AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Fibromyalgia (FM) and other chronic pain and fatigue syndromes constitute a huge societal burden that traditional Western medicine is currently failing to approach effectively. Although the hallmarks of FM (ie, chronic widespread pain, fatigue, multiple other somatic symptoms) have neurophysiologic and endocrinologic underpinnings, these biologic aspects likely derive significantly from psychologic, developmental, and sociocultural variables that lead to chronic unrelieved stress and distress. Female sex, adverse experiences during childhood, psychologic vulnerability to stress, and a stressful, often frightening, environment and culture are important antecedents of FM. To understand FM and related syndromes and to provide optimum care require a biopsychosocial, not a biomedical, viewpoint.

At a clinical level, fibromyalgia is much more than widespread pain. Substantial overlap exists in major depressive disorder, various anxiety disorders, and chronic fatigue syndrome and in multiple regional pain syndromes, such as headache, atypical chest pain (chest pain with normal cardiac evaluation findings), irritable bowel syndrome, chronic pelvic pain, temporomandibular joint pain (jaw pain with no underlying pathologic condition), and others. Indeed, the diagnostic label attached to a patient may be determined largely by the first specialist that he or she sees. For example, a rheumatologist might diagnosis fibromyalgia, whereas a gastroenterologist would diagnose irritable bowel syndrome.

Pathophysiology

Pain in patients with FM derives partly from a generalized decrease in the pain perception threshold, reflecting discrimination of a nociceptive quality from a nonnociceptive quality (eg, touch, warmth, cold), and in the threshold for pain tolerance, reflecting an unwillingness to receive more intense stimulation. This knowledge has been established by pressure algometry (dolorimetry) and by the application of heat, cold, and electricity as stimuli. Underlying these threshold changes is altered processing of nociceptive stimuli in the CNS (central sensitization). Recent research has identified many of the central mechanisms that underlie abnormal nociceptive processing in fibromyalgia, including recognition of discrete abnormalities in pro-nociception and antinociception pathways, serotonin-related and dopamine-related genes, and dysregulation of the stress response system.

The International Association for the Study of Pain defines pain as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage." Implicit here is the threat associated with pain, which can be trivial or profound. Neurophysiologically, the pain experience derives from a complex sensation-perception interaction involving the simultaneous parallel processing of nociceptive input from the spinal cord to multiple regions of the brain (see Image 1).

In addition to strictly sensory-discriminative elements of nociception and afferent input from somatic reflexes, major contributions from pathways and regions of the brain that are associated with emotional, motivational, and cognitive aspects of pain are evident and help determine the subjective intensity of pain. The 2 principal effectors of the stress response, the hypothalamic-pituitary-adrenocortical (HPA) axis and the sympathetic nervous system (SNS), are also activated. Although normally adaptive, the stress response may become maladaptive in patients with chronic pain and fatigue syndromes, such as FM.

Negative emotions (eg, depression, anxiety), other negative psychologic factors (eg, loss of control, unpredictability in one's environment), and certain cognitive aspects (eg, negative beliefs and attributions, catastrophizing) can all function as stressors with actions in these systems. In some patients with FM, such negative emotional, motivational, and cognitive stressors dominate the clinical picture and lead to a self-sustaining neuroendocrine cascade that contributes to flulike symptoms, depressed mood, fatigue, myalgias, cognitive difficulties, and poor sleep. The important biologic elements here include proinflammatory cytokines, the HPA axis, other neuroendocrine axes, and the autonomic nervous system.

Psychologic distress plays a central role in the pain experience and overall morbidity of patients with FM. First, increased psychologic distress is almost universal in patients with this illness. Second, psychologic distress strongly correlates with the number of tender points, both in patients with FM and in the general population. Third, high levels of anxiety and distress, less certainty of pain resolution, and a history of trauma are predictors of whether the patient will progress from acute pain to chronic pain. Consistent with this relationship between pain and distress is the improvement in measures of self-efficacy, coping, depression, pain, health status, and disease activity that accompany the application of stress management programs.

Frequency

United States

Chronic pain and fatigue are extremely prevalent in the general population, especially among women and persons of lower socioeconomic status, as follows: regional pain, 20%; widespread pain, 11%; FM according to the American College of Rheumatology (ACR) criteria, 3-5% in females and 0.5-1.6% in males; and chronic fatigue, approximately 20%.

Mortality/Morbidity

• FM is a chronic relapsing condition. In academic medical centers, long-term follow-up care of patients with FM reportedly averages 10 outpatient visits per year and 1 hospitalization every 3 years.
• Patients with FM have more comorbid medical conditions and more surgical interventions than patients with other rheumatic disorders. These patients consider themselves to be more ill and more impaired, reporting markedly abnormal scores for pain, functional disability, fatigue, sleep disturbance, and psychologic status.
• The mean cost per patient in 1996 was more than $2000, and more than 25% of the patients reported receiving some type of disability or compensation payment. After 7 years of follow-up care, the health status and disease severity of these patients did not change; 50% were dissatisfied with their health and 59% rated their health as fair or poor.

Sex

• FM, as defined by the ACR criteria, is more frequent in females than in males, with a female-to-male ratio of 9:1.
• This condition may be severe, particularly when it occurs in males.
• Some of the mechanisms that may contribute to increased pain sensitivity in women include (1) differences in primary afferent input to the CNS, with developmental and menstrual cycle–dependent enhancement; (2) developmental and phasic gonadal-hormonal modulation of pain regulatory systems, stress-induced analgesia, and opioid receptors; (3) higher levels of trait and state anxiety; (4) increased prevalence of depression; (5) use of maladaptive coping strategies; and (6) increased behavioral activity in response to pain.

Age

• Although usually considered a disorder of women aged 20-50 years, FM may be observed in pediatric populations, especially in adolescents, and older persons.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Fibromyalgia (FM) is a disorder of chronic widespread pain with associated fatigue, poor sleep, and multiple somatic symptoms.

