a high aggregation of fibromyalgia in families.[27][28] Using self-report of chronic widespread pain (CWP) as a surrogate marker for fibromyalgia, the Swedish Twin Registry reports:[29][30]
The mode of inheritance is currently unknown, but it is most probably polygenic.[13] Research has also demonstrated that fibromyalgia is potentially associated with polymorphisms of genes in the serotoninergic,[31] dopaminergic[32] and catecholaminergic systems.[33] However, these polymorphisms are not specific for fibromyalgia and are associated with a variety of allied disorders (e.g. chronic fatigue syndrome,[34] irritable bowel syndrome[35]) and with depression.[36] Individuals with the 5-HT2A receptor 102T/C polymorphism have been found to be at increased risk of developing fibromyalgia.[37]
Stress may be an important precipitating factor in the development of fibromyalgia.[38] Fibromyalgia is frequently comorbid with stress-related disorders such as chronic fatigue syndrome, posttraumatic stress disorder, irritable bowel syndrome and depression.[8] 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.[39] Poor lifestyles including being a smoker, obesity and lack of physical activity may increase the risk of an individual developing fibromyalgia.[11]
Two studies that employed single-voxel magnetic resonance spectroscopy (1H-MRS) reported metabolic abnormalities within the hippocampal complex in patients with fibromyalgia. As the hippocampus plays crucial roles in maintenance of cognitive functions, sleep regulation, and pain perception, it was suggested that metabolic dysfunction of the hippocampus may be implicated in the appearance of these symptoms.[40][41]
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.[42]
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" patients.[24] 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.[43] In one study it was found that the best predictor of the experience of pain in male fibromyalgia patients was sleep quality.[44]
There is strong evidence that major depression is associated with fibromyalgia (1999),[45] although the nature of the association is debated.[12] 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.[46] 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 fibromyalgia patients 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.[47]
Neck trauma has been reported to increase the risk of developing fibromyalgia.[48]
In a small 2004 double-blind study, all of the 42 FMS patients were found to have raised hydrogen levels in a lactulose hydrogen breath test, thought to indicate the presence of small bowel bacterial overgrowth syndrome.[49] It has been hypothesised that chronic activation of the immune system against pathogenic bacterial overgrowth may cause fibromyalgia symptoms.[50]
The "dopamine hypothesis of fibromyalgia" proposes that the central abnormality responsible for symptoms associated with fibromyalgia is a disruption of normal dopamine-related neurotransmission.[51] Insufficient dopamine in a part of the body is termed hypodopaminergia. Dopamine is a catecholamine neurotransmitter with roles in pain perception and natural analgesia. There is also strong evidence for a role of dopamine in restless leg syndrome,[52] which is a condition found frequently in patients with fibromyalgia.[53] Some fibromyalgia patients responded in controlled trials to pramipexole, a dopamine agonist that selectively stimulates dopamine D2/D3 receptors and is used to treat both Parkinson's disease and restless leg syndrome.[54]
In 1975, researchers hypothesized that serotonin, a neurotransmitter that regulates sleep patterns, mood, concentration and pain, could be involved in the pathophysiology of fibromyalgia-associated symptoms.[24] In 1992, decreased serotonin metabolites in patient blood samples[55] and cerebrospinal fluid were reported.[56] However, selective serotonin reuptake inhibitors (SSRIs) have met with limited success in alleviating the symptoms of the disorder, while drugs with activity as mixed serotonin-norepinephrine reuptake inhibitors (SNRIs) have been more successful.[57] However, the relevance of dysregulated serotonin metabolism to pathophysiology is a matter of debate.[58] Complicating the analysis, one of the more effective types of medication for the treatment of the disorder (i.e. serotonin 5-HT3 antagonists) actually blocks some of the effects of serotonin.[59]
Results from studies examining responses to experimental stimulation suggest that fibromyalgia patients may have heightened sensitivity of the nociceptive system, which senses pressure, heat, cold, electrical and chemical stimulation.[60] Experiments examining pain regulatory systems have shown that fibromyalgia patients display an exaggerated wind-up in response to repetitive stimulation[61] and an absence of exercise-induced analgesic response.[62]
