Fibromyalgia

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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
[hide]

• 1 History
• 2 Incidence
• 3 Symptoms
o 3.1 Variability of symptoms
• 4 Proposed causes and pathophysiology
o 4.1 Genetics
o 4.2 Stress
o 4.3 Dopamine abnormality
 o 4.4 Serotonin
o 4.5 Sleep disturbance
o 4.6 Human growth hormone
o 4.7 Deposition disease
o 4.8 Other hypotheses
o 4.9 Always a comorbid disease?
• 5 Diagnosis
o 5.1 Differentials
• 6 Treatment
o 6.1 Medications
 6.1.1 Pain relief
 6.1.2 Muscle relaxants
 6.1.3 Tricyclic antidepressants (TCAs)
 6.1.4 Selective serotonin reuptake inhibitors (SSRIs)
 6.1.5 Anti-seizure drugs
 6.1.6 Dopamine agonists
 6.1.7 Combination therapy
 6.1.8 Central Nervous System (CNS) Stimulants
 6.1.9 Cannabis and cannabinoids
o 6.2 Topical remedies
o 6.3 Non-drug treatment
 6.3.1 Physical treatments
 6.3.2 Psychological/behavioral therapies
 6.3.3 Dietary treatment
o 6.4 Investigational treatments
• 7 Living with fibromyalgia
• 8 Controversies
• 9 References
• 10 Further reading
• 11 See also

• 12 External links

[edit] History
Fibromyalgia has been studied since the early 1800s and referred to by a variety of
former names, including muscular rheumatism and fibrositis.[4] The term fibromyalgia
was coined in 1976 to more accurately describe the symptoms, from the Latin fibra
(fiber)[5] and the Greek words myo (muscle)[6] and algos (pain).[7]

In 1981, Dr. Muhammad B. Yunus published the "first controlled study of the clinical
characteristics" of the fibromyalgia syndrome, for which he is considered "the father of
our modern view of fibromyalgia."[8][9] His work was the "first controlled clinical study"
of fibromyalgia with validation of known symptoms and tender points, and he also
proposed "the first data-based criteria." In 1984, he proposed the important concept that
the fibromyalgia syndrome and other similar conditions are interconnected. In 1986, he
showed serotonergic and norepinephric drugs to be effective.[10]

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."[8][9]

Fibromyalgia was recognized by the American Medical Association as an illness and a

cause of disability in 1987.[citation needed] In an article the same year, in the Journal of the
American Medical Association, a physician named Dr. Don Goldenberg also called the
disorder fibromyalgia.[citation needed] The ACR published a criteria for fibromyalgia in 1990,
and developed neurohormonal mechanisms with central sensitization in the 1990s.[10]

[edit] Incidence
It affects more females than males, with a ratio of 9:1 by American College of
Rheumatology (ACR) criteria.[11] Fibromyalgia is seen in about 2% of the general
population.[12] It is most commonly diagnosed in individuals between the ages of 20 and
50, though onset can occur in childhood.

[edit] Symptoms
The defining symptoms of fibromyalgia are chronic, widespread pain and tenderness to
light touch. There is also typically moderate to severe fatigue. Those affected may also
experience heightened sensitivity of the skin (also called allodynia), tingling of the skin
(often needle-like), achiness in the muscle tissues, prolonged muscle spasms, weakness in
the limbs, and nerve pain. Chronic sleep disturbances are also characteristic of
fibromyalgia. Indeed, studies suggest that sleep disturbances are related to a phenomenon
called alpha-delta sleep, a condition in which deep sleep (associated with delta EEG
waves) is frequently interrupted by bursts of brain activity similar to wakefulness (i.e.
alpha waves). Deeper stages of sleep (stages 3 & 4) are often dramatically reduced.

