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Optimizing fibromyalgia management

Firestone, Kari A. MS, RN, CNS; Holton, Kathleen F. PhD, MPH; Mist, Scott D. PhD, MAcOM; Wright, Cheryl L. PhD, FNP-BC; Jones, Kim Dupree PhD, FNP-BC, FAAN

doi: 10.1097/01.NPR.0000412891.19933.48
Feature: FIBROMYALGIA: CE Connection

Fibromyalgia (FM) is a persistent pain state commonly diagnosed and managed by nurse practitioners. This article summarizes current information regarding the etiology, pathophysiology, clinical presentation, diagnostic standards, and pharmacologic and non-pharmacologic treatments necessary to successfully manage FM.

Kari A. Firestone is a PhD Student at Oregon Health & Sciences University School of Nursing in Portland, OR. She is also an assistant professor at Loma Linda University School of Nursing in Loma Linda, CA.

Kathleen F. Holton is a senior research associate at Oregon Health & Science University School of Medicine in Portland, OR.

Scott D. Mist is an assistant professor at Oregon Health & Sciences University in Portland, OR.

Cheryl L. Wright is an assistant professor at Oregon Health & Sciences University School of Nursing in Portland, OR.

Kim Dupree Jones is an associate professor at Oregon Health & Sciences University School of Nursing & School of Medicine Division of Arthritis and Rheumatic Diseases in Portland, OR.

The authors and planners have disclosed that they have no financial relationships related to this article.



Fibromyalgia (FM), a chronic widespread pain disorder, is common, costly, and debilitating, affecting approximately 5 million people in the United States.1 Women account for 80% to 90% of the cases.2 FM most commonly presents between the ages of 30 and 40, with a peak prevalence of 7% of females in their 60s.3 Misconceptions that the illness is psychosomatic in nature and has few visible signs often leads to underdiagnosis or misdiagnosis and delayed or inappropriate treatment. The average FM patient sees five different healthcare providers over an 8-year period before receiving a FM diagnosis. Over 27% of patients reported feeling that their healthcare provider did not view FM as a “very legitimate” disorder.4 FM is debilitating and affects patients' quality of life, socially and economically impairing their ability to work and maintain relationships with family and friends.5 The nurse practitioner (NP) is a vital component of the treatment team who can diagnose FM, identify comorbidities, and treat associated symptoms.6

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Predisposing factors associated with the increased incidence of FM include environmental stimuli and genetics. Environmental triggers may include viral infections (parvovirus, hepatitis, HIV, and possibly Lyme disease), adverse life events such as past history of painful conditions related to injury or trauma (motor vehicle trauma, regional pain syndromes, posttraumatic stress disorder), or traumas such as abuse.4,7,8

Additionally, research has shown a genetic correlation in the development of the disorder; patients with first-degree relatives who have FM have an eight times greater risk of developing the illness.9 Providers should be aware of family history of chronic pain and advise patients to minimize risk of environmental triggers. Many suggest more aggressive pharmacologic and nonpharmacologic treatment for these patients at the onset of symptoms.10,11

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Patients with FM have objective, reproducible findings of enhanced sensory processing. These findings are proposed to be the biological basis for most symptoms of FM and include altered pain processing in the central nervous system (CNS) or “central sensitization” that is characterized by hyperexcitable nociceptors. This leads to an increased pain response to nonpainful stimuli (allodynia), experiencing pain at lower levels of stimulation than a healthy individual (hyperalgesia), and the expansion of receptive fields outside the initial pain locus.6 Further supporting the theory of central sensitization is that FM patients exhibit abnormal windup or temporal summation; ongoing nociceptive input results in dorsal horn neurons exhibiting increased excitability and spontaneous activity, resulting in worsening pain with the repetition of pressure.12 Contributing to altered pain sensitivity in FM patients is increased levels of glutamate (excitatory neurotransmitter) and substance P (nociceptive neurotransmitter) at two to three times the level of a healthy individual.13 Increased levels of these neurotransmitters result in increased duration, amplification, and augmentation of the pain signal.14 In addition to central sensitization, FM patients have shown dysfunction in descending inhibitory pathways with absent or attenuated analgesic response in “pain inhibits pain” testing.15 Low levels of serotonin, norepinephrine, and dopamine in the cerebrospinal fluid of FM patients also support the idea of descending inhibitory pathway dysfunction. These biomarkers are commonly analyzed in research settings but are not useful in clinical practice as they do not alter treatment decisions.

