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

Immunoserological assays of patients with sudden deafness and progressive hearing losses have revealed the presence of different antibodies, leading to the assumption that immunological processes may be involved. Recent investigations have demonstrated that these patients have phospholipid antibodies that can cause venous or arterial vasculopathies. In the present study we analyzed the incidence of these antibodies in patients with inner ear disorders. Sera of 55 patients with sudden deafness and 80 patients with progressive hearing loss were tested. Phospholipid antibodies were demonstrable in 49% of the patients with sudden hearing loss and 50% of the patients with progressive hearing loss. Serotonin and ganglioside antibodies were found in 53% of the patients with sudden hearing loss and 63% of the patients with progressive hearing loss. Since these three antibodies are also frequently found in patients with fibromyalgia syndrome (FMS) and chronic fatigue syndrome (CFS), 28 of the patients studied displayed symptoms typical for these disorders, including fatigue, myalgia, arthralgia, depressions, sicca symptoms and diarrhea. We now recommend questioning patients suffering from inner ear disorders for symptoms typical for FMS or CFS, since these diseases are often closely related to inner ear disorders. If symptoms are present, antibodies should be tested against phospholipids, serotonin and gangliosides. If present, the antibodies are diagnostic for each syndrome. Additionally these immunologic and serologic findings show that these antibodies may play a role in the etiology of hearing loss disorders.
HNO 1998 Jun
PMID:[Incidence and clinical relevance of antibodies to phospholipids, serotonin and ganglioside in patients with sudden deafness and progressive inner ear hearing loss]. 967 86

Substance P (SP), a putative nociceptive transmitter, is increased in the CSF of patients with fibromyalgia syndrome (FMS). Because excitatory amino acids (EAAs) also appear to transmit pain, we hypothesized that CSF EAAs may be similarly involved in this syndrome. We found that the mean concentrations of most amino acids in the CSF did not differ amongst groups of subjects with primary FMS (PFMS), fibromyalgia associated with other conditions (SFMS), other painful conditions not exhibiting fibromyalgia (OTHER) or age-matched, healthy normal controls (HNC). However, in SFMS patients, individual measures of pain intensity, determined using an examination-based measure of pain intensity, the tender point index (TPI), covaried with their respective concentrations of glutamine and asparagine, metabolites of glutamate and aspartate, respectively. This suggests that re-uptake and biotransformation mask pain-related increases in EAAs. Individual concentrations of glycine and taurine also correlated with their respective TPI values in patients with PFMS. While taurine is affected by a variety of excitatory manipulations, glycine is an inhibitory transmitter as well as a positive modulator of the N-methyl-D-asparate (NMDA) receptor. In both PFMS and SFMS patients, TPI covaried with arginine, the precursor to nitric oxide (NO), whose concentrations, in turn, correlated with those of citrulline, a byproduct of NO synthesis. These events predict involvement of NO, a potent signaling molecule thought to be involved in pain processing. Together these metabolic changes that covary with the intensity of pain in patients with FMS may reflect increased EAA release and a positive modulation of NMDA receptors by glycine, perhaps resulting in enhanced synthesis of NO.
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PMID:Changes in the concentrations of amino acids in the cerebrospinal fluid that correlate with pain in patients with fibromyalgia: implications for nitric oxide pathways. 1092 13

Three types of overlap occur among the disease states chronic fatigue syndrome (CFS), fibromyalgia (FM), multiple chemical sensitivity (MCS) and posttraumatic stress disorder (PTSD). They share common symptoms. Many patients meet the criteria for diagnosis for two or more of these disorders and each disorder appears to be often induced by a relatively short-term stress which is followed by a chronic pathology, suggesting that the stress may act by inducing a self-perpetuating vicious cycle. Such a vicious cycle mechanism has been proposed to explain the etiology of CFS and MCS, based on elevated levels of nitric oxide and its potent oxidant product, peroxynitrite. Six positive feedback loops were proposed to act such that when peroxynitrite levels are elevated, they may remain elevated. The biochemistry involved is not highly tissue-specific, so that variation in symptoms may be explained by a variation in nitric oxide/peroxynitrite tissue distribution. The evidence for the same biochemical mechanism in the etiology of PTSD and FM is discussed here, and while less extensive than in the case of CFS and MCS, it is nevertheless suggestive. Evidence supporting the role of elevated nitric oxide/peroxynitrite in these four disease states is summarized, including induction of nitric oxide by common apparent inducers of these disease states, markers of elevated nitric oxide/peroxynitrite in patients and evidence for an inductive role of elevated nitric oxide in animal models. This theory appears to be the first to provide a mechanistic explanation for the multiple overlaps of these disease states and it also explains the origin of many of their common symptoms and similarity to both Gulf War syndrome and chronic sequelae of carbon monoxide toxicity. This theory suggests multiple studies that should be performed to further test this proposed mechanism. If this mechanism proves central to the etiology of these four conditions, it may also be involved in other conditions of currently obscure etiology and criteria are suggested for identifying such conditions.
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PMID:Common etiology of posttraumatic stress disorder, fibromyalgia, chronic fatigue syndrome and multiple chemical sensitivity via elevated nitric oxide/peroxynitrite. 1593 92