Levels of hormones under the direct or indirect control of growth hormone (GH), including insulin-like growth factor 1 (IGF-1), cortisol, leptin and neuropeptide Y may be abnormal in people with fibromyalgia.[63] Several authors have demonstrated low growth hormone levels or low IGF-I levels in patients with fibromyalgia compared with controls. Moreover, fibromyalgia patients have an abnormal sleep pattern involving stages 3 and 4 of non REM sleep during which growth hormone is predominantly secreted.[64] Further support for a causal role for growth hormone deficiency comes from observations that such deficiency in adults has been associated with many of the symptoms described by fibromyalgia patients. Growth hormone is important in maintaining muscle homeostasis, and it has been suggested that low levels may be responsible for delayed healing of muscle microtrauma in fibromyalgia.[65] Low (IGF-1) levels in some fibromyalgia patients have led to the theory that these patients may actually have a different, treatable syndrome, adult growth hormone deficiency.[66] However, there remains some disagreement about the role of HGH in fibromyalgia.[67]
Patients with fibromyalgia may have alterations of normal neuroendocrine function, characterized by mild hypocortisolemia,[68] hyperreactivity of pituitary adrenocorticotropin hormone release in response to challenge, and glucocorticoid feedback resistance.[69]
Other abnormalities include reduced responsivity of thyrotropin and thyroid hormones to thyroid-releasing hormone,[70] a mild elevation of prolactin levels with disinhibition of prolactin release in response to challenge[71] and hyposecretion of adrenal androgens.[72]
These changes might result from chronic stress, which, after being perceived and processed by the central nervous system, activates hypothalamic corticotrophin-releasing hormone neurons. Chronic overactivity of these neurons could disrupt normal function of the pituitary-adrenal axis and cause an increased stimulation of hypothalamic somatostatin secretion, which, in turn, could inhibit the secretion of other hormones.[73]
Functional analysis of the autonomic system in patients with fibromyalgia has demonstrated disturbed activity characterized by hyperactivity of the sympathetic nervous system at baseline[74] with reduced sympathoadrenal reactivity in response to a variety of stressors including physical exertion and mental stress.[75][76] Fibromyalgia patients demonstrate lower heart rate variability, an index of sympathetic/parasympathetic balance, indicating sustained sympathetic hyperactivity, especially at night.[77] In addition, plasma levels of neuropeptide Y, which is co-localized with norepinephrine in the sympathetic nervous system, have been reported as low in patients with fibromyalgia,[63] while circulating levels of epinephrine and norepinephrine have been variously reported as low, normal and high.[78][79] Administration of interleukin-6, a cytokine capable of stimulating the release of hypothalamic corticotropin-releasing hormone which in turn stimulates activity within the sympathetic nervous system, results in a dramatic increase in circulating norepinephrine levels and a significantly greater increase in heart rate over baseline in fibromyalgia patients as compared to healthy controls.[80]
One of the most reproduced laboratory finding in patients with fibromyalgia is an elevation in cerebrospinal fluid levels of substance P, a putative nociceptive neurotransmitter.[81][82][83] Metabolites for the monoamine neurotransmitters serotonin, norepinephrine, and dopamine—all of which play a role in natural analgesia—have been shown to be lower,[56] while concentrations of endogenous opioids (i.e., endorphins and enkephalins) appear to be higher.[84] The mean concentration of nerve growth factor, a substance known to participate in structural and functional plasticity of nociceptive pathways within the dorsal root ganglia and spinal cord, is elevated.[85] There is also evidence for increased excitatory amino acid release within cerebrospinal fluid, with a correlation demonstrated between levels for metabolites of glutamate and nitric oxide and clinical indices of pain.[86]
