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2008v17n2

Fibromyalgia Frontiers • 2010 (Volume 18, Number 1) Pathophysiology & Treatment
A GUIDE FOR PATIENTS & PHYSICIANS
By Russell Rothenberg, M.D.
Fibromyalgia remains an enigma to many term "fibrositis" in 1904. In 1978, Drs. Smythe and physicians despite its high prevalence in the U.S.
Moldofsky published the first scientific research on population. Why do people chronically hurt all over, the associated sleep pathology and the peripheral and feel fatigued, and wake up feeling non-rested despite central nervous system (CNS) pain sensitization that getting 6-8 hours of sleep? Why do these symptoms are important parts of the pathophysiology of FM.1 It often appear to coexist with painful bowel, bladder, was renamed fibromyalgia syndrome in 1990 with the and jaw (TMJ) symptoms, as well as symptoms of publication of official diagnostic criteria by the ACR.2 anxiety and cognitive impairment? The term Only recently have we learned that FM is pre- fibromyalgia (FM) was defined in 1990 by the dominately caused by abnormalities in CNS pain American College of Rheumatology (ACR). Since sensitization and abnormal levels of neurotransmitters then, the National Institutes of Health and other and pain processing in the pain centers of the brain institutions have dramatically increased their funding and spinal cord.
for FM research, and there have been significant FM is a relatively common illness estimated to increases in published articles on fibromyalgia and affect 4-10 million Americans. Demographic studies medical conferences that include FM research and show that it has a prevalence in the U.S. of 3 ½ % of treatment in the curriculum.
all women and ½ % of all men over the age of 18 The major purpose of this article is to provide years. These figures are similar to the prevalence of information that patients can take to their doctors to FM in other countries. It has been estimated that help them make an accurate diagnosis of fibromyalgia 10-20% of patients in a rheumatologist's practice have earlier and provide more effective treatment. With the FDA-approved drugs for FM as well as other There is a strong association between fibro- treatments shown to be effective for FM in scientific myalgia and many of the diseases rheumatologists studies, doctors can help most FM patients. This treat (rheumatoid arthritis, osteoarthritis, Sjögren's article can also be used to provide objective scientific syndrome, and systemic lupus) as well as certain evidence for doctors who still are uncertain whether infections (hepatitis C and Lyme disease). There is fibromyalgia is a real medical entity. I've treated over also a primary form of FM which appears to have 8,000 patients with FM and hope my experience can a genetic basis that can affect multiple members of help patients and doctors. Since my first article on certain families.
this subject published in 2007 in Fibromyalgia Despite all of the recent advances in the Frontiers, there have been significant advances in understanding of FM, the problem many patients still research and treatment.
experience is a long delay between the onset of their Fibromyalgia is not a new medical problem, it is symptoms and their diagnosis of FM. Since patients just better understood. It used to be called different often have multiple symptoms, and there are no names: "neurasthenia" and "muscular rheumatism" objective lab tests or imaging studies that are from the mid-1800's until Dr. Gowers created the National Fibromyalgia Partnership, Inc. (NFP). • www.fmpartnership.org Fibromyalgia Frontiers • 2010 (Volume 18, Number 1) commercially available to make the diagnosis, they anatomically specific tender points (See Figure 1) and often face years of multiple medical evaluations, requires the history of widespread pain being present multiple specialists, a lot of frustration and suffering, for at least three months. These tender points can be and no answers. It would benefit the FM patient if assessed by pressing on specific locations of the body more primary care doctors considered fibromyalgia with a pressure of 4 kg/m2 (enough pressure to blanch in their differential diagnosis when a patient presents the skin under the thumb nail). Pressing on these painful with chronic pain and fatigue.
points can cause a very painful response, and the FM is not an easy diagnosis to make. A careful doctor should press gently initially and stop when it history and complete physical examination are hurts. The tender point exam is a good diagnostic test necessary to make the diagnosis. It is essential for a (88.4% sensitive and 81.1% specific to FM),5 but doctor to do an adequate medical evaluation to "rule tender points are not the only tender areas FM patients out" other diseases that can mimic FM such as have. They also have generalized increased pain to hypothyroidism and rheumatic disease. There are also normal touch all over the body (allodynia). It is very numerous co-morbid conditions that can be the first upsetting not to want to be touched or hugged by your symptoms to appear in FM patients including irritable loved ones, but that is what FM patients experience.
