Fibromyalgia: An Overview of Etiology and Non-pharmaceutical Treatment Options
Fibromyalgia is a complex chronic pain disorder that can result in great personal1 and economic burden on the medical system,2 as well as strain on employers.3,4 The prevalence of fibromyalgia has been determined to range from 2% to 5% in the general population,5,6 with women seven times more likely than men to be affected.7 This article reviews the literature and examines the etiology, comorbid symptoms and disorders, and non-pharmacological treatment options for fibromyalgia.
The 1990 American College of Rheumatology (ACR) criteria for diagnosing fibromyalgia includes the presence of chronic widespread pain for a minimum of three months and the presence of at least 11 of 17 tender points with a manual tender point assessment.8 Chronic widespread pain is defined as pain above and below the waist, on the left and right side of the body, with at least one point along the axial skeleton. In 2010, the ACR proposed new diagnostic criteria, which eliminate the manual tender point evaluation, assess widespread pain somewhat differently, and include the assessment of additional symptoms of unrefreshed sleep, general fatigue, and cognitive deficits.8,9
Fibromyalgia is associated with a number of other similar syndromes, including chronic fatigue syndrome, irritable bowel syndrome, migraine/tension headache, and temporomandibular joint disorder.10,11 Common symptoms of these related syndromes include pain, fatigue, poor sleep, cognitive deficits, headaches, anxiety, and depression.12 The prevailing theory is that the root etiology of all of these related syndromes, including fibromyalgia, can be attributed to abnormal pain processing in the central nervous system. Within this central sensitization theory, central nervous system neurons become hyperexcitable, and descending inhibitory pathways in the spinal cord become suppressed, resulting in hypersensitivity to both noxious and non-noxious stimuli.13-20
Recent research, employing neuroimaging of fibromyalgia patients, has focused on specific regions of the brain, including the amygdala, the dorsal cingulate, and the nucleus accumbens.21 Using positron emission tomography (PET), studies of fibromyalgia patients have shown reduced binding potential of μ-opioid receptors in these brain regions. Harris et al posit that this finding explains why prescribed opioids are not as effective in fibromyalgia patients for pain management.21 There is also evidence of altered peripheral pain mechanisms,22 hypoactivity of the sympathetic-adrenal system, and hyporeactivity of the hypothalamic-pituitary system23,24 in patients with fibromyalgia.
How Does Fibromyalgia Develop?
The factors that cause the development of fibromyalgia are currently not well understood, but some predictive variables have been identified. Because central sensitization can be produced by physical trauma and/or sustained pain impulses, it has been proposed that fibromyalgia might develop from an acute injury.25-27 An association between whiplash/cervical injury and fibromyalgia has been identified by several researchers.28-30 In fact, one study reported that fibromyalgia was 13 times more frequent following a neck injury in patients than following a lower extremity injury.30
However, a more recent prospective study conducted on patients in automobile accidents showed that there was no association between neck injuries and the occurrence of fibromyalgia.31 These results were confirmed in a 3-year follow-up study.32 However, another study found that patients with regional pain syndromes, such as chronic neck or low back pain, are at risk for developing central sensitization, chronic widespread pain, and fibromyalgia.33 The study reported that 22.6% of patients presenting with neck or back pain had developed chronic widespread pain 5 years later.25
Emotional trauma has also been found to predict the onset of fibromyalgia.34 A recent study in Israel found that 15% of train wreck survivors had developed fibromyalgia, in addition to a number of other psychiatric and physical symptoms, 3 years after the wreck.35 A link between childhood abuse/trauma and the later development of fibromyalgia has also been suggested.36-38 In one study, subjects indicating psychological distress were given manual tender point examinations in conjunction with assessments regarding childhood traumas; those subjects with a greater number of tender points were found to have reported more aversive experiences.39
Finally, other factors including genetic predisposition, infections, neuroendocrine dysfunction, and even vaccinations have been implicated as precipitating factors in the development of fibromyalgia.11,40
It has been well documented that fibromyalgia is associated with increased psychosocial distress and psychiatric disorders, especially depression.41-44 The relationship between psychosocial distress and depression is bi-directional—as both a precipitating factor and a result of fibromyalgia.18
Stress has been suggested as a fibromyalgia symptom mediator. In one sample of fibromyalgia patients, 65% reported stress as a factor associated with their conditions. They demonstrated decreased reactivity to stress via the adrenal glands and the sympathetic nervous system, suggesting that fibromyalgia may be associated with a faulty stress-response system.24
Gracely et al investigated catastrophizing (ie, characterizations of pain as awful, horrible, and unbearable) in fibromyalgia patients.45 By using functional magnetic resonance imaging technology, patients with fibromyalgia reported elevated levels of catastrophizing and showed increased activation in multiple brain areas tied to the expectation of pain, concentration on pain, and the emotional facets associated with pain. Catastrophizing was seen to amplify the sensitivity to pain as a result of a heightened anticipation along with increased awareness of the pain source.
The Role of Sleep Disturbance
Fibromyalgia is highly associated with poor sleep quality and non-refreshing sleep. More than 75% of fibromyalgia subjects report disturbed sleep.46 A decrease in nighttime melatonin production and abnormalities in circadian rhythm of hormonal profiles and cytokines has been found in fibromyalgia subjects.47 Polysomnographic studies have confirmed that, compared to controls, fibromyalgia patients demonstrate more periodic limb movements and more superficial sleep, at the expense of deep sleep.48