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Fibromyalgia syndrome

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Fibromyalgia
ICD-10 M797
ICD-9 729.1
OMIM [1]
DiseasesDB [2]
MedlinePlus 000427
eMedicine med/790 med/2934 ped/777 pmr/47
MeSH {{{MeshNumber}}}
Main article: Muscular disorders

Fibromyalgia syndrome or Fibromyalgia (FM) is a disorder classified by the presence of chronic widespread pain and a heightened and painful response to gentle touch (tactile allodynia).[1] Other core features of the disorder include debilitating fatigue, sleep disturbance and joint stiffness. In addition, persons affected by the disorder frequently experience a range of other symptoms that involve multiple body systems, including difficulty with swallowing,[2] functional bowel and bladder abnormalities,[3] difficulty breathing,[4] diffuse sensations of numbness and tingling (non-dermatomal paresthesia),[5] abnormal motor activity (i.e. nocturnal myoclonus, sleep bruxism),[6] and cognitive dysfunction.[7] An increased prevalence of affective and anxiety-related symptoms is also well known.[8] 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".[9] Not all affected persons experience all the symptoms associated with the greater syndrome. Fibromyalgia is considered a controversial diagnosis, with some authors contending that the disorder is a ‘non-disease’, due in part to a lack of objective laboratory tests or medical imaging studies to confirm the diagnosis.[10] While historically considered either a musculoskeletal disease or neuropsychiatric condition, evidence from research conducted in the last three decades has revealed abnormalities within the central nervous system affecting brain regions that may be linked both to clinical symptoms and research phenomena.[11] Although there is as yet no generally accepted cure for fibromyalgia, there are treatments that have been demonstrated by controlled clinical trials to be effective in reducing symptoms, including medications, patient education, exercise and behavioral interventions.[12]

Signs and symptomsEdit

The defining symptoms of fibromyalgia are chronic, widespread pain and allodynia. Other symptoms can include moderate to severe fatigue, needle-like tingling of the skin, muscle aches, prolonged muscle spasms, weakness in the limbs, nerve pain, functional bowel disturbances,[13] and chronic sleep disturbances.[14] 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.[How to reference and link to summary or text]

Many patients experience cognitive dysfunction[15] (known as "brain fog" or "fibrofog"), which may be characterized by impaired concentration,[16] problems with short[17][16] and long-term memory, short-term memory consolidation[17], impaired speed of performance,[16][17] inability to multi-task, cognitive overload,[17][16] diminished attention span and anxiety and depressive symptoms.[17] "Brain fog" may be directly related to the sleep disturbances experienced by sufferers of fibromyalgia.[How to reference and link to summary or text]

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 (possibly linked to lower levels of ghrelin,[18] 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.[19] As 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. [How to reference and link to summary or text] Symptoms are often aggravated by unrelated illness or changes in the weather. [How to reference and link to summary or text]They can become more 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.[20]

An epidemiology study comprised of an internet-based survey of 2,596 people with fibromyalgia[21] reported that the most frequently cited factors perceived to worsen FM symptoms were emotional distress (83%), weather changes (80%), sleeping problems (79%), strenuous activity (70%), mental stress (68%), worrying (60%), car travel (57%), family conflicts (52%), physical injuries (50%) and physical inactivity (50%). Other factors included infections, allergies, lack of emotional support, perfectionism, side effects of medications, and chemical exposures.

Causation hypotheses Edit

The cause of fibromyalgia is currently unknown. However, several hypotheses have been developed, which are discussed below.

Genetic predisposition Edit

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.[22][23] The mode of inheritance is currently unknown, but it is most probably polygenic.[24] Research has demonstrated that FM is associated with polymorphisms of genes in the serotoninergic,[25] dopaminergic[26] and catecholaminergic systems.[27] However, these polymorphisms are not specific for FM and are associated with a variety of allied disorders (e.g. chronic fatigue syndrome,[28] irritable bowel syndrome[29]) and with depression.[30]

Stress-induced pathophysiology Edit

Studies have shown that stress is a significant precipitating factor in the development of fibromyalgia.[31] Accordingly, it has been proposed that fibromyalgia may result from stress-induced changes in the function and integrity of the hippocampus.[32] This proposition was based in part on the observation that preclinical studies in non-human primates have shown that exposure to psychosocial duress results in material changes to the very tissues of the brain, including atrophic and metabolic changes in the hippocampal complex.[33][34] Evidence in support of this hypothesis have been generated by two studies that employed single-voxel magnetic resonance spectroscopy (1H-MRS) to demonstrate metabolic abnormalities within the hippocampal complex in patients with fibromyalgia with significant correlations between hippocampal metabolic abnormalities and severity of clinical symptoms.[35][36]

Other 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.[37] This proposition is supported in part by the observation from a prospective epidemiology study by the same authors which found that variations in HPA function characterized by high levels of circulating cortisol following dexamethasone suppression testing, low levels of morning salivary cortisol and high levels of evening salivary cortisol are all associated with the development of chronic widespread pain.[38]

Consequence of sleep disturbanceEdit

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.[39] 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 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.

Central dopamine dysfunction (hypodopaminergia)Edit

The ‘dopamine hypothesis of fibromyalgia’ proposes that the central abnormality responsible for symptoms associate with FM is a disruption of normal dopamine-related neurotransmission. 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,[40] which is a common co-morbid condition in patients with fibromyalgia.[41] 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,[42] 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.[43][44] Patients with restless legs syndrome have also been demonstrated to have hyperalgesia to static mechanical stimulation.[45]

As noted above, FM 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.[46][47] Hence, it was proposed that FM 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).[48] This conclusion was based on three key observations; fibromyalgia is associated with stress, chronic exposure to stress results in a disruption of dopamine-related neurotransmission[49] and dopamine plays a critical role in modulating pain perception and central analgesia in such areas as the basal ganglia[50] including the nucleus accumbens,[51] insular cortex,[52] anterior cingulate cortex,[53] thalamus,[54] periaqueductal gray[55] and spinal cord.[56][57]

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.[58] 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),[59] fibromyalgia patients fail to release dopamine in response to pain and, in some cases, actually have a reduction in dopamine levels during painful stimulation.[60] 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.[61]

Abnormal serotonin metabolismEdit

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 (it was proposed) may explain in part many of the symptoms associated with the disorder.[62] This hypothesis is supported by the observation of decreased serotonin metabolites in patient plasma[63] and cerebrospinal fluid.[64] 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[65]. 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. It should be noted, however, that the relevance of dysregulated serotonin metabolism to the pathophysiology is a matter of debate.[66] 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.[67]

Deficient human growth hormone (HGH) secretionEdit

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.[How to reference and link to summary or text] 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,[68] In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep[69][70][71][72] though there is disagreement about the proposition.[73]

Psychological factorsEdit

There is strong evidence that major depression is associated with fibromyalgia, although the nature of the association is controversial. 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 FM refer to the same underlying construct or can be seen as subsidiaries of one disease concept.[74] Indeed, the sensation of pain has at least two dimensions: a sensory dimension which processes the magnitude 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 FM 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 indicate that the amplification of the sensory dimension of pain in FM occurs independently of mood or emotional processes.[75]

An alternative hypothesis regarding the development of fibromyalgia in relationship to psychological conflict proposes that the disorder may be a psychosomatic illness as described by John E. Sarno's writing related to "tension myositis syndrome", in which chronic pain is proposed to be a psychic diathesis of the mind's subconscious strategy of distracting painful or dangerous emotions. Education, attitude change, and in some cases, psychotherapy are proposed as treatments.[76]

Other hypothesesEdit

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.[How to reference and link to summary or text] 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.