Evidence of abnormal brain involvement in fibromyalgia has been provided via functional neuroimaging. The first findings reported were decreased blood flow within the thalamus and elements of the basal ganglia and mid-brain (i.e., pontine nucleus).[87][88] Differential activation in response to painful stimulation has also been demonstrated.[89][90] Brain centers showing hyperactivation in response to noxious stimulation include such pain-related brain centers as the primary and secondary somatosensory cortices, anterior cingulate cortex, and insular cortex. Patients also exhibit neural activation in brain regions associated with pain perception in response to nonpainful stimuli in such areas as the prefrontal, supplemental motor, insular, and cingulate cortices. Evidence of hippocampal disruption indicated by reduced brain metabolite ratios has been demonstrated by studies using single-voxel magnetic resonance spectroscopy (1H-MRS).[40][41] A significant negative correlation was demonstrated between abnormal metabolite ratios and a validated index of the clinical severity (i.e. the Fibromyalgia Impact Questionnaire).[91] Correlations between clinical pain severity and concentrations of the excitatory amino acid neurotransmitter glutamate within the insular cortex have also been demonstrated using 1H-MRS.[92] An acceleration of normal age-related brain atrophy has been demonstrated using voxel-based morphometry (VBM) with areas of reduced gray matter located in the cingulate cortex, insula and parahippocampal gyrus. Grey matter loss appears to increase 9.5 times the normal rate with each year.[93] Studies utilizing positron emission tomography have demonstrated reduced dopamine synthesis in the brainstem and elements of the limbic cortex.[94] A significant negative correlation between pain severity and dopamine synthesis was demonstrated within the insular cortex. A subsequent study demonstrated gross disruption of dopaminergic reactivity in response to a tonic pain stimulus within the basal ganglia with a significant positive correlation between the defining feature of the disorder (i.e. tender point index) and dopamine D2 receptor binding potential specifically in the right putamen.[95] Finally, reduced availability of mu-opioid receptors in the ventral striatum/nucleus accumbens and cingulate cortex has been demonstrated, with a significant negative correlation between affective pain levels and receptor availability in the nucleus accumbens.[96]
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, patients 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. In general, most doctors diagnose patients with a process called differential diagnosis, which means that doctors consider all of the possible things that might be wrong with the patient based on the patient's symptoms, gender, age, geographic location, medical history and other factors. They then narrow down the diagnosis to the most likely one. 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:
The ACR criteria for 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. It should be noted that the number of tender points that may be active at any one time may vary with time and circumstance. A controversial study 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 now question the useful validity of tender points in diagnosis.[99] 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 that patients complaining of pain all over should still have fibromyalgia considered as a diagnosis.[18] Since the ACR criteria were originally published, research with mechanical devices that exert defined pressure indicate that diagnosis of fibromyalgia cannot be done objectively by machine and require a physician's subjective estimate of how much pressure should be exerted.[citation needed]
Fibromyalgia is widely under-diagnosed with up to 75 percent of people suffering with fibromyalgia not being diagnosed.[14]
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, behavioural intervention and exercise. Indeed, integrated treatment plans that incorporate medication, patient education, aerobic exercise and cognitive-behavioural therapy have been shown to be effective in alleviating pain and other fibromyalgia-related symptoms.[100]
The Association of the Scientific Medical Societies in Germany,[101] the European League Against Rheumatism[102] and the Canadian Pain Society[103] currently publish guidelines for the diagnosis and management of FMS.
Cognitive behavioural therapy (CBT) and related psychological and behavioural therapies have a small to moderate effect in reducing symptoms of fibromyalgia.[104][105] The greatest benefit occurs when CBT is used along with exercise.[100][106]
A meta-analysis of 1,119 subjects found "strong evidence that multicomponent treatment has beneficial short-term effects on key symptoms of FMS." [107] 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 followup. Depressed mood was also improved but this could not be distinguished from some risks of bias.[108] A multidisciplinary approach, often including CBT is sometimes considered to be the "gold standard" of treatment for chronic pain syndromes such as fibromyalgia.