bowel syndrome, interstitial cystitis, vulvodynia, Research doctors have shown in studies that the temporomandibular joint syndrome, chronic fatigue tender point exam is reproducible in FM patients. Dr.
syndrome, hyper-extensible joints/Ehlers Danlos Bradley has demonstrated that lower pain threshold Syndrome, non-restorative sleep disturbances, and responses to thermal stimuli consistently are present neurally mediated hypotension. When the diagnosis in FM patients compared to normal controls, and this of a patient with chronic musculoskeletal pain and scientific finding has been reproduced by Dr. Geisser.6 fatigue is unclear, rheumatologists are available for Drs. Gracely and Clauw have demonstrated with functional brain MRI's that a FM patient's responseto painful stimuli consistently activates the areas of the Scientific Findings That Support
brain associated with pain recognition at lower pain Fibromyalgia As A Medical Entity
thresholds than in normal controls.7 Tender Point Exam & Pain Threshold Studies
The ACR definition of fibromyalgia includes the Fatigue is an important FM symptom, and it is often identification of at least 11 of a possible 18 multi-modal in cause. Chronic pain, non-restorative OCCIPUT: bilateral, at the suboccipital muscle
LOW CERVICAL: bilateral, at the anterior aspects of
the intertransverse spaces at C5-C7.
TRAPEZIUS: bilateral, at the midpoint of the upper
border.
SUPRASPINATUS: bilateral, at origins, above the
scapula spine near the medial border.
SECOND RIB: bilateral, at the second costochondral
junctions, just lateral to the junctions on upper
surfaces.
LATERAL EPICONDYLE: bilateral, 2 cm distal to the
epicondyles.
GLUTEAL: bilateral, in upper outer quadrants of
buttocks in anterior fold of muscle.
GREATER TROCHANTER: bilateral, posterior to the
KNEE: bilateral, at the medial fat pad proximal to the
joint line.
National Fibromyalgia Partnership, Inc. (NFP). • www.fmpartnership.org Fibromyalgia Frontiers • 2010 (Volume 18, Number 1) sleep disturbances, autonomic nervous system dysfunction, chronic anxiety and depression, Myofascial pain is a big problem for many FM exercise deconditioning, sedative effects of patients. Patients with this condition get palpable prescribed medications, and poor management of "knots" in their muscles and soft tissues that cause available energy can cause patients to be fatigued.
significant pain which at first glance may be mistaken While sleep medications such as zolpidem (Ambien) for painful muscle spasms. I have had patients that induce sleep while preserving normal sleep misdiagnosed as having fibrocystic breast disease who architecture are effective in treating the fatigue of really had tender myofascial nodules in their breast fibromyalgia, they are not effective in treating FM tissue that could be eliminated with massage therapy pain for most patients.
techniques! I've seen orthopedic surgeons want to The sleep abnormalities in FM are reproducible operate on moderately severe osteoarthritis of the knee in overnight sleep studies (this test may be ordered when the real problem was severe myofascial pain but is not necessary for the diagnosis of FM). One around the knee that responded to medication and sees alpha wave intrusion in delta sleep and a physical therapy.
decrease in stage 3 and 4 sleep in many FM patients Doctors of physical medicine and rehabilitation (though these findings may not be present in treated often describe myofascial pain as originating in painful patients). These findings appear to be responsible tissue which contains nodules associated with "trigger for the non-restorative sleep and daytime som- points" (not to be confused with the diagnostic "tender nolence often described by those with fibromyalgia, points" of fibromyalgia!) which are palpable, tense, and they can also be seen in patients with or taut bands of muscle and surrounding tissue. These rheumatoid arthritis, osteoarthritis, and Sjögren's trigger points are often so painful that the patient is syndrome as well as other illnesses.8 very uncomfortable. There can also be "latent triggerpoints" that the patient doesn't report as tender, but can be very painful upon examination. Trigger points There is a growing body of scientific evidence which are typically associated with a referred pain pattern, suggests that a subset of FM patients have genetic sometimes at distant sites from the primary pain source, factors that predispose them to develop FM. Dr.