Other hypotheses have been proposed related to various toxins from the patient's environment,[How to reference and link to summary or text] viral causes such as the Epstein-Barr Virus,[How to reference and link to summary or text] an aberrant immune response to intestinal bacteria,[77] and erosion of the protective chemical coating around sensory nerves.[How to reference and link to summary or text] Still another hypothesis regarding the cause of FM symptoms proposes that affected individuals suffer from vasomotor dysregulation resulting in sluggish or improper vascular flow.[78]

PathophysiologyEdit

Sleep disturbancesEdit

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.[62] 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.[79] Since that time a variety of other EEG sleep abnormalities have also been reported in subgroups of fibromyalgia patients.[80]

Poly-modal sensitivityEdit

Results from studies examining responses to experimental stimulation have shown that fibromyalgia patients display sensitivity to pressure, heat, cold, electrical and chemical stimulation.[81] Experiments examining pain regulatory systems have shown that fibromyalgia patients also display a dysregulation of diffuse noxious inhibitory control,[82] an exaggerated wind-up in response to repetitive stimulation,[83] and an absence of exercise-induced analgesic response.[84] Together these results point to dysregulation of the nociceptive system at the central level.

Neuroendocrine disruptionEdit

Patients with fibromyalgia have been demonstrated to have a disruption of normal neuroendocrine function, characterized by mild hypocortisolemia,[85] hyperreactivity of pituitary adrenocorticotropin hormone release in response to challenge, and glucocorticoid feedback resistance.[86] 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.[87] Other abnormalities include reduced responsivity of thyrotropin and thyroid hormones to thyroid-releasing hormone,[88] a mild elevation of prolactin levels with disinhibition of prolactin release in response to challenge[89] and hyposecretion of adrenal androgens.[90] 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.[91]

Sympathetic HyperactivityEdit

Functional analysis of the autonomic system in patients with fibromyalgia has demonstrated disturbed activity characterized by hyperactivity of the sympathetic nervous system at baseline[92] with reduced sympathoadrenal reactivity in response to a variety of stressors including physical exertion and mental stress.[93][94] Fibromyalgia patients demonstrate lower heart rate variability, an index of sympathetic/parasympathetic balance, indicating sustained sympathetic hyperactivity, especially at night.[95] 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,[96] while circulating levels of epinephrine and norepinephrine have been variously reported as low, normal and high.[97][98] 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.[99]

Cerebrospinal fluid abnormalitiesEdit

The most reproduced laboratory finding in patients with fibromyalgia is an elevation in cerebrospinal fluid levels of substance P, a putative nociceptive neurotransmitter.[100][101][102] Metabolites for the monoamine neurotransmitters serotonin, norepinephrine, and dopamine—all of which play a role in natural analgesia—have been shown to be lower,[103] while concentrations of endogenous opioids (i.e., endorphins and enkephalins) appear to be higher.[104] 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.[105] 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.[106]

Brain imaging studiesEdit

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).[107][108] Differential activation in response to painful stimulation has also been demonstrated.[109][110] 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. 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).[35] [36] A significant negative correlation was demonstrated between abnormal metabolite ratios and a validated index of the clinical severity (i.e. the Fibromyalgia Impact Questionnaire).[111] 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.[112] 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.[113] Studies utilizing positron emission tomography have demonstrated reduced dopamine synthesis in the brainstem and elements of the limbic cortex.[114] 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 [115] 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.[116]

DiagnosisEdit

File:Tender points fibromyalgia.gif

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 the patient based on the patient's 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 was 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.[117] 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.

TreatmentEdit

As with many other syndromes, there is no universally accepted cure for fibromyalgia, though some physicians claim to have found cures[118], and treatment is typically aimed at symptom management. Developments in the understanding of the pathophysiology of the disorder have led to improvements in treatment, which include prescription medication, behavioral intervention, excercise, and alternative and complementary medicine. Indeed, integrated treatment plans that incorporate medication, patient education, aerobic exercise and cognitive-behavioral therapy have been shown to be effective in alleviating pain and other fibromyalgia-related symptoms.[12] In 2005, the American Pain Society produced the first comprehensive guidelines for patient evaluation and management.[119] More recently, the European League Against Rheumatism (EULAR) issued updated treatment guidelines. [120]

PharmaceuticalEdit

AnalgesicsEdit

A number of analgesics are used to treat the pain symptoms resulting from fibromyalgia, including nonsteroidal anti-inflammatory drugs (NSAID), COX-2 inhibitors, and tramadol.[How to reference and link to summary or text]

Selective serotonin reuptake inhibitors Edit

Research data consistently contradict the utility of agents with specificity as serotonin reuptake inhibitors for the treatment of core symptoms of fibromyalgia.[121][122][123] Moreover, SSRIs are known to aggravate many of the comorbidities that commonly affect patients with fibromyalgia including restless legs syndrome and sleep bruxism.[124][125][126]

Note that a controlled clinical trial of the tricyclic antidepressant amitriptyline and the SSRI fluoxetine demonstrated superior utility when used in combination than either drug used in isolation, although neither drug is labeled for use in treatment of fibromyalgia.[127]

Anti-seizure medicationEdit

Anti-seizure drugs are also sometimes used, such as gabapentin (Neurontin)[128] and pregabalin (Lyrica). Gabapentin is not approved or labeled for use in treatment of neuropathic pain or fibromyalgia. Pregabalin, originally labeled for the treatment of nerve pain suffered by diabetics, has been cleared by the US Food and Drug Administration for treatment of fibromyalgia.[129] 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.[130]

Dopamine agonistsEdit

Dopamine agonists (e.g. pramipexole (Mirapex) and ropinirole(ReQuip) have been studied for use in the treatment of fibromyalgia with good results.[61] A trial of transdermal rotigotine is currently on going[131].

Investigational medicationsEdit

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, 2007Template:Dated maintenance category, 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, 2008Template:Dated maintenance category.[132]

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;[133][134] however, there are no controlled trials of safety or efficacy in clinical use.

