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Query: UMLS:C0016053 (fibromyalgia)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent reports have not emphasized the presence of paresthesias in fibromyalgia syndrome. In our retrospective review of 161 patients with fibromyalgia we found that 84% complained of numbness or tingling at initial evaluation. Most had either bilateral upper and lower extremity or bilateral upper extremity paresthesias. None had concurrent diseases commonly associated with peripheral neuropathy. Thirty-six patients with paresthesias had electromyograms performed before the diagnosis of fibromyalgia and 32 were normal. At a second assessment performed at a mean of 25 months from time of diagnosis, 56 of these 57 patients reported current paresthesias. Paresthesias are common in fibromyalgia and may mimic a neurologic disorder, although objective abnormalities are rare. Judicious use of neurodiagnostic tests are therefore indicated in the clinical setting of fibromyalgia.
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PMID:Symptoms mimicking neurologic disorders in fibromyalgia syndrome. 318 73

Pain properties of 50 fibromyalgia patients were examined and compared with pain properties of 50 rheumatoid arthritis patients. In both fibromyalgia and rheumatoid arthritis, pain was bilateral, involved multiple sites, and was of equal intensity (60.8 versus 58.7, respectively, on a scale of 100). Fibromyalgia pain, however, was less localized to the joints and suggested greater spatial diffusion. It involved more kinds of pain experiences (radiating, steady, spreading, spasms, gnawing, unlocalized, pricking, crushing, shooting, pressing, splitting, cramping, nagging, and pins and needles), and was dispersed over larger areas of the body. The anatomic sites best for discrimination between patients with fibromyalgia and patients with rheumatoid arthritis were the lower back, thigh, abdomen, head, and hips for fibromyalgia, and wrist, foot, and fingers for rheumatoid arthritis. The traditional clinical description of aching and stiffness does not appear to accurately describe the complexity of the fibromyalgia pain syndrome.
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PMID:Comparison of pain properties in fibromyalgia patients and rheumatoid arthritis patients. 348 24

Fibromyalgia (FM) is a costly and debilitating pain syndrome which is commonly encountered by advanced practice nurses working in acute care settings. Fibromyalgia affects nearly 6 million people in the United States, approximately 80% to 90% of whom are women. Symptoms of FM include widespread and localized pain, disrupted sleep, fatigue, visceral pain and other pain syndromes, neurological symptoms (eg, dizziness, numbness, tingling, impaired cognition), and exercise-induced pain. Difficulties remaining active with FM may lead to extreme deconditioning, inability to remain employed, and eventually even impaired ability in complete activities of daily living. Exercise that combats deconditioning without triggering pain is, therefore, a key component in treating FM. Clinicians who understand FM pain and associated symptoms can minimize the negative impact of deconditioning by prescribing disease-specific exercise for people with FM.
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PMID:Prescribing exercise for people with fibromyalgia. 1201 99

Every pain syndrome has an inflammatory profile consisting of the inflammatory mediators that are present in the pain syndrome. The inflammatory profile may have variations from one person to another and may have variations in the same person at different times. The key to treatment of Pain Syndromes is an understanding of their inflammatory profile. Pain syndromes may be treated medically or surgically. The goal should be inhibition or suppression of production of the inflammatory mediators and inhibition, suppression or modulation of neuronal afferent and efferent (motor) transmission. A successful outcome is one that results in less inflammation and thus less pain. We hereby briefly describe the inflammatory profile for several pain syndromes including arthritis, back pain, neck pain, fibromyalgia, interstitial cystitis, migraine, neuropathic pain, complex regional pain syndrome/reflex sympathetic dystrophy (CRPS/RSD), bursitis, shoulder pain and vulvodynia. These profiles are derived from basic science and clinical research performed in the past by numerous investigators and serve as a foundation to be built upon by other researchers and will be updated in the future by new technologies such as magnetic resonance spectroscopy. Our unifying theory or law of pain states: the origin of all pain is inflammation and the inflammatory response. The biochemical mediators of inflammation include cytokines, neuropeptides, growth factors and neurotransmitters. Irrespective of the type of pain whether it is acute or chronic pain, peripheral or central pain, nociceptive or neuropathic pain, the underlying origin is inflammation and the inflammatory response. Activation of pain receptors, transmission and modulation of pain signals, neuro plasticity and central sensitization are all one continuum of inflammation and the inflammatory response. Irrespective of the characteristic of the pain, whether it is sharp, dull, aching, burning, stabbing, numbing or tingling, all pain arise from inflammation and the inflammatory response. We are proposing a re-classification and treatment of pain syndromes based upon their inflammatory profile.
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PMID:The biochemical origin of pain: the origin of all pain is inflammation and the inflammatory response. Part 2 of 3 - inflammatory profile of pain syndromes. 1772 71