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Clinical presentation

The FM patient may appear healthy with no outward signs of illness, but will report multiple symptoms with varying degrees of physical dysfunction. The chief complaint is widespread body pain described as originating from muscles and joints.16 Other common presenting complaints including fatigue, sleep disturbances, cognitive dysfunction, stiffness (morning stiffness being reported as having the most significant impact on daily activities)tenderness, and lower fitness levels than age-expected norms.16 Patient's with FM often report perceived exaggerated symptoms from changes in weather, sleep deprivation, increase in activities, or strenuous activity and stress.4

The clinical presentation of FM includes symptoms that may be related to alterations in central processing. Fatigue and sleep disturbances in the form of nonrestorative sleep or insomnia are cited as a significant factor for morbidity.17 Cognitive symptoms include the presentation of “Fibro Fog” a phenomena of forgetfulness, short-term memory loss, decreased mental alertness, concentration difficulties, and difficulty multitasking under distraction.17 Approximately 45% to 69% of FM patients have concurrent mood disorders; the most common are anxiety disorder and depression.17 Many FM patients also experience difficulty with other common comorbidities such as restless legs syndrome, irritable bowel or painful bladder syndrome, chronic headaches, and temporomandibular disorders (TMDs).17

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Diagnostic criteria

Formal recognition of FM began in 1990 with the American College of Rheumatology (ACR) classification criteria. The combination of widespread pain and tenderness in greater than or equal to 11 of 18 tender point sites yields a sensitivity of 88.4% and a specificity of 81.1%. Arguments for adopting the preliminary 2010 criteria include the assumption that the tender point exam is often either performed incorrectly or rarely performed. For these reasons some experts think that FM has become a symptom-based diagnosis.18 Rheumatologists and other pain related health care providers are concerned that the proposed 2010 criteria may misdiagnose highly symptomatic patients with regional pain, as FM (see 1990 vs. 2010 ACR diagnostic criteria).

Table 1990

Table 1990

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Differential diagnosis

Few disorders present at midlife with long-standing, widespread pain. Nonetheless, the NP must be certain that patients not only meet diagnostic criteria for FM but also have no preexisting illnesses that mimic FM or its common comorbidities. Differential diagnosis labs rule out autoimmune and other medical disorders. Specialized rheumatic or autoimmune lab tests (antinuclear antibody test [ANA], rheumatoid factor, anti-dsDNA antibody test, anti-Smith [anti-Sm], anti-phospholipid antibodies) are more sensitive and specific when ordered after a positive history or physical exam, and are not recommended for screening. Systemic lupus erythematosus (SLE) and other autoimmune disorders are diagnosed in part by tests such as anti-phospholipid antibodies. Other diagnostic tests may be indicated based on specific positive history or physical exam findings (see Differential diagnosis).

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The management of the FM is patient-centered and highly individualized including both pharmacologic and non-pharmacologic treatment modalities aimed at achieving optimal functional health status. Treatment is complex, and it often takes trial and error to find a combination of modalities to alleviate symptoms.

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Pharmacologic management of FM