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,[138][139] 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, and they propose that the disorder may be associated with an underlying clinical deficiency of the endocannabinoid system.[140][141]

Among the more controversial therapies involves the use of guaifenesin; called St. Amand's protocol or the guaifenesin protocol[142] 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,[143] and the lead researcher has suggested that the anecdotally reported benefits were due to placebo suggestion.[144] The results of the study have since been contested by Dr St. Amand, who was a co-author of the original research report.[145]

Physical treatmentsEdit

Studies have found exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia.[146] Many patients find temporary relief by applying heat to painful areas. Those with access to chiropractic,physical therapy, massage, or acupuncture may find them beneficial.[147] Most patients find exercise, even low intensity exercise to be extremely helpful.[148] Osteopathic manipulative therapy can also temporarily relieve pain due to fibromyalgia.[149]

Whirlpool therapy is very beneficial. It's important that the water temperature be at least 95 degrees Fahrenheit. This therapy was recommended by the Fibromyalgia Clinic at Mayo.[How to reference and link to summary or text]

Psychological/behavioural therapiesEdit

Cognitive behavioural therapy has been shown to improve quality of life and coping in fibromyalgia patients and other sufferers of chronic pain.[150] Neurofeedback has also shown to provide temporary and long-term relief.[How to reference and link to summary or text] Biofeedback and self-management techniques such as pacing and stress management may also be helpful for some patients. [How to reference and link to summary or text] Because the nature of fibromyalgia is not well understood, some physicians believe that it may be psychosomatic or psychogenic.[151] Accordingly, some doctors have claimed to have successfully treated fibromyalgia when a psychological cause is accepted.[152]

PrognosisEdit

Although neither degenerative nor fatal, the chronic pain of fibromyalgia is pervasive and persistent. Most fibromyalgia patients report that their symptoms do not change over time. Recovery is dependent on psychosocial factors, including current or past psychological issues, the ability to work, and disability.[153] Of those diagnosed with fibromyalgia, 10% to 30% report being work-impaired,[153] and patients often need accommodations to fully participate in their education or remain active in their careers.[How to reference and link to summary or text]

EpidemiologyEdit

Fibromyalgia is seen in about 2% of the general population[150] and affects more females than males, with a ratio of 9:1 by ACR criteria.[154] It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood.

HistoryEdit

Fibromyalgia has been studied since the early 1800s and referred to by a variety of former names, including muscular rheumatism and fibrositis.[155] The term fibromyalgia was coined in 1976 to more accurately describe the symptoms, from the Latin fibra (fiber)[156] and the Greek words myo (muscle)[157] and algos (pain).[158]

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.[159][160] 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.[161] 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.[159][160]

Fibromyalgia was recognized by the American Medical Association as an illness and a cause of disability in 1987.[How to reference and link to summary or text] In an article the same year, the Journal of the American Medical Association also called the disorder fibromyalgia.[162] The American College of Rheumatology (ACR) published criteria for fibromyalgia in 1990 and developed neurohormonal mechanisms with central sensitization in the 1990s.[161]

ControversiesEdit

Several controversial issues exist with regard to fibromyalgia that range from questions regarding the validity of the disorder as a clinical entity, to issues regarding primary pathophysiology and the potential existence of fibromyalgia sub-types. Dr. Frederick Wolfe, the lead author of the 1990 paper that first defined the classification criteria for fibromyalgia, has been since quoted as saying he has become cynical and discouraged about the diagnosis and that he now considers the condition a physical response to stress, depression, and economic and social anxiety[163]. Opponents of the fibromyalgia concept argue that fibromyalgia represents a ‘non-disease’ and that giving it a label simply legitimizes patients' sickness behavior[10]. In contrast, findings from the London Fibromyalgia Epidemiology Study, which comprised a 36 month prospective, within-group comparison of 100 individuals identified as having fibromyalgia (72 of whom were newly diagnosed with the disorder), demonstrated that although physical functioning decreased slightly over time, there was also a statistically significant improvement in satisfaction with health, and newly diagnosed FM cases reported fewer symptoms and major symptoms over the long term. No other differences in clinical status or health service use occurred over time.[164] The authors of the study concluded that the ‘fibromyalgia label’ does not have a meaningful adverse affect on clinical outcome over the long term.

The validity of fibromyalgia as a unique clinical entity is also a matter of some contention among researchers in the field. Contradictory findings from clinical research, compounded by differences in psychological and autonomic profiles among affected individuals, have been interpreted by different groups to indicate the existence of fibromyalgia sub-types.[165][166]. There is also considerable overlap between fibromyalgia and other clinical disorders, which are frequently referred to collectively as "functional somatic syndromes" (e.g. irritable bowel syndrome, chronic fatigue syndrome).[167] Others have proposed that the clinical phenomena that fall under the label ‘fibromyalgia syndrome' might actually comprise several clinical entities, ranging from mild, idiopathic inflammatory processes in some individuals, to somatoform disorders resulting from neuropsychiatric processes in others, with probable overlaps in between.[165]