(See Figure 2) and are responsible for musculoskeletal Arnold and colleagues showed that the first-degree stiffness, weakness, and limitation of motion.
relatives of FM patients had an eight-fold greater risk Scientific evidence has demonstrated that painful of developing FM than did the general population.9 myofascial tissue has increased levels of the pain These patients tend to have primary FM which has neurotransmitters Substance P and glutamate as well usually been present since the teenage years, though as other mediators of pain and inflammation.12,13 Dr.
the symptoms may not be clinically apparent until the Jay Shah at the NIH is involved in much of the recent patient is exposed to significant physical or emotional investigations into the pathophysiology of these stressors. Secondary FM is usually secondary to an palpable, hyperirritable nodules that cause myofascial overwhelming infection, injury, or a significant pain- pain.13 There appears to be an association between generating problem that causes increased CNS pain myofascial pain and low levels of Vitamin B12 and D called central sensitization. Genetic abnormalities in as well as iron deficiency, and these common the serotonin transporter promoter gene have been deficiencies should be treated if present in FM noted in FM.10 Patients with adequate serotonin transporter promoter genes seem to be lesssusceptible to the adverse effects of chronic stress Autonomic Nervous System Abnormalities
and depressive events. Another gene, catecholamine- There is research that suggests that autonomic 0- methyltransferase (COMT) has been shown to be nervous system dysfunction, which includes associated with pain regulation and myofascial pain increased sympathetic tone, is an important factor of the jaw, and there is an increased association of in the pathophysiology of FM as well.14 FM COMT deficiency in FM patients.11 National Fibromyalgia Partnership, Inc. (NFP). • www.fmpartnership.org

Fibromyalgia Frontiers • 2010 (Volume 18, Number 1) patients commonly have autonomic nervous system abnormalities that make them vulnerable tocoexistent conditions such as neurally-mediated Examples Of
hypotension/reduced heart rate variability, irritablebowel and bladder syndromes, and vascular headaches. Autonomic dysfunction may be partially Points & Their
due to neuroendocrine abnormalities in the hypothalamic-pituitary-adrenal (HPA) axis foundin FM. Documented abnormalities include low AM Zones Of Referred
cortisol and 24-hour urinary cortisol levels, Pain In The Body*
inappropriately high levels of adrenocortical trophic Trapezius Muscle Trigger Points hormones (ACTH), and failure to suppress ACTHwith dexamethasone. The physician needs to beaware of the need to treat neurally-mediatedhypotension in FM patients with adequate salt andfluids as well as explaining the need for conservationof energy. If the hypotension is more severe,cardiac consultation for tilt table testing can berequested.
Central Sensitization, CNS "Windup" &
Trapezius Muscle Trigger Points Hyperalgesia
The central nervous system is the major source of
pain in FM, and treatment of CNS pain is essential.
FM patients get a phenomenon called central
Supraspinatus Muscle sensitization, the amplification of CNS pain transmission and processing, that causes hyperalgesia(increased sensitivity to pain) and allodynia (painfulperception of normal situations). We now understandthat increased afferent pain pathways in the CNS areassociated with elevated levels of the neurotransmittersSubstance P and glutamate. There is also a reductionof pain modulating neurotransmitters (serotonin andnorepinephrine) in the descending CNS pain pathwaysthat normally dampen pain transmission. Theseabnormal changes occur in the dorsal horn of the spinalcord and contribute to the hyperalgesic state.
Functional brain MRI studies show increased painprocessing activity in the brain in response to noxiousstimuli in FM, confirming central sensitization.
Drs. Price and Staud have demonstrated that with increasing nociceptive inputs, there is an increased Sternocleidomastoid Muscle Trigger Points temporal summation of CNS pain discharges or"windup."15 This increased activity of the nociceptive *Trigger points are marked by "X's" above. Pain referral
neurons in the spinal cord involves increased NMDA zones are marked by solid blotches of dark ink with
receptor activity and neural plasticity of nociceptive stippling showing spillover portions of pain.