Pharmacologic management of FM is influenced by the severity, functional disabilities, and presence of comorbidities and will require frequent follow-up and modifications dependent on patient response. The pharmacologic agents that have shown the strongest evidence of efficacy in FM management include duloxetine, milnacipran, and pregabalin, which are FDA-approved for FM, and tramadol, which is indicated for the treatment of moderate to moderately severe chronic pain, but is not specifically approved for FM.1921 Other off-label medications with less conclusive research data in current use include tricyclic antidepressants (TCAs) such as amitriptyline and the skeletal muscle relaxant, cyclobenzaprine.22 Sodium oxybate, a CNS depressant that is indicated for excessive daytime sleepiness and cataplexy in patients with narcolepsy, has shown statistically significant improvement in multisite phase III clinical trials. However, it has failed to attain an FDA indication for FM, perhaps due to concerns about diversion.23 This agent is not easily reimbursed by third-party payers without extensive prior authorization, unless the patient also has narcolepsy (marked by excessive daytime sleepiness). Notably absent from the list of recommended agents are corticosteroids and nonsteroidal anti-inflammatory drugs (NSAIDs) since they have not shown therapeutic benefit in FM. Unless the provider is using NSAIDs or corticosteroids for an acute injury or concurrent inflammatory condition, clinicians may consider removing these from the medication regimen. Rationale polypharmacy may include pairing drugs with activity in ascending pathways such as anticonvulsants with agents that target descending pathways such as serotonin-norepinephrine reuptake inhibitors (SNRIs).24

Table Diffe

Table Diffe

Antidepressants. Antidepressants are used in FM to treat pain and address the common comorbidities of depression and anxiety disorders. The use of SNRIs such as duloxetine and milnacipran has been shown to enhance transmission in the descending inhibitory pain pathways resulting in the reduction of pain severity, stiffness, and improvement in function.20,21 SNRIs lack the adverse reaction profile, drug interaction, and efficacy issues of the TCAs making them a more desirable treatment option. Selective serotonin reuptake inhibitors (SSRIs), while commonly prescribed in FM for mood disorder, have not tested positively in clinical trials for FM pain.25 One treatment option is to consider SNRIs over SSRIs for patients with FM.

Older medications such as amitriptyline and cyclobenzaprine (a skeletal muscle relaxant that is structurally related to TCAs) have shown moderate benefit for FM symptoms and are used off-label mainly at nighttime due to their effect on sleep quality.22

Anticonvulsants. Anticonvulsants have long been used in the treatment of neuropathic pain and have been shown in recent studies to be effective in the management of FM. Pregabalin, approved in 2007 for the treatment of FM, inhibits the release of substance P and glutamate in the CNS and has shown significant improvement in pain severity, fatigue, sleep, and functionality (see Pharmacologic agents commonly used to treat FM).26,27

Analgesics. Tramadol, a centrally acting analgesic used alone or when combined with acetaminophen, was found to significantly improve pain and functionality.19 Tramadol is not recommended in patients with seizure disorder as it may lower the seizure threshold. It should also be used cautiously in patients on SSRIs, SNRIs, or other agents that activate serotonin pathways.

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Nonpharmacologic management

The cornerstones of nonpharmacologic management in FM are exercise and cognitive behavioral strategies. Patients are increasingly choosing other nonpharmacologic modalities such as complementary and alternative therapies as well as requesting dietary counseling. Therefore, emerging evidence for these therapies is presented. Long-term management of chronic illnesses such as FM often use a multidisciplinary approach that includes:

  • NPs-primary management
  • Physicians-evaluate and manage refractory comorbidities
  • Psychologists-counseling, cognitive behavioral strategies
  • Physical therapists-individualize exercise prescription and provide specific rehabilitation plans
  • Occupational therapists-modify work and home environment
  • Speech therapists-employ cognitive therapy for Fibro Fog
  • Exercise specialists-carry out exercise classes long term.3,28

Exercise. Promoting structured exercise that targets aerobic, strength, flexibility, and balance training are critical in treating FM. When supervised multimodal exercise sessions can be successfully performed without triggering an exercise-induced flare, efforts to increase physical activity can be added. Multiple physiologic deficits in central and peripheral pain processing, autonomic dysfunction, and neuroendocrine and inflammatory processes are known to hinder exercise success in FM.2931 Modifying the exercise prescription to accommodate these deficits will increase the likelihood that a patient can tolerate exercise that will eventually improve most FM symptoms and help them to regain physical function.6,32 Both land-based and water-based (balneotherapy) programs are recommended, providing that the programs are modified for FM.