ReferencesEdit

  1. Wolfe F, Smythe HA, Yunus MB et al (Feb 1990). The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 33 (2): 160–72.
  2. Wallace DJ, Hallegua DS. (Oct 2002). Fibromyalgia: the gastrointestinal link.. Curr Pain Headache Rep. 8 (5): 364-8.
  3. Clauw DJ, Schmidt M, Radulovic D, Singer A, Katz P, Bresette J. (Jan-Feb 1997). The relationship between fibromyalgia and interstitial cystitis.. J Psychiatr Res. 31 (1): 125–31.
  4. Lurie M, Caidahl K, Johansson G, Bake B. (1990). Respiratory function in chronic primary fibromyalgia.. Scand J Rehabil Med. 22 (3): 151-5.
  5. Simms RW, Goldenberg DL. (Aug 1988). Symptoms mimicking neurologic disorders in fibromyalgia syndrome.. J Rheumatol. 15 (8): 1271-3.
  6. Moldofsky H, Tullis C, Lue FA, Quance G, Davidson J. (Mar-Apr 1984). Sleep-related myoclonus in rheumatic pain modulation disorder (fibrositis syndrome) and in excessive daytime somnolence.. Psychosom Med. 46 (2): 145-51.
  7. Glass JM. (Dec 2006). Cognitive dysfunction in fibromyalgia and chronic fatigue syndrome: new trends and future directions.. Curr Rheumatol Rep. 8 (6): 425-9.
  8. Buskila D, Cohen H. (Oct 2007). Comorbidity of fibromyalgia and psychiatric disorders.. Curr Pain Headache Rep. 11 (5): 333-8.
  9. Yunus MB. (Dec 1983). Fibromyalgia syndrome: a need for uniform classification.. J Rheumatol. 10 (6): 841.
  10. 10.0 10.1 Goldenberg DL (January 1995). Fibromyalgia: why such controversy?. Ann. Rheum. Dis. 54 (1): 3–5.
  11. Schweinhardt P, Sauro KM, Bushnell MC. (Oct 2008). Fibromyalgia: a disorder of the brain?. Neuroscientist. 14 (5): 415-21.
  12. 12.0 12.1 Goldenberg DL (2008). Multidisciplinary modalities in the treatment of fibromyalgia. J Clin Psychiatry 69: 30–4.
  13. Wallace DJ, Hallegua DS (October 2004). Fibromyalgia: the gastrointestinal link. Curr Pain Headache Rep 8 (5): 364–8.
  14. Moldofsky H, Scarisbrick P, England R, Smythe H (1975). Musculosketal symptoms and non-REM sleep disturbance in patients with "fibrositis syndrome" and healthy subjects. Psychosom Med 37 (4): 341–51.
  15. Glass JM (December 2006). Cognitive dysfunction in fibromyalgia and chronic fatigue syndrome: new trends and future directions. Curr Rheumatol Rep 8 (6): 425–9.
  16. 16.0 16.1 16.2 16.3 Leavitt F, Katz RS, Mills M, Heard AR (2002). Cognitive and Dissociative Manifestations in Fibromyalgia. J Clin Rheumatol. 8 (2): 77–84.
  17. 17.0 17.1 17.2 17.3 17.4 Buskila D, Cohen H (Oct 2007). Comorbidity of fibromyalgia and psychiatric disorders. Curr Pain Headache Rep 11 (5): 333–8.
  18. Tander B, Atmaca A, Aliyazicioglu Y, Canturk F (Oct 2007). Serum ghrelin levels but not GH, IGF-1 and IGFBP-3 levels are altered in patients with fibromyalgia syndrome. Joint Bone Spine 74 (5): 477–81.
  19. Does Fibromyalgia Affect Eyesight?. URL accessed on 2008-08-06.
  20. Shannon Erstad. Nonsteroidal anti-inflammatory drugs for fibromyalgia. Health Yahoo. URL accessed on 2007-10-25.
  21. Bennett RM, Jones J, Turk DC, Russell IJ, Matallana L. (Mar 2007). An internet survey of 2,596 people with fibromyalgia.. BMC Musculoskelet Disord. 9;8:27. 9 (6): 27.
  22. Stormorken H, Brosstad F (1992). Fibromyalgia: family clustering and sensory urgency with early onset indicate genetic predisposition and thus a "true" disease. Scand J Rheumatol. 21 (4): 207.
  23. Arnold LM, Hudson JI, Hess EV, et al (Mar 2004). Family study of fibromyalgia. Arthritis Rheum. 50 (3): 944–52.
  24. Buskila D, Sarzi-Puttini P (2006). Biology and therapy of fibromyalgia. Genetic aspects of fibromyalgia syndrome. Arthritis Res Ther. 8 (5): 218.
  25. Cohen H, Buskila D, Neumann L, Ebstein RP (Mar 2002). Confirmation of an association between fibromyalgia and serotonin transporter promoter region (5- HTTLPR) polymorphism, and relationship to anxiety-related personality traits. Arthritis Rheum. 46 (3): 845–7.
  26. Buskila D, Dan B, Cohen H, et al (Aug 2004). An association between fibromyalgia and the dopamine D4 receptor exon III repeat polymorphism and relationship to novelty seeking personality traits. Mol. Psychiatry 9 (8): 730–1.
  27. Zubieta JK, Heitzeg MM, Smith YR, et al (Feb 2003). COMT val158met genotype affects mu-opioid neurotransmitter responses to a pain stressor. Science (journal) 299 (5610): 1240–3.
  28. Narita M, Nishigami N, Narita N, et al (Nov 2003). Association between serotonin transporter gene polymorphism and chronic fatigue syndrome. Biochem Biophys Res Commun. 311 (2): 264–6.
  29. Camilleri M, Atanasova E, Carlson PJ, et al (Aug 2002). Serotonin-transporter polymorphism pharmacogenetics in diarrhea-predominant irritable bowel syndrome. Gastroenterology 123 (2): 425–32.
  30. Hudson JI, Mangweth B, Pope HG JR, De COL C, Hausmann A, Gutweniger S, Laird NM, Biebl W, Tsuang MT. Family study of affective spectrum disorder. Arch Gene Psychiatry. 2003;60:170–177. doi: 10.1001/archpsyc.60.2.170.
  31. Anderberg UM, Marteinsdottir I, Theorell T, von Knorring L (Aug 2000). The impact of life events in female patients with fibromyalgia and in female healthy controls. Eur Psychiatry 15 (5): 33–41.
  32. Wood PB (2004). Fibromyalgia: A Central Role for the Hippocampus – A Theoretical Construct. J Musculoskeletal Pain 12 (1): 19-26.
  33. Uno H, Tarara R, Else JG, Suleman MA, Sapolsky RM. (May 1989). Hippocampal damage associated with prolonged and fatal stress in primates.. J Neurosci. 9 (5): 1705-11.
  34. Lucassen PJ, Vollmann-Honsdorf GK, Gleisberg M, Czéh B, De Kloet ER, Fuchs E. (Ju1 2001). Chronic psychosocial stress differentially affects apoptosis in hippocampal subregions and cortex of the adult tree shrew.. Eur J Neurosci. 14 (1): 161-6.
  35. 35.0 35.1 Emad Y, Ragab Y, Zeinhom F, El-Khouly G, Abou-Zeid A, Rasker JJ. (Jul 2008). Hippocampus dysfunction may explain symptoms of fibromyalgia syndrome. A study with single-voxel magnetic resonance spectroscopy.. J Rheumatol. 35 (7): 1371-7.