spinal cord pathways, and it is an important factor in National Fibromyalgia Partnership, Inc. (NFP). • www.fmpartnership.org Fibromyalgia Frontiers • 2010 (Volume 18, Number 1) central sensitization. The pain in FM is not due to the physician use inflammation, and traditional pain medications such to assess the sta- as non-steroidal anti-inflammatory drugs (NSAID's) tus of the FM pa- or corticosteroids which treat pain and inflammation tient? First, it is are not effective in treating FM pain.16 important for thephysician to see Treatment of Fibromyalgia By The
the patient oftenuntil his or her Patient's Primary Care Doctor
I've listed below some of the most commonly prescribed treatments for FM. I've tried to emphasize the patient keep a the FDA- approved drugs and other evidence-based, pain and activity successful therapies. No one therapy is successful for all FM patients. It is very important for physicians to see patients on a regular basis and carefully determine which therapies are most successful for each particular her functional sta- patient. Since patients often have multiple symptoms, tus (activities of daily living, exercise, and work) and it is important to treat FM holistically rather than treat recording the patient's subjective pain score ( 0-10), each symptom separately with a polypharmacy the physician will have a better idea of how the patient approach. However, since no one drug in clinical trials appears to successfully treat FM in more than 50% Important non-pain symptoms associated with FM of cases, multiple drug therapy is necessary for many usually include chronic fatigue, non-restorative sleep FM patients.
disturbances and daytime somnolence, neurally- Many FM patients have problems with multiple mediated hypotension, cognitive dysfunction, irritable chemical sensitivities. Part of the problem could be bowel syndrome, increased anxiety, and reactive due to how they metabolize or eliminate certain depression (which is distinguished from major medications. I often tell patients if they could tolerate depressive disorder). In my clinical experience as a the full dose of a prescribed drug their FM problems rheumatologist who has treated FM patients for over would be much less severe. Another problem is that 25 years, successful treatment of these other co- the FDA-approved FM drugs were tested as morbid FM problems is essential to a good clinical monotherapies, meaning that patients were not allowed to take other FM medications during the It is also important to identify the patient's pain clinical trials. Patients on more than one medication generators. These pain generators can come from co- can experience drug-drug interactions which require existing osteoarthritis, rheumatoid arthritis, systemic them to use a lower dose of medication due to lupus, myofascial pain, or other mechanical problems increased side effects on the full dose. Some drugs such as degenerative disc disease or spinal stenosis.
have generic alternatives that may be absorbed Adequate control of these additional sources of pain, differently than the brand name drug. These problems if present, is an important therapeutic challenge.
can often cause FM patients to have difficulty takingstandard doses of medication due to intolerable side When a FM patient has a pain flare, it usually effects. It is not uncommon for FM patients to need involves a CNS windup and central sensitization. In to start at lower than standard doses of medications.
my experience, it is essential to aggressively treat thistype of pain before it causes a chronic escalation ofthe patient's pain syndrome. It also gives the patient a Medical Management For Fibromyalgia
sense of control and avoids unnecessary emergency In addition to a tender points exam and an assessment room visits. I encourage my patients to have adequate of the patient's myofascial pain, range of motion, pain medication at home for the short-term treatment posture, and gait, what other diagnostic criteria should of this type of emergency, breakthrough pain.
National Fibromyalgia Partnership, Inc. (NFP). • www.fmpartnership.org Fibromyalgia Frontiers • 2010 (Volume 18, Number 1) PHARMACOLOGY FOR FIBROMYALGIA
by the U.S. Drug Enforcement Agency (DEA) . They These drugs block the biogenic amines that are also have TCA effects and are FDA-approved for abnormal in the CNS in FM.
the treatment of moderate to severe pain. Clinical trials a. Tricyclic Antidepressant Drugs (TCA): Bedtime
show them to be effective in the treatment of FM pain.
doses of low-dose amitriptyline (Elavil) and doxepin My experience is that Ultracet is more effective than (Sinequan) have been effective in FM.
Ultram with fewer adverse effects, and Ultram ERoffers the important benefit of 24-hour pain control b. Selective Serotonin Reuptake Inhibitors (SSRI):
Only 40-80 mg. of fluoxetine (Prozac) has been
without breakthrough pain when the short acting drug shown to be effective in small FM studies. The other wears off in 6-8 hours.
SSRI's are effective in treating anxiety and depression, b. Long-Acting Opioids: Fentanyl patch and time-
but not effective treating pain in FM studies.
release morphine have been shown to be effective for c. Serotonin-Norepinephrine Reuptake Inhibitors
long-term use in chronic low back pain and (SNRI): Duloxetine (Cymbalta) and milnacipran
osteoarthritis pain, but their use should be limited to (Savella) are now FDA-approved for the manage- only the most severe chronic pain patients due to ment of fibromyalgia. Cymbalta is also approved for concerns about addictive potential and adverse effects.
the treatment of diabetic neuropathic pain, generalized The EULAR (European League Against Rheumatism) anxiety disorder, and major depressive disorder.