An example of tactile allodynia is when a person perceives light pressure or the

movement of clothes over the skin as painful, whereas a healthy individual would not feel
pain. Fibromyalgia patients are often affected by a number of symptoms other than pain,
including debilitating fatigue, abnormal sleep architecture, [13] (meaning the brain does
not reach all the restorative levels of sleep necessary for overall health), functional bowel
disturbances,[14] and a variety of neuropsychiatric problems including cognitive
dysfunction, [15] which can mean short and/or long term memory problems, slowed
information processing ability, diminished attention span and anxiety and depressive
symptoms.[16]
In addition, many patients experience cognitive dysfunction (known as "brain fog" or
"fibrofog"), which may be characterized by impaired concentration and short-term
memory consolidation, impaired speed of performance, inability to multi-task, and
cognitive overload.[17][18] Many experts suspect that "brain fog" is directly related to the
sleep disturbances experienced by sufferers of fibromyalgia.[citation needed]

Other symptoms often attributed to fibromyalgia that may possibly be due to a comorbid
disorder include myofascial pain syndrome, diffuse non-dermatomal paresthesias,
functional bowel disturbances and irritable bowel syndrome (possibly linked to lower
levels of ghrelin[2], genitourinary symptoms and interstitial cystitis), dermatological
disorders, headaches, myoclonic twitches, and symptomatic hypoglycemia. Although
fibromyalgia is classified based on the presence of chronic widespread pain, pain may
also be localized in areas such as the shoulders, neck, low back, hips, or other areas.
Many sufferers also experience varying degrees of facial pain and have high rates of
comorbid temporomandibular joint disorder. Not all patients have all symptoms.

Symptoms can have a slow onset, and many patients have mild symptoms beginning in
childhood, that are often misdiagnosed as growing pains.[citation needed] Symptoms are often
aggravated by unrelated illness or changes in the weather.[citation needed]They can become
more tolerable or less tolerable throughout daily or yearly cycles; however, many people
with fibromyalgia find that, at least some of the time, the condition prevents them from
performing normal activities such as driving a car or walking up stairs. The disorder does
not cause inflammation as is characteristic of rheumatoid arthritis, although some
NSAIDs may temporarily reduce pain symptoms in some patients. Their use, however, is
limited, and often of little to no value in pain management.[19]

[edit] Variability of symptoms

The following factors have been proposed to exacerbate symptoms of pain in patients:

• Increased psychosocial stress Meador, MD, Clifton K. (May 2008). Puzzling

Symptoms. Cable Publishing. ISBN 13:978-1-934980-11-8.
• Excessive physical exertion (exercise seems to decrease the pain threshold of
people with fibromyalgia but increase it in healthy individuals)[20]
• Lack of slow-wave sleep
• Changes in humidity and barometric pressure[citation needed]

[edit] Proposed causes and pathophysiology

The cause of fibromyalgia is unknown. Fibromyalgia can, but does not always, start as a
result of some trauma such as a traffic accident, major surgery, or disease. Some evidence
shows that Lyme Disease may be a trigger of fibromyalgia symptoms.[21] Another study
suggests that more than one clinical entity may be involved, ranging from a mild,
idiopathic inflammatory process to clinical depression[22]
[edit] Genetics

By using self-reported "Chronic Widespread Pain" (CWP) as a surrogate marker for

fibromyalgia, the Swedish Twin Registry found that a modest genetic contribution may
exist:[23][24]

• Monozygotic twins with CWP have a 15% chance that their twin sibling has CWP
• Dizygotic twins with CWP have a 7% chance that their twin sibling has CWP

[edit] Stress

Studies have shown that stress is a significant precipitating factor in the development of
fibromyalgia,[25] and that PTSD is linked with fibromyalgia.[26][27] The Amital study found
that 49% of PTSD patients fulfilled the criteria for FMS, compared with none of the
controls.

A non-mainstream hypothesis that fibromyalgia may be a psychosomatic illness has been

described by John E. Sarno's "tension myositis syndrome". He believes many cases of
chronic pain result from changes in the body caused by the mind's subconscious strategy
of distracting painful or dangerous emotions. Education, attitude change, and, in some
cases, psychotherapy are treatments proposed to stop the brain from using that
strategy.[28][29][30][31]

[edit] Dopamine abnormality

Dopamine is a catecholamine neurotransmitter perhaps best known for its role in the
pathology of schizophrenia, Parkinson's disease and addiction. There is also strong
evidence for a role of dopamine in restless leg syndrome [32], which is a common co-
morbid condition in patients with fibromyalgia. [33] 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 [34], 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.[35][36] Interestingly, patients with restless legs syndrome have
also been demonstrated to have hyperalgesia to static mechanical stimulation.[37]