Fibromyalgia syndrome (FMS) is characterised by diffuse muscle pain, poor sleep and unrelenting fatigue. Individuals with FMS may also experience headaches, anxiety, depression, poor memory, numbness and tingling in the extremities, cold hands and feet, irritable bowel syndrome and lowered immune function. FMS is a common chronic pain syndrome of unknown etiology and limited treatment options. Previous studies have reported oxidative stress in FMS patients, but the results were inconsistent. Oxidative stress and nitric oxide is involved in FMS pathophysiology, however, it is still not clear whether oxidative stress abnormalities are the cause of FMS. There are several studies indicating oxidative stress in patients with FMS. Oxidant (Malondialdehyde) and antioxidant (Superoxide dismutase) balances were found to be changed in FMS patients. Furthermore, increased free radical levels may be responsible for the development of FMS and free radical-mediated oxidative stress including inflammatory cytokines may also play important roles in its pathogenesis. Moreover, oxidative stress is supposed to be increased in patients with FMS which is related to the severity of FMS symptoms. Therefore, it is important to understand whether the oxidative stress parameters are involved in FMS and what is the relationship between these and antioxidants in FMS patients. In this review we will elucidate the importance of oxidative stress and antioxidants and its possible relationship with FMS. Moreover, as metal toxicity is also reported to be involved in the pathogenesis of FMS, therefore we will also try to establish the role of toxic metals in the pathogenesis of FMS.
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PMID:Oxidative stress and antioxidative parameters and metal ion content in patients with fibromyalgia syndrome: implications in the pathogenesis of the disease. 2437 71

Fibromyalgia is a chronic musculoskeletal pain disorder that affects an estimated 5 million adults in the U.S. The hallmark is burning, searing, tingling, shooting, stabbing, deep aching, or sharp pain. Fibromyalgia is generally considered to be a "central sensitivity syndrome" where central sensitization is regarded as the cause of pain in its own right. Nonetheless, the case continues to be made that all central and spatially distributed peripheral components of fibromyalgia pain would fade if the peripheral generators could be silenced. Although neural mechanisms are clearly important in pain sensitivity, cognitive and social mechanisms also need to be considered. The aim of this review is to examine four mechanisms responsible for heightened pain sensitivity in fibromyalgia: peripheral sensitization, central sensitization, cognitive-emotional sensitization, and interpersonal sensitization. The purpose of framing the review in terms of pain sensitivity in fibromyalgia is to highlight that different mechanisms of sensitization are appropriately regarded as intervening variables when it comes to understanding individual differences in the experience of pain. The paper concludes by considering the implications of the findings of the review for explanations of fibromyalgia pain by nurses working in multidisciplinary teams. The trend appears to be able to explain the cause of fibromyalgia pain in terms of sensitization per se. The recommended alternative is to explain fibromyalgia pain in terms of changes in pain sensitivity and the role of underlying neural and psychosocial mechanisms.
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PMID:Neural and psychosocial mechanisms of pain sensitivity in fibromyalgia. 2488 30