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

Pain dominates the lives of many patients with hyperlaxity syndromes, most commonly the Benign Joint Hypermobility Syndrome (BJHS/EDS). As a result they may experience psychosocial problems, which in many cases severely affects their healthy functioning. Above all is the overriding chronic pain in joints, muscles and ligaments, which arises from an inherent predisposition to the effects of everyday trauma, but other factors such as associated osteoarthritis or fibromyalgia are also important. There may also be neurophysiological factors at play producing nociceptive enhancement. Pain and distress of visceral origin can result from laxity of connective tissue within or providing support for the abdominal, thoracic or pelvic viscera leading to hernia, uterine and/or rectal prolapse, mitral valve prolapse or spontaneous pneumothorax. In children joint hyperlaxity is an important (and often unrecognised) source of rheumatic symptoms, which may be ignored or erroneously ascribed to juvenile idiopathic arthritis. The management of pain and distress in the hyperlaxity syndromes requires skill, patience, compassion and understanding. Often the results of conventional anti-rheumatic therapy (including anti-rheumatic drugs and surgery) as applied to other rheumatic diseases are disappointing and innovative approaches are required. Amongst these, for which evidence of efficacy is available, are physiotherapeutic and orthotic stabilisation of hyperlax joints, proprioceptive enhancement and the newer pain management techniques including cognitive behavioural therapy.
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PMID:Pain, distress and joint hyperlaxity. 1087 11

This structured review addresses the issue of whether antidepressants have an antinociceptive (analgesic) effect for chronic pain independent of their antidepressant effect. In order to answer this question, human acute pain studies, individual placebo-controlled studies for the treatment of specific chronic pain syndromes, and metaanalytic studies were reviewed and placed into table format. Analysis of this evidence led to the following conclusions: The evidence was consistent in indicating that overall antidepressants may have an antinociceptive effect in chronic pain, and that these drugs were effective for neuropathic pain. There was also some evidence that these drugs could be effective for psychogenic or somatoform disorder-associated pain. This evidence also strongly suggested that serotonergic-noradrenergic antidepressants may have a more consistent antinociceptive effect than the serotonergic antidepressants. Finally, this evidence indicated that antidepressants could be effective for pain associated with some specific pain syndromes, such as chronic low back pain, osteoarthritis or rheumatoid arthritis, fibrositis or fibromyalgia, and ulcer healing. Possible reasons for the conflicting results of studies in this area are presented, and problems that could limit the validity of the conclusions of this review are discussed.
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PMID:Evidence-based data on pain relief with antidepressants. 1094 61

The validity of the fibromyalgia syndrome (FMS) as a distinct clinical entity has been challenged for several reasons. Many skeptics express concern about the subjective nature of chronic pain, the subjectivity of the tender point (TeP) examination, the lack of a gold standard laboratory test, and the absence of a clear pathogenic mechanism by which to define FMS. Another expressed concern has been the relative nature of the pain-distress relationship in the rheumatology clinic. The apparently continuous relationship between TePs and somatic distress across a variety of clinical disorders is said to argue against FMS as a separate clinical disorder. The most aggressive challenges of the FMS concept have been from legal defenses of insurance carriers motivated by economic concerns. Other forms of critique have presented as psychiatric dogma, uninformed posturing, suspicion of malingering, ignorance of nociceptive physiology, and occasionally have resulted from honest misunderstanding. It is not likely that a few paragraphs of data and logic will cause an unbeliever to change an ingrained opinion. Therefore, this review describes the clinical manifestations of FMS, responds to some of the theoretic arguments against it, and discusses some possible pathophysiologic mechanisms by which FMS may develop and persist as a unique syndrome.
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PMID:Is fibromyalgia a distinct clinical syndrome? 1095 76

Fibromyalgia and other chronic pain and fatigue syndromes constitute an increasingly greater societal burden that currently is not being approached effectively by traditional Western medicine. Although the hallmarks of fibromyalgia--chronic widespread pain, fatigue, and multiple other somatic symptoms--have neurophysiologic and endocrinologic underpinnings, these biological aspects derive primarily from psychological variables. Female gender, adverse experiences during childhood, psychological vulnerability to stress, and a stressful, often frightening environment and culture are important antecedents of fibromyalgia. To understand fibromyalgia and related syndromes and to provide optimum care requires a biopsychosocial, not a biomedical, viewpoint.
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PMID:Psychological determinants of fibromyalgia and related syndromes. 1095 75