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.[38][39] It was
therefore proposed that fibromyalgia may represent a condition characterized by low
levels of central dopamine that likely results from a combination of genetic factors and
exposure to environmental stressors, including psychosocial distress, physical trauma,
systemic viral infections or inflammatory disorders (e.g. rheumatoid arthritis, systemic
lupus erythematosus).[40] This conclusion was based on three key observations: (1)
fibromyalgia is associated with stress; (2) chronic exposure to stress results in a
disruption of dopamine-related neurotransmission[41]; and (3) dopamine plays a critical
role in modulating pain perception and central analgesia in such areas as the basal
ganglia[42] including the nucleus accumbens[43], insular cortex[44], anterior cingulate
cortex[45], thalamus[46], periaqueductal gray[47], and spinal cord[48] [49].

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.[50] 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)[51], fibromyalgia patients fail to release dopamine in
response to pain and, in some cases, actually have a reduction in dopamine levels during
painful stimulation. [52] 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.[53] Trials of other dopamine agonists are currently ongoing.

[edit] Serotonin

Serotonin is a neurotransmitter that is known to play a role in regulating sleep patterns,

mood, feelings of well-being, concentration and descending inhibition of pain.
Accordingly, it has been hypothesized that the pathophysiology underlying the symptoms
of fibromyalgia may be a dysregulation of serotonin metabolism, which may explain (in
part) many of the symptoms associated with the disorder. This hypothesis is derived in
part by the observation of decreased serotonin metabolites in patient plasma [54] and
cerebrospinal fluid.[55] 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[56]. 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.[57] 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.[58]

[edit] Sleep disturbance

Electroencephalography studies have shown that people with fibromyalgia lack slow-
wave sleep and circumstances that interfere with stage four sleep (pain, depression,
serotonin deficiency, certain medications or anxiety) may cause or worsen the
condition.[59] According to the sleep disturbance hypothesis, an event such as a trauma or
illness causes sleep disturbance and possibly initial chronic pain that may initiate the
disorder. The hypothesis supposes that stage 4 sleep is critical to the function of the
nervous system, as it is during that stage that certain neurochemical processes in the body
'reset'. In particular, pain causes the release of the neuropeptide substance P in the spinal
cord which has the effect of amplifying pain and causing nerves near the initiating ones to
become more sensitive to pain. Under normal circumstances, areas around a wound to
become more sensitive to pain but if pain becomes chronic and body-wide this process
can run out of control. The sleep disturbance hypothesis holds that deep sleep is critical to
reset the substance P mechanism and prevent this out-of-control effect.

The sleep disturbance/substance P hypothesis could explain "tender points" that are
characteristic of fibromyalgia but which are otherwise enigmatic, since their positions
don't correspond to any particular set of nerve junctions or other obvious body
structures.[citation needed] The hypothesis proposes that these locations are more sensitive
because the sensory nerves that serve them are positioned in the spinal cord to be most
strongly affected by substance P. This hypothesis could also explain some of more
general neurological features of fibromyalgia, since substance P is active in many other
areas of the nervous system. The sleep disturbance hypothesis could also provide a
possible connection between fibromyalgia, chronic fatigue syndrome (CFS) and post-
polio syndrome through damage to the ascending reticular activating system of the
reticular formation. This area of the brain, in addition to apparently controlling the
sensation of fatigue, is known to control sleep behaviors and is also believed to produce
some neuropeptides, and thus injury or imbalance in this area could cause both CFS and
sleep-related fibromyalgia.

Critics of the hypothesis argue that it does not explain slow-onset fibromyalgia,
fibromyalgia present without tender points, or patients without heightened pain
symptoms, and a number of the non-pain symptoms present in the disorder.[citation needed]

[edit] Human growth hormone

An alternate hypothesis suggests that stress-induced problems in the hypothalamus may

lead to reduced sleep and reduced production of human growth hormone (HGH) during
slow-wave sleep. People with fibromyalgia tend to produce inadequate levels of HGH.
Most patients with FM with low IGF-I levels failed to secrete HGH after stimulation with
clonidine and l-dopa.[citation needed]