  36. 36.0 36.1 Wood PB, Ledbetter CR, Glabus MF, Broadwell LK, Patterson JC 2nd. Hippocampal Metabolite Abnormalities in Fibromyalgia: Correlation With Clinical Features.. J Pain..
  37. McBeth J, Chiu YH, Silman AJ, Ray D, Morriss R, Dickens C, Gupta A, Macfarlane GJ. (2005). Hypothalamic-pituitary-adrenal stress axis function and the relationship with chronic widespread pain and its antecedents. Arthritis Res Ther. 7 (5): R992-R1000.
  38. McBeth J, Silman AJ, Gupta A, Chiu YH, Ray D, Morriss R, Dickens C, King Y, Macfarlane GJ. (2007). Moderation of psychosocial risk factors through dysfunction of the hypothalamic-pituitary-adrenal stress axis in the onset of chronic widespread musculoskeletal pain: findings of a population-based prospective cohort study.. Arthritis Rheum. 2007 Jan;56(1):360-71.. 56 (1): 360-71.
  39. (2004). Fibromyalgia – An Information Booklet. Arthritis Research Campaign.
  40. Cervenka S, Pålhagen SE, Comley RA, et al (Aug 2006). Support for dopaminergic hypoactivity in restless legs syndrome: a PET study on D2-receptor binding. Brain 129 (Pt 8): 2017–28.
  41. Yunus MB, Aldag JC (May 1996). Restless legs syndrome and leg cramps in fibromyalgia syndrome: a controlled study. BMJ 312 (7042): 1339.
  42. Sage JI (May 2004). Pain in Parkinson's Disease. Curr Treat Options Neurol 6 (3): 191–200.
  43. Potvin S, Stip E, Tempier A, et al (Dec 2007). Pain perception in schizophrenia: No changes in diffuse noxious inhibitory controls (DNIC) but a lack of pain sensitization. J Psychiatr Res 42: 1010.
  44. Potvin S, Marchand S (Dec 2007). Hypoalgesia in schizophrenia is independent of antipsychotic drugs: A systematic quantitative review of experimental studies. Pain 138: 70.
  45. Stiasny-Kolster K, Magerl W, Oertel WH, Möller JC, Treede RD (Apr 2004). Static mechanical hyperalgesia without dynamic tactile allodynia in patients with restless legs syndrome. Brain 127 (Pt 4): 773–82.
  46. Van Houdenhove B, Egle U, Luyten P (Oct 2005). The role of life stress in fibromyalgia. Curr Rheumatol Rep 7 (5): 365–70.
  47. Clauw DJ, Crofford LJ (Aug 2003). Chronic widespread pain and fibromyalgia: what we know, and what we need to know. Best Pract Res Clin Rheumatol 17 (4): 685–701.
  48. Wood PB (2004). Stress and dopamine: implications for the pathophysiology of chronic widespread pain. Med. Hypotheses 62 (3): 420–4.
  49. Finlay JM, Zigmond MJ (Nov 1997). The effects of stress on central dopaminergic neurons: possible clinical implications. Neurochem. Res. 22 (11): 1387–94.
  50. Chudler EH, Dong WK (Jan 1995). The role of the basal ganglia in nociception and pain. Pain 60 (1): 3–38.
  51. Altier N, Stewart J (1999). The role of dopamine in the nucleus accumbens in analgesia. Life Sci. 65 (22): 2269–87.
  52. Burkey AR, Carstens E, Jasmin L (May 1999). Dopamine reuptake inhibition in the rostral agranular insular cortex produces antinociception. J. Neurosci. 19 (10): 4169–79.
  53. López-Avila A, Coffeen U, Ortega-Legaspi JM, del Angel R, Pellicer F (Sep 2004). Dopamine and NMDA systems modulate long-term nociception in the rat anterior cingulate cortex. Pain 111 (1-2): 136–43.
  54. Shyu BC, Kiritsy-Roy JA, Morrow TJ, Casey KL (Feb 1992). Neurophysiological, pharmacological and behavioral evidence for medial thalamic mediation of cocaine-induced dopaminergic analgesia. Brain Res. 572 (1-2): 216–23.
  55. Flores JA, El Banoua F, Galán-Rodríguez B, Fernandez-Espejo E (Jul 2004). Opiate anti-nociception is attenuated following lesion of large dopamine neurons of the periaqueductal grey: critical role for D1 (not D2) dopamine receptors. Pain 110 (1-2): 205–14.
  56. Lindvall O, Björklund A, Skagerberg G (Sep 1983). Dopamine-containing neurons in the spinal cord: anatomy and some functional aspects. Ann. Neurol. 14 (3): 255–60.
  57. Tamae A, Nakatsuka T, Koga K, et al (Oct 2005). Direct inhibition of substantia gelatinosa neurones in the rat spinal cord by activation of dopamine D2-like receptors. J. Physiol. (Lond.) 568 (Pt 1): 243–53.
  58. Wood PB, Patterson JC, Sunderland JJ, Tainter KH, Glabus MF, Lilien DL (Jan 2007). Reduced presynaptic dopamine activity in fibromyalgia syndrome demonstrated with positron emission tomography: a pilot study. J Pain 8 (1): 51–8.
  59. Scott DJ, Heitzeg MM, Koeppe RA, Stohler CS, Zubieta JK (Oct 2006). Variations in the human pain stress experience mediated by ventral and dorsal basal ganglia dopamine activity. J. Neurosci. 26 (42): 10789–95.
  60. Wood PB, Schweinhardt P, Jaeger E, et al (Jun 2007). Fibromyalgia patients show an abnormal dopamine response to pain. Eur. J. Neurosci. 25 (12): 3576–82.
  61. 61.0 61.1 Holman AJ, Myers RR (Aug 2005). A randomized, double-blind, placebo-controlled trial of pramipexole, a dopamine agonist, in patients with fibromyalgia receiving concomitant medications. Arthritis Rheum. 52 (8): 2495–505.
  62. 62.0 62.1 Moldofsky H, Scarisbrick P, England R, Smythe H (Jul-Aug 1975). Musculosketal symptoms and non-REM sleep disturbance in patients with "fibrositis syndrome" and healthy subjects. Psychosom Med 37 (4): 341–51.
  63. Russell IJ, Michalek JE, Vipraio GA, Fletcher EM, Javors MA, Bowden CA (Jan 1992). Platelet 3H-imipramine uptake receptor density and serum serotonin levels in patients with fibromyalgia/fibrositis syndrome. J Rheumatol. 19 (1): 104–9.
  64. Russell IJ, Vaeroy H, Javors M, Nyberg F (May 1992). Cerebrospinal fluid biogenic amine metabolites in fibromyalgia/fibrositis syndrome and rheumatoid arthritis. Arthritis Rheum. 35 (5): 550–6.
  65. Arnold LM (2006). Biology and therapy of fibromyalgia. New therapies in fibromyalgia. Arthritis Res Ther. 8 (4): 212.
  66. Jaschko G, Hepp U, Berkhoff M, et al (Sep 2007). Serum serotonin levels are not useful in diagnosing fibromyalgia. Ann Rheum Dis. 66 (9): 1267–8.
  67. Späth M (May 2002). Current experience with 5-HT3 receptor antagonists in fibromyalgia. Rheum Dis Clin North Am. 28 (2): 319–28.