• Pain in patients with FM diffusely radiates from the axial skeleton over large areas of the body, predominantly involving muscles, and is described as exhausting, burning, miserable, or unbearable. Pain may also be multifocal and can wax and wane in a migratory fashion. Patients frequently describe "pain all over."
• Fatigue and poor sleep are virtually universal. Most patients with FM also meet the classification criteria for chronic fatigue syndrome.
• Other frequent symptoms include the following:
• • Cognitive difficulties with attention and memory
  • Weight fluctuations
  • Allergic symptoms (eg, nasal congestion) and hypersensitivity to environmental stimuli (eg, odors, bright lights, loud noises) and medications
  • A series of regional pains, including noncardiac chest pain, dyspepsia, headache, abdominal cramping (irritable bowel syndrome), temporomandibular pain, and chronic pelvic pain
  • Syncope
  • Shortness of breath
  • Urinary frequency and urgency
• The 1990 ACR classification criteria for FM include (1) the presence of widespread pain for more than 3 months and (2) pain, not just tenderness, that can be elicited by manual pressure of approximately 4 kg/cm² at 11 or more defined tender points. The number of painful tender points is correlated strongly with psychologic distress, not only in patients with FM but also in the general population. These criteria are classification criteria for the selection of subjects for research studies, not diagnostic criteria. They should not be used for clinic diagnosis.
• FM is considered by some to be one of a series of symptom-based conditions.
• • Primarily associated with fatigue (eg, chronic fatigue syndrome)
  • Primarily associated with pain and fatigue (eg, FM)
  • Regional pain syndromes (eg, myofascial pain syndrome, atypical chest pain, irritable bowl syndrome)
  • Attributed to chemical, food, yeast sensitivity (at least 21 in all)
  • Associated with silicone breast implants (probably mostly FM)
  • Related to modern office buildings (sick building syndrome)
  • Related to service in the Persian Gulf War (mostly men)
  • Following infectious illnesses (eg, post–Lyme disease syndrome)

Physical

Except for evidence of deconditioning, physical examination findings are normal. Pain, not just tenderness, is present at multiple FM tender points when pressure (approximately 4 kg/cm²) is manually applied (see Image 2). However, pain with light pressure may not be restricted to specific tender points. Many patients feel pain virtually anywhere that pressure is applied, including control areas (eg, forehead, thumbnail), which are relatively insensitive to pain in patients who are healthy.

• Clinical assessment
• • Clinical assessment may reveal objective evidence for a discrete illness, such as hypothyroidism, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), polymyalgia rheumatica, or another autoimmune disorder. Such findings do not exclude the presence of comorbid FM. Indeed, approximately 25% of patients with rheumatoid arthritis and approximately 50% of patients with SLE also have fibromyalgia, and the provision of optimum care in such cases impels recognition and treatment of both illnesses.
  • A useful device for rough quantitation of pain sensitivity in the clinic is a pressure algometer, or dolorimeter (see Image 3). With this instrument or with multiple other laboratory approaches, such as the use of a thermode, a generalized decrease in the pain perception threshold and in the pain tolerance threshold has been demonstrated unequivocally in patients with FM and related pain syndromes. This reflects altered central nociceptive processing and is expressed in the patient as (1) allodynia (ie, pain with stimuli that should not cause pain, such as gentle touching) and/or (2) hyperalgesia (ie, amplification of pain experienced from peripheral stimuli that are expected to be painful).

Causes

The cause of FM remains unknown but appears to be multifactorial. Engel's biopsychosocial model of chronic illness (ie, health status and outcomes in chronic illness are influenced by the interaction of biologic, psychologic, and sociologic factors) is a useful way to approach FM (see Image 4).

