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Abstract This article presents a brief review of the physiologic abnormalities seen in fibromyalgia, current theories of widespread pain, and treatment options, including emerging therapeutics, with a focus Aopen FM56-PA the use of duloxetine to manage fibromyalgia symptoms. Major clinical trials that examine the efficacy and effectiveness of duloxetine to date are reviewed, and safety issues are discussed. A search was conducted using the following databases: Fibromyalgia is a common, chronic and often debilitating syndrome characterized by muscle pain and stiffness, nonrestorative sleep and fatigue [ 1 ]. Many patients also experience a range of other somatic complaints that may include irritable bowel syndrome, cognitive impairment, headache, anxiety and depression, among others [ 2 ].
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For these reasons, medical management of symptoms is a high priority. Fibromyalgia diagnosis Inthe American College of Rheumatology ACR developed classification criteria for FM, which were formally established Aopen FM56-PA a multicenter study. These criteria included a subjective report of widespread pain, above and below the waist, and on the left and right side of the body, including the axial spine.
Furthermore, on physical examination, 4 kg or less of pressure applied slowly over 4 s to at least 11 out of 18 predefined tender points should elicit pain [ 8 ]. This Aopen FM56-PA has allowed FM to become established as a legitimate clinical entity and has created subsequent research opportunities, which have led to an increased understanding of FM and other forms of chronic pain [ 9 ].
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Recently, a revised diagnostic criterion was proposed [ 2 ]; however, the original criteria remains the gold standard with the most stringent criteria as well as commendable sensitivity and specificity [ 8 ]. To date, no single etiology of FM Aopen FM56-PA has been identified; however, in the past three decades, there has been progress in identifying physiologic abnormalities seen in patients with FM. Current theories underpinning the pathophysiology responsible for the increased pain and sensitivity in those with FM include abnormal sensitization from a peripheral pain stimulus, perhaps originating from deep muscle tissue or fascia [ 1011 ], which may lead to sensitization of the CNS as a final common pathway for FM, as well as other chronic pain conditions [ 12 ]. This in turn may lead to more acute somatosensory perception or allodynia, a dysregulated autonomic nervous system [ 13 ], as well as altered CNS physiology [ 14 - 18 ].
Additional abnormal physiologic findings include abnormal sleep electroencephalography [ 1920 ], neuroendocrine perturbations [ 21 ], abnormal changes in the neurochemistry of cerebrospinal fluid suggestive of a proexcitatory state [ 22 ], cortical hyperactivation in response to both noxious and non-noxious stimuli [ 1014 ], disruptions in central dopaminergic neurotransmission [ 2324 ] and apparent acceleration in age-associated brain atrophy correlated with illness duration [ 25 ]. In addition, FM seems to aggregate in families, so a genetic predisposition seems likely.
Several genes have been identified as possible Aopen FM56-PA, principally those that involve neurotransmitter physiology [ 26 ]. As with all chronic illnesses, there is no known curative therapy for FM.
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At best, symptoms and functionality have been managed with varying degrees of success through a combination of pharmacological therapy [ 27 ], lifestyle Aopen FM56-PA [ 28 ] and complementary and alternative medicine therapies [ 2930 ]. The group identified research papers that offered Aopen FM56-PA best evidence to support the most effective interventions for FM. Nine major conceptual and therapeutic realms were identified and included pharmacologic and nonpharmacologic approaches, ideally in the form of a comprehensive multimodal approach. Providers should understand that FM is a chronic pain syndrome, with abnormal pain processing and associated features.
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In addition, the provider should perform a comprehensive evaluation of pain, function and psychosocial coping. Finally, the Aopen FM56-PA must offer symptom-specific pharmacological and nonpharmacological Aopen FM56-PA, with close attention paid to individual symptoms and subsequent response to treatment plans, and be willing to make adjustments as necessary [ 28 ].
There Aopen FM56-PA also evidence-based nonpharmacological interventions that deserve consideration. Less conventional interventions that could be considered include biofeedback [ 37 ], heart rate variability feedback [ 38 ] and transcranial direct current stimulation [ 3940 ]. Despite lack of formal approval, patients and prescribers use other, unapproved agents with varying degrees of success to manage FM symptoms.
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However, only four of the aforementioned pharmaceutical agents have multicenter research-backed clinical trial evidence to support their use: Mechanism of action For widespread chronic pain conditions such as FM, the mechanism of action for SNRIs is not fully understood, but is thought to be directly related to serotonin and norepinephrine reuptake inhibition at the level of the dorsal horn in descending pain pathways. The triad of chronic pain, depression and anxiety that lead to inter-related symptoms is well described, but our Aopen FM56-PA understanding of neurophysiology in chronic pain, while not clear, suggests a direct role for neurotransmitters in analgesia [ 4445 ].
The neuromatrix theory is bolstered by CNS imaging studies that suggest CNS neural networks, rather than any single region, are engaged in those with chronic pain [ 1517 ]. The characteristic Aopen FM56-PA pain and decreased pressure pain thresholds e.
Importantly, the analgesic effect associated with SNRIs has been demonstrated to be independent of effect on mood [ 51 - 53 ]. Overview of the market To date, managing the chronic pain of FM has represented a major challenge for healthcare providers [ 54 ]. FM studies suggest that chronic pain management responds best to multidisciplinary approaches [ 2854 ], and from these models, strategic uses of pharmaceuticals play an important role. In general, regular use of opioids is discouraged for chronic pain management as they are generally not as effective as other agents and may lead to a paradoxical hyperalgesia in a subset of patients, which may in part be due to a saturation of opioid receptors Aopen FM56-PA endogenous opioids [ 55 ].
Finally, common opioid side effects such as constipation, drowsiness and tolerance usually result in their limited Aopen FM56-PA for chronic pain [ 5557 ].
NSAIDs alone often fail to relieve chronic muscle pain of FM [ 27 ], but may be useful in reducing peripheral pain Aopen FM56-PA regional pain generators, such as bursitis, tendonitis or plantar fasciitis, as an adjunct therapy. In clinical practice, providers often combine pharmacologic agents based on rational mechanisms of action without the benefit of empiric data. Aopen FM56-PA small-scale study illustrates this point. Zucker et al.
Zucker and colleagues examined 58 N-of-1 trials designed to look at combination therapy for FM, using amitriptyline alone or in combination with fluoxetine. The results illustrate a practice-based research design that may more accurately reflect clinical practice, while also examining the question of best patient outcomes. Currently, we know that noradrenaline reuptake has better antinociceptive qualities than serotonin reuptake alone; however, these study results are important for methods as most patients suffering with chronic pain will not be on monotherapy [ 58 ].
Competitor compounds that are in clinical or late-phase development There are four emerging therapies on the horizon for FM symptom management: Sodium oxybate is a schedule III compound approved by the FDA for the treatment of cataplexy and excessive daytime sleepiness. The FCC has established rules which permit Aopen FM56-PA device to be directly connected to the telephone network.
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