This view is supported by the fact that those hormones under the direct or indirect control
of HGH, including IGF-1, cortisol, leptin and neuropeptide Y are abnormal in people
with fibromyalgia,[60] In addition, treatment with exogenous HGH or growth hormone
secretagogue reduces fibromyalgia related pain and restores slow wave sleep[61][62][63][64]
though there is disagreement about the proposition.[65]

[edit] Deposition disease

The 'deposition hypothesis of fibromyaglia' posits fibromyalgia is due to intracellular

phosphate and calcium accumulations that eventually reaches levels sufficient to impede
the ATP process, possibly caused by a kidney defect or missing enzyme that prevents the
removal of excess phosphates from the blood stream. Accordingly, proponents of this
hypothesis suggest that fibromyalgia may be an inherited disorder, and that phosphate
build-up in cells is gradual but can be accelerated by trauma or illness. Calcium is
required for the excess phosphate to enter the cells.[citation needed]The additional phosphate
slows down the ATP process; however the excess calcium prods the cell to continue
producing ATP.[66]

Diagnosis is made with a specialized technique called mapping, a gentle palpitation of the
muscles to detect lumps and areas of spasm thought to be caused by an excess of calcium
in the cytosol of the cells. The mapping technique is notably different from the manual
tenderpoint examination[67] upon which a diagnosis of fibromyalgia depends and is
purportedly different from the detection of trigger points that characterize the myofascial
pain syndrome.[citation needed]

While this hypothesis does not identify the causative mechanism in the kidneys, it
proposes a treatment known as guaifenesin therapy. This treatment involves
administering the drug guaifenesin to a patient's individual dosage, avoiding salicylic
acid in medications or on the skin. Often products for salicylate sensitivity are very
helpful. If the patient is also hypoglycemic, a diet is designed to keep insulin levels low.

The phosphate build-up hypothesis explains many of the symptoms present in

fibromyalgia.[citation needed]and proposes an underlying cause. The guaifenesin treatment,
based on this hypothesis, has received mixed reviews, with some practitioners claiming
many near-universal successes[citation needed] and others reporting no success. Of note,
guaifenesin is also a central acting muscle relaxant used in veterinary anaesthesia[68] 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. [69] 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.[70] As of 2005, further studies to test the protocol's
effectiveness are in the planning stages, with funding for independent studies largely
collected from groups which advocate the hypothesis. It should be noted that nothing in
the scientific literature supports the proposition that fibromyalgia patients have excessive
levels of phosphate in their tissues.

[edit] Other hypotheses

Other hypotheses have been proposed related to various toxins from the patient's
environment, viral causes such as the Epstein-Barr Virus, growth hormone deficiencies
possibly related to an underlying (maybe autoimmune) disease affecting the
hypothalamus gland, an aberrant immune response to intestinal bacteria,[71][72]
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.[73][74] This association has
not repeated in a number of related studies,[75] 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."[76] Due to the multi-systemic nature of
illnesses such as fibromyalgia and chronic fatigue syndrome (CFS/ME), an emerging
branch of medical science called psychoneuroimmunology (PNI) is looking into how the
various hypotheses fit together.

Another hypothesis on the cause of symptoms in fibromyalgia states that patients suffer
from vasomotor dysregulation causing improper vascularflow and hypoperfusion
(decreased blood flow to a given tissue or organ).[77]

[edit] Always a comorbid disease?

Cutting across several of the above hypotheses is the proposition that fibromyalgia is
almost always a comorbid disorder, occurring in combination with some other disorder
that likely served to "trigger" the fibromyalgia in the first place. Two possible triggers are
gluten sensitivity and/or irritable bowel. Irritable bowel is found at high frequency in
fibromyalgia,[78] and a large coeliac support group survey of adult celiacs revealed that
7% had fibromyalgia and also has a co-occurrence with chronic fatique.[79]

According to this hypothesis, some other disorder (or trauma) occurs first, and
fibromyalgia follows as a result. In some cases, the original disorder abates on its own or
is separately treated and cured, but the fibromyalgia remains. This is especially apparent
when fibromyalgia seems triggered by major surgery. In other cases the two disorders
coexist.