• Biologic variables: Certain biologic variables may contribute to the development and persistence of FM. None of the variables, as single elements, explains all facets of FM. Some of the variables (eg, trauma) are highly controversial, and additional evidence is required before an etiologic role can be assigned.
• • Inheritance: With regard to inheritance, altered serotonin metabolism in at least one subgroup of patients with FM has been linked to a genotype of the promoter region of the serotonin transporter gene.
  • Sex
    • Sex-related effects are important with FM, which has a female-to-male ratio of 9:1, and with pain in general.
    • Central pain modulatory systems in females are influenced by phasic alterations in reproductive hormone levels.
    • Aversive stimuli and stressful tasks more likely evoke SNS, HPA axis, and psychologic responses in females compared to males.
  • Age
  • Sleep: Almost all patients with FM sleep poorly, and the frequent complaint that a night of poor sleep is followed by a more painful day is supported in the research. Although not the proximate cause of FM, abnormal sleep affects both limbs of the stress response system and contributes to negative mood and cognitive difficulties.
  • Trauma and tissue injury
    • Trauma as a trigger of FM has been a highly contentious and medicolegally charged issue in American society today. Until very recently, physical trauma as a causative factor in the development of fibromyalgia was an open question because properly designed prospective studies had not been performed and little experimental evidence explained the presence of pain in the absence of tissue injury. Setting aside case series and other anecdotal observations that do not provide valid evidence concerning causation, a number of controlled investigations bearing on this issue are now available.
    • In addition, clinical neurophysiological investigations have begun to clarify, at least potentially, how physical injury could result in central sensitization (induced functional alterations in the brain that disrupt normal mechanisms of pain control).
    • At the clinical level, patients who attribute their FM to trauma have more perceived disability, self-reported pain, life interference, and affective distress than patients with idiopathic onset.
  • Physical conditioning
  • Stress/neuroendocrine and autonomic dysregulation
    • A large body of data suggests that FM, chronic fatigue syndrome, regional chronic pain syndromes, and certain emotional disorders that frequently coexist with FM all involve central dysregulation of the stress response system. Here, various forms of stress function as initiators or perpetuators of functional alterations in the corticotropin-releasing hormone (CRH) neuron, with associated effects on the HPA axis, other neuroendocrine axes, and the SNS.
    • Subtle abnormalities in the stress response system, which cannot be detected by routine clinical and laboratory assessments, may contribute to the diverse clinical manifestations in this spectrum of illnesses. Although incomplete, the emerging evidence is beginning to clarify how the brain, endocrine, and immune systems (especially proinflammatory cytokines) interact in the pathophysiology of pain, fatigue, neurally mediated hypotension, depression, anxiety, and poor sleep.
    • The extremely high prevalence of stress-related disorders in society may reflect maladaption of the stress response system in the face of chronic unrelieved stress and distress in modern life.
    • Both neurally mediated hypotension and FM are female-associated disorders and exhibit similar symptomatology; however, exercise and emotional distress can precipitate these conditions. Neurally mediated hypotension is demonstrated in patients with FM by tilt-table testing, which, in turn, provokes pain. Although still poorly understood, current investigations are focusing on a role for inhibition of arterial baroreceptors in the setting of hypotension, or some other type of baroreceptor dysfunction, in the genesis of increased pain and anxiety. Consistent with this idea is evidence that arterial baroreceptor activation by increased blood pressure results in a decreased pain threshold, pain tolerance, and anxiety.
  • Neurotransmitter abnormalities/neuronal activation leading to central sensitization, low calcium levels, low serotonin levels, elevated levels of substance P, elevated levels of cerebrospinal fluid (CSF) nerve growth factor, elevated levels of CSF dynorphin A, elevated levels of CSF calcitonin gene-related peptide, and various other antinociceptive molecules
  • Functional brain activity abnormalities (decreased regional blood flow in thalamus and caudate nucleus): These variables (eg, those involved in abnormal central nociceptive processing and functional brain abnormalities) may also be part of the pathophysiology of FM but likely are derivative or secondary.
  • Neurally mediated hypotension
  • Viruses or other infections: While considered unlikely to be sole triggers, they may contribute to exacerbation of symptomatology via cytokine-vagus nerve stimulation of the CRH neuron/stress response system in bidirectional brain-immune system communication.
  • Decreased collagen cross-linking, hypermobility, Chiari malformation, environmental chemicals: These variables are conjectural, of limited significance, or just plain wrong.
• Cognitive-behavioral variables: Cognitive-behavioral variables may be pivotal in the development and maintenance of persistent pain and functional disability. The repertoire of cognitive-behavioral variables that are operant in adults may have antecedents in earlier life (eg, childhood abuse, parental alcoholism, learned behaviors from living as children with dysfunctional or chronically ill parents). By early adulthood, a failure in goal-oriented behavior may develop, leading to lower self-efficacy, the inability to achieve goals, and a fear of failure. In turn, this may presage reporting of chronic pain as a socially acceptable excuse for failure to achieve goals in later life.
• • Meaning structures
    • Qualitative research shows that patients with FM exhibit meaning structures that facilitate their invisible and capricious illness, for which they cannot be blamed.
    • Unwittingly, this may serve as an excuse for not meeting the demands and challenges of life, with accompanying strong rejection of any notion that FM could have psychologic antecedents.
    • Rather, patients with FM need their physicians and family to confirm that they are ill and that their symptoms are explained as being organically based rather than psychologically based. Therefore, physicians should assist patients with somatic symptoms to not choose illness as a way to deal with difficult personal life situations.
  • Pain beliefs and attributions
    • Negative beliefs (eg, self-blame for the mysterious enduring pain) are associated with increased subjective pain intensity, reduced compliance with treatment, low self-esteem, somatization, and psychologic distress. In patients with chronic pain, the expected tolerance to stimuli or activities that evoke pain or fatigue predicts actual tolerance. Expected danger (damage) predicts avoidance.
    • Self-assessed inability to work, helplessness, low perceived control over pain, and maladaptive coping all affect pain severity and the overall impact of FM. Thus, patients with FM perceive that they are using excessive effort during formal exercise testing of muscle, even though their actual muscle function is electrophysiologically normal. Similarly, the discordance between disability by self-report versus observed functional disability is high in patients with FM but low or absent in patients with other rheumatic diseases, such as ankylosing spondylitis and RA.
  • Hypervigilance
    • Certain data support a hypervigilance model of pain in patients with FM. Heightened sensitivity to pain occurs, at least in part, because of increased attention to external stimuli and a preoccupation with pain sensations.
    • Here, pain is amplified by hypervigilance to pain. Patients with FM become what they perceive themselves to be.
  • Self-efficacy and coping
    • Perceived self-efficacy is the level of confidence that the patient requires to control pain effectively. People with high self-efficacy beliefs engage in coping behaviors until success is achieved. People with low self-efficacy beliefs anticipate failure and stop using effective coping strategies. Higher coping self-efficacy is associated with less negative mood and pain conditions associated with pain generally. Treatments that improve coping reduce pain and enhance a positive mood, although the use of active coping actually may be detrimental in patients with FM who have low self-efficacy for pain control.
    • Self-efficacy may be a significant determinant of pain itself, particularly with respect to its emotional arousal and unpleasant effects. In a study of patients with osteoarthritis, those scoring high for self-efficacy about arthritis pain control exhibited higher thresholds and tolerance for thermal pain compared to those with low scores. Conversely, maladaptive coping strategies, such as catastrophizing about pain, make the pain experience worse, especially with respect to the development of depression.
  • Mood, depression, and anxiety
    • Mood encompasses sadness, fear, anger, joy, interest, and surprise. Depression and anxiety are emotional disorders. A consensus is emerging that depression is a common denominator in chronic pain and fatigue. In addition, unrelieved stress is believed to be the underlying element linking depression, pain, and fatigue. As discussed above, neurohumoral dysfunction consequent to chronic stress provides, at least in part, a biologic explanation for mood disorders and subjective pain and fatigue in patients with FM and related disorders.
    • FM and major depressive disorder are similar with respect to symptomatology, lifetime prevalence of depression, patterns of comorbidity in individual patients, family history, and response to antidepressant medications. However, chronic pain is not simply a manifestation of depression. Despite frequent complaints of pain and other somatic symptoms, patients with pure major depression actually have increased pain thresholds and more stoical responses to pain stimuli. Similarly, patients with major depression have markedly fewer tender points compared to patients with FM.
  • Personality traits and disorders: Personality traits have the largest effect on the cognitive processes by which people attach meanings and implications to their pain. For example, neuroticism, which is associated with hypochondriasis, irritability, and emotional disturbance, has no influence on the discrimination of thermal pain but exerts powerful influences in the delayed, reflective stage of pain (ie, at the level of emotions related to suffering, including depression, anxiety, and, especially, frustration).
  • Pain behaviors
    • At one level, pain behaviors are the various signals that serve to communicate the pain experience to the outside world and include nonverbal expressions of pain (eg, grimacing, bracing, sighing, rubbing, groans, histrionic behavior). Increased pain behaviors are associated with more depression, reduced self-efficacy for pain control, and more negative thoughts. Pain behaviors can be important perpetuators of illness through reinforcement of the responses that the patients induce as a means to get attention, obtain medication, or avoid work or activity. This can lead to limited physical and social activity, dependence on narcotics and alcohol, and unemployment.
    • A common pain behavior in patients with FM is excessive use of medical services. Care seekers exhibit lower pain thresholds and greater psychiatric morbidity compared to patients without FM who do not have chronic pain, an observation consistent with the idea that care seeking reduces the emotional distress consequent to symptoms and life stressors.
    • Models of pain behavior that interrelate biologic, cognitive, emotional, and behavioral variables form the basis for cognitive-behavioral approaches to pain management.
• Environmental and sociocultural variables: Multiple experiences and forces in a person's environment and social culture influence the pain experience, either positively (eg, job satisfaction in a person who strains his or her back at work) or negatively (eg, physician who medicalizes a minor injury by diagnostic waffling and inappropriate diagnostic testing). Environmental and sociocultural variables include (1) psychosocial experiences during childhood, (2) spousal and family support, (3) ethnological factors, (4) focus on definable causes, (5) media hype, and (6) primary and secondary gain.
• • Developmental variables
    • These include the psychosocial experiences during childhood, including school stress, role models, unhappy families, and abuse, that shape the cognitive, affective, and behavioral aspects of pain in adults.
    • Some studies show that two thirds of patients with chronic pain have first-degree relatives with chronic pain, one third have a family member with an affective illness, and one third have a family member with alcohol abuse.
    • Childhood physical, emotional, or sexual abuse appears to be a common antecedent of anxiety, somatization, and chronic pain in many adults.
    • In this regard, biologic vulnerability may derive from persisting effects of early life stresses on the stress response system.
  • Interpersonal variables
    • Spousal and family support can either mitigate or adversely impact the various dimensions of chronic pain.
    • Training of spouses to enhance their ill partner's coping skills improves self-efficacy for pain control and reduces pain and psychologic distress. Spousal reinforcement of pain behaviors can lower experimentally determined pain thresholds.
  • Work environment and job satisfaction
    • Job satisfaction and a healthy work environment lessen the emotional distress associated with chronic pain.
    • Conversely, job dissatisfaction strongly predicts the progression of acute back pain to chronic low back pain. Similarly, workers' compensation and disability benefits can be significant disincentives for recovery from chronic pain.
  • Sociocultural factors
    • Pain tolerance may be profoundly influenced by culture (eg, greater emotional and behavioral responses to pain in Jewish and Italian patients in New York City relative to native-born Anglo-Saxons). The prevalence of widespread chronic pain is zero in Pima Indians but is approximately 10% for white populations on both sides of the Atlantic.
    • The current epidemic of FM, chronic fatigue syndrome, sick building syndrome, and multiple chemical sensitivity syndrome arguably is, at least in part, due to media hype, fear, suggestibility, and a focus on definable causes by patients and physicians.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Migraine headache
Atypical chest pain
Chronic fatigue syndrome
Multiple chemical sensitivity
Sick building syndrome
Temporomandibular disorder
Vulvar vestibulitis
Mitral valve prolapse
Dysmenorrhea
Vulvodynia