evidenced-based guidelines do not recommend these Savella has a higher concentration of norepinephrine drugs for the treatment of FM pain.17 than Cymbalta and may be more effective in the c. Short-Acting Opioids: Hydrocodone and
treatment of FM fatigue. In clinical trials, both drugs oxycodone, in combination with acetaminophen or appear to be very effective in 30% of FM patients ibuprofen, are excellent short-acting analgesics for and partially effective in 50% of FM patients.
acute peripheral and CNS pain. They should not beused for chronic pain except in rare instances due toconcerns about addictive potential and adverse effects, including the potential for withdrawal-related (Calcium Channel Inhibitor Drugs) These drugs symptoms of increased pain.
block the release of neurotransmitters Substance Pand Glutamate in hyper-excited nerve fibers.
4. MUSCLE RELAXANTS
a. Pregabalin (Lyrica) is now FDA-approved for
the management of fibromyalgia. It is also approved
Muscle relaxants are commonly used both chronically for the treatment of shingles and diabetic neuropathic and for acute pain flares in FM. Cyclobenzaprine pain. In clinical trials, it appears to be very effective (Flexeril) is effective in FM due to its tricyclic anti- in 30% of FM patients and partially effective in 50% depressant and muscle relaxant properties, and it is of FM patients.
often used to help with sleep. There is now a 24-hour time release form of cyclobenzaprine, Amrix, b. Gabapentin (Neurontin) is commonly used in the
which usually causes less sedation than cyclo- treatment of FM and neuropathic pain. It is FDA- benzaprine if used during the day.
indicated for shingles neuropathic pain and was shownto be effective for the treatment of FM in one clinicaltrial funded by the National Institutes of Health.
5. SEDATIVE HYPNOTICS
a. Non-Benzodiazepines: Zolpidem (Ambien) has
3. OPIOIDS
been shown to improve FM sleep disturbances andfatigue.
a. Tramadol (Ultram), Tramadol with Aceta-
minophen (Ultracet), and Tramadol Extended
b. Benzodiazepines: Alprazolam (Xanax) has been
Release (Ultram ER): are weak opioids, but they are
shown to be effective in FM.
not considered controlled substances as determined National Fibromyalgia Partnership, Inc. (NFP). • www.fmpartnership.org

Fibromyalgia Frontiers • 2010 (Volume 18, Number 1) NON-PHARMACOLOGIC TREATMENT FOR FIBROMYALGIA
1. EDUCATION:
When a FM diagnosis is made, and the condition
their pain (by increasing endorphins in the CNS), is properly explained to the patient and family, the mood, physical conditioning, and functional status.
intensity of symptoms will often be reduced by It is important to combine exercise with adequate one-third due to reduction in patient anxiety which stretching as well as energy conservation to prevent contributes to abnormal pain processing. An injury or FM flare. I find core and Pilates exercises essential goal of FM treatment is to empower the as well as warm water aquatic exercises (when patient to understand his or her illness and learn possible) to be very effective for most of my FM how to best manage the disease.
2. PHYSICAL THERAPY:
4. COGNITIVE BEHAVIORAL THERAPY &
Proper posture, balance, muscle tone, and BEHAVIORAL MODIFICATION THERAPY:
physical conditioning are important needs to These are being used in FM with increasing correct in many FM patients, much more so than frequency and success. Proper conservation of your for their non-fibromyalgia friends with similar poor available energy and development of coping skills posture, muscle tone, and physical conditioning.
to reduce anxiety over dealing with chronic pain are It is often necessary to prescribe physical therapy important goals in the management of FM.
with a therapist skilled in FM, myofascial release,and neuromuscular re-education before the patient can successfully progress to an appropriate This discipline has been shown to be an effective exercise program.
FM treatment in small clinical studies. It shouldbe considered a supplemental therapy for FM 3. EXERCISE:
patients and can be very beneficial in selected Low impact, aerobic exercise is an important treatment for almost all FM patients to improve Important Note: Before attempting any new form of medication or treatment, be sure to check with your physician.
National Fibromyalgia Partnership, Inc. (NFP). • www.fmpartnership.org Fibromyalgia Frontiers • 2010 (Volume 18, Number 1) June 23, 2003. Website: www.fda.gov/ oh rms/dockets/ac/03/transcripts/3967T1.htm , pp. 26-45.