Health Canada and the US Food and Drug Administration (FDA) have approved pregabalin[109] and duloxetine, for the management of fibromyalgia. The FDA also approves milnacipran, but the European Medicines Agency refused marketing authority.[110]
Antidepressants are "associated with improvements in pain, depression, fatigue, sleep disturbances, and health-related quality of life in patients with FMS."[111] 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 (such as amitriptyline) however many people experience more adverse effects than benefits.[112][113] While amitriptyline has been used as a first line treatment, the quality of evidence to support this use is poor.[114]
The anti-convulsant drugs gabapentin[115] and pregabalin[116] may be used. Gabapentin is of a significant benefit in about 30% of people who take it however is commonly associated with adverse effects.[115] A Cochrane review of pregabalin use in chronic pain concluded that "A minority of patients will have substantial benefit with pregabalin, and more will have moderate benefit. Many will have no or trivial benefit, or will discontinue because of adverse events."[117] A meta-analysis of four trials of pregabalin in fibromyalgia found that, for people who did respond to pregabalin, there was a reduction in their time off work of greater than 1 day per week.[118]
The Association of the Scientific Medical Societies in Germany makes 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.[101] The European League Against Rheumatism recommends the weak opioid tramadol but not strong opioids.[102] The Canadian Pain Society says that opioids, starting with a weak opioid like tramadol, can be tried but only for patients with moderate to severe pain that is not well-controlled by non-opioid pain-killers. They discourage the use of strong opioids, and only recommend using them while they continue to provide improved pain and functioning. Healthcare providers must monitor patients on opioids for ongoing effectiveness, side effects and possible unwanted drug behaviours.[103]
The combination of tramadol and paracetemol has demonstrated efficacy, safety and tolerability (for up to two years in the management of other pain conditions) without the development of tolerance. It is as effective as a combination of codeine (another mild opioid) and paracetamol but produces less sleepiness and constipation.[119]
A large study of US fibromyalgia patients found that between 2005 and 2007 37.4% were prescribed short-acting opioids and 8.3% were prescribed long-acting opioids,[120] with around 10% of those prescribed short-acting opioids using tramadol;[121] and a 2011 Canadian study of 457 FM patients found 32% used opioids and two thirds of those used strong opioids.[103]
Initial studies on the use of human growth hormone for fibromyalgia yielded promising results.[122][123] A 2007 literature review, reported on the results of 3 randomized placebo controlled studies, this concluded that a long period of 9 months of growth hormone was required to reduce fibromyalgia symptoms and normalize IGF-1. It was recommended that further study be conducted before any solid recommendations can be made.[124] However, in 2012 the largest and longest clinical trial of this hormone for fibromyalgia, concluded that adding growth hormone to the standard treatment was effective in reducing pain, and showed sustained action over time.[125]
The narcolepsy medication sodium oxybate has been studied in those with fibromyalgia. This drug was shown to reduce the symptoms of pain and fatigue, and dramatically reduce the sleep abnormalities (alpha intrusion and decreased slow-wave sleep).[126] Subsequent stage 3 trials for this drug supported these findings which found the drug provided important benefits across multiple symptoms in subjects with fibromyalgia.[127] Since Sodium Oxybate was shown to increase natural growth hormone production levels through increased slow-wave sleep patterns, these studies provide further support that supplementing growth hormone may be beneficial for fibromyalgia sufferers. However, this medication was not approved by the FDA for the indication for use in fibromyalgia patients due to the concern for abuse.[128]
The muscle relaxants cyclobenzaprine and tizanidine are sometimes used off-label to treat fibromyalgia.[129][130]
Dopamine agonists (e.g. pramipexole (Mirapex) and ropinirole (ReQuip)) resulted in some improvement in a minority of patients,[54] but numerous side effects, including the onset of impulse control disorders like compulsive gambling and shopping, have led to concern about this approach.[131]
The use of NSAIDs is not recommended as first line therapy.[132] It can take up to three months to derive benefit from the antidepressant amitriptyline and up to six months to gain 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.[18]
Evidence exists that fibromyalgia is a neuro-immuno-endocrine disorder. Elevations in substance P, IL-6 and IL-8 as well as corticotropin-releasing hormone have been found in the cerebral spinal fluid of fibromyalgia suffering individuals. Increased numbers of mast cell numbers have been found in skin biopsies of some individuals with fibromyalgia. Quercetin, a pharmacologically active natural product which possesses anti-inflammatory in addition to mast cell inhibiting properties may be a useful treatment.[133]
Exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia.[134][135] In particular, there is strong evidence that cardiovascular exercise is effective for some patients.[136] Long-term aquatic-based exercise has been proven beneficial as it combines cardiovascular exercise with resistance training.[137] However, due to the cold sensitivities of people with fibromyalgia syndrome, aquatic therapy must take place in a warm pool. Not only that, but the air outside of the pool must also be heated to prevent fibromyalgia patients from getting chills and aches when out of the water. This involves a specialised pool facility, which makes this therapy more expensive and less accessible than regular swimming exercise.
In children and teens, fibromyalgia is often treated with an intense physical and occupational therapy program for amplified musculoskeletal pain syndromes. These programs also employ counseling, art therapy, and music therapy. Such programs can be found at The Children's Hospital of Philadelphia (University of Pennsylvania), Boston Children's Hospital (Harvard University) and several other children's hospitals around the US. These programs are evidence-based and report long term total pain resolution rates as high as 88%.[138] The efficacy of such a program has not been studied in adults with fibromyalgia.