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Patients with fibromyalgia (FM) do not have characteristic or consistent abnormalities as determined by laboratory test results. Laboratory studies are important to help rule out diseases that have similar manifestations.
• Thyroid-stimulating hormone: Hypothyroidism shares many clinical features with FM, especially diffuse muscle pain and fatigue.
• Erythrocyte sedimentation rate (ESR): The normal ESR in patients with FM contrasts with the high ESR in elderly patients with polymyalgia rheumatica. Obtaining an ESR can assist in identifying an underlying inflammatory disorder.
• Antinuclear antibodies (ANAs): Many patients with SLE have comorbid FM. A low-titer ANA is common in the general population and may be of no clinical significance if diagnostic features of SLE or related autoimmune disorders are not present.
• Rheumatoid factor: Many patients with RA have comorbid FM. A positive result for rheumatoid factor does not support a diagnosis of RA unless objective evidence of characteristic joint inflammation is present. A positive result for rheumatoid factor is diagnostically nonspecific in other clinical settings.
• The ACR classification criteria have no exclusions. FM frequently coexists with well-defined diseases (eg, SLE) and should be specifically sought to allow optimum therapy.

Other Tests

• Laboratory sleep assessment: If sleep does not improve with usual conservative measures (eg, elimination of caffeine, prescription of hypnotics or nighttime tricyclics), obtaining a formal assessment by a neurologist experienced in sleep disorders may be useful.
• Although unusual, diffuse arthralgias and myalgias have been described in patients with hemochromatosis. Consider screening with a serum transferrin saturation and a serum ferritin concentration in patients aged 40-60 years, especially if small joint arthropathy in the hands and/or calcium pyrophosphate dihydrate deposition disease (CPPD) is present.

Procedures

• Obtain a verbal or numerical rating scale or a visual analog scale for pain intensity and the degree of fatigue.
• While waiting to see the physician, the patient, in a few minutes, can complete a simple self-report form that incorporates visual analog scales for pain and fatigue and a global self-assessment of how the patient is doing, along with validated scales for physical and psychologic health status (eg, modified Health Assessment Questionnaire, Fibromyalgia Impact Questionnaire, a checklist of current symptoms, scales for helplessness and cognitive performance). Easily adaptable to a busy practice, such information is invaluable for the psychosocial assessment of pain, both for aiding with diagnosis and in monitoring the response to therapy.
• Using pressure algometry (dolorimetry) for a simple determination of pressure pain thresholds at 4 tender points associated with FM (ie, both lateral epicondyles, midpoints of the trapezii) may be useful both as an aid for diagnosis and as a semiquantitative guide to therapy. Normal values are equal to or greater than 4 kg/cm².
• Psychometric testing includes the Minnesota Multiphasic Personality Inventory, the Social Support Questionnaire, the Sickness Impact Profile, and the Multidimensional Pain Inventory (MPI). In multidisciplinary settings, information obtained from these tests is useful for a more comprehensive assessment. For example, subgroups of patients with chronic pain were identified based on MPI responses that appear to predict response to interdisciplinary therapeutic interventions.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical Care