As my experience treating FM patients grows, and thescience regarding the disease and treatment options 7) Williams DA and Gracely RH. Biology and therapyof fibromyalgia. Functional magnetic resonance increases, I find myself becoming more and more imaging findings in fibromyalgia. Arthritis Res Ther optimistic about good patient outcomes. Most FM 2006; 8(6): 224.
patients have symptoms that do not worsen over time, 8) Arnold LM et al. Family study of fibromyalgia.
and many patients improve to a level of pain they can Arthritis Rheum 2004 Mar;50(3):944-52 tolerate and be functional. The mainstay of treatment is 9) Drewes AM. Pain and sleep disturbances with the use of evidence-based treatments which include special reference to fibromyalgia and rheumatoid patients' active participation to fine tune their treatment arthritis. Rheumatology 1999 Nov;38(11):1035-8.
plans to their particular needs, as part of the medical 10) Buskila D, Neumann L, Epstein RP. Confirmation of team. This formula ensures a successful and positive an association between fibromyalgia and serotonin relationship for both doctor and patient.
transporter promoter region (5-HTTLRPR)polymorphism, and relationship to anxiety-relatedpersonality traits. Arthritis Rheum 2002 Mar;46(3):845-7.
Dr. Rothenberg is Board Certified in
Rheumatology and Internal Medicine and
11) Gursoy S, Erdal E, Herken H, Madenci E, Alasehirli B, is Chair of the Medical Advisory Board of
Erdal N. Significance of catecho-O-methyltransferase the National Fibromyalgia Partnership, Inc.
gene polymorphism in fibromyalgia syndrome.
He is in private practice in Bethesda, MD.
Rheumatol Int 2003 May;23(3):104-7.
You can contact him at:
12) De Stefano R, Selvi E, Villanova M., et al. Imageanalysis quantification of substance P immunoreactivity The Camalier Building
in the trapezius muscle of patients with fibromyalgia and 10215 Fernwood Road, Suite 401
myofascial pain syndrome. J Rheumatol 2000;27(12): Bethesda, MD 20817-1106
Telephone: (301) 571-2273
13) Shah J et al. Biochemicals associated with pain andinflammation are elevated in sites near to and remotefrom active myofascial trigger points. Arch Phys MedRehabil 2008 Jan;89(1):16-23.
14) Martínez-Lavín M. A novel holistic explanation forthe fibromyalgia enigma: autonomic nervous systemdysfunction. Fibromyalgia Frontiers 2001; Vol 10(1).
1) Smythe HA, Moldofsky H. Two contributions to under-standing the "fibrositis" syndrome. Bull Rheum Dis 1977- 15) Price D and Staud R. Neurobiology of fibromyalgia syndrome. J Rheumatol Suppl 2005 Aug;32(75):22-8.
2) Wolfe F, Smythe HA, Yunus MB, et al. The American 16) Mease P. Fibromyalgia syndrome: review of clinical College of Rheumatology 1990 Criteria for the classification presentation, pathogenesis, outcome measures and of fibromyalgia. Arthritis Rheum 1990 Feb;33(2):160-72.
treatment. J Rheumatol 2005;32(75):6-21. 3) Goldenberg DL, Simms RW, Geiger A, Komaroff AL. High 17) Carville SF et al. EULAR evidence-based frequency of fibromyalgia in patients with chronic fatigue recommendations for the management of fibromyalgia seen in a primary care practice. Arthritis Rheum 1990 Mar; syndrome. Ann Rheum Dis July 20, 2007; dol, p.1522.
4) Wolfe F, Ross K, Anderson J. The prevalence andcharacteristics of fibromyalgia in the general population.
This article may be photocopied in its
Arthritis Rheum 1995 Jan;38(1):19-28. Also,Weir PT, et al. J entirety, and distributed without per-
Clin Rheumatol 2006 Jun;12(3):124-8.
mission, if used for non-commercial,
5) Ibid. Wolfe F, Smythe HA, Yunus MB, et al. The educational purposes. It may not be
American College of Rheumatology 1990 Criteria for the reprinted or reproduced in any publi-
classification of fibromyalgia.
cation, website, or other media without
prior permission.
6) Bradley L. FDA Center for Drug Evaluation andResearch, Meeting of the Arthritis Advisory Committee, National Fibromyalgia Partnership, Inc. (NFP). • www.fmpartnership.org

Source: http://russellrothenbergmd.com/pdf/fibro2.pdf