[edit] Diagnosis
There is still debate over what should be considered essential diagnostic criteria. The
most widely accepted set of classification criteria for research purposes were elaborated
in 1990 by the Multicenter Criteria Committee of the the American College of
Rheumatology. These criteria, which are known informally as "the ACR 1990" define
fibromyalgia according to the presence of the following criteria:

• A history of widespread pain lasting more than three months—affecting all four
quadrants of the body, i.e., both sides, and above and below the waist.
• Tender points—there are 18 designated possible tender or trigger points (although
a person with the disorder may feel pain in other areas as well). During diagnosis,
four kilograms-force (39 newtons) of force is exerted at each of the 18 points; the
patient must feel pain at 11 or more of these points for fibromyalgia to be
considered.[80] Four kilograms of force is about the amount of pressure required to
blanch the thumbnail when applying pressure. This set of criteria was developed
by the American College of Rheumatology as a means of classifying an individual
as having fibromyalgia for both clinical and research purposes. While these
criteria for classification of patients were originally established as inclusion
criteria for research purposes and were not intended for clinical diagnosis, they
 have become the de facto diagnostic criteria in the clinical setting. It should be
noted that the number of tender points that may be active at any one time may
vary with time and circumstance.

[edit] Differentials

A number of other disorders can produce similar symptoms to fibromyalgia:

• Chronic fatigue • Lupus erythematosus • Thyroid disease

syndrome • Lyme disease • Vitamin B12
• Depression • Mercury poisoning deficiency
• Ehlers-Danlos • Myofascial pain • Vitamin D deficiency
syndrome syndrome • Whiplash-associated
• Gulf War syndrome disorder
• Influenza • Tendinitis
• Multiple chemical
• Lead poisoning sensitivity

[edit] Treatment
As with many other syndromes, there is no universally accepted cure for fibromyalgia,
though some physicians claim to have found cures.[81] 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 guidelines[82] for the
treatment of fibromyalgia syndrome (FMS) and published them in the September 17th
On-line First issue of the Annals of the Rheumatic Diseases.

[edit] Medications

Many medications are used to treat specific symptoms of fibromyalgia, such as muscle
pain and insomnia.

[edit] Pain relief

A number of pain relievers have been prescribed for fibromyalgia. This includes NSAID
medications over the counter, COX-2 inhibitors, and tramadol in prescription form for
more advanced cases. Recently, pregabalin (marketed as Lyrica) has been given FDA
approval for the treatment of diagnosed Fibromyalgia.[83]

[edit] Muscle relaxants

Muscle relaxants, such as cyclobenzaprine (Flexeril) or tizanidine (Zanaflex), may be
used to treat the muscle pain associated with the disorder.[84][85][86]

[edit] Tricyclic antidepressants (TCAs)

Traditionally, low doses of sedating antidepressants (e.g. amitriptyline and trazodone)

have been used to reduce the sleep disturbances that are associated with fibromyalgia and
are believed by some practitioners to alleviate the symptoms of the disorder. Because
depression often accompanies chronic illness, these antidepressants may provide
additional benefits to patients suffering from depression. Amitriptyline is often favoured
as it can also have the effect of providing relief from neuralgenic or neuropathic
pain.[citation needed] It is to be noted that Fibromyalgia is not considered a depressive disorder;
antidepressants are used for their sedating effect to aid in sleep.

[edit] Selective serotonin reuptake inhibitors (SSRIs)

Research data consistently contradict the utility of agents with specificity as serotonin
reuptake inhibitors for the treatment of core symptoms of fibromyalgia. [87][88][89]
Moreover, SSRIs are known to aggravate many of the comorbidities that commonly
affect patients with fibromyalgia including restless legs syndrome and sleep
bruxism[90][91][92].

[edit] Anti-seizure drugs

Anti-seizure drugs are also sometimes used, such as gabapentin[93] 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.[94]

[edit] Dopamine agonists

Dopamine agonists (e.g. pramipexole (Mirapex) and ropinirole(ReQuip)) have been

studied for use in the treatment of fibromyalgia with good results. [95] A trial of
transdermal rotigotine is currently on going [96].