This study reports an improved approach for the determination of neuropeptide levels in human cerebrospinal fluid (CSF). The method is based on sample acidification followed by liquid-liquid extraction (LLE) combined with radioimmunoassay. It was applied to study the recovery and level of some opioid peptides (Met-enkephalin-Arg(6)-Phe(7) and Leu-enkephalin-Arg(6)), substance P and the substance P(1-7) fragment, which are all compounds known to be present in human CSF. The results indicated that the use of LLE highly improved the recovery of these peptides compared to current liquid-solid-phase extraction methods by using silica gel cartridges or mini-columns for ion-exchange chromatography. Peptides added to CSF in concentrations down to 10 fmol/ml were recovered in yields exceeding 80%. The mean recovery of synthetic peptides as recorded by radioimmunoassay in the LLE procedure was significantly improved when HCl was added to the sample. In contrast, when the (125)I-labeled analogues of the peptides were added to CSF samples, the mean recovery of the four labeled peptides using the LLE procedure was markedly reduced in acidified samples. We also found that the inclusion of HCl effectively improved the removal of proteins present in the samples. As an application the levels of substance P and Met-enkephalin-Arg(6)-Phe(7) in CSF samples from patients with chronic pain (fibromyalgia syndrome) were measured using the new procedure. It was possible to confirm a significant difference in the CSF levels of both peptides when comparing patients and controls.
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PMID:A high-recovery extraction procedure for quantitative analysis of substance P and opioid peptides in human cerebrospinal fluid. 1095 8

The symptomatology of the fibromyalgia syndrome (FMS) often resembles an alteration in central nervous set points at least in three systems. The patients suffer under chronic pain in the region of the locomotor system, presumably reflecting a disturbed central processing of pain. Anxiety and depression often characterizes the clinical picture. Almost all of the hormonal feedback mechanisms controlled by the hypothalamus are altered. Characteristic for FMS patients are the elevated basal values of ACTH, follicle-stimulating hormone (FSH), and cortisol as well as lowered basal values of insulin-like growth factor 1 (IGF-1, somatomedin C), free triiodothyronine (FT3), and oestrogen. In FMS patients, the systemic administration of the relevant releasing hormones of corticotropin-releasing hormone (CRH), growth hormone-releasing hormone (GHRH), thyreotropin-releasing hormone (TRH), and luteinizing hormone-releasing hormone (LHRH) leads to increased secretion of ACTH and prolactin, whereas the degree to which TSH can be stimulated is reduced. The stimulation of the hypophysis with LHRH in female FMS patients during their follicular phase results in a significantly reduced LH response. All in all, the typical alterations in set points of hormonal regulation that are typical for FMS patients can be explained as a primary stress activation of hypothalamic CRH neurons caused by the chronic pain. In addition to the stimulation of pituitary ACTH secretion, CRH activates somatostatin on the hypothalamic level, which in turn inhibits the release of GH and TSH on the hypophyseal level. The lowered oestrogen levels could be accounted for both via an inhibitory effect of the CRH on the hypothalamic release of LHRH or via a direct CRH-mediated inhibition of the FSH-stimulated oestrogen production in the ovary. Serotonin (5HT), precursors like tryptophan (5HTP), drugs which release 5HT or act directly on 5HT receptors stimulate HPA axis, indicating a stimulatory serotonergic influence on HPA axis function. Therefore activation of the HPA axis may reflect an elevated serotonergic tonus in the central nervous system of FMS patients.
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PMID:Neuroendocrine and hormonal perturbations and relations to the serotonergic system in fibromyalgia patients. 1102 24

Venlafaxine is a medication available by prescription in the U.S. both in an immediate release and an extended release formulation. Preclinical studies indicate it has the effect of potently blocking the serotonin and norepinephrine transporters. Venlafaxine is approved by the FDA for the treatment of major depressive disorder and generalized anxiety disorder. Suggestive evidence, mostly from open label case series, indicates efficacy of venlafaxine in several other conditions including panic disorder, social anxiety disorder, obsessive compulsive disorder, trichotillomania, ADHD, chronic pain, and fibromyalgia. The limited evidence supporting efficacy in these conditions is reviewed. Additional randomized clinical trials with placebo controls are indicated.
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PMID:Use of venlafaxine in other psychiatric disorders. 1109 21