Drugs that inhibit reuptake of monoamines are frequently used to treat pain syndromes, e.g. neuropathy or fibromyalgia, where mechanical allodynia is present. Several lines of evidence suggest the involvement of supraspinal sites of action of these drugs. However, a direct study of supraspinal serotonin (5-HT) or norepinephrine (NE) release in an animal model in which allodynia is expressed, e.g. neuropathy, has not been done. The ventrobasal (VB) thalamus and the hypothalamus are major supraspinal projection regions for spinal neurons that transmit nociceptive information and are innervated by monoaminergic fibers. This study determined if peripheral neuropathy would induce changes in extracellular monoamines in VB thalamus and hypothalamus. Male Sprague-Dawley rats had spinal nerve roots L5 and L6 tightly ligated (neuropathic rats; NP) or sham (SHAM) surgery; contralateral and ipsilateral VB thalamus and contralateral hypothalamus were dialyzed with modified artificial cerebral spinal fluid (aCSF), with and without fluoxetine. NP rats had significantly decreased 5-HT content in dialysates of the contralateral VB thalamus compared with SHAM rats with (82% decrease) or without (63% decrease) fluoxetine in the perfusion medium over the 180 min of the study. There were no differences in the ipsilateral VB thalamus. In contrast, release of 5-HT was unchanged in the hypothalamic dialysates of SHAM vs. NP rats. NE release was not different in dialysates of either the VB thalamus or hypothalamus of SHAM vs. NP rats. Synthesis of 5-HT, as assessed by accumulation of 5-hydroxytrytophan after treatment with an L-amino acid decarboxylase inhibitor, was not different between NP and SHAM rats in VB thalamic and hypothalamic brain tissue. This study is the first to demonstrate changes in monoamine release supraspinally in NP rats. The differential effect between VB thalamus and hypothalamus suggests that a terminal field change may be involved. Putative mechanisms for mediating this change include alterations of GABA-ergic systems and/or plasticity related to alterations in N-methyl-D-aspartate receptor activation and nitric oxide release related to afferent hyperactivity induced by neuropathic pain.
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PMID:Reduced basal release of serotonin from the ventrobasal thalamus of the rat in a model of neuropathic pain. 1223 15

MECHANISMS IN THE LESIONED MUSCLE: The peripheral mechanism underlying the tenderness and pain during movement of a damaged muscle is the sensitization of muscle nociceptors. Ongoing activity of nociceptors causes spontaneous pain in addition to tenderness. Muscle pain (particularly that originating in myofascial trigger points) is often mislocalized because it is referred to other deep somatic tissues. The development of trigger points is a purely peripheral event, whereas the referral of muscle pain is based on central nervous mechanisms. MECHANISMS AT THE SPINAL LEVEL: The input from muscle nociceptors induces neuroplastic changes in the spinal cord and higher centres of the central nervous system. These changes are associated with an overexcitability of neurones (central sensitization) and contribute to hyperalgesia of patients. Resting activity of spinal neurones (and hence spontaneous pain) is strongly dependent on nitric oxide (NO). A muscle lesion is likely to lead to an inhibition of the homonymous muscle, it can, however, elicit spasm in another muscle. SUPRASPINAL MECHANISMS: Spinal neurones that mediate muscle pain are subjected to a strong descending inhibitory influence. The inhibitory tracts originate in the mesencephalon and medulla oblongata. A dysfunction of this inhibitory system might be involved in the pathogenesis of fibromyalgia.
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PMID:[Neurobiological basis of muscle pain]. 1279 45

Increased shear stress to the endothelium increases activity of endothelial nitric oxide synthase (eNOS) with subsequent release of small quantities (nMol) of nitric oxide (NO) into the circulation. It occurs during moderate aerobic exercise mostly as a result of laminar shear stress and with whole body, periodic acceleration as a result of pulsatile shear stress. The latter is administered by means of a new, non-invasive, passive exercise device. Moderate exercise has long been known to alleviate the symptoms of fibromyalgia and chronic fatigue syndrome and in the current study, whole body, periodic acceleration did as well. Since NO through action of eNOS has potent anti-inflammatory properties mainly by suppressing nuclear factor kappabeta activity, it is hypothesized that both diseases have chronic inflammation as their basis. Whole body periodic acceleration can be applied separately or supplementary to aerobic exercise in the treatment of fibromyalgia and chronic fatigue syndrome.
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PMID:Say NO to fibromyalgia and chronic fatigue syndrome: an alternative and complementary therapy to aerobic exercise. 1519 62

