Musculoskeletal side effects were common in AI-treated patients, resulting in therapy discontinuation in more than 10% of patients. There are no identifiable pre-therapy indicators of risk, and the etiology remains elusive.
Researchers studying fibromyalgia strive to identify objective, measurable biomarkers that may identify susceptible individuals, may facilitate diagnosis, or that parallel activity of the disease. Candidate objective measures range from sophisticated functional neuroimaging to office-ready measures of the pressure pain threshold. A systematic literature review was completed to assess highly investigated, objective measures used in fibromyalgia studies. To date, only experimental pain testing has been shown to coincide with improvements in clinical status in a longitudinal study. Concerted efforts to systematically evaluate additional objective measures in research trials will be vital for ongoing progress in outcome research and translation into clinical practice. IntroductionFibromyalgia (FM) is a chronic condition characterized by widespread pain and tenderness on examination, along with symptoms of nonrestorative sleep, fatigue, and cognitive difficulties. Recent familial studies have suggested an underlying genetic susceptibility on which environmental factors trigger the expression of symptoms [1,2]. Despite the myalgias that patients experience, no abnormality in muscle has been reliably found [3]. Instead, aberrant pain and sensory processing probably caused by alterations in the central nervous system function are being consistently recognized in FM and related syndromes. Investigations into the autonomic nervous system and the hypothalamic-pituitary-adrenal axis also suggest a role of these stress-response systems in vulnerability to FM or in symptom expression in FM.Our improved understanding of FM has stimulated the search for biomarkers to be used to identify individuals susceptible to the syndrome, for the diagnosis of FM, for objective measures of disease activity, or as surrogate endpoints of GeneticsIncreasing evidence supports a genetic predisposition to FM. First-degree relatives of individuals with FM display an eightfold greater risk of developing the syndrome than those in the general population [1]. As such, a genetic study using multicase families has been completed that identified an HLA linkage not yet replicated [4].Polymorphisms in the serotonergic 5-hydroxy tryptamine 2A receptor (T/T phenotype), the serotonin transporter, the dopamine 4 receptor and the catecholamine o-methyl transferase enzyme have also been evaluated in patients with FM [5][6][7][8][9][10]. Notably, these polymorphisms all affect the metabolism or transport of monoamines, compounds that have a critical role in both sensory processing and the human stress response. With the exception of the catecholamine omethyl transferase finding and the dopamine-4-receptor gene polymorphism, however, which have not been replicated or
In the past decade, we have made tremendous progress in our understanding of fibromyalgia, which is now recognized as one of many 'central' pain syndromes that are common in the general population. Specific genes that might confer an increased risk of developing fibromyalgia syndrome are beginning to be identified and the environment (in this case exposure to stressors) might also have a significant effect on triggering the expression of symptoms. After developing the syndrome, the hallmark aberration noted in individuals with fibromyalgia is augmented central pain processing. Insights from research suggest that fibromyalgia and related syndromes require a multimodal management program that is different from the standard used to treat peripheral pain (i.e. acute or inflammatory pain). Instead of the nonsteroidal anti-inflammatory drugs and opioids commonly used in the treatment of peripheral pain, the recommended drugs for central pain conditions are neuroactive compounds that downregulate sensory processing. The most efficacious compounds that are currently available include the tricyclic drugs and mixed reuptake inhibitors that simultaneously increase serotonin and norepinephrine concentrations in the central nervous system. Other compounds that increase levels of single monoamines (serotonin, norepinephrine or dopamine), and anticonvulsants also show efficacy in this condition. In addition to these pharmacologic therapies, which are useful in improving symptoms, nonpharmacologic therapies such as exercise and cognitive behavioral therapy are useful treatments for restoring function to an individual with fibromyalgia.
Objective. To examine effects of activity strategy training (AST), a structured rehabilitation program taught by occupational therapists and designed to teach adaptive strategies for symptom control and engagement in physical activity (PA). Methods. A randomized controlled pilot trial was conducted at 4 sites (3 senior housing facilities and 1 senior center) in southeastern, lower Michigan. Fifty-four older adults with hip or knee osteoarthritis (mean ؎ SD age 75.3 ؎ 7.1 years) participated. At each site, older adults were randomly assigned to 1 of 2 programs: exercise plus AST (Ex ؉ AST) or exercise plus health education (Ex ؉ Ed). The programs involved 8 sessions over 4 weeks with 2 followup sessions over a 6-month period, and were conducted concurrently within each site. Pain, total PA and PA intensity (measured objectively by actigraphy and subjectively by the Community Healthy Activities Model Program for Seniors questionnaire), arthritis self-efficacy, and physical function were assessed at baseline and posttest. Results. At posttest, participants who received Ex ؉ AST had significantly higher levels of objective peak PA (P ؍ 0.02) compared with participants who received Ex ؉ Ed. Although not statistically significant, participants in Ex ؉ AST tended to have larger pain decreases, increased total objective and subjective PA, and increased physical function. No effects were found for arthritis self-efficacy. Conclusion. Although participants were involved in identical exercise programs, participants who received AST tended to have larger increases in PA at posttest compared with participants who received health education. Future studies will be needed to examine larger samples and long-term effects of AST.
Fibromyalgia is a frequent cause of chronic widespread pain and affects up to 5% of the general population. Diagnosis and treatment have been especially challenging due to limited knowledge of etiology and poor response to conventional treatment of pain. Appreciation for the interactions of neurobiologic, psychologic, and behavioral factors in the disease pathogenesis has led to improved treatment options that can be effective in individual patients. Current evidence advocates a multifaceted program emphasizing patient education, medications for improving symptoms, and aggressive use of exercise and cognitive-behavioral approaches to retain or restore function.
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