eMedicine Specialties > Rheumatology > Soft Tissue and Regional Rheumatic Disease

Fibromyalgia

Author: John Buckner Winfield, MD, Herman and Louise Smith Distinguished Professor of Medicine in Arthritis Emeritus, Department of Medicine, Senior Member, Neurosensory Disorders Center, University of North Carolina at Chapel Hill; Consulting Rheumatologist, Appalachian Regional Rheumatology
Contributor Information and Disclosures

Updated: Feb 20, 2009

Introduction

Background

Fibromyalgia (FM) typically presents in young or middle-aged females as persistent widespread pain, stiffness, fatigue, disrupted unrefreshing sleep, and cognitive difficulties, often accompanied by multiple other unexplained symptoms, anxiety and/or depression, and functional impairment of daily living activities.

Fibromyalgia was once often dismissed by physicians and the public as a psychological disorder or "waste basket" diagnosis because of an absence of objective findings on physical examination and usual laboratory and imaging evaluations. Many physicians still do not accept fibromyalgia as a discrete illness. However, recent basic and clinical investigation has rapidly clarified the neurophysiologic bases for fibromyalgia and has led to its new classification as a central sensitivity syndrome (CSS).¹ Indeed, fibromyalgia can now be considered a neurosensory disorder characterized, in part, by abnormalities in CNS pain processing.² Increased understanding of the biological bases underlying fibromyalgia is rapidly leading to a new era of specific pharmacologic therapy for the condition.

At a clinical level, fibromyalgia is much more than widespread pain. It overlaps substantially with the following:

• Other central sensitivity syndromes (eg, chronic fatigue syndrome, irritable bowel syndrome, chronic pelvic pain syndrome/primary dysmenorrhea, temporomandibular joint pain, tension-type headaches/migraine, posttraumatic stress disorder [PTSD], multiple chemical sensitivity, periodic limb movement disorder/restless legs syndrome, interstitial cystitis)
• Other regional pain syndromes
• Mood and anxiety disorders

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 may diagnose irritable bowel syndrome. Wood (2008) published a useful summary of therapeutic approaches to CSS comorbidities in fibromyalgia.³ In addition, fibromyalgia coexists in unusually high frequency with certain illnesses characterized by systemic inflammation, such as rheumatoid arthritis (RA),⁴ systemic lupus erythematosus (SLE),⁵ and chronic hepatitis C infection,⁶ among others. In such cases, both disorders must be recognized and treated for optimum therapeutic outcome.

Pathophysiology

The prevailing paradigm for the development of fibromyalgia involves (1) certain vulnerability elements (female sex, genes,⁷ abuse or other adverse experiences during childhood when the brain is still developing) and (2) persistent stress or distress.^8,9,10 Psychologic variables (eg, distress, mood and anxiety disorders, personality traits and disorders, catastrophizing, coping, self-efficacy for pain control) play a central role in the pain experience, overall morbidity, and prognosis in patients with fibromyalgia.¹¹

High levels of anxiety and distress, less certainty of pain resolution, and a history of trauma are predictors of whether the acute pain will progress to chronic pain. Consistent with the 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.

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" (Merskey, 1986). 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 two 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 fibromyalgia.^12,13,14,15 Negative emotions (eg, depression and anxiety) and 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 fibromyalgia, such negative emotional, motivational, and cognitive stressors may dominate the clinical picture, potentially leading to a self-sustaining neuroendocrine cascade that contributes to flu-like 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. Growth-hormone abnormalities are also thought to contribute to symptomatology in fibromyalgia.¹⁶

Pain in patients with fibromyalgia 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. These phenomena can be demonstrated clinically by pressure algometry (dolorimetry) or in research settings with quantitative sensory testing (QST) using pressure, heat, cold, or electricity as stimuli. Underlying these changes in thresholds is altered processing of nociceptive stimuli in the CNS (central sensitization).

Demonstrated abnormalities in pain processing in fibromyalgia include (1) excess excitatory (pronociceptive) neurotransmitters (eg, substance P, glutamate levels in the insula), (2) low levels of inhibitory neurotransmitters (eg, serotonin and norepinephrine) in descending antinociceptive pathways in the spinal cord, (3) maintained enhancement of temporal summation of second pain, (4) altered endogenous opioid analgesic activity in several brain regions known to play a role in pain modulation, and (5) dopamine dysregulation, among others.^{17,18,19,20,21}

High throughput genotyping is rapidly identifying a series of single nucleotide polymorphism (SNP) haplotypes that influence neurotransmitter levels and receptor levels in the brain that contribute to the various abnormalities in pain processing.²² Such SNP haplotypes constitute vulnerability elements in the development of fibromyalgia and other central sensitivity syndromes. Pharmacologic agents known to be effective in reducing pain in fibromyalgia function in this regard by either increasing levels of inhibitory neurotransmitters (eg, duloxetine) or decreasing levels of excitatory neurotransmitters, in turn increasing levels of substance P (eg, gabapentin or pregabalin).^17,23 Because fibromyalgia is a polygenic syndrome with multiple different underlying genetic polymorphisms, genetic testing to tailor therapy and to predict response to therapy will soon become available.

