From Wikipedia, the free encyclopedia
Classification and external resources
ICD-10
M79.7
ICD-9
729.1
MedlinePlus
000427
eMedicine
med/790 med/2934 ped/777 pmr/47
MeSH
D005356
Fibromyalgia (FM) is a disorder classified by the presence of chronic widespread pain and tactile allodynia.[1] An example of tactile allodynia is when a person perceives light pressure or the movement of clothes over the skin as painful, whereas a healthy individual would not feel pain. Fibromyalgia patients are often affected by a number of symptoms other than pain, including debilitating fatigue, abnormal sleep architecture [2] meaning the brain does not reach all the restorative levels of sleep necessary for overall health, functional bowel disturbances[3] and a variety of neuropsychiatric problems including cognitive dysfunction [4] which can mean short and/or long term memory problems, slowed information processing ability, diminished attention span and anxiety and depressive symptoms[5]. While the criteria for such an entity have not yet been thoroughly developed, the recognition that fibromyalgia involves more than just pain has led to the frequent use of the term “fibromyalgia syndrome.” It is not contagious, and recent studies suggest that people with fibromyalgia may be genetically predisposed.[6] It affects more females than males, with a ratio of 9:1 by American College of Rheumatology (ACR)criteria.[7] Fibromyalgia is seen in about 2% of the general population.[8] It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood.
The disorder is not directly life-threatening. The degree of symptoms may vary greatly from day to day with periods of flares (severe worsening of symptoms) or remission; however, the disorder is generally perceived as non-progressive.[9]
The validity of fibromyalgia as a unique clinical entity is a matter of some contention among researchers in the field. For example, it has been proposed that the pathophysiology responsible for the symptoms that are collectively classified as representing "fibromyalgia" is poorly understood, thereby suggesting that the fibromyalgia phenotype which is the difference between an individual’s heredity and what that heredity produces, may result from several different disease processes that have global hyperalgesia - an increased sensitivity to pain - and allodynia in common, [10][11][12] an observation that has led to the proposition that current diagnostic criteria are insufficient to differentiate patient groups from each other.[13] Alternatively, there is evidence for the existence of differing pathophysiological - which is the study of the disturbance of normal mechanical, physical, and biochemical functions of the body - within the greater fibromyalgia construct[14][15], which may be interpreted to represent evidence for the existence of biologically distinct "sub-types" of the disorder akin to conditions such as epilepsy, schizophrenia and major depressive disorder. In a January 14, 2008 article in the New York Times, the controversy of the reality of the disease and its proposed cures are discussed, while citing that the American College of Rheumatology, the Food and Drug Administration and insurers recognize fibromyalgia as a diagnosable disease. Drug companies are aggressively pursuing fibromyalgia treatments, seeing the potential for a major new market.[16]
History
Fibromyalgia has been studied since the early 1800s and referred to by a variety of former names, including muscular rheumatism and fibrositis.[17] The term fibromyalgia was coined in 1976 to more accurately describe the symptoms, from the Latin fibra (fiber)[18] and the Greek words myo (muscle)[19] and algos (pain).[20]
In 1981, Dr. Muhammad B. Yunus published the "first controlled study of the clinical characteristics" of the fibromyalgia syndrome, for which he is considered "the father of our modern view of fibromyalgia."[21][22] His work was the "first controlled clinical study" of fibromyalgia with validation of known symptoms and tender points, and he also proposed "the first data-based criteria." In 1984, he proposed the important concept that the fibromyalgia syndrome and other similar conditions are interconnected. In 1986, he showed serotonergic and norepinephric drugs to be effective.[23]
Yunus later emphasized a "biopsychosocial perspective" of fibromyalgia, which is considered the "only way to synthesize the disparate contributions of such variables as genes and adverse childhood experiences, life stress and distress, posttraumatic stress disorder, mood disorders, self-efficacy for pain control, catastrophizing, coping style, and social support into the evolving picture of central nervous system dysfunction vis-a-vis chronic pain and fatigue."[21][22]
Fibromyalgia was recognized by the American Medical Association as an illness and a cause of disability in 1987.[citation needed] In an article the same year, in the Journal of the American Medical Association, a physician named Dr. Don Goldenberg also called the disorder fibromyalgia.[citation needed] The ACR published a criteria for fibromyalgia in 1990, and developed neurohormonal mechanisms with central sensitization in the 1990s.[23]
Symptoms
The defining symptoms of fibromyalgia are chronic, widespread pain and tenderness to light touch. There is also typically moderate to severe fatigue. Those affected may also experience heightened sensitivity of the skin (also called allodynia), tingling of the skin (often needle-like), achiness in the muscle tissues, prolonged muscle spasms, weakness in the limbs, and nerve pain. Chronic sleep disturbances are also characteristic of fibromyalgia. Indeed, studies suggest that sleep disturbance are related to a phenomenon called alpha-delta sleep, a condition in which deep sleep (associated with delta EEG waves) is frequently interrupted by bursts of brain activity similar to wakefulness (i.e. alpha waves). Deeper stages of sleep (stages 3 & 4) are often dramatically reduced.
