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14-September-2008 18:02:36 - Fibromyalgia Fibromyalgia 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 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.2 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.3 Contents 1 Signs and symptoms 1.1 Variability of symptoms 2 Causes 2.1 Genetic predisposition 2.2 Stress 2.3 Sleep disturbance 2.4 Dopamine abnormality 2.5 Serotonin 2.6 Human growth hormone 2.7 Comorbidity 2.8 Deposition disease 2.9 Other hypotheses 3 Pathophysiology 4 Diagnosis 5 Treatment 5.1 Pharmaceutical 5.1.1 Hormones 5.1.2 Analgesics 5.1.3 Muscle relaxants 5.1.4 Tricyclic antidepressants 5.1.5 Selective serotonin reuptake inhibitors 5.1.6 Anti-seizure medication 5.1.7 Dopamine agonists 5.1.8 Combination therapy 5.1.9 Central nervous system stimulants 5.1.10 Cannabis and cannabinoids 5.2 Non-drug treatment 5.2.1 Physical treatments 5.2.2 Psychological/behavioral therapies 5.2.3 Dietary treatment 5.3 Investigational treatments 6 Prognosis 7 Epidemiology 8 History 9 Controversies 10 Timeline 11 References 12 External links Signs and symptoms The defining symptoms of fibromyalgia are chronic, widespread pain and tenderness to light touch. Other symptoms can include moderate to severe fatigue, a heightened and painful response to gentle touch allodynia, needle-like tingling of the skin, muscle aches, prolonged muscle spasms, weakness in the limbs, nerve pain, functional bowel disturbances,4 and chronic sleep disturbances.5 Sleep disturbances may be related to a phenomenon called alpha-delta sleep, a condition in which deep sleep associated with delta waves is frequently interrupted by bursts of alpha waves, which normally occur during wakefulness. Slow-wave sleep is often dramatically reduced.citation needed Many patients experience cognitive dysfunction6 known as brain fog or fibrofog, which may be characterized by impaired concentration,7 problems with short87 and long-term memory, short-term memory consolidation,8 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. Eye problems such as eye pain, sensitivity to light, blurred vision, and fluctuating visual clarity, can also be a symptom of the condition. 9As a consequence of this sufferers may have to change their lens prescription more often. 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 neededThey 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 non-steroidal anti-inflammatory drugs may temporarily reduce pain symptoms in some patients. Their use, however, is limited, and often of little to no value in pain management.10 Not all patients have all symptoms. Variability of symptoms The following factors have been proposed to exacerbate symptoms of pain in patients: Increased psychosocial stress11 Excessive physical exertion exercise seems to decrease the pain threshold of people with fibromyalgia but increase it in healthy individuals12 Lack of slow-wave sleep Changes in humidity and barometric pressurecitation needed Lack of normal energy Causes The cause of fibromyalgia is unknown. However, several hypotheses have been developed, which are discussed below. Genetic predisposition There is evidence that genetic factors may play a role in the development of fibromyalgia. For example, there is a high aggregation of FM in families.1314 The mode of inheritance is currently unknown , but it is most probably polygenic.15 Research has demonstrated that FM is associated with polymorphisms of genes in the serotoninergic,16 dopaminergic17 and catecholaminergic systems.18 However, these polymorphisms are not specific for FM and are associated with a variety of allied disorders e.g. chronic fatigue syndrome,19 irritable bowel syndrome20 and with depression.21 Stress Studies have shown that stress is a significant precipitating factor in the development of fibromyalgia,22 and that PTSD is linked with fibromyalgia.2324 The Amital study found that 49% of PTSD patients fulfilled the criteria for FMS, compared with none of the controls. Stress can alter the function of the HPA axis and change cortisol levels in the body, leading to widespread pain.25 An alternate hypothesis regarding the development of fibromyalgia in relationship to stress proposes that the disorder may be a psychosomatic illness has been described by John E. Sarno's tension myositis syndrome, which hypothesizes that chronic pain is caused by the mind's subconscious strategy of distracting painful or dangerous emotions. Education, attitude change, and in some cases, psychotherapy are proposed as treatments.26 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.27 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 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,28 which is a common co-morbid condition in patients with fibromyalgia.29 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,30 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.3132 Patients with restless legs syndrome have also been demonstrated to have hyperalgesia to static