• General approach to management
• • The first crucial element in the treatment of pain, fatigue, and other diverse symptomatology in patients with fibromyalgia (FM) is empathetic listening and acknowledgment that the patient is indeed experiencing pain (ie, validate the patient's illness).
  • Accurately assess possible causal or perpetuating factors, including attention to psychologic and sociocultural factors and identification of specific regional sources of ongoing nociceptive pain (eg, degenerative spondylosis, bursitis).
  • Avoid diagnostic waffling, frightening testing, excessive use of physical therapy modalities after minor trauma, excessive activity limitation, and over-liberal work release.
  • Comments such as "it's all in your mind" or "I cannot find anything wrong with you" only add to the patient's frustration.
  • Be aware of confounders to recovery, such as pending litigation or compensation claims.
  • If significant nociceptive pain coexists with the diffuse chronic pain of FM, manage it pharmacologically with analgesics using the same stepwise approach used for acute pain.
  • The overall approach for chronic pain in FM involves a multifaceted treatment plan that incorporates various adjuvant medicines, aerobic exercise, and psychologic and behavioral approaches to reduce distress and promote self-efficacy and self-management (eg, relaxation training, activity pacing, visual imagery, distraction).
  • For associated regional chronic pain syndromes (eg, temporomandibular disorder), referral to an experienced specialist who advocates holistic, nonsurgical approaches is recommended.
• Assessment of pain (see Physical and Procedures)
• Pharmacologic management (see Medication)
• Psychologic and behavioral approaches
• • Depression, anxiety, stress, sleep disturbance, pain beliefs and coping strategies, and self-efficacy all are central to the pain experience in many patients and frequently determine the outcome of chronic pain. Depression must be treated aggressively.
  • Unless psychosocial and behavioral variables are recognized and approached, strictly pharmacologic interventions are of limited benefit.
  • Cognitive behavior therapy, which includes components for education, training in relaxation and coping skills, rehearsals of the skills learned, and relapse prevention, shows promise but should be considered experimental at this time.
  • Other useful strategies to improve coping skills include relaxation training, activity pacing, visual imagery, and distraction strategies. Instruction in proper sleep hygiene may be beneficial.
• Physical therapy/physical modalities
• • Massage is beneficial in patients with FM; however, excessive dependence on administration of physical therapy and modalities by another person may confound the patient's efforts to achieve self-efficacy for pain control.
  • The benefits of exercise for patients with FM include improvement in subjective and objective measures of pain and in an overall sense of well-being. Because many patients with chronic pain fear that activity will make their pain and fatigue worse, they become deconditioned. Graded aerobic exercise (eg, low-impact aerobics, walking, water aerobics, stationary bicycle) should start gently and progress gradually to endurance and strength training. Encouragement and positive reinforcement can improve compliance. Obesity, poor posture, and overloading activities at work and at home should be addressed.
  • Heat, massage, and other treatments are useful. Diffuse and regional pain is improved by strategies such as sauna, hot baths and showers, hot mud, and massage.
  • Trigger point injections, acupuncture, chiropractic manipulation, and myofascial release are well received by patients but are passive modalities of questionable long-term efficacy and do not promote self-efficacy for pain control.

Surgical Care

Generally accepted evidence indicating that skull surgery for correction of Chiari malformations is of benefit for patients with FM is lacking.

Consultations

• Consultation with a rheumatologist experienced in the diagnosis and treatment of FM is appropriate. In addition, a rheumatologist can assist in the differential diagnosis of chronic pain and fatigue syndromes and in the assessment of comorbid rheumatologic disorders.
• Referral to a neurologist, dentist, or other specialist may be of benefit in patients with prominent regional pain disorders that coexist with FM.
• Psychologic counseling is useful. If a psychiatric disorder is suggested, consult a psychiatrist.

Diet

Patients with FM are generally interested in diet and are influenced heavily by information promoting complementary and alternative approaches to this disorder; therefore, promote sound general nutrition, appropriate vitamin supplementation, bone health, and weight reduction, if needed.

Activity

Graded aerobic exercise is an integral part of optimum treatment for patients with FM. With the exceptions of pacing and avoidance of prolonged, overly strenuous physical exercise before reconditioning is established, limitations on activity, including work release, generally should be avoided.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Always combine pharmacologic approaches with nonpharmacologic therapy, especially stress management, aerobic exercise, and, in some cases, psychotherapy. Aggressively treat comorbid depression. Opioids, hypnotics, anxiolytics, and certain skeletal muscle relaxants must be used with caution because of the potential for abuse. Tricyclic antidepressants (TCAs) are of proven benefit. Certain newer anticonvulsants appear to decrease pain sensitivity. Corticosteroids and nonsteroidal anti-inflammatory medications are useful only as management for coexisting inflammatory processes. Pharmacologic and nonpharmacologic treatment of poor sleep is crucial for improving the patient's overall sense of well-being.

Anecdotally, dextromethorphan, an N-methyl-D-aspartate (NMDA) receptor antagonist available as an over-the-counter (OTC) antitussive, is beneficial as adjunctive therapy for patients with fibromyalgia (FM). Topical capsaicin, obtained from red chili peppers, is essentially free of toxicity, other than mild burning at the site of application, and is useful as adjunctive therapy in combination with gentle massage. Beta-blockers and/or increased fluid and sodium/potassium intake may benefit a subset of patients with orthostatic hypotension, palpitation, and vasomotor instability. Growth hormone and cytokine therapies are still experimental.

Complementary and alternative medicine (CAM) is immensely popular for patients with FM, possibly because of the frustration that many patients have with traditional medicine. Many physicians are ignorant of, if not overtly hostile toward, CAM. Patients are reluctant to inform their physician about their use of CAMs. This can be dangerous because of unsuspected drug-to-drug interactions. A practical approach is to inquire about CAM usage, refrain from expression of negative opinions if a particular CAM treatment is relatively inexpensive and appears to be safe, and encourage whatever works in the context of the power of the placebo effect and promotion of self-efficacy for pain control.

Nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen usually have limited efficacy in pain due to fibromyalgia but are important adjuncts for nociceptive pain generators, such as osteoarthritis and degenerative spondylosis. Topical anesthesia with lidocaine (5% Lidoderm patch) can also be very helpful in this regard. An occasional patient with severe allodynia may require tramadol or opioid analgesics in order to improve quality of life and to restore function.

Opioids bind opioid receptors in regions of the brain involved in integrating pain and to presynaptic and postsynaptic terminals of peripheral sensory fibers where they inhibit the release of substance P and other mediators. Older persons are more sensitive to opioids with respect to both efficacy for pain relief and vulnerability to adverse effects; therefore, the starting dose should be reduced 25-50%. Expect several weeks or months for titration after initiating opioid therapy in the outpatient setting. Tapering takes 2-3 weeks; clonidine, 0.2-0.4 mg/d, is helpful for controlling withdrawal symptoms.

Monitoring of patients receiving opioid medications requires frequent reevaluation for efficacy, improvement in daily functioning, and adverse effects during initiation, titration, and maintenance therapy. The patient should sign a narcotics contract that specifies one prescribing physician, one dispensing pharmacy, and acceptance of no early prescription of opioids if medication runs out early or is lost or stolen.

Drug Category: Anxiolytics/hypnotics

Agents of varying durations of action are used frequently for anxiety and panic and as sleep aids (poor sleep is nearly universal in FM). These agents may also have antinociceptive effects in patients with chronic pain. Anxiolytics/hypnotics are often used in combination with antidepressants and antiepileptic drugs and include benzodiazepines such as alprazolam (Xanax, <12-h half-life), temazepam (Restoril, 10- to 15-h half-life), or clonazepam (Klonopin, 25- to 100-h half-life), buspirone (BuSpar), and trazodone (Desyrel).

In considering an anxiolytic drug, remember that many antidepressants also have indications for anxiety. Zolpidem (Ambien), trazodone, zaleplon (Sonata), and eszopiclone (Lunesta), along with careful attention to optimum sleep hygiene, are useful for insomnia. An effective combination is zolpidem hs prn in combination with very-short–half-life zaleplon (5 mg) for awakenings in the middle of the night. Patients who fail to have improved sleep with the above should be referred for polysomnography.

Drug Name	Clonazepam (Klonopin)
Description	Suppresses muscle contractions by facilitating inhibitory GABA neurotransmission and other inhibitory transmitters. Long half-life (25-100 h).
Adult Dose	Initial: 1.5 mg PO divided tid Maintenance: Increase dose by 0.5-1 mg PO q3d to 0.05-0.2 mg/kg in divided doses; not to exceed 20 mg/d
Pediatric Dose	<10 years: 0.01-0.03 mg/kg/d PO bid/tid; increase dose by 0.5 mg q3d to 0.1-0.2 mg/kg/d divided tid; not to exceed 0.2 mg/kg/d >10 years: Administer as in adults
Contraindications	Documented hypersensitivity; severe liver disease; acute narrow-angle glaucoma
Interactions	Phenytoin and barbiturates may reduce effects; coadministration of CNS depressants increases toxicity
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Caution in chronic respiratory disease or impaired renal function; withdrawal symptoms can result from abrupt discontinuation

Drug Name	Zolpidem (Ambien)
Description	Indicated for insomnia. Structurally dissimilar to benzodiazepines but similar in activity, with the exception of having reduced effects on skeletal muscle and seizure threshold.
Adult Dose	10 mg PO hs; not to exceed 10 mg
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; lactation
Interactions	Increases toxicity of alcohol and CNS depressants
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	Monitor elderly patients for impaired cognitive or motor performance

Drug Name	Trazodone (Desyrel)
Description	Useful as an alternative to improve sleep and to treat anxiety and panic disorders that may be associated with FM. Antagonist at the 5-HT2 receptor and inhibits the reuptake of 5-HT. Also has negligible affinity for cholinergic and histaminergic receptors. In animals, selectively inhibits serotonin uptake by brain synaptosomes and potentiates behavioral changes induced by serotonin precursor, 5-hydroxytryptophan.
Adult Dose	Initial: 50 mg/d PO and may increase by 50 mg/d q3-4d; not to exceed 400 mg/d in divided doses; average dose is 300 mg/d Maintenance: Once an adequate response has been achieved, dosage may be reduced gradually with subsequent adjustment depending on response; keep dose at the lowest effective level
Pediatric Dose	<6 years: Not established 6-18 years: 1.5-2 mg/kg/d PO in divided doses; increase dose gradually q3-4d prn; not to exceed 6 mg/kg/d
Contraindications	Documented hypersensitivity
Interactions	May enhance response to alcohol, barbiturates, and other CNS depressants; digoxin and phenytoin serum levels may increase in patients receiving trazodone concurrently; may decrease hypoprothrombinemic effects of warfarin
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	Hypotension, including orthostatic hypotension and syncope, has occurred; may produce drowsiness, dizziness, or blurred vision; patients should observe caution while driving or performing other tasks requiring alertness, coordination, or dexterity

Drug Name	Buspirone (BuSpar)
Description	5-HT1 agonist with serotonergic neurotransmission and some dopaminergic effects in CNS. Has anxiolytic effect but may take as long as 2-3 wk for full efficacy.
Adult Dose	15 mg/d PO divided tid; increase by 5 mg/d q2-4d; not to exceed 60 mg/d
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	Toxicity is increased with MAOIs, phenothiazines, and CNS depressants; increases toxicity of digoxin and haloperidol
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Caution in hepatic or renal impairment

Drug Name	Temazepam (Restoril)
Description	Indicated for insomnia. Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.
Adult Dose	15 mg PO hs
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; narrow-angle glaucoma; untreated obstructive sleep apnea; history of substance abuse; severe uncontrolled pain
Interactions	Increases CNS toxicity of benzodiazepines with coadministration of phenothiazines, barbiturates, alcohol, and MAOIs
Pregnancy	D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions	Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Drug Category: Skeletal muscle relaxants

Have modest short-term benefit as adjunctive therapy for nociceptive pain associated with muscle strains and, used intermittently, for diffuse and certain regional chronic pain syndromes;. Long-term improvement over placebo has not been established in fibromyalgia. Cyclobenzaprine, a tricyclic, can be helpful for sleep and pain control as a single nighttime dose in combination with an anxiolytic/hypnotic agent. Sedation and other CNS effects occur frequently. Abuse may occur, particularly with carisoprodol (not recommended in fibromyalgia), and abrupt cessation may be associated with withdrawal symptoms.