[edit] Combination therapy

A controlled clinical trial of amitriptyline and fluoxetine demonstrated utility when used
in combination.[97]

[edit] Central Nervous System (CNS) 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,
Provigil, Methylphenidate (Ritalin, Ritalin SR, Methylin, Methylin ER.) These non-
amphetamine stimulants are also used to treat the chronic fatigue that is characteristic of
fibromyalgia.[98] [99]

Stimulants may be habit forming and can have other serious side effects, so it is
important to note that other treatments may be effective.[100] Care should be taken with
any prescription, as people with fibromyalgia are known to be sensitive to medications.
[101]

[edit] Cannabis and cannabinoids

Fibromyalgia patients frequently self-report using cannabis therapeutically to treat

symptoms of the disorder.[102] 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.[103] Previous clinical and preclinical
trials have shown that both naturally occurring and endogenous cannabinoids hold
analgesic qualities,[104] particularly in the treatment of cancer pain and neuropathic
pain,[105][106] 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.[107][108]

[edit] Topical remedies

Users of Epsom Salts in the gel form (Magnesium Sulfate), have reported significant and
lasting relief from pain associated with fibromyalgia. Epsom Salts have long been touted
for their ability to reduce pain and swelling. [109]

[edit] Non-drug treatment

[edit] Physical treatments

Studies have found exercise improves fitness and sleep and may reduce pain and fatigue
in some people with fibromyalgia.[110] Many patients find temporary relief by applying
heat to painful areas. Those with access to physical therapy, massage, or acupuncture
may find them beneficial.[111] Most patients find exercise, even low intensity exercise to
be extremely helpful.[112] Osteopathic manipulative therapy can also temporarily relieve
pain due to fibromyalgia.[113]

A holistic approach—including managing diet, sleep, stress, activity, and pain—is used
by many patients. Dietary supplements, massage, chiropractic care, managing blood
sugar levels, and avoiding known triggers when possible means living as well as it is in
the patient's power to do.[citation needed]

[edit] Psychological/behavioral therapies

As the nature of fibromyalgia is not well understood, some physicians believe that it may
be psychosomatic or psychogenic.[114] Although there is no universally accepted cure,
some doctors have claimed to have successfully treated fibromyalgia when a
psychological cause is accepted.[115]

Cognitive behavioral therapy has been shown to improve quality of life and coping in
fibromyalgia patients and other sufferers of chronic pain.[12] Neurofeedback has also
shown to provide temporary and long-term relief.

Biofeedback and self-management techniques such as pacing and stress management may
be helpful for some patients. The use of medication to improve sleep helps some patients,
as does supplementation with folic acid and ginkgo biloba.[citation needed]

[edit] Dietary treatment

In a 2001 review of four case studies, symptom alleviation was found by minimizing
consumption of monosodium glutamate.[116]

[edit] Investigational treatments

Milnacipran, a serotonin-norepinephrine reuptake inhibitor (SNRI), is available in parts

of Europe where it has been safely prescribed for other disorders. On May 22nd, 2007, a
Phase III study demonstrated statistically significant therapeutic effects of Milnacipran as
a treatment of fibromyalgia syndrome. At this time, only initial top-line results are
available and further analyses will be completed in the coming weeks. If ultimately
approved by the FDA, Milnacipran could be distributed in the United States as early as
summer, 2008.[117]

Among the more controversial therapies involves the use of guaifenesin; called St.
Amand's protocol or the guaifenesin protocol[66] 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,[69] and the lead researcher
has suggested that the anecdotally reported benefits where due to placebo suggestion.[118]
The results of the study have since been contested by Dr St. Amand, who was a co-author
or the original research report.[119]

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[120][121]; however, there are no controlled trials of safety or efficacy in
clinical use.
[edit] Living with fibromyalgia
Fibromyalgia can affect every aspect of a person's life. While neither degenerative nor
fatal, the chronic pain associated with fibromyalgia is pervasive and persistent. FMS can
severely curtail social activity and recreation, and as many as 30% of those diagnosed
with fibromyalgia are unable to maintain full-time employment.[citation needed] Like others
with disabilities, individuals with FMS often need accommodations to fully participate in
their education or remain active in their careers.

In the United States, those who are unable to maintain a full-time job due to the condition
may apply for Social Security Disability benefits. Although fibromyalgia has been
recognized as a genuine, severe medical condition by the government, applicants are
often denied benefits, since there are no formal diagnostic criteria or medically provable
symptoms.