  68. Anderberg UM, Liu Z, Berglund L, Nyberg F (1999). Elevated plasma levels of neuropeptide Y in female fibromyalgia patients. Eur J Pain 3 (1): 19–30.
  69. Jones KD, Deodhar P, Lorentzen A, Bennett RM, Deodhar AA (2007). Growth hormone perturbations in fibromyalgia: a review. Seminars in Arthritis and Rheumatism 36 (6): 357–79.
  70. Shuer, ML (2003). Fibromyalgia: symptom constellation and potential therapeutic options. Endocrine 22 (1): 67–76.
  71. Yuen, KC, Bennett RM, Hryciw CA, Cook MB, Rhoads SA, Cook DM (2007). Is further evaluation for growth hormone (GH) deficiency necessary in fibromyalgia patients with low serum insulin-like growth factor (IGF)-I levels?. Growth hormone & IGF research 17 (1): 82–8.
  72. Bennett, RM, Cook DM, Clark SR, Burckhardt CS, Campbell SM.. Hypothalamic-pituitary-insulin-like growth factor-I axis dysfunction in patients with fibromyalgia. J Rheumatology 24 (7): 1384–9.
  73. McCall-Hosenfeld, JS, Goldenberg DL, Hurwitz S, Adler GK.. Growth hormone and insulin-like growth factor-1 concentrations in women with fibromyalgia. Journal of Rheumatology 30: 809–14.
  74. Pae CU, Luyten P, Marks DM, Han C, Park SH, Patkar AA, Masand PS, Van Houdenhove B (Aug 2008). The relationship between fibromyalgia and major depressive disorder: a comprehensive review.. Curr Med Res Opin 24 (8): 2359–71.
  75. Giesecke T, Gracely RH, Williams DA, Geisser ME, Petzke FW, Clauw DJ (May 2005). The relationship between depression, clinical pain, and experimental pain in a chronic pain cohort.. Arthritis Rheum. 52 (5): 1577–84.
  76. Sarno, Dr. John E. et al, (2006). The Divided Mind: The Epidemic of Mindbody Disorders, 21–2, 235–7, 294–8.
  77. Pimental M, Wallace D, Hallegua D et.al (April 2004). A link between irritable bowel syndrome and fibromyalgia may be related to findings on lactulose breath testing. Ann Rheum Dis. 63 (4): 450–2.
  78. Katz DL, Greene L, Ali A, Faridi Z (2007). The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation. Med. Hypotheses 69 (3): 517–25.
  79. Moldofsky H, Scarisbrick P (Jan-Feb 1976). Induction of neurasthenic musculoskeletal pain syndrome by selective sleep stage deprivation. Psychosom Med 38 (1): 35–44.
  80. Drewes AM, Gade K, Nielsen KD, Bjerregård K, Taagholt SJ, Svendsen L (Dec 1995). Clustering of sleep electroencephalographic patterns in patients with the fibromyalgia syndrome. Br J Rheumatol. 34 (12): 1151–6.
  81. Desmeules JA, Cedraschi C, Rapiti E, et al (May 2003). Neurophysiologic evidence for a central sensitization in patients with fibromyalgia. Arthritis Rheum. 48 (5): 1420–9.
  82. Kosek E, Hansson P (Mar 1997). Modulatory influence on somatosensory perception from vibration and heterotopic noxious conditioning stimulation (HNCS) in fibromyalgia patients and healthy subjects. Pain 70 (1): 41–51.
  83. Staud R, Vierck CJ, Cannon RL, Mauderli AP, Price DD (Mar 2001). Abnormal sensitization and temporal summation of second pain (wind-up) in patients with fibromyalgia syndrome. Pain 91 (1-2): 165–75.
  84. Staud R, Robinson ME, Price DD (Nov 2005). Isometric exercise has opposite effects on central pain mechanisms in fibromyalgia patients compared to normal controls. Pain 118 (1-2): 176–84.
  85. Gur A, Cevik R, Sarac AJ, Colpan L, Em S (Nov 2004). Hypothalamic-pituitary-gonadal axis and cortisol in young women with primary fibromyalgia: the potential roles of depression, fatigue, and sleep disturbance in the occurrence of hypocortisolism. Ann. Rheum. Dis. 63 (11): 1504–6.
  86. Griep EN, Boersma JW, Lentjes EG, Prins AP, van der Korst JK, de Kloet ER (Jul 1998). Function of the hypothalamic-pituitary-adrenal axis in patients with fibromyalgia and low back pain. J. Rheumatol. 25 (7): 1374–81.
  87. Bennett RM (Aug 2002). Adult growth hormone deficiency in patients with fibromyalgia. Curr Rheumatol Rep 4 (4): 306–12.
  88. Neeck G, Riedel W (Jul 1992). Thyroid function in patients with fibromyalgia syndrome. J. Rheumatol. 19 (7): 1120–2.
  89. Riedel W, Layka H, Neeck G (1998). Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol 57 Suppl 2: 81–7.
  90. Dessein PH, Shipton EA, Joffe BI, Hadebe DP, Stanwix AE, Van der Merwe BA (Nov 1999). Hyposecretion of adrenal androgens and the relation of serum adrenal steroids, serotonin and insulin-like growth factor-1 to clinical features in women with fibromyalgia. Pain 83 (2): 313–9.
  91. Neeck G, Crofford LJ (Nov 2000). Neuroendocrine perturbations in fibromyalgia and chronic fatigue syndrome. Rheum. Dis. Clin. North Am. 26 (4): 989–1002.
  92. Martinez-Lavin M. Biology and therapy of fibromyalgia. Stress, the stress response system, and fibromyalgia. Arthritis Res Ther. 2007;9(4):216.
  93. Giske L, Vøllestad NK, Mengshoel AM, Jensen J, Knardahl S, Røe C (Apr 2008). Attenuated adrenergic responses to exercise in women with fibromyalgia--a controlled study. Eur J Pain 12 (3): 351–60.
  94. Nilsen KB, Sand T, Westgaard RH, Stovner LJ, White LR, Bang Leistad R, Helde G, Rø M. Autonomic activation and pain in response to low-grade mental stress in fibromyalgia and shoulder/neck pain patients. Eur J Pain. 2007 Oct;11(7):743-55.
  95. Martínez-Lavín M, Hermosillo AG, Mendoza C, et al (Apr 1997). Orthostatic sympathetic derangement in subjects with fibromyalgia. J. Rheumatol. 24 (4): 714–8.
  96. Anderberg UM, Liu Z, Berglund L, Nyberg F (Mar 1999). Elevated plasma levels of neuropeptide Y in female fibromyalgia patients. Eur J Pain 3 (1): 19–30.
  97. van Denderen JC, Boersma JW, Zeinstra P, Hollander AP, van Neerbos BR (1992). Physiological effects of exhaustive physical exercise in primary fibromyalgia syndrome (PFS): is PFS a disorder of neuroendocrine reactivity?. Scand. J. Rheumatol. 21 (1): 35–7.
  98. Adler GK, Kinsley BT, Hurwitz S, Mossey CJ, Goldenberg DL (May 1999). Reduced hypothalamic-pituitary and sympathoadrenal responses to hypoglycemia in women with fibromyalgia syndrome. Am J Med. 106 (5): 534–43.