Nine evidence-based strategies an exercise instructor can employ include (1) keep movement near the body's midline and limit time spent with arms overhead to decrease muscle microtrauma and delayed onset muscle soreness; (2) gradually increase standing time to maximize the use of the large muscles of the hips and thighs (however, chair exercises are usually employed initially); (3) allow muscles to return to baseline resting state by alternating limbs, rather than working one side for 8 counts; (4) reverse pain posture with the following movements: chin back, shoulders down, crown of head lift, deep breathing, anterior chest stretches, and back strengthening exercises; (5) modify poses for joint hypermobility, which is common in FM; (6) limit fast or pivot turns and use a cane, wall, or chair to reduce fall risk- eventually retrain balance with foam balance trainers and one-legged standing activities; (7) find an instructor who is willing to modify the exercise routine as outlined above and who uses kind self-talk as part of the class, rather than body-shape-oriented verbiage; (8) find an FM exercise friendly environment, namely one that minimizes bright light, loud noise, cold temperatures, has close proximity to restrooms, and does not allow strong smells such as cigarette smoke or perfume; and (9) start-low, go slow, but eventually get there, meaning keep working toward a full-scope exercise program (see Strategies to decrease pain and fatigue in daily activities).32



Cognitive behavioral therapy. Formal testing of cognitive behavioral strategies in FM is often positive for improving mood, reducing stress and pain-related behavior, coping, and enhancing physical function.33 These studies generally added CBT to standard care (medications). In clinical practice, patients sometimes have access to therapists, but often use strategies employed in CBT at home, in a small group, or with a therapist with less FM expertise. Some of the helpful CBT strategies include reframing problems to decrease catastrophic thinking, time-based rather than task-based pacing (energy conservation), and scheduling pleasurable activities. It is noted that CBT is not a replacement for accurate diagnosis and treatment for Axis I or II disorders.34

Complementary and alternative medicine (CAM). Many patients with FM frequently seek CAM, such as acupuncture, as a treatment option; national surveys indicate that 15% of FM patients have sought acupuncture treatment.4 The evidence is mixed on how effective acupuncture treatments are for the treatment of FM.35 However, all of the reviews agree that true needle placement acupuncture is a successful adjunct short-term treatment.36 Acupuncture may be a useful treatment option in patients who do not respond to biomedical approaches, who may be sensitive to the adverse reactions of medications. One should base their referrals on professional credentials and personal knowledge; acupuncturists are generally licensed by a state credentialing board. There is less research available on the treatment of FM with herbal or nutraceutical treatments, which many patients utilize. Research indicates that 43% of women with FM were taking at least one herb or supplement compared to 23% of healthy women.37 Herb-drug interactions are a serious concern. One should inform patients about possible interactions and communicate with any practitioner that might be offering such treatments to ensure the safety of the patient.

The most promising bodywork data to date supports the use of a massage technique called myofascial release. Studies indicate that this type of massage reduces anxiety and pain, while improving sleep patterns and quality of life. Those exercise therapies that naturally incorporate mindfulness such as certain yoga therapies and Tai chi have been demonstrated to improve many symptoms in FM including pain.38,39

Diet. Although many FM patients report that they seek dietary guidance for helping to manage their symptoms, dietary manipulation in FM is still a relatively new treatment option. A few studies have examined the effect of a raw food vegan diet in FM subjects.4,4042 These studies were demonstrated symptom improvement; however, no subjects were able to continue the diets poststudy due to their highly restrictive nature. It is possible that the restrictive diets may have caused improvement by inadvertently removing food additives from the diet. A study examining the effects of a class of food additives, including monosodium glutamate (MSG) and aspartame, recently demonstrated that those who experienced over 30% remission of symptoms on a 4-week additive-free diet had a significant return of symptoms when challenged with MSG as compared to challenge with placebo.43 Published case series also support the idea that food additives such as MSG and aspartame could be contributing to symptoms in FM.44,45

Various studies have also suggested that FM patients may be low in certain nutrients important to neurologic function including iron, magnesium, zinc, vitamin B12, and antioxidants.46,49 A nutritious, whole food diet, which is also low in food additives, could optimize nutrient intake, has no risk of harm, and could help prevent other diet-related comorbidities. Referral to a registered dietitian should be considered to aid patients in optimizing their diets and to help screen for reactions to certain foods/additives.

