Pathoetiology. The prevalence and severity of fibromyalgia are determined by impaired slow-wave sleep, the magnitude of mood disturbance, and gene polymorphisms. These factors influence the brain and dorsal horns of the spinal cord, resulting in abnormally low pain thresholds, also known as allodynia. They also activate the stress response, which, in turn, negatively affects the endocrine and autonomic nervous system.

Clinical Manifestations/Diagnosis. Fibromyalgia has a prevalence of about 2%, is more often seen in women, and usually begins as a subacute illness, often with a prior history of related symptoms such as irritable bowel syndrome present before diffuse pain and fatigue become prominent. When it appears after a traumatic event or remembered illness, it is likely that these events marked the onset of the proximate cause of fibromyalgia, which is chronic stress.

The new preliminary diagnostic criteria highlight the core symptoms of fibromyalgia and emphasize the point that fibromyalgia is not just pain. Other symptoms of multisystem amplification responses occur that include increased sensitivity to light, odors, and sound, headache, temporomandibular facial pain, orthostatic hypotension, subjective shortness of breath, intermittent constipation and diarrhea, urinary frequency, subjective weakness, and diffuse paresthesias.

The key finding at physical examination is diffuse articular and nonarticular pain with palpation. Certain tools/questionnaires can be used to better characterize the patient, including the Symptom Intensity Scale and Fibromyalgia Impact Questionnaire, to establish diagnosis and severity. Other tools, including the Brief Patient Health Questionnaire-9, are used to determine the presence and severity of depression; and the Epworth Sleepiness Scale is used to investigate possible sleep apnea.

Serologic testing is unnecessary to confirm diagnosis and is only indicated to test for comorbid disease.

Differential Diagnosis. Some diseases bear superficial resemblance to fibromyalgia but do have their own unique signs and symptoms used to “rule them in” as the correct diagnosis. In real-life situations, many patients carry more than one diagnosis. For instance, a patient is free to have both gout and a fractured tibia. Each separate diagnosis is confirmed using a logical clinical approach, referenced to individual past clinical experience as well as published criteria for each separate disorder. The same is true with fibromyalgia. It is not a “diagnosis of exclusion” but in fact has a distinct phenotype, its own set of highly specific signs and symptoms. These are “unmasked” by using the approach just discussed. When it accompanies other illnesses, fibromyalgia can complicate the diagnosis and determination of disease severity. For instance, comorbid fibromyalgia will falsely elevate the number of tender joints, patient global assessment, and Health Assessment Questionnaire results used in the evaluation of rheumatoid arthritis.

Treatment. Three agents are approved by the U.S. Food and Drug Administration for the treatment of fibromyalgia and include the antidepressants duloxetine and milnacipran as well as the antiepileptic drug pregabalin. Although they have been shown to be more effective than placebo, they are usually not “curative.” Other agents that are superior to placebo include fluoxetine, citalopram, and tricyclic antidepressants. Neither corticosteroids nor narcotics are beneficial.

Of at least equal importance are aerobic exercise and education, often combined with some form of cognitive therapy. A discussion of sleep hygiene is often also important.

Fibromyalgia is a syndrome most often associated with distress. Treating underlying depression and anxiety and sleep problems and deconditioning is the basis of therapy. A dismissive attitude on the part of the treating physician can be a major iatrogenic perpetuating factor.