Drug Category: Antidepressants

Low-dose TCAs are of proven short-term efficacy for pain control and improved sleep in patients with FM, but adverse effects (eg, dry mouth, drowsiness, weight gain) limit patient acceptance. SSRIs and certain dual reuptake inhibitors also have been shown to improve symptoms in fibromyalgia independently of their effects on depression. SSRIs include fluoxetine (Prozac), citalopram (Celexa), escitalopram (Lexapro), fluvoxamine, paroxetine (Paxil), and sertraline (Zoloft). A useful combination is a TCA, such as amitriptyline in low dosage at bedtime and an SSRI, such as fluoxetine, every morning or one of the newer dual serotonin/norepinephrine reuptake inhibitors, such as venlafaxine (Effexor) or duloxetine (Cymbalta), all of which have been shown to improve many symptoms in fibromyalgia irrespective of comorbid depression. Carefully monitor the patients for worsening depression or emergence of suicidal thoughts.

Drug Name	Duloxetine (Cymbalta)
Description	Potent inhibitor of neuronal serotonin and norepinephrine reuptake. Antidepressive action is theorized to be due to serotonergic and noradrenergic potentiation in CNS.
Adult Dose	20 mg PO bid; may increase to 60 mg/d administered qd or divided as 30 mg bid
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity; uncontrolled narrow-angle glaucoma; within 14 d of stopping MAOI use (do not initiate MAOIs within 5 d of stopping duloxetine)
Interactions	Metabolized by CYP1A2 and CYP2D6; coadministration with drugs that inhibit CYP1A2 (eg, fluvoxamine, cimetidine, ciprofloxacin, enoxacin) may increase duloxetine blood levels and toxicity; coadministration with drugs that inhibit CYP2D6 (eg, paroxetine, fluoxetine, quinidine) may increase duloxetine blood levels and toxicity; duloxetine moderately inhibits CYP2D6 and may decrease elimination of CYP2D6 substrates (eg, tricyclic antidepressants, phenothiazines [eg, thioridazine], type 1C antiarrhythmics [eg, propafenone, flecainide]); coadministration with MAOIs may cause serious, sometimes fatal reactions that include hyperthermia, rigidity, myoclonus, autonomic instability, and mental status changes such as extreme agitation, delirium, and coma (see contraindications)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	Observe closely for clinical worsening and suicidality when initiating treatment or following dosage change; gradually decrease dose when discontinuing, do not abruptly discontinue; caution with hepatic impairment or end-stage renal disease; recommended not to prescribe to patients with substantial alcohol use or evidence of chronic liver disease; may cause slight blood pressure increase; may activate mania or hypomania; common adverse effects include nausea, dry mouth, constipation, decreased appetite, fatigue, somnolence, and increased sweating

Drug Category: Anticonvulsants

These agents are useful for chronic pain states, including FM and related syndromes and various types of neuropathic pain, and serve as adjunctive medications for disturbed sleep and depression. Multiple choices are available, including gabapentin (Neurontin), topiramate (Topamax, also useful for migraine prophylaxis), tiagabine (Gabitril), and recently released pregabalin (Lyrica), which has been particularly well-studied in fibromyalgia. Knowledge of idiosyncrasies of these drugs is helpful in patient care. For example, gabapentin may cause weight gain, while topiramate is associated with weight loss.

Drug Name	Pregabalin (Lyrica)
Description	Structural derivative of GABA. Mechanism of action unknown. Binds with high affinity to alpha2-delta site (a calcium channel subunit). In vitro, reduces calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. FDA approved for neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, or fibromyalgia. Also indicated as adjunctive therapy in partial-onset seizures.
Adult Dose	75 mg PO bid initially; increase to 150 mg PO bid within 1 wk based on efficacy and tolerability; may further increase dose to 225 mg bid if needed
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	May cause additive effects on cognitive and gross motor functioning when coadministered with drugs that cause dizziness or somnolence
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	Discontinue gradually (over a minimum of 1 wk) to minimize increased seizure frequency in patients with seizure disorders; may cause insomnia, nausea, headache, or diarrhea with abrupt withdrawal; common adverse effects include dizziness, somnolence, blurred vision, weight gain, and peripheral edema; may elevate creatinine kinase level, decrease platelet count, and increase PR interval; doses >300 mg/d associated with higher rate of adverse effects and treatment discontinuation; decrease dose with renal impairment (ie, CrCl <60 mL/min); angioedema has been reported during postmarketing surveillance

Drug Name	Topiramate (Topamax)
Description	Sulfamate-substituted monosaccharide with broad spectrum of antiepileptic activity that may have state-dependent sodium channel–blocking action, potentiates inhibitory activity of neurotransmitter GABA. May block glutamate activity. Effectiveness in West syndrome has been investigated in one open-label study with promising results.
Adult Dose	50 mg/d PO; titrate by 50 mg/d at 1-wk intervals to target dose of 200 mg bid, not to exceed 1600 mg/d
Pediatric Dose	Initial starting dose: 2 -3 mg/kg/d PO; increment of 2-3 mg/kg q3-4d Maintenance dose: 15-20 mg/kg/d PO
Contraindications	Documented hypersensitivity
Interactions	Phenytoin, carbamazepine, and valproic acid can significantly decrease topiramate levels; when administered concomitantly, topiramate reduces digoxin and norethindrone levels; concomitant use with carbonic anhydrase inhibitors may increase risk of renal stone formation and should be avoided; use topiramate with extreme caution when administering concurrently with CNS depressants since may have an additive effect in CNS depression, as well as other cognitive or neuropsychiatric adverse events
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	Risk of developing a kidney stone formation is increased 2-4 times that of untreated population (risk may be reduced by increasing fluid intake); caution in renal or hepatic impairment; patients taking topiramate should seek immediate medical attention if they experience blurred vision or periorbital pain (continued usage after symptoms develop can lead to glaucoma); primary treatment is discontinuation of topiramate; if left untreated, serious sequelae, including permanent vision loss, may occur; oligohidrosis and hyperthermia has been reported predominantly in children during vigorous exercise or exposure to warm environmental temperatures (ensure proper hydration prior and during activity and warm temperatures) May cause hyperchloremic, non–anion gap metabolic acidosis or acute or chronic metabolic acidosis resulting in hyperventilation and nonspecific symptoms, such as fatigue and anorexia, or more severe adverse effects including cardiac arrhythmias or stupor; chronic untreated metabolic acidosis may increase nephrolithiasis or nephrocalcinosis risk, osteomalacia (ie, rickets in pediatric patients), or osteoporosis, with an increased risk for bone fractures; chronic metabolic acidosis in pediatric patients may also reduce growth rates; measure baseline and periodic serum bicarbonate; sprinkle capsules should be swallowed whole or carefully open capsule and sprinkle contents on soft food immediately before ingestion, do not chew or crush