Frequency

United States

Chronic pain and fatigue are extremely prevalent in the general population,^24,25,26 especially among women and persons of lower socioeconomic status. The prevalence of regional pain is 20%; widespread pain, 11%; fibromyalgia according to the American College of Rheumatology (ACR) criteria,²⁷ 3-5% in females and 0.5-1.6% in males; and chronic fatigue, approximately 20%. Because the ACR criteria are relatively insensitive, the actual prevalence of fibromyalgia is higher.

Mortality/Morbidity

• Fibromyalgia is a chronic relapsing condition. In academic medical centers, long-term follow-up care of patients with fibromyalgia reportedly averages 10 outpatient visits per year and 1 hospitalization every 3 years. Chronic pain and fatigue in fibromyalgia increases the risk for metabolic syndrome.
• A subset of patients with fibromyalgia consider themselves to be more ill and more impaired, reporting markedly abnormal scores for pain, functional disability, fatigue, sleep disturbance, and psychologic status.²⁸ They have significantly higher levels of comorbid illness and healthcare utilization and costs than matched controls. The annual economic burden of fibromyalgia in 2005 was $10,199 (US dollars) per patient per year, nearly double that of matched controls.²⁹

Sex

• Fibromyalgia as defined by the ACR criteria is more common in females than in males, with a female-to-male ratio of approximately 9:1.
• Males with fibromyalgia tend to have lower health perception and more physical limitations than females. Females with fibromyalgia have greater pain sensitivity³⁰ and may exhibit greater life interference due to pain.
• 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.¹¹

Age

• Although usually considered a disorder of women aged 20-50 years, fibromyalgia is observed in pediatric populations,³¹ especially in adolescents, and in older persons.³² Fibromyalgia in children responds to a combination of psychotherapy, exercise, relaxation techniques, and education. Pharmacotherapy is generally not indicated.

Clinical

History

Fibromyalgia (FM) is a disorder of chronic widespread pain with associated fatigue, poor sleep, stiffness, cognitive difficulties, multiple somatic symptoms, and, not infrequently, anxiety and/or depression.

• Pain in patients with fibromyalgia radiates diffusely from the axial skeleton over large areas of the body, predominantly involving muscles and musculoskeletal junctions, but also in joints (arthralgia without actual synovitis) and is described as exhausting, burning, miserable, or unbearable. The pain may also be multifocal and can wax and wane in a migratory fashion. Patients with fibromyalgia usually describe "pain all over." However, multifocal pain or recurrent episodes of regional pain are essentially equivalent to the classic "pain all over" description.
• Fatigue and poor sleep are virtually universal in individuals with fibromyalgia. Most patients with fibromyalgia also meet the classification criteria for chronic fatigue syndrome.
• Cognitive problems (known as "fibrofog") may be a primary symptom of fibromyalgia, reflecting impairments in working, episodic, and semantic memory that are roughly equivalent to 20 years of aging.³³ Cognitive symptoms associated with fibromyalgia are exacerbated by pain, mood and anxiety disorders, and poor sleep.
• Other common symptoms associated with fibromyalgia include the following:
  • Weight fluctuations
  • Allergic symptoms (eg, nasal congestion) and hypersensitivity to environmental stimuli (eg, odors, bright lights, loud noises) and medications
  • Regional pains, including noncardiac chest pain, dyspepsia, headache, abdominal cramping (irritable bowel syndrome), temporomandibular pain, chronic pelvic pain, and others (Patients with fibromyalgia may meet criteria for 3 or more central sensitivity syndromes.)¹
  • Syncope or dizziness
  • Shortness of breath
  • Urinary frequency and urgency (female urethral syndrome, interstitial cystitis)
• The 1990 ACR classification criteria for fibromyalgia 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.²⁷ These are classification criteria for selection of subjects for research studies rather than diagnostic criteria and should not be used for clinical diagnosis. Efforts to develop and validate improved criteria suitable for diagnosis by nonspecialist clinicians are currently underway.
• Attention to certain aspects of the history is of particular relevance in fibromyalgia. These include details of the social and development history (abuse, alcoholism in a parent during childhood, past and ongoing stressors, belief regarding triggers of illness, ongoing compensation claims, work status), previous treatment modalities and their efficacy, and opioid prescription.