The brain and the immune system are the two major adaptive systems of the body. During an immune response the brain and the immune system "talk to each other" and this process is essential for maintaining homeostasis. Two major pathway systems are involved in this cross-talk: the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS). This overview focuses on the role of SNS in neuroimmune interactions, an area that has received much less attention than the role of HPA axis. Evidence accumulated over the last 20 years suggests that norepinephrine (NE) fulfills the criteria for neurotransmitter/neuromodulator in lymphoid organs. Thus, primary and secondary lymphoid organs receive extensive sympathetic/noradrenergic innervation. Under stimulation, NE is released from the sympathetic nerve terminals in these organs, and the target immune cells express adrenoreceptors. Through stimulation of these receptors, locally released NE, or circulating catecholamines such as epinephrine, affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells. Although there exists substantial sympathetic innervation in the bone marrow, and particularly in the thymus and mucosal tissues, our knowledge about the effect of the sympathetic neural input on hematopoiesis, thymocyte development, and mucosal immunity is extremely modest. In addition, recent evidence is discussed that NE and epinephrine, through stimulation of the beta(2)-adrenoreceptor-cAMP-protein kinase A pathway, inhibit the production of type 1/proinflammatory cytokines, such as interleukin (IL-12), tumor necrosis factor-alpha, and interferon-gamma by antigen-presenting cells and T helper (Th) 1 cells, whereas they stimulate the production of type 2/anti-inflammatory cytokines such as IL-10 and transforming growth factor-beta. Through this mechanism, systemically, endogenous catecholamines may cause a selective suppression of Th1 responses and cellular immunity, and a Th2 shift toward dominance of humoral immunity. On the other hand, in certain local responses, and under certain conditions, catecholamines may actually boost regional immune responses, through induction of IL-1, tumor necrosis factor-alpha, and primarily IL-8 production. Thus, the activation of SNS during an immune response might be aimed to localize the inflammatory response, through induction of neutrophil accumulation and stimulation of more specific humoral immune responses, although systemically it may suppress Th1 responses, and, thus protect the organism from the detrimental effects of proinflammatory cytokines and other products of activated macrophages. The above-mentioned immunomodulatory effects of catecholamines and the role of SNS are also discussed in the context of their clinical implication in certain infections, major injury and sepsis, autoimmunity, chronic pain and fatigue syndromes, and tumor growth. Finally, the pharmacological manipulation of the sympathetic-immune interface is reviewed with focus on new therapeutic strategies using selective alpha(2)- and beta(2)-adrenoreceptor agonists and antagonists and inhibitors of phosphodiesterase type IV in the treatment of experimental models of autoimmune diseases, fibromyalgia, and chronic fatigue syndrome.
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PMID:The sympathetic nerve--an integrative interface between two supersystems: the brain and the immune system. 1112 11

A considerable proportion of chronic non-organic pain patients suffer from insomnia, and alpha sleep has been suggested to be specifically associated with fibromyalgia. However, the clinical significance of those symptoms is not clear. This study was carried out to investigate this question. Twenty-six middle-aged, non-organic pain patients complaining of persistent insomnia were compared with 25 chronic primary insomniacs in a polysomnographic investigation. Alpha sleep was measured by automatic EEG analysis. A postsleep inventory allowed a separation of those pain patients with actual pain in the recording night to examine its possible influence on sleep. Both groups of patients displayed severe disturbance of sleep maintenance. The pain group did not differ in any of the insomnia variables or in sleep stages from chronic primary insomniacs. The occurrence of alpha sleep was high in either group which suggests that this is not a phenomenon specifically related to pain syndromes. A comparison of the pain subgroups revealed no difference between those with or without actual pain in the recording night. It is concluded that insomnia in chronic pain is of the same type and degree as primary insomnia. Apparently, the chronic process made insomnia so persistent that there was no response to actual night-time pain. Our study suggests that the interpretation of insomnia as secondary to pain, as it is usually made by the pain patients themselves, is a misattribution. It is suggested that insomnia in chronic pain patients should be taken seriously and treated by its specific methods.
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PMID:Insomnia and alpha sleep in chronic non-organic pain as compared to primary insomnia. 1115 Sep

Patients with fibromyalgia syndrome (FS) experience a decreased ability to participate in both vocational and avocational activities. Although many treatment programs advocate activity pacing techniques, 'pacing' is a poorly understood concept for which there are no available measures. The present study describes a brief six-item pacing scale that can be administered as part of the Chronic Pain Coping Inventory (CPCI). Preliminary data indicate that this scale is a valid, reliable index of the pacing construct that is associated with physical impairment in patients with FS and is unrelated to simple task persistence.
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PMID:An activity pacing scale for the chronic pain coping inventory: development in a sample of patients with fibromyalgia syndrome. 1116 66


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