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Implications for practice

NPs are ideally suited to diagnose and manage patients with FM. It often requires a collaborative multidisciplinary approach including medications, exercise, cognitive strategies, and an open mind when evaluating the efficacy of newer CAM-related treatments as they emerge in the literature. It is critical for the NP to provide hope and gently redirect patients away from unsafe treatments or therapies that have tested negatively, and toward a healthier, individualized treatment plan.

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Strategies to decrease pain and fatigue in daily activities

  • Take shorter steps when walking downhill
  • Avoid carrying a heavy shoulder bag
  • Always use handrails and canes if needed
  • Take breaks often when reaching overhead repeatedly
  • Use a grabber for reaching objects on high shelves
  • Rearrange kitchen by placing frequently used items near waist level
  • Change positions frequently
  • Sit in the middle of an auditorium to keep from twisting
  • Use a telephone headset and other ergonomic aids
  • Use a wheeled shopping cart rather than a hand basket
  • Balance rest with exercise
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1. Lawerence RC, Felson DT, Helmick CG, et al.Estimates of the prevalence of arthritis and other rheumatic conditions in the Unites States. Part II. Arthritis Rheum. 2008;58(1):26–35.
2. Weir PT, Harlan GA, Nkoy FL, et al.The incidence of fibromyalgia and its associated comorbidities: a population-based retrospective cohort study based on International Classification of Disease, 9th Revision CODES. J Clin Rheumatol. 2006;12(3):124–128.
3. Jones KD, Bennett RM, Ward RL, Deodhar AADescription of a half-day interprofessional fibromyalgia clinic with an evaluation of patient satisfaction. Am J Phys Med Rehabil. 2011;90(10):825–833.
4. Bennett RM, Jones J, Turk DC, Russell IJ, Matallana LAn Internet survey of 2,596 people with fibromyalgia. BMC Musculoskel Dis. 2007;8:27.
5. Arnold LM, Crofford LJ, Mease PJ, et al.Patient perspectives on the impact of fibromyalgia. Patient Educ Couns. 2008;73(1):114–120.
6. Paiva ES, Jones KDRational treatment of fibromyalgia for a solo practitioner. Best Pract Res Clin Rheumatol. 2010;24(3):341–352.
7. Hauser W, Kosseva M, Uceyler N, Klose P, Sommer CEmotional, physical, and sexual abuse in fibromyalgia syndrome: a systematic review with meta-analysis. Arthritis Care Res. 2011;63(6):808–820.
8. Buskila D, Atzeni F, Sarzi-Puttini PEtiology of fibromyalgia: the possible role of infection and vaccination. Autoimmun Rev. 2008;8(1):41–43.
9. Arnold LM, Hudson JI, Hess EV, et al.Family study of fibromyalgia. Arthritis Rheum. 2004;50(3):944–952.
10. Kindler LL, Jones KD, Perrin N, Bennett RMRisk factors predicting the development of widespread pain from chronic back or neck pain. J Pain. 2010;11(12):1320–1328.
11. Williams DA, Clauw DJUnderstanding fibromyalgia: lessons from the broader pain research community. J Pain. 2009;10(8):777–791.
12. Staud R, Vierck CJ, Cannon RL, Mauderli AP, Price DDAbnormal sensitization and temporal summation of second pain (wind up) in patients with fibromyalgia syndrome. Pain. 2001;91(1–2):165–175.
13. Harris RE, Sundgren PC, Pang Y, et al.Dynamic levels of glutamate within the insula are associated with improvements in multiple pain domains in fibromyalgia. Arthritis Rheum. 2008;58(3):903–907.