We proposed to assess the oxidant/antioxidant status, lipid peroxidation and nitric oxide (NO) in untreated fibromyalgia (FM) patients and controls. The effect of amitriptyline (A, 20 mg daily) and sertraline (S, 100 mg daily) treatment on patients' superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (ADA) enzyme activities, thiobarbituric acid reactive substances (TBARS) and NO levels was investigated. Thirty female patients with primary FM and age-matched 16 healthy female controls were included. Patients received an 8-week course of treatment with either A or S. FM patients had higher serum levels of TBARS (particularly malondialdehyde) and lower levels of nitrite compared to controls whereas enzyme activities were similar. A and S significantly improved Fibromyalgia Impact Questionnaire (FIQ) pain scores, Hamilton anxiety and depression rating scales. But neither A nor S had significant effects on measured oxidative stress parameters, except SOD activity that was significantly reduced after S treatment. Total myalgic scores negatively correlated with XO activity, and depression scales negatively correlated with levels of TBARS. Our results indicate that patients with FM are under oxidative stress. These findings represent a rationale for further research assessing the effect of free radical scavengers or antioxidant agents like vitamins and omega-3 fatty acids on peripheral and central mechanisms in FM.
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PMID:Antioxidant status, lipid peroxidation and nitric oxide in fibromyalgia: etiologic and therapeutic concerns. 1628 18

Fibromyalgia (FM) is a common chronic pain syndrome with an unknown etiology. Recent years added new information to our understanding of FM pathophysiology. Researches on genetics, biogenic amines, neurotransmitters, hypothalamic-pituitary-adrenal axis hormones, oxidative stress, and mechanisms of pain modulation, central sensitization, and autonomic functions in FM revealed various abnormalities indicating that multiple factors and mechanisms are involved in the pathogenesis of FM. Oxidative stress and nitric oxide may play an important role in FM pathophysiology, however it is still not clear whether oxidative stress abnormalities documented in FM are the cause or the effect. This should encourage further researches evaluating the potential role of oxidative stress and nitric oxide in the pathophysiology of FM and the efficacy of antioxidant treatments (omega-3 and -6 fatty acids, vitamins and others) in double blind and placebo controlled trials. These future researches will enhance our understanding of the complex pathophysiology of this disorder.
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PMID:Current concepts in the pathophysiology of fibromyalgia: the potential role of oxidative stress and nitric oxide. 1632 20

Although the underlying mechanism responsible for muscular fatigue and exercise intolerance remains to be elucidated, it is reported two major mechanisms, central and peripheral hypothesis. As a peripheral mechanism, there are few reports on abnormalities of the microcirculation in patients with fibromyalgia. The key point to note is that ischemia associated with a modest decline in tissue oxygen causes muscle fatigue. It has been shown that have been found low muscle levels of phosphates and abnormalities in microcirculation in fibromyalgia. Based on several novel data, production abnormalities of nitric oxide level might lead to symptoms of fatigue as a long term effect. There a vicious cycle concerning impairment of microcirculation in FM. The cycle is firstly initiated decrease of production of nitric oxide in the endothelial level by some trigger factors. Changed level of nitric oxide may cause microcirculation abnormalities in the tissue levels, muscular region. At the end of these phases, muscular fatigue and exercise intolerance may progressively develop in the FM. It is possible that this theory appears to provide a physiopathological explanation for decreased exercise capacity in patients with fibromyalgia. This paper describes a plausible mechanism for the development of exercise intolerance on microcirculation abnormalities.
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PMID:Reduced tolerance of exercise in fibromyalgia may be a consequence of impaired microcirculation initiated by deficient action of nitric oxide. 1641 81

The objective of this study was to analyze the genotype distributions and allele frequencies for the Glu298Asp (G894T) polymorphism of the eNOS gene and the serum nitric oxide level among the patients with fibromyalgia syndrome (FS). Ninety-six fibromyalgia patients and 79 unrelated healthy volunteer controls were included in the study. All patients and controls were females. Genomic DNA from 96 patients meeting the American College of Rheumatology 1990 criteria for FS and 79 healthy controls was analyzed by polymerase chain reaction. A polymerase chain reaction-restriction fragment-length polymorphism analysis of eNOS gene polymorphism was performed, and the results of the patients with FS and healthy controls were compared. Ozone-based chemiluminescence assay with Sievers NO Analyzer was used to measure the serum nitric oxide levels. Neither the frequencies of the Glu298Asp genotypes nor the serum nitric oxide levels showed a significant difference between the groups. These results suggested that FS of the Turkish population seemed to develop without any alterations in eNOS Glu298Asp genotype frequency and the serum nitric oxide level.
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PMID:No evidence for an association between the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene and fibromyalgia syndrome. 1695 45


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