In addition, many patients experience cognitive dysfunction (known as "brain fog" or "fibrofog"), which may be characterized by impaired concentration and short-term memory consolidation, impaired speed of performance, inability to multi-task, and cognitive overload.[24][25] Many experts suspect that "brain fog" is directly related to the sleep disturbances experienced by sufferers of fibromyalgia.[citation needed]
Other symptoms often attributed to fibromyalgia that may possibly be due to a comorbid disorder include myofascial pain syndrome, diffuse non-dermatomal paresthesias, functional bowel disturbances and irritable bowel syndrome (possibly linked to lower levels of ghrelin[2], 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 facial pain and have high rates of comorbid temporomandibular joint disorder. Not all patients have all symptoms.
Symptoms can have a slow onset, and many patients have mild symptoms beginning in childhood, that are often misdiagnosed as growing pains.[citation needed] Symptoms are often aggravated by unrelated illness or changes in the weather.[citation needed]They can become more tolerable or less tolerable throughout daily or yearly cycles; however, many people with fibromyalgia find that, at least some of the time, the condition prevents them from performing normal activities such as driving a car or walking up stairs. The disorder does not cause inflammation as is characteristic of rheumatoid arthritis, although some NSAIDs may temporarily reduce pain symptoms in some patients. Their use, however, is limited, and often of little to no value in pain management.[26]
[edit] Variability of symptoms
The following factors have been proposed to exacerbate symptoms of pain in patients:
Increased psychosocial stress[citation needed]
Excessive physical exertion (exercise seems to decrease the pain threshold of people with fibromyalgia but increase it in healthy individuals)[27]
Lack of slow-wave sleep
Changes in humidity and barometric pressure[citation needed]
[edit] Proposed causes and pathophysiology
The cause of fibromyalgia is unknown. Fibromyalgia can, but does not always, start as a result of some trauma such as a traffic accident, major surgery, or disease. Some evidence shows that Lyme Disease may be a trigger of fibromyalgia symptoms.[28] Another study suggests that more than one clinical entity may be involved, ranging from a mild, idiopathic inflammatory process to clinical depression[29]
[edit] Genetics
By using self-reported "Chronic Widespread Pain" (CWP) as a surrogate marker for fibromyalgia, the Swedish Twin Registry found that a modest genetic contribution may exist:[30][31]
Monozygotic twins with CWP have a 15% chance that their twin sibling has CWP
Dizygotic twins with CWP have a 7% chance that their twin sibling has CWP
[edit] Stress
Studies have shown that stress is a significant precipitating factor in the development of fibromyalgia,[32] and that PTSD is linked with fibromyalgia.[33][34] The Amital study found that 49% of PTSD patients fulfilled the criteria for FMS, compared with none of the controls.
A non-mainstream hypothesis that fibromyalgia may be a psychosomatic illness has been described by John E. Sarno's "tension myositis syndrome". He believes many cases of chronic pain result from changes in the body caused by the mind's subconscious strategy of distracting painful or dangerous emotions. Education, attitude change, (and in some cases, psychotherapy) are treatments proposed to stop the brain from using that strategy.[35][36][37][38]
[edit] Dopamine abnormality
Dopamine is a catecholamine neurotransmitter perhaps best known for its role in the pathology of schizophrenia, Parkinson's disease and addiction. There is also strong evidence for a role of dopamine in restless leg syndrome [39], which is a common co-morbid condition in patients with fibromyalgia. [40] In addition, dopamine plays a critical role in pain perception and natural analgesia. Accordingly, musculoskeletal pain complaints are common among patients with Parkinson's disease [41], which is characterized by drastic reductions in dopamine owing to neurodegeneration of dopamine-producing neurons, while patients with schizophrenia, which is thought to be due (in part) to hyperactivity of dopamine-producing neurons, have been shown to be relatively insensitive to pain.[42][43] Interestingly, patients with restless legs syndrome have also been demonstrated to have hyperalgesia to static mechanical stimulation.[44]
Fibromyalgia has been commonly referred to as a "stress-related disorder" due to its frequent onset and worsening of symptoms in the context of stressful events.[45][46] It was therefore proposed that fibromyalgia may represent a condition characterized by low levels of central dopamine that likely results from a combination of genetic factors and exposure to environmental stressors, including psychosocial distress, physical trauma, systemic viral infections or inflammatory disorders (e.g. rheumatoid arthritis, systemic lupus erythematosus).[47] This conclusion was based on three key observations: (1) fibromyalgia is associated with stress; (2) chronic exposure to stress results in a disruption of dopamine-related neurotransmission[48]; and (3) dopamine plays a critical role in modulating pain perception and central analgesia in such areas as the basal ganglia[49] including the nucleus accumbens[50], insular cortex[51], anterior cingulate cortex[52], thalamus[53], periaqueductal gray[54], and spinal cord[55] [56].
In support of the 'dopamine hypothesis of fibromyalgia', a reduction in dopamine synthesis has been reported by a study that used positron emission tomography (PET) and demonstrated a reduction in dopamine synthesis among fibromyalgia patients in several brain regions in which dopamine plays a role in inhibiting pain perception, including the mesencephalon, thalamus, insular cortex and anterior cingulate cortex.[57] A subsequent PET study demonstrated that, whereas healthy individuals release dopamine into the caudate nucleus and putamen during a tonic experimental pain stimulus (i.e. hypertonic saline infusion into a muscle bed)[58], fibromyalgia patients fail to release dopamine in response to pain and, in some cases, actually have a reduction in dopamine levels during painful stimulation. [59] Moreover, a substantial subset of fibromyalgia patients respond well 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 legs syndrome.[60] Trials of other dopamine agonists are currently ongoing.
[edit] Serotonin
Serotonin is a neurotransmitter that is known to play a role in regulating sleep patterns, mood, feelings of well-being, concentration and descending inhibition of pain. Accordingly, it has been hypothesized that the pathophysiology underlying the symptoms of fibromyalgia may be a dysregulation of serotonin metabolism, which may explain (in part) many of the symptoms associated with the disorder. This hypothesis is derived in part by the observation of decreased serotonin metabolites in patient plasma [61] and cerebrospinal fluid.[62] 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[63]. Accordingly, duloxetine (Cymbalta), a SNRI originally used to treat depression and painful diabetic neuropathy, has been demonstrated by controlled trials to relieve symptoms of some patients. Eli Lilly and Company, the manufacturer of duloxetine has submitted a supplementary new drug application (sNDA) to the FDA for approval of it use in the treatment of FM. The relevance of dysregulated serotonin metabolism to the pathophysiology is a matter of debate.[64] Ironically, one of the more effective types of medication for the treatment of the disorder (i.e. serotonin 5-HT3 antagonists) actually block some of the effects of serotonin.[65]
[edit] Sleep disturbance
Electroencephalography studies have shown that people with fibromyalgia lack slow-wave sleep and circumstances that interfere with stage four sleep (pain, depression, serotonin deficiency, certain medications or anxiety) may cause or worsen the condition.[66] According to the sleep disturbance hypothesis, an event such as a trauma or illness causes sleep disturbance and possibly initial chronic pain that may initiate the disorder. The hypothesis supposes that stage 4 sleep is critical to the function of the nervous system, as it is during that stage that certain neurochemical processes in the body 'reset'. In particular, pain causes the release of the neuropeptide substance P in the spinal cord which has the effect of amplifying pain and causing nerves near the initiating ones to become more sensitive to pain. Under normal circumstances, areas around a wound to become more sensitive to pain but if pain becomes chronic and body-wide this process can run out of control. The sleep disturbance hypothesis holds that deep sleep is critical to reset the substance P mechanism and prevent this out-of-control effect.
The sleep disturbance/substance P hypothesis could explain "tender points" that are characteristic of fibromyalgia but which are otherwise enigmatic, since their positions don't correspond to any particular set of nerve junctions or other obvious body structures.[citation needed] The hypothesis proposes that these locations are more sensitive because the sensory nerves that serve them are positioned in the spinal cord to be most strongly affected by substance P. This hypothesis could also explain some of more general neurological features of fibromyalgia, since substance P is active in many other areas of the nervous system. The sleep disturbance hypothesis could also provide a possible connection between fibromyalgia, chronic fatigue syndrome (CFS) and post-polio syndrome through damage to the ascending reticular activating system of the reticular formation. This area of the brain, in addition to apparently controlling the sensation of fatigue, is known to control sleep behaviors and is also believed to produce some neuropeptides, and thus injury or imbalance in this area could cause both CFS and sleep-related fibromyalgia.
Critics of the hypothesis argue that it does not explain slow-onset fibromyalgia, fibromyalgia present without tender points, or patients without heightened pain symptoms, and a number of the non-pain symptoms present in the disorder.[citation needed]
[edit] Human growth hormone
An alternate hypothesis suggests that stress-induced problems in the hypothalamus may lead to reduced sleep and reduced production of human growth hormone (HGH) during slow-wave sleep. People with fibromyalgia tend to produce inadequate levels of HGH. Most patients with FM with low IGF-I levels failed to secrete HGH after stimulation with clonidine and l-dopa.[citation needed]
This view is supported by the fact that those hormones under the direct or indirect control of HGH, including IGF-1, cortisol, leptin and neuropeptide Y are abnormal in people with fibromyalgia,[67] In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep[68][69][70][71] though there is disagreement about the proposition.[72]
[edit] Deposition disease
The 'deposition hypothesis of fibromyaglia' posits fibromyalgia is due to intracellular phosphate and calcium accumulations that eventually reaches levels sufficient to impede the ATP process, possibly caused by a kidney defect or missing enzyme that prevents the removal of excess phosphates from the blood stream. Accordingly, proponents of this hypothesis suggest that fibromyalgia may be an inherited disorder, and that phosphate build-up in cells is gradual but can be accelerated by trauma or illness. Calcium is required for the excess phosphate to enter the cells.[citation needed]The additional phosphate slows down the ATP process; however the excess calcium prods the cell to continue producing ATP.[73]
Diagnosis is made with a specialized technique called mapping, a gentle palpitation of the muscles to detect lumps and areas of spasm thought to be caused by an excess of calcium in the cytosol of the cells. The mapping technique is notably different from the manual tenderpoint examination[74] upon which a diagnosis of fibromyalgia depends and is purportedly different from the detection of trigger points that characterize the myofascial pain syndrome.[citation needed]
While this hypothesis does not identify the causative mechanism in the kidneys, it proposes a treatment known as guaifenesin therapy. This treatment involves administering the drug guaifenesin to a patient's individual dosage, avoiding salicylic acid in medications or on the skin. Often products for salicylate sensitivity are very helpful. If the patient is also hypoglycemic, a diet is designed to keep insulin levels low.
The phosphate build-up hypothesis explains many of the symptoms present in fibromyalgia.[citation needed]and proposes an underlying cause. The guaifenesin treatment, based on this hypothesis, has received mixed reviews, with some practitioners claiming many near-universal successes[citation needed] and others reporting no success. Of note, guaifenesin is also a central acting muscle relaxant used in veterinary anaesthesia[75] that is structurally related to methocarbamol, a property that might explain its utility in some fibromyalgia patients. A controlled trial of guaifenesin for the treatment of fibromyalgia demonstrated no evidence for efficacy of this medication. [76] However, this study has been criticized by the chief proponent of the deposition hypothesis for not limiting salicylic acid exposure in patients, and for studying the effectiveness of only guaifenesin, not the entire treatment method.[77] As of 2005, further studies to test the protocol's effectiveness are in the planning stages, with funding for independent studies largely collected from groups which advocate the hypothesis. It should be noted that nothing in the scientific literature supports the proposition that fibromyalgia patients have excessive levels of phosphate in their tissues.
[edit] Other hypotheses
Other hypotheses have been proposed related to various toxins from the patient's environment, viral causes such as the Epstein-Barr Virus, growth hormone deficiencies possibly related to an underlying (maybe autoimmune) disease affecting the hypothalamus gland, an aberrant immune response to intestinal bacteria,[78][79] neurotransmitter disruptions in the central nervous system, and erosion of the protective chemical coating around sensory nerves. A 2001 study suggested an increase in fibromyalgia among women with extracapsular silicone gel leakage, compared to women whose implants were not broken or leaking outside the capsule.[80][81] This association has not repeated in a number of related studies,[82] and the US-FDA concluded "the weight of the epidemiological evidence published in the literature does not support an association between fibromyalgia and breast implants."[83] Due to the multi-systemic nature of illnesses such as fibromyalgia and chronic fatigue syndrome (CFS/ME), an emerging branch of medical science called psychoneuroimmunology (PNI) is looking into how the various hypotheses fit together.
Another hypothesis on the cause of symptoms in fibromyalgia states that patients suffer from vasomotor dysregulation causing improper vascularflow and hypoperfusion (decreased blood flow to a given tissue or organ).[84]
[edit] Always a comorbid disease?
Cutting across several of the above hypotheses is the proposition that fibromyalgia is almost always a comorbid disorder, occurring in combination with some other disorder that likely served to "trigger" the fibromyalgia in the first place. Two possible triggers are gluten sensitivity and/or irritable bowel. Irritable bowel is found at high frequency in fibromyalgia,[85] and a large coeliac support group survey of adult celiacs revealed that 7% had fibromyalgia and also has a co-occurrence with chronic fatique.[86]
According to this hypothesis, some other disorder (or trauma) occurs first, and fibromyalgia follows as a result. In some cases, the original disorder abates on its own or is separately treated and cured, but the fibromyalgia remains. This is especially apparent when fibromyalgia seems triggered by major surgery. In other cases the two disorders coexist.
[edit] Diagnosis
There is still debate over what should be considered essential diagnostic criteria. The most widely accepted set of classification criteria for research purposes were elaborated in 1990 by the Multicenter Criteria Committee of the 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 or trigger points (although a person with the disorder may feel pain in other areas as well). During diagnosis, four kilograms-force (39 newtons) of force is exerted at each of the 18 points; the patient must feel pain at 11 or more of these points for fibromyalgia to be considered.[87] Four kilograms of force is about the amount of pressure required to blanch the thumbnail when applying pressure. This set of criteria was developed by the American College of Rheumatology as a means of classifying an individual as having fibromyalgia for both clinical and research purposes. While these criteria for classification of patients were originally established as inclusion criteria for research purposes and were not intended for clinical diagnosis, they have 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.
[edit] Differentials
A number of other disorders can produce similar symptoms to fibromyalgia:
Chronic fatigue syndrome
Depression
Ehlers-Danlos syndrome
Gulf War syndrome
Influenza
Lead poisoning
Lupus erythematosus
Lyme disease
Mercury poisoning
Myofascial pain syndrome
Tendinitis
Thyroid disease
Vitamin B12 deficiency
Vitamin D deficiency
Whiplash-associated disorder
Multiple chemical sensitivity
[edit] Treatment
As with many other syndromes, there is no universally accepted cure for fibromyalgia, though some physicians claim to have found cures.[88] However, a steady interest in the disorder on the part of academic researchers as well as pharmaceutical interests has led to improvements in its treatment, which ranges from symptomatic prescription medication to alternative and complementary medicine.
[edit] Medications
Many medications are used to treat specific symptoms of fibromyalgia, such as muscle pain and insomnia.
[edit] Pain Relief
A number of pain relievers have been prescribed for fibromyalgia. This includes NSAID medications over the counter, COX-2 inhibitors, and tramadol in prescription form for more advanced cases. Recently, pregabalin (marketed as Lyrica) has been given FDA approval for the treatment of diagnosed Fibromyalgia.[16]
[edit] Muscle Relaxants
Muscle relaxants, such as cyclobenzaprine (Flexeril) or tizanidine (Zanaflex), may be used to treat the muscle pain associated with the disorder.[89][90][91]
[edit] Tricyclic antidepressants (TCAs)
Traditionally, low doses of sedating antidepressants (e.g. amitriptyline and trazodone) have been used to reduce the sleep disturbances that are associated with fibromyalgia and are believed by some practitioners to alleviate the symptoms of the disorder. Because depression often accompanies chronic illness, these antidepressants may provide additional benefits to patients suffering from depression. Amitriptyline is often favoured as it can also have the effect of providing relief from neuralgenic or neuropathic pain.[citation needed] It is to be noted that Fibromyalgia is not considered a depressive disorder; antidepressants are used for their sedating effect to aid in sleep.
[edit] Selective serotonin reuptake inhibitors (SSRIs)
Research data consistently contradict the utility of agents with specificity as serotonin reuptake inhibitors for the treatment of core symptoms of fibromyalgia. [92][93][94] Moreover, SSRIs are known to aggravate many of the comorbidities that commonly affect patients with fibromyalgia including restless legs syndrome and sleep bruxism[95][96][97].
[edit] Anti-seizure drugs
Anti-seizure drugs are also sometimes used, such as gabapentin[98] and pregabalin (Lyrica). Pregabalin, originally used for the nerve pain suffered by diabetics, has been approved by the American Food and Drug Administration for treatment of fibromyalgia. A randomized controlled trial of pregabalin 450 mg/day found that a number needed to treat of 6 patients for one patient to have 50% reduction in pain.[99]
[edit] Dopamine agonists
Dopamine agonists (e.g. pramipexole (Mirapex) and ropinirole(ReQuip)) have been studied for use in the treatment of fibromyalgia with good results. [100] A trial of transdermal rotigotine is currently on going [101].
[edit] Combination therapy
A controlled clinical trial of amitriptyline and fluoxetine demonstrated utility when used in combination.[102]
[edit] Cannabis and cannabinoids
Fibromyalgia patients frequently self-report using cannabis therapeutically to treat symptoms of the disorder.[103] Writing in the July 2006 issue of the journal Current Medical Research and Opinion, investigators at Germany's University of Heidelberg evaluated the analgesic effects of oral THC (∆9-tetrahydrocannabinol) in nine patients with fibromyalgia over a 3-month period. Subjects in the trial were administered daily doses of 2.5 to 15 mg of THC, but received no other pain medication during the trial. Among those participants who completed the trial, all reported a significant reduction in daily recorded pain and electronically induced pain.[104] Previous clinical and preclinical trials have shown that both naturally occurring and endogenous cannabinoids hold analgesic qualities,[105] particularly in the treatment of cancer pain and neuropathic pain,[106][107] both of which are poorly treated by conventional opioids. As a result, some experts have suggested that cannabinoid agonists would be applicable for the treatment of chronic pain conditions unresponsive to opioid analgesics such as fibromyalgia, and they propose that the disorder may be associated with an underlying clinical deficiency of the endocannabinoid system.[108][109]
[edit] Topical Remedies
Users of Epsom Salts in the gel form (Magnesium Sulfate), have reported significant and lasting relief from pain associated with fibromyalgia. Epsom Salts have long been touted for its ability to reduce pain and swelling. [110]
[edit] Non-drug treatment
[edit] Physical treatments
Studies have found exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia.[111] Many patients find temporary relief by applying heat to painful areas. Those with access to physical therapy, massage, or acupuncture may find them beneficial.[112] Most patients find exercise, even low intensity exercise to be extremely helpful.[113] Osteopathic manipulative therapy can also temporarily relieve pain due to fibromyalgia.[114]
A holistic approach—including managing diet, sleep, stress, activity, and pain—is used by many patients. Dietary supplements, massage, chiropractic care, managing blood sugar levels, and avoiding known triggers when possible means living as well as it is in the patient's power to do.[citation needed]
[edit] Psychological/Behavioral Therapies
As the nature of fibromyalgia is not well understood, some physicians believe that it may be psychosomatic or psychogenic.[115] Although there is no universally accepted cure, some doctors have claimed to have successfully treated fibromyalgia when a psychological cause is accepted.[116]
Cognitive behavioral therapy has been shown to improve quality of life and coping in fibromyalgia patients and other sufferers of chronic pain.[8] Neurofeedback has also shown to provide temporary and long-term relief.
Treatment for the "brain fog" has not yet been developed, however biofeedback and self-management techniques such as pacing and stress management may be helpful for some patients. The use of medication to improve sleep helps some patients, as does supplementation with folic acid and ginkgo biloba.[citation needed]
[edit] Dietary treatment
In a 2001 review of four case studies, symptom alleviation was found by minimizing consumption of monosodium glutamate.[117]
[edit] Investigational treatments
Milnacipran, a serotonin-norepinephrine reuptake inhibitor (SNRI), is available in parts of Europe where it has been safely prescribed for other disorders. On May 22nd, 2007, a Phase III study demonstrated statistically significant therapeutic effects of Milnacipran as a treatment of fibromyalgia syndrome. At this time, only initial top-line results are available and further analyses will be completed in the coming weeks. If ultimately approved by the FDA, Milnacipran could be distributed in the United States as early as summer, 2008.[118]
Among the more controversial therapies involves the use of guaifenesin; called St. Amand's protocol or the guaifenesin protocol[73] the efficacy of guaifenesin in treating fibromyalgia has not been proven in properly designed research studies. Indeed, a controlled study conducted by researchers at Oregon Health Science University in Portland failed to demonstrate any benefits from this treatment,[76] and the lead researcher has suggested that the annecdotaly reported benefits where due to placebo suggestion.[119] The results of the study have since been contested by Dr St. Amand, who was a co-author or the original research report.[120]
Dextromethorphan is an over-the-counter cough medicine with activity as an NMDA receptor antagonist. It has been used in the research setting to investigate the nature of fibromyalgia pain[121][122]; however, there are no controlled trials of safety or efficacy in clinical use.
[edit] Living with fibromyalgia
Fibromyalgia can affect every aspect of a person's life. While neither degenerative nor fatal, the chronic pain associated with fibromyalgia is pervasive and persistent. FMS can severely curtail social activity and recreation, and as many as 30% of those diagnosed with fibromyalgia are unable to maintain full-time employment.[citation needed] Like others with disabilities, individuals with FMS often need accommodations to fully participate in their education or remain active in their careers.
In the United States, those who are unable to maintain a full-time job due to the condition may apply for Social Security Disability benefits. Although fibromyalgia has been recognized as a genuine, severe medical condition by the government, applicants are often denied benefits, since there are no formal diagnostic criteria or medically provable symptoms. Because of this, if an applicant does have a medically verifiable condition that would justify disability benefits in addition to fibromyalgia, it is recommended that they not list fibromyalgia in their claim. However, most are awarded benefits at the judicial level; the entire process often takes two to four years.[citation needed]
In the United Kingdom, the Department for Work and Pensions recognizes fibromyalgia as a condition for the purpose of claiming benefits and assistance.[123]
Fibromyalgia is often referred to as an "invisible" illness or disability due to the fact that generally there are no outward indications of the illness or its resulting disabilities. The invisible nature of the illness, as well as its relative rarity and the lack of understanding about its pathology, often has psychosocial complications for those that have the disorder. Individuals suffering from invisible illnesses in general often face disbelief or accusations of malingering or laziness from others that are unfamiliar with the disorder.
There are a variety of support groups on the Web that cater to fibromyalgia sufferers.
[edit] References
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^ The Fibromyalgia Association of the UK
[edit] Further reading
Fibromyalgia for Pharmacists, a medication guide
[edit] See also
Somatosensory Amplification
[edit] External links
American College of Rheumatology Fibromyalgia factsheet
US Food and Drug Administration Living with Fibromyalgia, First Drug ApprovedJune 21, 2007
Fibromyalgia at the Open Directory Project
National Institute of Arthritis and Musculoskeletal and Skin Diseases. Questions and Answers About Fibromyalgia. Retrieved on 2008-03-18.
The National Fibromyalgia Association U.S (2007). Retrieved on 2007-06-01.
Fibromyalgia Resource Information (2005). Retrieved on 2007-06-01.
[hide]
v • d • eDiseases of the musculoskeletal system and connective tissue (M, 710-739)
Arthropathies
Arthritis (Septic arthritis, Reactive arthritis, Rheumatoid arthritis, Psoriatic arthritis, Felty's syndrome, Juvenile idiopathic arthritis, Still's disease) - crystal (Gout, Chondrocalcinosis) - Osteoarthritis (Heberden's node, Bouchard's nodes)
acquired deformities of fingers and toes (Boutonniere deformity, Bunion, Hallux rigidus, Hallux varus, Hammer toe) - other acquired deformities of limbs (Valgus deformity, Varus deformity, Wrist drop, Foot drop, Flat feet, Club foot, Unequal leg length, Winged scapula)
patella (Luxating patella, Chondromalacia patellae)Protrusio acetabuli - Hemarthrosis - Arthralgia - Osteophyte
Systemic connectivetissue disorders
Polyarteritis nodosa - Churg-Strauss syndrome - Kawasaki disease - Hypersensitivity vasculitis - Goodpasture's syndrome - Wegener's granulomatosis - Arteritis (Takayasu's arteritis, Temporal arteritis) - Microscopic polyangiitis - Systemic lupus erythematosus (Drug-induced) - Dermatomyositis (Juvenile dermatomyositis) - Polymyositis - Scleroderma - Sjögren's syndrome - Behçet's disease - Polymyalgia rheumatica - Eosinophilic fasciitis - Hypermobility
Dorsopathies
Kyphosis - Lordosis - Scoliosis - Scheuermann's disease - Spondylolysis - Torticollis - Spondylolisthesis - Spondylopathies (Ankylosing spondylitis, Spondylosis, Spinal stenosis) - Schmorl's nodes - Degenerative disc disease - Coccydynia - Back pain (Radiculopathy, Neck pain, Sciatica, Low back pain)
Soft tissue disorders
muscle: Myositis - Myositis ossificans (Fibrodysplasia ossificans progressiva)
synovium and tendon: Synovitis/Tenosynovitis (Calcific tendinitis, Stenosing tenosynovitis, Trigger finger, DeQuervain's syndrome) - Irritable hip - Ganglion cyst
bursa: bursitis (Olecranon, Prepatellar, Trochanteric) - Baker's cyst
fibroblastic disorders (Dupuytren's contracture, Plantar fasciitis, Nodular fasciitis, Necrotizing fasciitis, Fasciitis, Fibromatosis)
shoulder lesions: Adhesive capsulitis - Rotator cuff tear - Subacromial bursitis
enthesis: enthesopathies (Iliotibial band syndrome, Achilles tendinitis, Patellar tendinitis, Golfer's elbow, Tennis elbow, Metatarsalgia, Bone spur, Tendinitis)other, NEC: Muscle weakness - Rheumatism - Myalgia - Neuralgia - Neuritis - Panniculitis - Fibromyalgia
Osteopathies
disorders of bone density and structure: Osteoporosis - Osteomalacia - continuity of bone (Pseudarthrosis, Stress fracture) - Monostotic fibrous dysplasia - Skeletal fluorosis - Aneurysmal bone cyst - Hyperostosis - OsteosclerosisOsteomyelitis - Avascular necrosis - Paget's disease of bone - Algoneurodystrophy - Osteolysis - Infantile cortical hyperostosis
Chondropathies
Juvenile osteochondrosis (Legg-Calvé-Perthes syndrome, Osgood-Schlatter disease, Köhler disease, Sever's disease) - Osteochondritis - Tietze's syndrome
See also congenital conditions (Q65-Q79, 754-756)
Retrieved from "http://en.wikipedia.org/wiki/Fibromyalgia"
Categories: Rheumatology Diseases involving the fasciae Syndromes Ailments of unknown etiology
For information on another disease, click on Digestive Diseases Library.