14. Desmeules JA, Cedraschi C, Rapiti E, et al.Neurophysiologic evidence for central sensitization in patients with fibromyalgia. Arthritis Rheum. 2003;48(5):1420–1429.
15. de Souza JB, Potvin S, Goffaux P, Charest J, Marchand SThe deficit of pain inhibition in fibromyalgia is more pronounced in patients with comorbid depressive symptoms. Clin J Pain. 2009;25(2):123–127.
16. Bennett RMClinical manifestation and diagnosis of fibromyalgia. Rheum Dis Clin North Am. 2009;35(2):215–232.
17. Arnold LMThe pathophysiology, diagnosis and treatment of fibromyalgia. Psychiartr Clin North Am. 2010;33(2):375–408.
18. Staud R, Price DD, Robinson METhe provisional diagnostic criteria for fibromyalgia: one step forward, two steps back: comment on the article by Wolfe et al. Arthritis Care Res. 2010;62(11):1675–1676.
19. Bennett R, Kamin M, Karin R, Rosenthal NTramadol and acetopminophen combination tablets in the treatment of fibromyalgia pain: a double-blind, randomized, placebo-controlled study. Am J Med. 2003;114(7):537–545.
20. Arnold LM, Lu Y, Crofford LJ, et al.A double-blind, multicenter trial comparing duloxetine with placebo in the treatment of fibromyalgia patients with or without major depressive disorder. Arthritis Rheum. 2004;50(9):2974–2984.
21. Vitton O, Gendreau M, Gendreau J, Kranzler J, Rao SGA double-blind placebo controlled trial of milnacipran in the treatment of fibromyalgia. Hum Psychopharmacol. 2004;19(suppl 1):S27–S35.
22. Arnold LM, Keck PE Jr, Welge JAAntidepressant treatment of fibromyalgia. A meta-analysis and review. Psychosomatics. 2000;41(2):104–113.
23. Russell IJ, Holman AJ, Swick TJ, Alvarez-Horine S, Wang YG, Guinta DSodium oxybate reduces pain, fatigue, and sleep disturbance and improves functionality in FM: results from a 14-week, randomized, double-blind, placebo-controlled study. Pain. 2011:152(5):1007–1017.
24. Russell IJFibromyalgia syndrome: approach to management. CNS Spectr. 2008;13(3 suppl 5):27–33.
25. Mease P J, Choy E HPharmacotherapy of fibromyalgia. Rheum.Dis.Clin.North Am 2009;35:359–372.
26. Mease PJ, Russel IJ, Arnold LM, et al.A randomized, double blind, placebo controlled, phase III trial of pregabalin in the treatment of patients with fibromyalgia. J Pain. 2008;35(3):502–514.
27. Arnold LM, Russell IJ, Diri EW, et al.A 14-week, randomized double blinded, placebo controlled monotherapy trial of pregabalin in patients with fibromyalgia. J Pain. 2008;9(9):792–805.
28. Casanueva-Fernandez B, Llorca J, Rubio JB, Rodero-Fernandez B, Gonzalez-Gay MAAn efficacy of a multidisciplinary treatment program in patients with severe fibromyalgia. Rheumatol Int. 2011 Jul 23. [Epub ahead of print].
29. Jones KD, Deodhar P, Lorentzen A, Bennett RM, Deodhar AAGrowth hormone perturbations in fibromyalgia: a review. Semin Arthritis Rheum. 2007;36(6):357–379.
30. Elvin A, Siosteen AK, Nilsson A, Kosek EDecreased muscle blood flow in fibromyalgia patients during standardized muscle exercise: a contrast media enhanced colour Doppler study. Eur J Pain. 2006;10(2):137–144.
    31. Staud R, Robinson ME, Price DDIsometric exercise has opposite effects on central pain mechanisms in fibromyalgia patients compared to normal controls. Pain. 2005;118(1–2):176–184.
    32. Jones KD, Liptan GLExercise interventions in fibromyalgia: clinical applications from the evidence. Rheum Dis Clin North Am. 2009;35(2):373–391.
    33. Bernardy K, Fuber N, Kollner V, Hauser WEfficacy of cognitive-behavioral therapies in fibromyalgia syndrome—a systematic review and meta-analysis of randomized controlled trials. J Rheumatol. 2010;37(10):1991–2005.