mechanical stimulation.33 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.3435 It was 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.36 This conclusion was based on three key observations; fibromyalgia is associated with stress, chronic exposure to stress results in a disruption of dopamine-related neurotransmission37 and dopamine plays a critical role in modulating pain perception and central analgesia in such areas as the basal ganglia38 including the nucleus accumbens,39 insular cortex,40 anterior cingulate cortex,41 thalamus,42 periaqueductal gray43 and spinal cord.4445 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.46 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,47 fibromyalgia patients fail to release dopamine in response to pain and, in some cases, actually have a reduction in dopamine levels during painful stimulation.48 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.49 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 plasma50 and cerebrospinal fluid.51 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 successful52. 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.53 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.54 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,55 In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep56575859 though there is disagreement about the proposition.60 Comorbidity 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 or trauma that likely served to trigger the fibromyalgia in the first place. 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.citation needed A large percentage of chronic fatigue syndrome patients are reported to develop fibromyalgia between onset and the second year of illness.61 Other possible triggers are gluten sensitivity and/or irritable bowel. Irritable bowel is found at high frequency in fibromyalgia,62 and a large support group survey of adult celiacs revealed that 9% had fibromyalgia.63 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. 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 examination64 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. Of note, guaifenesin is also a central acting muscle relaxant used in veterinary anaesthesia65 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.66 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.67 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,6869 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.7071 This association has not repeated in a number of related studies,72 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.73 Still another hypothesis on the cause of symptoms in fibromyalgia states that patients suffer from vasomotor dysregulation causing sluggish or improper vascular flow.74 Pathophysiology Sleep disturbances The first objective findings associated with the disorder were reported in 1975 by Moldofsky and colleagues who reported the presence of anomalous alpha wave activity typically associated with arousal states on sleep electroencephalogram EEG during non-rapid-eye-movement sleep.75 In fact, by disrupting stage IV sleep consistently in young, healthy subjects Moldofsky was able to reproduce a significant increase in muscle tenderness similar to that experienced by fibromyalgia but which resolved when the subjects were able to resume their normal sleep patterns.76 Since that time a variety of other EEG sleep abnormalities have also been reported in subgroups of fibromyalgia patients.77 Poly-modal sensitivity Results from studies examining responses to experimental stimulation have shown that fibromyalgia patients display sensitivity to pressure, heat, cold, electrical and chemical stimulation.78 Experiments examining pain regulatory systems have shown that fibromyalgia patients also display a dysregulation of diffuse noxious inhibitory control,79 an exaggerated wind-up in response to repetitive stimulation,80 and an absence of exercise-induced analgesic response.81 Together these results point to dysregulation of the nociceptive system at the central level. Neuroendocrine disruption Patients with fibromyalgia have been demonstrated to have a disruption of normal neuroendocrine function, characterized by mild hypocortisolemia,82 hyperreactivity of pituitary adrenocorticotropin hormone release in response to challenge, and glucocorticoid feedback resistance.83 A progressive reduction of serum growth hormone levels has also been documented-at baseline in a minority of patients, while most demonstrate reduced secretion in response to exercise or pharmacological challenge.84 Other abnormalities include reduced responsivity of thyrotropin and thyroid hormones to thyroid-releasing hormone,85 a mild elevation of prolactin levels with disinhibition of prolactin release in response to challenge86 and hyposecretion of adrenal androgens.87 These changes might be attributed to the effects of chronic stress, which, after being perceived and processed by the central nervous system, activates hypothalamic corticotrophin-releasing hormone neurons. Thus, the multiple neuroendocrine changes evident in fibromyalgia have been proposed to stem from chronic overactivity of corticotropin-releasing hormone releasing neurons, resulting in a disruption of normal function of the pituitary-adrenal axis and an increased stimulation of hypothalamic somatostatin secretion, which, in turn, inhibits the secretion of a multiplicity of other hormones.88 Sympathetic Hyperactivity Functional analysis of the autonomic system in patients with fibromyalgia has demonstrated disturbed activity characterized by hyperactivity of the sympathetic nervous system at baseline89 with reduced sympathoadrenal reactivity in response to a variety of stressors including physical exertion and mental stress.9091 Fibromyalgia patients demonstrate lower heart rate variability, an index of sympathetic/parasympathetic balance, indicating sustained sympathetic hyperactivity, especially at night.92 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,93 while circulating levels of epinephrine and norepinephrine have been variously reported as low, normal and high.9495 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.96 Cerebrospinal fluid abnormalities The most reproduced laboratory finding in patients with fibromyalgia is an elevation in cerebrospinal fluid levels of substance P, a putative nociceptive neurotransmitter.979899 Metabolites for the monoamine neurotransmitters serotonin, norepinephrine, and dopamine-all of which play a role in natural analgesia-have been shown to be lower,100 while concentrations of endogenous opioids i.e., endorphins and enkephalins appear to be higher.101 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.102 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.103 Brain imaging studies 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.104105 Differential activation in response to painful stimulation has also been demonstrated.106 Brain centers showing hyperactivation in response to noxious stimulation include such pain-related brain centers as the primary and secondary somatosensory cortex, anterior cingulate cortex and insular cortex, while relative hypoactivation at subjectively equal pain levels appears to occur within the thalamus and basal ganglia. In addition, patients 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.107 Patients with fibromyalgia have evidence of hippocampal disruption indicated by reduced brain metabolite ratios.108 An acceleration of normal age-related brain atrophy has likewise been demonstrated using voxel-based morphometry VBM with areas of reduced gray matter located in the cingulate cortex, insula and parahippocampal gyrus.109 Studies utilizing positron emission tomography have demonstrated reduced dopamine synthesis in the brainstem and elements of the limbic cortex,110 disruption of dopaminergic reactivity to tonic pain stimulus111 and a reduced availability of mu-opioid receptors in the ventral striatum/nucleus accumbens and cingulate cortex.112 Diagnosis There is still debate over what should be considered essential diagnostic criteria. The difficulty with diagnosing fibromyalgia is that, in most cases, laboratory testing appears normal and that many of the symptoms 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 you based on your symptoms, gender, age geographic location, medical history and other factors. They then narrow down the diagnosis down to the most likely one. 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.113 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. Treatment As with many other syndromes, there is no universally accepted cure for fibromyalgia, though some physicians claim to have found cures.114 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. The European League Against Rheumatism EULAR issued the first guidelines115 for the treatment of fibromyalgia syndrome FMS and published them in the September 17 On-line First issue of the Annals of the Rheumatic Diseases. Pharmaceutical Hormones A recent review and study published in February 2008 by Kent Holtorf, reviewed all previous hydrocortisone trials regarding safety and effectiveness, and concluded that because treatment with low physiological doses of cortisol less than 15mg has been shown to be safe and effective and routine dynamic ACTH testing does not have adequate diagnostic sensitivity, it is reasonable to give a therapeutic trial of physiologic doses of cortisol to the majority of patients with CFS and FM, especially to those who have symptoms that are consistent with adrenal dysfunction, have low blood pressure or have baseline cortisol levels in the low or low-normal range. 116 Analgesics A number of analgesics are used to treat the pain symptoms resulting from 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.117 Muscle relaxants Muscle relaxants, such as cyclobenzaprine Flexeril or tizanidine Zanaflex, may be used to treat the muscle pain associated with the disorder.118119120 Tricyclic antidepressants 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. Selective serotonin reuptake inhibitors Research data consistently contradict the utility of agents with specificity as serotonin reuptake inhibitors for the treatment of core symptoms of fibromyalgia.121122123 Moreover, SSRIs are known to aggravate many of the comorbidities that commonly affect patients with fibromyalgia including restless legs syndrome and sleep bruxism.124125126 Anti-seizure medication Anti-seizure drugs are also sometimes used, such as gabapentin127 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.128 Dopamine agonists Dopamine agonists e.g. pramipexole Mirapex and ropiniroleReQuip have been studied for use in the treatment of fibromyalgia with good results.49 A trial of transdermal rotigotine is currently on going129. Combination therapy A controlled clinical trial of amitriptyline and fluoxetine demonstrated utility when used in combination.130 Central nervous system stimulants Cognitive dysfunction in fibromyalgia, often referred to as brain fog, may be treated with low doses of central nervous system CNS stimulants such as modafinil, adderall or methylphenidate. These stimulants are also used to treat the chronic fatigue that is characteristic of fibromyalgia.131132 Stimulants may be habit forming and can have other serious side effects, so it is important to note that other treatments may be effective.133 Care should be taken with any prescription, as people with fibromyalgia are known to be sensitive to medications.134 Cannabis and cannabinoids Fibromyalgia patients frequently self-report using cannabis therapeutically to treat symptoms of the disorder.135 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.136 Previous clinical and preclinical trials have shown that both naturally occurring and endogenous cannabinoids hold analgesic qualities,137 particularly in the treatment of cancer pain and neuropathic pain,138139 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.140141 Non-drug treatment NEW RESEARCH undertaken at the Human Performance Laboratory at Karlstad University by Swedish PHD, Sven-Åke Bood 142concludes that regular floatation tank sessions can drastically relieve chronic stress related ailments. Studies involving 140 people with long-term conditions such as anxiety, stress, depression and fibromyalgia found that more than three quarters experienced noticeable improvements. Mr Bood commented: Through relaxing in floating tanks, people with long-term fibromyalgia, for instance, or depression and anxiety felt substantially better after only 12 treatments. Research targeted the effectiveness of floatation treatment with regard to stress related pain and anxiety over the period of seven weeks. 22 percent of the participants became entirely free of pain and 56 percent experienced clear improvement. The research also confirms the findings of an earlier thesis that floatation, after only twelve sessions, substantially improves sleep patterns leaving users more optimistic and with reduced nervousness, tension and pain. Relaxing in a weightless state in the silent warmth of a floatation tank activates the body's own system for recuperation and healing, said Sven-Ake Bood. What researchers find particularly gratifying is that the positive effects were still in evidence 4 months after the floating treatment ended. While many health professionals still associate Fibromyalgia as a stress related condition, there is no such clear connection. The above study seems to suggest it is a stress-connected condition, and it is not. It is a physical pain disorder. Physical treatments Studies have found exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia.143 Many patients find temporary relief by applying heat to painful areas. Those with access to physical therapy, massage, or acupuncture may find them beneficial.144 Most patients find exercise, even low intensity exercise to be extremely helpful.145 Osteopathic manipulative therapy can also temporarily relieve pain due to fibromyalgia.146 Whirlpool therapy is very beneficial. It's important that the water temperature be at least 95 degrees. This therapy was recommended by the Fibromyalgia Clinic at Mayo. Psychological/behavioral therapies Cognitive behavioral therapy has been shown to improve quality of life and coping in fibromyalgia patients and other sufferers of chronic pain.147 Neurofeedback has also shown to provide temporary and long-term relief.citation needed Biofeedback and self-management techniques such as pacing and stress management may also be helpful for some patients.citation needed Because the nature of fibromyalgia is not well understood, some physicians believe that it may be psychosomatic or psychogenic.148 Accordingly, some doctors have claimed to have successfully treated fibromyalgia when a psychological cause is accepted.149 Dietary treatment In a 2001 review of four case studies, symptoms were alleviated by minimizing consumption of monosodium glutamate.150 There are few other studies linking diet and the disease. 