  99. Torpy DJ, Papanicolaou DA, Lotsikas AJ, Wilder RL, Chrousos GP, Pillemer SR (Apr 2000). Responses of the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis to interleukin-6: a pilot study in fibromyalgia. Arthritis Rheum. 43 (4): 872–80.
  100. Russell IJ, Orr MD, Littman B, et al (Nov 1994). Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Arthritis Rheum. 37 (11): 1593–601.
  101. Vaerøy H, Helle R, Førre O, Kåss E, Terenius L (Jan 1988). Elevated CSF levels of substance P and high incidence of Raynaud phenomenon in patients with fibromyalgia: new features for diagnosis. Pain 32 (1): 21–6.
  102. Evengard B, Nilsson CG, Lindh G, et al (Nov 1998). Chronic fatigue syndrome differs from fibromyalgia. No evidence for elevated substance P levels in cerebrospinal fluid of patients with chronic fatigue syndrome. Pain 78 (2): 153–5.
  103. Russell IJ, Vaeroy H, Javors M, Nyberg F (May 1992). Cerebrospinal fluid biogenic amine metabolites in fibromyalgia/fibrositis syndrome and rheumatoid arthritis. Arthritis Rheum. 35 (5): 550–6.
  104. Vaerøy H, Nyberg F, Terenius L (Aug 1991). No evidence for endorphin deficiency in fibromyalgia following investigation of cerebrospinal fluid (CSF) dynorphin A and Met-enkephalin-Arg6-Phe7. Pain 46 (2): 139–43.
  105. Giovengo SL, Russell IJ, Larson AA (Jul 1999). Increased concentrations of nerve growth factor in cerebrospinal fluid of patients with fibromyalgia. J Rheumatol. 26 (7): 1564–9.
  106. Larson AA, Giovengo SL, Russell IJ, Michalek JE (Aug 2000). Changes in the concentrations of amino acids in the cerebrospinal fluid that correlate with pain in patients with fibromyalgia: implications for nitric oxide pathways. Pain 87 (2): 201–11.
  107. Mountz JM, Bradley LA, Modell JG, et al (Jul 1995). Fibromyalgia in women. Abnormalities of regional cerebral blood flow in the thalamus and the caudate nucleus are associated with low pain threshold levels. Arthritis Rheum. 38 (7): 926–38.
  108. Kwiatek R, Barnden L, Tedman R, et al (Dec 2000). Regional cerebral blood flow in fibromyalgia: single-photon-emission computed tomography evidence of reduction in the pontine tegmentum and thalami. Arthritis Rheum. 43 (12): 2823–33.
  109. Gracely RH, Petzke F, Wolf JM, Clauw DJ (May 2002). Functional magnetic resonance imaging evidence of augmented pain processing in fibromyalgia. Arthritis Rheum. 46 (5): 1333–43.
  110. Cook DB, Lange G, Ciccone DS, Liu WC, Steffener J, Natelson BH (Feb 2004). Functional imaging of pain in patients with primary fibromyalgia. J Rheumatol. 31 (2): 364–78.
  111. Burckhardt CS, Clark SR, Bennett RM. (May 1991). The fibromyalgia impact questionnaire: development and validation.. J Rheumatol. 18 (5): 728-33.
  112. Harris RE, Sundgren PC, Pang Y, Hsu M, Petrou M, Kim SH, McLean SA, Gracely RH, Clauw DJ. (Mar 2008). Dynamic levels of glutamate within the insula are associated with improvements in multiple pain domains in fibromyalgia.. Arthritis Rheum. 58 (3): 903-7.
  113. Kuchinad A, Schweinhardt P, Seminowicz DA, Wood PB, Chizh BA, Bushnell MC (Apr 2007). Accelerated brain gray matter loss in fibromyalgia patients: premature aging of the brain?. J Neurosci. 27 (15): 4004–7.
  114. Wood PB, Patterson JC, Sunderland JJ, Tainter KH, Glabus MF, Lilien DL (Jan 2007). Reduced presynaptic dopamine activity in fibromyalgia syndrome demonstrated with positron emission tomography: a pilot study. J Pain 8 (1): 51–8.
  115. Wood PB, Schweinhardt P, Jaeger E, et al (Jun 2007). Fibromyalgia patients show an abnormal dopamine response to pain. Eur J Neurosci. 25 (12): 3576–82.
  116. Harris RE, Clauw DJ, Scott DJ, McLean SA, Gracely RH, Zubieta JK (Sep 2007). Decreased central mu-opioid receptor availability in fibromyalgia. J Neurosci. 27 (37): 10000–6.
  117. National Institute of Arthritis and Musculoskeletal and Skin Diseases (2004). Questions and Answers About Fibromyalgia – How Is Fibromyalgia Diagnosed?. National Institutes for Health.
  118. Selfridge, Dr. Nancy, and Peterson, Franklynn (2001). Freedom from Fibromyalgia: The 5-Week Program Proven to Conquer Pain.
  119. Burkhardt C, Goldenberg DL, Crofford LJ, et al. Guideline for the Management of Fibromyalgia Syndrome Pain in Adults and Children. APS Clinical Practice Guidelines Series, No. 4, 2005.
  120. Carville SF, Arendt-Nielsen S, Bliddal H, et al. (2008). EULAR evidence-based recommendations for the management of fibromyalgia syndrome.. Ann Rheum Dis. 67: 536-41.
  121. Nørregaard J, Volkmann H, Danneskiold-Samsøe B (Jun 1995). A randomized controlled trial of citalopram in the treatment of fibromyalgia. Pain 61 (3): 445–9.
  122. Anderberg UM, Marteinsdottir I, von Knorring L (2000). Citalopram in patients with fibromyalgia—a randomized, double-blind, placebo-controlled study. Eur J Pain 4 (1): 27–35.
  123. Patkar AA, Masand PS, Krulewicz S, et al (May 2007). A randomized, controlled, trial of controlled release paroxetine in fibromyalgia. Am. J. Med. 120 (5): 448–54.
  124. Caley CF (Dec 1997). Extrapyramidal reactions and the selective serotonin-reuptake inhibitors. Ann Pharmacother 31 (12): 1481–9.
  125. Leo RJ (Oct 1996). Movement disorders associated with the serotonin selective reuptake inhibitors. J Clin Psychiatry 57 (10): 449–54.
  126. Gerber PE, Lynd LD (June 1998). Selective serotonin-reuptake inhibitor-induced movement disorders. Ann Pharmacother 32 (6): 692–8.
  127. Goldenberg D, Mayskiy M, Mossey C, Ruthazer R, Schmid C (1996). A randomized, double-blind crossover trial of fluoxetine and amitriptyline in the treatment of fibromyalgia. Arthritis Rheum. 39 (11): 1852–9.
  128. Arnold LM, Goldenberg DL, Stanford SB, et al (Apr 2007). Gabapentin in the treatment of fibromyalgia: a randomized, double-blind, placebo-controlled, multicenter trial. Arthritis Rheum. 56 (4): 1336–44.
  129. U.S. Food and Drug Administration (June 21 2007). FDA Approves First Drug for Treating Fibromyalgia. Press release. Retrieved on 2008-01-14.