In the United Kingdom, the Department for Work and Pensions recognizes fibromyalgia
as a condition for the purpose of claiming benefits and assistance.[122]

Fibromyalgia is often referred to as an "invisible" illness or disability due to the fact that
generally there are no outward indications of the illness or its resulting disabilities. The
invisible nature of the illness, as well as its relative rarity and the lack of understanding
about its pathology, often has psychosocial complications for those that have the disorder.
Individuals suffering from invisible illnesses in general often face disbelief or accusations
of malingering or laziness from others that are unfamiliar with the disorder.

There are a variety of support groups on the Web that cater to fibromyalgia sufferers.

[edit] 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 which is the difference between an individual’s heredity and
what that heredity produces, may result from several different disease processes that have
global hyperalgesia - an increased sensitivity to pain - and allodynia in common,
[123][124][125]
an observation that has led to the proposition that current diagnostic criteria are
insufficient to differentiate patient groups from each other.[126] Alternatively, there is
evidence for the existence of differing pathophysiological processes within the greater
fibromyalgia construct[127][128], which may be interpreted to represent evidence for the
existence of biologically distinct "sub-types" of the disorder akin to conditions such as
epilepsy, schizophrenia and major depressive disorder. In a January 14, 2008 article in
the New York Times, the controversy of the reality of the disease and its proposed cures
are discussed, while citing that the American College of Rheumatology, the Food and
Drug Administration and insurers recognize fibromyalgia as a diagnosable disease. Drug
companies are aggressively pursuing fibromyalgia treatments, seeing the potential for a
major new market.[83]

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[edit] Further reading

• Fibromyalgia for Pharmacists, a medication guide

[edit] See also

• Somatosensory Amplification

[edit] External links

• American College of Rheumatology Fibromyalgia factsheet
• Living with Fibromyalgia, First Drug 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
 [hide]
v•d•e
Diseases of the musculoskeletal system and connective tissue (M, 710-739)

Arthritis (Septic arthritis, Reactive arthritis, Rheumatoid

arthritis, Psoriatic arthritis, Felty's syndrome, Juvenile
idiopathic arthritis, Still's disease) - crystal (Gout,
Chondrocalcinosis) - Osteoarthritis (Heberden's node,
Bouchard's nodes)

acquired deformities of fingers and toes (Boutonniere

Arthropathies deformity, Bunion, Hallux rigidus, Hallux varus, Hammer
toe) - other acquired deformities of limbs (Valgus deformity,
Varus deformity, Wrist drop, Foot drop, Flat feet, Club foot,
Unequal leg length, Winged scapula)

patella (Luxating patella, Chondromalacia patellae)

Protrusio acetabuli - Hemarthrosis - Arthralgia - Osteophyte

vasculitis: Polyarteritis nodosa - Churg-Strauss syndrome -

Kawasaki disease - Hypersensitivity vasculitis -
Goodpasture's syndrome - Wegener's granulomatosis -
Arteritis (Takayasu's arteritis, Temporal arteritis) -
Microscopic polyangiitis
Systemic CT disorders
Systemic lupus erythematosus (Drug-induced) -
Dermatomyositis (Juvenile dermatomyositis) - Polymyositis
- Scleroderma - Sjögren's syndrome - Behçet's disease -
Polymyalgia rheumatica - Eosinophilic fasciitis -
Hypermobility

Kyphosis - Lordosis - Scoliosis - Scheuermann's disease -

Spondylolysis - Torticollis - Spondylolisthesis -
Spondylopathies (Ankylosing spondylitis, Spondylosis,
Dorsopathies
Spinal stenosis) - Schmorl's nodes - Degenerative disc
disease - Coccydynia - Back pain (Radiculopathy, Neck
pain, Sciatica, Low back pain)

muscle: Myositis (Pyomyositis) - Myositis ossificans

(Fibrodysplasia ossificans progressiva)

synovium and tendon: Synovitis/Tenosynovitis (Calcific

tendinitis, Stenosing tenosynovitis, Trigger finger,
DeQuervain's syndrome) - Irritable hip - Ganglion cyst

bursa: bursitis (Olecranon, Prepatellar, Trochanteric) -

Retrieved from "http://en.wikipedia.org/wiki/Fibromyalgia"
Categories: Rheumatology | Diseases involving the fasciae | Syndromes | Ailments of
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