Although in itself neither degenerative nor fatal, the chronic pain of fibromyalgia is pervasive and persistent. Most fibromyalgia patients report that their symptoms do not improve over time. An evaluation of 332 consecutive new fibromyalgia patients 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.[139]
Fibromyalgia is seen in about 2% of the general population[140] and affects more females than males, with a ratio of 7:1 by ACR criteria.[22] It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood.
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.[18] Many names, including "muscular rheumatism", "fibrositis", "psychogenic rheumatism", and "neurasthenia" were applied historically to symptoms resembling those of fibromyalgia.[141] The term fibromyalgia was coined by researcher Mohammed Yunus as a synonym for fibrositis and was first used in a scientific publication in 1981.[142] Fibromyalgia is from the Latin fibra (fiber)[143] and the Greek words myo (muscle)[144] and algos (pain).[145]
Historical perspectives on the development of the fibromyalgia concept note the "central importance" of a 1977 paper by Smythe and Moldofsky on fibrositis.[146][147] The first clinical, controlled study of the characteristics of fibromyalgia syndrome was published in 1981,[148] providing support for symptom associations. In 1984, an interconnection between fibromyalgia syndrome and other similar conditions was proposed,[149] and in 1986, trials of the first proposed medications for fibromyalgia were published.[149]
A 1987 article in the Journal of the American Medical Association used the term "fibromyalgia syndrome" while saying it was a "controversial condition".[150] The American College of Rheumatology (ACR) published its first classification criteria for fibromyalgia in 1990,[151] although these are not strictly diagnostic criteria.[21]
Patients 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 persons 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.[152]
Being a disorder defined relatively recently and still not completely understood, fibromyalgia continues to be a diagnosis that sometimes is disputed. 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.[146][153] Yunus has referred to some physicians' belief that FM is psychological in nature as disturbed physician syndrome (DPS): "It is the physicians who are psychologically disturbed because they ignore the data, and whatever data there is, they manipulate it to say what they want it to say."[154]
Rheumatologists, neurologists, and pain specialists tend to view fibromyalgia as a pathology due to dysfunction of muscles, connective tissue as well as being due to functional abnormalities in the central nervous system. On the other hand, psychiatrists often view fibromyalgia as being a type of affective disorder whereas specialists in psychosomatic medicine tend to view fibromyalgia as being somatoform disorder. However, there is extensive research evidence to support the view that the central symptom of fibromyalgia, namely pain, has a neurogenic origin. The controversies don't just involve healthcare specialists but also patients who often object to fibromyalgia being described in purely somatic terms.[14][18]
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."[136][155] Because of this considerable symptomatic overlap, some researchers have proposed that fibromyalgia and other syndromes with overlapping symptoms be classified as functional somatic syndromes for some purposes.[156]
Investigational medications include cannabinoids and the 5-HT3 receptor antagonist tropisetron.[157] A controlled study of guaifenesin failed to demonstrate any benefits from this treatment.[158][159] Quercetin, a flavanoid and pharmacologically active natural compound, which acts as an anti-inflammatory and has mast cell inhibitory properties may be effective in the treatment of fibromyalgia.[133] Preliminary research on naltrexone at very low dosage has been found to be effective in reducing fibromyalgia symptoms by more than 30 percent in one small pilot study of 10 women. Naltrexone, an opioid antagonist also acts at very low dosage, to inhibit microglia cells thereby reducing proinflammatory cytokines and neurotoxic superoxides.[1]
|displayauthors= suggested (help)|date= (help)|displayauthors= suggested (help)| Wikimedia Commons has media related to Fibromyalgia. |
|
||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||||||
全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.
| リンク元 | 「線維筋痛症」「FMS」「線維性筋痛症候群」 |
| 関連記事 | 「syndrome」 |
| 1 | 後頭部 |
| 2 | 下部頚椎 |
| 3 | 僧帽筋 |
| 4 | 棘上筋 |
| 5 | 第2肋骨 |
| 6 | 外側上顆 |
| 7 | 臀部 |
| 8 | 大転子 |
| 9 | 膝 |
[★] 線維性筋痛症候群 fibromyalgia syndrome