Physical

Except for painful tender points and, perhaps, signs of deconditioning, physical examination findings are normal in patients with fibromyalgia. Pain, not just tenderness, is present at multiple fibromyalgia tender points when pressure (approximately 4 kg/cm²) is applied manually, with pressure increasing gradually at the rate of 1 kg per second over 4 seconds (see Image 2). However, pain upon 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) that are relatively insensitive to pain in healthy patients.

• Clinical assessment
  • The clinical assessment may reveal objective evidence for a discrete illness, such as hypothyroidism, RA, SLE, polymyalgia rheumatica, or another inflammatory or autoimmune disorder. Such findings do not exclude comorbid fibromyalgia. Indeed, approximately 25% of patients with RA 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 is a pressure algometer, or dolorimeter (see Image 3). Applied to several tender points, a pressure algometer enables rapid and simple demonstration of decreased thresholds for pain perception and pain tolerance in the clinic examining room. Pressure algometry can also serve as a useful tool for educating the patient regarding the nature of altered central nociceptive processing, allodynia (pain with stimuli that should not cause pain, such as gentle touching) and hyperalgesia (amplification of pain experienced from peripheral stimuli that are expected to be painful).

Causes

The etiology of fibromyalgia is multifactorial. While the causes of fibromyalgia have not yet been fully clarified, remarkable progress in the understanding of this disorder has recently been made. 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) provides a useful way to conceptualize fibromyalgia (see Image 4).³⁴