  130. Crofford LJ, Rowbotham MC, Mease PJ, et al (2005). Pregabalin for the treatment of fibromyalgia syndrome: results of a randomized, double-blind, placebo-controlled trial. Arthritis Rheum. 52 (4): 1264–73.
  131. A Double-Blind Multicenter Proof of Concept Trial to Assess the Efficacy and Safety of Rotigotine in Subjects With Fibromyalgia Syndrome - Full Text View - ClinicalTrials.gov
  132. Forest Laboratories. Forest Laboratories, Inc. and Cypress Bioscience, Inc. Announce Positive Results of Phase III Study for Milnacipran as a Treatment for Fibromyalgia Syndrome.
  133. Staud R, Vierck CJ, Robinson ME, Price DD (2005). Effects of the N-methyl-D-aspartate receptor antagonist dextromethorphan on temporal summation of pain are similar in fibromyalgia patients and normal control subjects. The journal of pain: official journal of the American Pain Society 6 (5): 323–32.
  134. Salynn Boyles. Cough Drug May Help Fibromyalgia Pain: Findings Could Affect Other Chronic Pain Conditions. WebMD.
  135. Swift W, Gates P, Dillon P (2005). Survey of Australians using cannabis for medical purposes. Harm reduction journal 2: 18.
  136. Schley M, Legler A, Skopp G, Schmelz M, Konrad C, Rukwied R (2006). Delta-9-THC based monotherapy in fibromyalgia patients on experimentally induced pain, axon reflex flare, and pain relief. Current medical research and opinion 22 (7): 1269–76.
  137. Burnes TL, Ineck JR (2006). Cannabinoid Analgesia as a Potential New Therapeutic Option in the Treatment of Chronic Pain. Annals of Pharmacotherapy 40 (2): 251–60.
  138. Radbruch L, Elsner F (2005). Emerging analgesics in cancer pain management. Expert opinion on emerging drugs 10 (1): 151–71.
  139. Notcutt W, Price M, Miller R, et al (2004). Initial experiences with medicinal extracts of cannabis for chronic pain: results from 34 'N of 1' studies. Anaesthesia 59 (5): 440–52.
  140. Russo EB (2004). Clinical endocannabinoid deficiency (CECD): can this concept explain therapeutic benefits of cannabis in migraine, fibromyalgia, irritable bowel syndrome and other treatment-resistant conditions?. Neuro Endocrinol. Lett. 25 (1-2): 31–9.
  141. Fibromyalgia. NORML (The National Organization for the Reform of Marijuana Laws). URL accessed on 2007-10-25.
  142. Kathy Longley (2004). Are phosphates the hidden enemy?. (PDF) Fibromyalgia Association UK.
  143. Bennett RM, De Garmo P, Clark SR (1996). A Randomized, Prospective, 12 Month Study To Compare The Efficacy Of Guaifenesin Versus Placebo In The Management Of Fibromyalgia. Arthritis and Rheumatism 39: S212.
    Lay summary and report:
  144. Robert Bennett. Speculation as to the mechanism whereby some of Dr. St. Amand's fibromyalgia patients experienced improvement while taking guaifenesin. Fibromyalgia Information Foundation. URL accessed on 2008-01-06.
  145. St. Amand, R. Paul (1997). A Response To The Oregon Study's Implication. Clinical Bulletin of Myofascial Therapy 2 (4).
  146. Busch A, Schachter CL, Peloso PM, Bombardier C (2002). Exercise for treating fibromyalgia syndrome. Cochrane database of systematic reviews (Online) (3): CD003786.
  147. Berman BM, Ezzo J, Hadhazy V, Swyers JP (1999). Is acupuncture effective in the treatment of fibromyalgia?. The Journal of family practice 48 (3): 213–8.
  148. Gowans SE, deHueck A (2004). Effectiveness of exercise in management of fibromyalgia. Current opinion in rheumatology 16 (2): 138–42.
  149. Gamber RG, Shores JH, Russo DP, Jimenez C, Rubin BR (2002). Osteopathic manipulative treatment in conjunction with medication relieves pain associated with fibromyalgia syndrome: results of a randomized clinical pilot project. The Journal of the American Osteopathic Association 102 (6): 321–5.
  150. 150.0 150.1 Chakrabarty, S, Zoorob R (Jul 2007). Fibromyalgia. American Family Physician 76 (2): 247–254.
  151. Sarno, Dr. John E, et al (2006). The Divided Mind: The Epidemic of Mindbody Disorders, 21–2, 235–7, 264–5, 294–8, 315, 319–20, 363, ReganBooks.
  152. Leonard-Segal, Dr. Andrea (2006). "A Rheumatologist's Experience With Psychosomatic Disorders" The Divided Mind: The Epidemic of Mindbody Disorders, 264–5, ReganBooks.
  153. 153.0 153.1 Goldenberg DL (Apr 1999). Fibromyalgia syndrome a decade later: what have we learned?. Arch Intern Med. 159 (8): 777–85.
  154. eMedicine med/790
  155. Health Information Team (2004). Fibromyalgia.
  156. Fibro-. Dictionary.com. URL accessed on 2008-05-21.
  157. Meaning of myo
  158. Meaning of algos
  159. 159.0 159.1 Winfield JB (Jun 2007). Fibromyalgia and related central sensitivity syndromes: twenty-five years of progress. Semin. Arthritis Rheum. 36 (6): 335–8.
  160. 160.0 160.1 includeonly>"Further Legitimization Of Fibromyalgia As A True Medical Condition", Science Daily, 2007-06-25. Retrieved on 2008-05-21.
  161. 161.0 161.1 Inanici F, Yunus MB (Oct 2004). History of fibromyalgia: past to present. Curr Pain Headache Rep 8 (5): 369–78.
  162. Goldenberg DL (May 1987). Fibromyalgia syndrome. An emerging but controversial condition. JAMA 257 (20): 2782–7.
  163. http://www.nytimes.com/2008/01/14/health/14pain.html
  164. White KP et al (Jun 2002). Does the label "fibromyalgia" alter health status, function, and health service utilization? A prospective, within-group comparison in a community cohort of adults with chronic widespread pain.. Arthritis Rheum. 47 (3): 260-5.
  165. 165.0 165.1 Müller W, Schneider EM, Stratz T (Sep 2007). The classification of fibromyalgia syndrome. Rheumatol Int. 27 (11): 1005–10.
  166. Thieme K, Turk DC (2006). Heterogeneity of psychophysiological stress responses in fibromyalgia syndrome patients. Arthritis Res. Ther. 8 (1): R9.
  167. Kanaan RA, Lepine JP, Wessely SC (Dec 2007). The association or otherwise of the functional somatic syndromes. Psychosom Med 69 (9): 855–9.

External linksEdit

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