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, 2008.151 Among the more controversial therapies involves the use of guaifenesin; called St. Amand's protocol or the guaifenesin protocol152 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,66 and the lead researcher has suggested that the anecdotally reported benefits where due to placebo suggestion.153 The results of the study have since been contested by Dr St. Amand, who was a co-author or the original research report.67 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;154155 however, there are no controlled trials of safety or efficacy in clinical use. Prognosis 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.citation needed 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 governmentcitation needed, applicants are often denied benefits, since there are no formal diagnostic criteria or medically provable symptoms. In the United Kingdom, the Department for Work and Pensions recognizes fibromyalgia as a condition for the purpose of claiming benefits and assistance.156 Epidemiology Fibromyalgia is seen in about 2% of the general population147 and affects more females than males, with a ratio of 9:1 by ACR criteria.157 It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood. History Fibromyalgia has been studied since the early 1800s and referred to by a variety of former names, including muscular rheumatism and fibrositis.158 The term fibromyalgia was coined in 1976 to more accurately describe the symptoms, from the Latin fibra fiber159 and the Greek words myo muscle160 and algos pain.161 Dr. Muhammad B. Yunus, considered the father of the modern view of fibromyalgia, published the first clinical, controlled study of the characteristics of fibromyalgia syndrome in 1981.162163 Yunus' work validated the known symptoms and tender points that characterise the condition, and proposed data-based criteria for diagnosis. In 1984, Yunus proposed the interconnection between fibromyalgia syndrome and other similar conditions, and in 1986 demonstrated the effectiveness of serotonergic and norepinephric drugs.164 Yunus later emphasized the biopsychosocial perspective of fibromyalgia, which synthesized the contributions of genes, personal and medical history, stress, posttraumatic and mood disorders, coping skills, self-efficacy of pain management and social support towards the functioning and dysfunctioning of the central nervous system in relation to pain and fatigue.162163 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 American College of Rheumatology ACR published a criteria for fibromyalgia in 1990, and developed neurohormonal mechanisms with central sensitization in the 1990s.164 Controversies 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 may result from several different disease processes that have global hyperalgesia and allodynia in common,165166167 an observation that has led to the proposition that current diagnostic criteria are insufficient to differentiate patient groups from each other.168 Alternatively, there is evidence for the existence of differing pathophysiological processes within the greater fibromyalgia construct169170, 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 essence, fibromyalgia may actually be composed of several clinical entities, ranging from a mild, idiopathic inflammatory process in some individuals, to a somatoform disorder resulting from clinical depression in others, with probable overlaps in between.165 Current diagnostic criteria are insufficient to differentiate these entities. Timeline This section may contain original research or unverified claims. Please help by adding references. June 2008 Please wikify this article or section. Help improve this article by adding relevant internal links. August 2008 1800s The study of muscular rheumatism begins. 1976 The term fibromyalgia was coined to more accurately describe the symptoms, from the Latin fibra fiber, the Greek words myo muscleand algos pain. 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. 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. 1984 Dr. Muhammad B. Yunus proposed the important concept that the fibromyalgia syndrome and other similar conditions are interconnected. 1986 Dr. Muhammad B. Yunus showed serotonergic and norepinephric drugs to be effective. 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. 1987 Fibromyalgia was recognized by the American Medical Association as an illness and a cause of disability. 1987 In an article of the Journal of the American Medical Association, a physician named Dr. Don Goldenberg also called the disorder 'fibromyalgia'. 1990 The ACR American College of Rheumatology published a criteria for fibromyalgia and developed neurohormonal mechanisms with central sensitization. 1997 National Fibromyalgia Association NFA is founded in Orange, California, by Lynne Matallana and Karen Lee Richards. It is the largest nonprofit organization working to support people with fibromyalgia and other chronic pain illnesses. 1999 The Annual Fibromyalgia Awareness Day Proclamation Program is established. 2000 May - 2006 March The National Fibromyalgia Association hosted six international conferences, each providing a venue for leading fibromyalgia authorities to share their research and expertise with patients and health care professionals alike. 2001 In a review of four case studies, symptom alleviation was found by minimizing consumption of monosodium glutamate. 2002 The National Fibromyalgia Association publishes the first and only consumer magazine, Fibromyalgia AWARE providing information on research, lifestyle and health for people affected by fibromyalgia. AWARE is now available at Barnes Noble Bookstores. 2005 Pfizer began selling Lyrica in the United States. 2006 July In the issue of 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. 2007 June 21 The F.D.A. approves Pfizer's request to market the drug Lyrica as a fibromyalgia treatment. 2007 July Facing Fibromyalgia, Finding Hope, a national educational campaign aimed at increasing the understanding of fibromyalgia among patients, healthcare providers and the public, was launched. The public service announcement, distributed through print, radio and television outlets, reached more than 37 million people in the United States. 2008 Monday, May 10th To garner support for ACR 112, more than 100 fibromyalgia patients and their supporters from across California turned out at the state capitol of Sacramento to participate in the first Fibromyalgia Legislation Day coordinated by the National Fibromyalgia Association. 2008 Monday, May 19th Resolution ACR 112 continues on its successful path, passing the California Assembly. It will now go before the California Senate for a vote. The resolution, written by Assembly member Mervyn Dymally, calls on members of the State Assembly, State Senate and the National Fibromyalgia Association to appoint a 14-member task force. 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Fibromyalgia and related central sensitivity syndromes: twenty-five years of progress. Semin. Arthritis Rheum. 36 6: 335-8. doi:10.1016/j.semarthrit.2006.12.001. PMID 17303220. Retrieved on 2008-05-21. ^ a b Further Legitimization Of Fibromyalgia As A True Medical Condition, Science Daily 2007-06-25. Retrieved on 2008-05-21. ^ a b Inanici F, Yunus MB October 2004. History of fibromyalgia: past to present. Curr Pain Headache Rep 8 5: 369-78. PMID 15361321. Retrieved on 2008-05-21. ^ a b http://www.springerlink.com/content/1271314042w8405g/ Mueller W, et al. The classification of fibromyalgia syndrome. Rheumatol Int. July 25, 2007 ^ The association or otherwise of the functional somatic syndromes.Psychosom Med. 2007 Dec;699:855-9. Review. PMID: 180400 ^ Comorbidity of fibromyalgia and psychiatric disorders.Curr Pain Headache Rep. 2007 Oct;115:333-8. Review. PMID: 17894922 ^ An integrated model of group psychotherapy for patients with fibromyalgia.Int J Group Psychother. 2007 Oct;574:451-74 ^ Psychophysiological responses in patients with fib...J Psychosom Res. 2006 - PubMed Result ^ Heterogeneity of psychophysiological stress responses in fibromyalgia syndrome patients External links Fibromyalgia Topics A-Z from the National Fibromyalgia Association American College of Rheumatology Fibromyalgia factsheet Living with Fibromyalgia: Two Drugs Approved at US Food and Drug Administration Questions and Answers About Fibromyalgia by the National Institute of Arthritis and Musculoskeletal and Skin Diseases Fibromyalgia at the Open Directory Project v d e Soft tissue disorders M60-M79, 725-729 Muscle Myositis Pyomyositis - Myositis ossificans Fibrodysplasia ossificans progressiva - Muscle weakness - Myalgia - Myopathy Fascia/fibroblastic Fasciitis Plantar fasciitis, Nodular fasciitis, Necrotizing fasciitis - Dupuytren's contracture - Fibromatosis Enthesis Enthesitis/Enthesopathies Iliotibial band syndrome, Achilles tendinitis, Patellar tendinitis, Golfer's elbow, Tennis elbow, Metatarsalgia, Bone spur, Tendinitis Other, NEC Rheumatism - Neuralgia/Neuritis - Panniculitis - Fibromyalgia see also neoplasia Retrieved from http://en..org/wiki/Fibromyalgia Categories: Rheumatology | Diseases involving the fasciae | Syndromes | Ailments of unknown etiologyHidden categories: All articles with dead external links | Articles with dead external links since June 2008 | All articles with statements | Articles with statements since May 2008 | Articles with statements since January 2008 | Articles with statements since June 2007 | Articles with statements since June 2008 | Articles with statements since November 2007 | Articles that may contain original research since June 2008 | All pages needing to be wikified | Wikify from August 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Català Dansk Deutsch Español Euskara Français Italiano עברית Nederlands 日本語 Norsk bokmål Polski Português Suomi Svenska This page was last modified on 11 September 2008, at 19:24
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