• Biologic variables: Certain biologic variables contribute to the development and persistence of fibromyalgia, although none, as a single element, explains all facets of fibromyalgia. Certain variables (eg, physical trauma, exposure to toxins) have been widely incriminated by the public, particularly in medicolegal settings, but are actually of little significance in the etiology of fibromyalgia as shown by recent prospective research studies.
  • Inheritance: Family studies³⁵ initially pointed to a role for genes in fibromyalgia. With application of sophisticated genotyping and statistical methodology, the extremely important genetic contribution to fibromyalgia and related central sensitivity syndromes is becoming increasingly recognized.⁷ For example, altered serotonin metabolism in a subgroup of patients with fibromyalgia has been linked to a genotype of the promoter region of the serotonin transporter gene.³⁶ SNP haplotypes in the catecholamine-O-methyltransferase and β2-adrenergic receptor genes have been linked to increased pain perception.^22,37
  • Female sex³⁰
    • Sex-related effects are important in fibromyalgia 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 are more likely to evoke SNS, HPA axis, and psychologic responses in females than in males.
  • Age
  • Sleep: Almost all patients with fibromyalgia sleep poorly, hence the common report that a night of poor sleep is followed by a more painful day. Indeed, intrusion of alpha waves into slow delta wave stage III/IV (deep) sleep was the first objective abnormality observed in fibromyalgia.³⁸ Although not the proximate cause of fibromyalgia, 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 fibromyalgia has been a highly contentious and medicolegally charged issue in American society. 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, numerous controlled investigations on this issue are now available. The preponderance of current evidence does not support physical trauma as a significant causative factor in the development of fibromyalgia.^{39,40,41,42,43} At a clinical level, however, patients who attribute their fibromyalgia to trauma have more perceived disability, self-reported pain, life interference, and affective distress than patients with idiopathic onset.
  • Physical deconditioning
  • Stress/neuroendocrine and autonomic dysregulation^9,8,13,7,15
    • A large body of data suggests that fibromyalgia, chronic fatigue syndrome, regional chronic pain syndromes, and certain emotional disorders that frequently coexist with fibromyalgia 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 maladaptation of the stress response system in the face of the almost universal stress and consequent distress that characterizes modern life.
  • Central sensitization and abnormal central nociceptive processing: Fibromyalgia pain can now be classified as a neurosensory disorder.
  • Viruses or other infections: While considered unlikely to be sole triggers, infection may contribute to exacerbation of symptomatology via cytokine-vagus nerve stimulation of the CRH neuron/stress response system in bidirectional brain–immune system communication.⁶
  • Decreased collagen cross-linking, hypermobility, Chiari malformation, and environmental chemicals: The relationship of these variables to the development of fibromyalgia is unclear.
• Cognitive-behavioral variables: While not significant in all patients with fibromyalgia, cognitive-behavioral variables can be pivotal in the development and maintenance of persistent pain and functional disability.¹¹ The repertoire of operant cognitive-behavioral variables in adults 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 some patients with fibromyalgia exhibit meaning structures that facilitate their "invisible," "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 fibromyalgia could have psychologic antecedents. When this occurs, physicians and/or counselors should assist the patient in avoiding to 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 fibromyalgia. Thus, some patients with fibromyalgia 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 self-reported disability versus observed functional disability can be high in some patients with fibromyalgia but is generally low or absent in patients with other rheumatic diseases, such as ankylosing spondylitis and RA.
  • Hypervigilance:⁴⁴ Certain data support a hypervigilance model of pain in patients with fibromyalgia. Heightened sensitivity to pain is due, at least in part, to increased attention to external stimuli and a preoccupation with pain sensations. Here, pain is amplified by hypervigilance to pain. Patients with fibromyalgia may 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 less pain. Treatments that improve coping reduce pain and enhance a positive mood. Excessive use of active coping may actually be detrimental in patients with fibromyalgia 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.⁴⁵ Conversely, maladaptive coping strategies, such as catastrophizing about pain, worsen the pain experience, especially with respect to the development of depression.
    • Pain catastrophizing, defined as characterizing pain as unbearable or horrible, is an important factor in the experience of pain. Recent research using functional magnetic resonance imaging (fMRI) to measure regional cerebral blood flow (rCBF) and quantitative sensory testing (QST) techniques has demonstrated that pain perception is augmented by increased activity in response to painful stimuli in brain areas involved in anticipation of pain (medial frontal cortex, cerebellum), attention to pain (dorsal anterior cingulate gyrus, dorsolateral prefrontal cortex), and emotional aspects of pain (claustrum, closely connected to the amygdala) in persons with high catastrophizing.⁴⁶
  • Depression and anxiety
    • Lifetime psychiatric comorbidity is common in individuals with fibromyalgia, including mood disorders (bipolar disorder, major depressive disorder), anxiety disorders (generalized anxiety disorder, obsessive-compulsive disorder, panic disorder, PTSD, social phobia), eating disorders, and substance use disorders.^47,48 Patients with fibromyalgia can be subgrouped based on pressure-pain thresholds (degree of tenderness with application of pressure) and such psychological factors.⁴⁹ Low tenderness is associated with moderate depression/anxiety, moderate catastrophizing, and moderate control over pain; high tenderness is associated with high depression/anxiety, high catastrophizing, and low control over pain; extremely high tenderness is associated with normal levels of depression/anxiety, very low catastrophizing, and highest control over pain.
    • Depression contributes to the subjective unpleasantness and distress of pain through parallel, somewhat independent neural pain processing networks for purely sensory and affective pain elements. This has been demonstrated in studies combining QST and fMRI in healthy subjects, subjects with fibromyalgia and no depression, and subjects with fibromyalgia and comorbid depression.⁵⁰ The first two groups exhibit increased rCBF only in the somatosensory cortices and the anterior insula; the group with fibromyalgia and depression shows, in addition, increased rCBF in the amygdala and contralateral anterior insula, which are involved in affective pain processing.
    • However, chronic pain is not simply a manifestation of depression. Despite common reports of pain and other somatic symptoms, patients with pure major depression actually have fewer tender points than patients with fibromyalgia,⁵¹ increased pain thresholds, and more stoical responses to pain stimuli.
  • Personality traits and disorders¹¹
    • 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).
    • Several personality styles among patients with fibromyalgia are encountered in clinical practice.⁵² Most common is a perfectionism-compulsiveness personality, characterized by a rigid belief system in the need to be perfect, high underlying anxiety, and an unawareness of feelings and emotions. Another common personality style is the self-sacrificing type, characterized by a tendency to put everyone else’s needs before their own. Less common is the "wounded warrior" type, who may be totally helpless and disabled physically and psychologically, carrying a great burden of adverse psychosocial experiences and psychiatric comorbidity. Theses three personality styles are difficult to treat and often require counseling or psychiatric intervention. The "resilient" patient who lacks maladaptive schemas and psychiatric comorbidity has a much better prognosis.
  • 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 patients with fibromyalgia induce as a means to get attention, to obtain medication, or to 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 fibromyalgia is an excessive use of medical services. Care seekers exhibit lower pain thresholds and greater psychiatric morbidity than patients without fibromyalgia 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 and operant-behavioral approaches to pain management.
• Environmental and sociocultural variables:¹¹ 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 (eg, school stress, role models, unhappy families, 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. For example, in a community population-based screening survey, the association of childhood abuse and the presence of more than 5 tender points (a characteristic of fibromyalgia) in adults was very strong (OR, 6.9; 95% CI, 2.0-24.6).⁵³ Biologic vulnerability likely derives, in part, from persisting effects of early life stresses on the stress response system.
  • Interpersonal variables
    • Spousal and family support can either mitigate or adversely affect 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% in white populations on both sides of the Atlantic.
    • The current epidemic of fibromyalgia, chronic fatigue syndrome, sick building syndrome, and multiple chemical sensitivity syndrome is arguably due, at least in part, to media hype, fear, suggestibility, and a focus on definable causes by patients and physicians.

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