    34. Bennett R, Nelson DCognitive behavioral therapy for fibromyalgia. Nat Clin Pract Rheumatol. 2006;2:416–424.
    35. Mayhew E, Ernst EAcupuncture for fibromyalgia—a systematic review of randomized clinical trials. Rheumatology (Oxford). 2007;46(5):801–804.
    36. Duncan B, White A, Rahman AAcupuncture in the treatment of fibromyalgia in tertiary care: a case series. Acupunct Med. 2007;25(4):137–147.
    37. Shaver JL, Wilbur J, Lee H, Robinson FP, Wang ESelf-reported medication and herb/supplement use by women with and without fibromyalgia. J Womens Health (Larchmt). 2009;18(5):709–716.
    38. Carson JW, Carson KM, Jones KD, Bennett RM, Wright CL, Mist SDA randomized controlled clinical trial of the yoga of awareness program in the management of fibromyalgia. Pain. 2010;151(2):530–539.
    39. Wang C, Schmid CH, Rones R, et al.A randomized trial of tai chi for fibromyalgia. N Engl J Med. 2010;363(8):743–754.
    40. Donaldson MS, Speight N, Loomis SFibromyalgia syndrome improved using a mostly raw vegetarian diet: an observational study. BMC Complement Altern Med. 2001;1:7.
    41. Hanninen O, Kaartinen K, Rauma AL, et al.Antioxidants in vegan diet and rheumatic disorders. Toxicology. 2000;155(1–3):45–53.
      42. Kaartinen K, Lammi K, Hypen M, Nenonen M, Hanninen O, Rauma ALVegan diet alleviates fibromyalgia symptoms. Scand J Rheumatol. 2000;29(5):308–313.
      43. Holton KF, Taren DL, Thomson CA, Bennett RM, Jones KDThe effect of dietary glutamate on fibromyalgia and irritable bowel symptoms. Clin Exper Rheum. 2012. (In Press).
      44. Smith JD, Terpening CM, Schmidt SO, Gums JGRelief of fibromyalgia symptoms following discontinuation of dietary excitotoxins. Ann Pharmacother. 2001;35(6):702–706.
      45. Ciappuccini R, Ansemant T, Maillefert JF, Tavernier C, Ornetti PAspartame-induced fibromyalgia, an unusual but curable cause of chronic pain. Clin Exp Rheumatol. 2010;28(6 suppl 63):S131-S133.
      46. Ortancil O, Sanli A, Eryuksel R, Basaran A, Ankarali HAssociation between serum ferritin level and fibromyalgia syndrome. Eur J Clin Nutr. 2010;64(3):308–312.
      47. Sendur OF, Tastaban E, Turan Y, Ulman CThe relationship between serum trace element levels and clinical parameters in patients with fibromyalgia. Rheumatol Int. 2008;28(11):1117–1121.
        48. Regland B, Andersson M, Abrahamsson L, Bagby J, Dyrehag LE, Gottfries CGIncreased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome. Scand J Rheumatol. 1997;26(4):301–307.
          49. Altindag O, Celik HTotal antioxidant capacity and the severity of the pain in patients with fibromyalgia. Redox Rep. 2006;11(3):131–135.
          50. Wolfe F, Smythe HA, Yunus MB, et al.The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the Multicenter Criteria Committee. Arthritis Rheum. 1990;33(2):160–172.
            51. Wolfe F, Clauw DJ, Fitzcharles MA, et al.The American College of Rheumatology of preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity. Arthritis Care Res. 2010;62(5):600–610.
            52. Russell IJ, Kamin M, Bennett RM, Schnitzer TJ, Green JA, Katz WAEfficacy of tramadol in treatment of pain in fibromyalgia. J Clin Rheumatol. 2000;6(5):250–257.
              53. Goldenberg DL, Burckhardt C, Crofford LManagement of fibromyalgia syndrome. JAMA. 2004;292(19):2388–2395.

                chronic pain disorder; fibromyalgia; management of fibromyalgia

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