Drug Name	Tiagabine (Gabitril)
Description	Mechanism of antiseizure effect unknown. However, believed to be related to its ability to enhance activity of GABA, major inhibitory neurotransmitter in CNS. May block GABA uptake into presynaptic neurons, permitting more GABA to be available for receptor binding on surfaces of postsynaptic cells and possibly prevents propagation of neural impulses that contribute to seizures by GABAergic action. Modification of concomitant AEDs not necessary, unless clinically indicated.
Adult Dose	4 mg PO qd divided bid/qid; increase by 4-8 mg/wk until clinical response achieved or until total daily dose of 56 mg/d administered; doses >56 mg/d have not been systematically evaluated in adequate well-controlled trials
Pediatric Dose	<12 years: Not established 12-18 years: 4 mg PO qd; increase by 4 mg at beginning of wk 2; thereafter, total daily dose may be increased by 4-8 mg/wk until clinical response achieved or until 32 mg/d administered; doses >32 mg/d have been tolerated in small number of adolescent patients for relatively short duration
Contraindications	Documented hypersensitivity
Interactions	Cleared more rapidly in patients treated with carbamazepine, phenytoin, primidone, and phenobarbital than in patients who have not received these drugs
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studies in humans; may use if benefits outweigh risk to fetus
Precautions	Patients receiving valproate monotherapy may require lower doses or a slower dose titration of tiagabine for clinical response; moderately severe to incapacitating generalized weakness has been reported following administration of tiagabine in up to 1% of patients with epilepsy; weakness may resolve after a reduction in dose or discontinuation of tiagabine; tiagabine should be withdrawn slowly to reduce potential for increased seizure frequency

Drug Category: Antihypertensive Agent

Helpful in controlling withdrawal symptoms during tapering of opioids, which may take 2-3 wk.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Outpatient Care

• Follow-up care is greatly facilitated by the following:
• • Maintaining rapport
  • Encouraging compliance with exercise regimens
  • Paying attention to current psychologic and physical stressors
  • Obtaining self-report questionnaire information that provides semiquantitative data concerning the patient's function, levels of pain and fatigue, and global self-assessment of how the patient is doing

Complications

• Patients may develop extreme allodynia with high levels of distress, opioid or alcohol dependence, marked disability, and severe depression and anxiety.
• Opioid or alcohol dependence
• Marked functional impairment
• Severe depression and anxiety
• Obesity and physical deconditioning

Prognosis

• Although entirely reversing the allodynia and hyperalgesia in patients with fibromyalgia (FM) may not be possible, many patients improve significantly in response to therapy if ongoing stressors are relieved and self-efficacy for pain control can be achieved.
• Prognosis is guarded for patients who are highly distressed and have long-standing FM, major psychiatric disease, an ingrained pattern of work avoidance, or established disability compensation.
• Prognosis is poor in patients with opioid or alcohol dependence, marked functional impairment despite multidisciplinary approaches to treatment, and severe depression and anxiety that responds poorly to treatment.

Patient Education

• Education is an essential element in therapy. It begins with an empathetic manner on the part of the physician, who must affirm the patient's pain, explore social and behavioral variables (both in childhood and current) that influence this illness, and explain to the patient how stress and distress can amplify pain and fatigue. Front loading of time to accomplish this saves time in subsequent visits. Effort should be made by the patient to foster self-efficacy, with diminishing dependence on health care providers.
• Excellent educational resources include the Arthritis Foundation, various FM advocacy groups, and certain Internet sites, such as Arthritis Foundation; MedlinePlus Health Information, a service of the US National Library of Medicine and the National Institutes of Health; American College of Rheumatology; Missouri Arthritis Rehabilitation Research and Training Center; A Physician's Guide to Fibromyalgia Syndrome; The American Fibromyalgia Syndrome Association; Chronic Fatigue Syndrome and
  Fibromyalgia; Fibromyalgia.com; Health information for the whole family from the American Academy of Family Physicians; and Friends International Support. Local patient support groups can also be helpful if the overall tenor of meetings is one of optimism and realism rather than pessimism and quick-fix orientation.
• For excellent patient education resources, visit eMedicine's Muscle Disorders Center; Mental Health and Behavior Center; and Back, Ribs, Neck, and Head Center. Also, see eMedicine's patient education articles Fibromyalgia, Chronic Fatigue Syndrome, Chronic Pain, Fatigue, and Pain Medications.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• Secondary gain becomes a major perpetuator of illness in people with fibromyalgia (FM) if injury at work or in minor motor vehicle accidents is inappropriately identified as a trigger of their illness. Well-meaning physicians, unaware of the biopsychosocial nature of FM and current clinical and epidemiologic research data that, in the aggregate, fail to support trauma as a cause or trigger of FM, unwittingly create legal imbroglios that adversely affect the patient's long-term prognosis. Importantly, remember that associations of events do not establish causality.
• The ACR criteria for classification of FM have created a major pitfall with respect to diagnosis. These are classification criteria, not diagnostic criteria, and have not been validated in compensation settings. Pain at tender points is subject to manipulation by the patient. The ACR criteria have no place for diagnosis in clinical settings.
• Although no basis for many of the multiple symptoms of patients with FM will be found upon physical examination or laboratory testing, the physician must remain alert for organic illness (eg, colon carcinoma in a patient with irritable bowel syndrome).

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment