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

Using 31P nuclear magnetic resonance, the following parameters were determined in the resting musculus erector spinae of five patients suffering from chronic low back pain, five patients with fibromyalgia, and five healthy controls: Inorganic phosphate (Pi), phosphocreatine (PCr), ATP gamma, ATP alpha, ATP beta. The intracellular pH was derived from the chemical shift of Pi referenced to the PCr resonance. In addition, the Pi-Index was calculated according to the formula: Pi/(Pi + PCr). We discovered a tendency towards a shift of the Pi resonance in the alcalic direction, which was the larger, the stronger muscle spasm was found on palpation. The pH showed the most reliable relationship to the clinical status of muscle spasm. The surprising finding that there is no acidification within the spasmed muscle indicates that generalized hypoxia does not exist in this tissue. This has already been shown with PO2 measurements. An intracellular acidification is only recorded during maximal isometric contraction. Thus, ischemia cannot be responsible for pain experienced during muscle spasm.
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PMID:[Recording muscle spasm in the musculus erector spinae using in vivo 31P magnetic resonance spectroscopy in patients with chronic lumbalgia and generalized tendomyopathies]. 147 7

This study was performed to test the existing notion that an increased muscle sympathetic nerve discharge is part of the underlying mechanism for the chronic pain syndrome of primary fibromyalgia. Muscle sympathetic nerve activity was recorded in the peroneal nerve in eight patients with primary fibromyalgia and eight age-matched controls. No difference in baseline sympathetic activity was observed between patients and controls. Furthermore, patients did not show exaggerated sympathetic nerve responses to static handgrip or jaw muscle contractions, postcontraction ischemia or mental stress. Thus the results do not indicate muscle sympathetic nerve overactivity in primary fibromyalgic patients.
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PMID:Do patients with primary fibromyalgia have an altered muscle sympathetic nerve activity? 159 59

The fibromyalgia syndrome (FMS) is an extraarticular rheumatic disease. Typical features are the chronic, polytopic pain in the musculoskeletal system and the provocation of pain by pressure on defined tender points. Mainly medium age women are affected by the disease. In histomorphological studies of muscle tissue non-specific changes were demonstrated, which were thought to be due to ischemia. Furthermore, sleep disturbance and a reduced pain threshold, which may be related to psychological factors, are discussed in the etiology. In FMS a primary and a secondary form related to other diseases can be differentiated. The treatment consists mainly of behaviour therapy and physiotherapy.
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PMID:[Fibromyalgia syndrome. Current contributions to the etiology, diagnosis and therapy of so-called "soft tissue rheumatism"]. 220 20

Upper medial trapezius muscle biopsy was obtained from 12 primary fibromyalgia syndrome (PFS) patients (age 17 to 40 years) and studied with histochemistry, light and electron microscopy (EM). No evidence of inflammation was found in any case. Significant histochemical abnormalities were Type II fiber atrophy in 7 and moth-eaten appearance of Type I fibers in 5. EM revealed segmental muscle fiber necrosis with lipid and glycogen deposition as well as subsarcolemmal mitochondrial accumulation in all cases. Papillary projections of sarcolemmal membrane were seen in 11 patients. These observations in 12 PFS cases without obvious muscle trauma indicate definite but nonspecific muscle changes which we suspect are secondary to chronic muscle spasm and ischemia of unknown etiology.
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PMID:Muscle pathology in primary fibromyalgia syndrome: a light microscopic, histochemical and ultrastructural study. 659 30

This study aimed at evaluating the influence of submaximal isometric contraction on pressure pain thresholds (PPTs) in 14 fibromyalgia (FM) patients and 14 healthy volunteers, before and after skin hypoesthesia. PPTs were determined with pressure algometry over m. quadriceps femoris before, during and following an isometric contraction. Maximum voluntary contraction (MVC) was assessed using a computerized dynamometer. A contraction of 22% MVC on average was held until exhaustion (max. 5 min) and PPTs were assessed every 30 sec. A local anesthetic cream and a control cream were applied following a double-blind design and PPTs were reassessed. In healthy volunteers PPTs increased during contraction (P < 0.001), then decreased after the end of contraction (P < 0.001) but remained above precontraction values during the 5 min of post-contraction assessments (P < 0.001). In FM patients PPTs decreased in the middle of the contraction period (P < 0.05) and remained below precontraction levels during the rest of the contraction period (P < 0.05) and during the 5 min of post-contraction assessment (immediately post-contraction NS; 2.5 min post-contraction P < 0.01; 5 min post-contraction P < 0.05). The normalized PPTs were significantly lower in patients than in controls during contraction (start P < 0.01; middle P < 0.001; end P < 0.001) and at all times during post-contraction assessments (P < 0.001). Anesthetic cream raised PPTs at rest in controls (P < 0.01) but not in FM patients, and did not influence contraction or post-contraction PPTs in either group. Therefore, the increased pressure pain sensibility in FM patients is more pronounced deep to the skin. The observed decrease of PPTs during isometric contraction in FM patients could be due to sensitization of mechanonociceptors caused by muscle ischemia and/or dysfunction in pain modulation during muscle contraction.
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PMID:Modulation of pressure pain thresholds during and following isometric contraction in patients with fibromyalgia and in healthy controls. 878 4

The aim of the study was to investigate if contrast enhanced ultrasound (US) imaging of muscular blood flow during and following exercise could detect alterations in vascularity in fibromyalgia (FM) patients. Ten FM patients and 10 matched controls were examined with US during standardised static and directly following static and dynamic muscular contractions of the infraspinatus muscle. Doppler ultrasound evaluation was performed before and after the administration of ultrasound contrast media. The FM patients had lower magnitude of muscle vascularity following dynamic (p<0.001) and during (p<0.002) static exercise compared to controls. The immediate flow response to muscular activity was not only of a lower magnitude, but also of a shorter duration in FM patients following dynamic exercise (p<0.001) and during static exercise (p<0.01). There were no statistically significant group differences in blood flow intensity or duration following static contraction. In conclusion, contrast enhanced US was found useful to study real-time muscle blood flow changes during and following standardised, low-intensity exercise in FM patients and healthy controls. Our results support the suggestion that muscle ischemia can contribute to pain in FM, possibly by maintaining the central nervous changes such as central sensitisation/disinhibition. US with contrast can be a new valuable approach to assess muscle perfusion in pain patients during standardised exercise.
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PMID:Decreased muscle blood flow in fibromyalgia patients during standardised muscle exercise: a contrast media enhanced colour Doppler study. 1631 Jul 17

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

Fibromyalgia syndrome (FMS) is a condition of chronic muscle pain and fatigue of unknown etiology and pathogenesis. There is limited support for the various hypotheses espoused to account for the manifestations of FMS, including immunogenic, endocrine, and neurological mechanisms. Treatment, partially effective at best, is directed toward symptomatic relief without the benefit of targeting known, underlying pathology. A noteworthy commonality among partially effective therapies is a vasodilatory effect. This is true both of conventional treatments, unconventional treatments such as intravenous micronutrient therapy, and lifestyle treatments, specifically graduated exercise. The pain of fibromyalgia is described in terms suggestive of the pain in muscles following extreme exertion and anaerobic metabolism. Taken together, these characteristics suggest that the pain could be induced by vasomotor dysregulation, and vasoconstriction in muscle, leading to low-level ischemia and its metabolic sequelae. Vasodilatory influences, including physical activity, relieve the pain of FMS by increasing muscle perfusion. There are some preliminary data consistent with this hypothesis, and nothing known about FMS that refutes it. The hypothesis that the downstream cause of FMS symptoms is muscle hypoperfusion due to regional vasomotor dysregulation has clear implications for treatment; is testable with current technology; and should be investigated.
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PMID:The pain of fibromyalgia syndrome is due to muscle hypoperfusion induced by regional vasomotor dysregulation. 1737 1

Chronic widespread pain (CWP) conditions such as fibromyalgia and myofascial syndromes are characterized by generalized pain, tenderness, morning stiffness, disturbed sleep, and pronounced fatigue. However, CWP pathophysiology is still unclear. A number of hypotheses have been proposed as the underlying pathophysiology of CWP: muscular dysfunction/ischemia, central sensitization, and a deficit in endogenous pain-modulating systems. This article reviews the current and emerging literature about the pathophysiology and neurobiology of chronic widespread -musculoskeletal pain. Widespread musculoskeletal pain results in changes in the central nervous system in human subjects and animal models. These changes likely reflect alterations in supraspinal modulation of nociception, and include increases in excitatory and decreases in inhibitory modulation pathways. These alterations in excitation and inhibition likely drive changes observed in the spinal cord to result in central sensitization, and the consequent pain and hyperalgesia.
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PMID:Central mechanisms in the maintenance of chronic widespread noninflammatory muscle pain. 1876 38

Fibromyalgia syndrome (FMS) is characterized by pain referred to deep tissues. Diagnosis and treatment of FMS are complicated by a variable coexistence with regional pain, fatigue, sleep disruption, difficulty with mentation, and depression. The widespread, deep pain of FMS can be a consequence of chronic psychological stress with autonomic dysregulation. Stress acts centrally to facilitate pain and acts peripherally, via sympathetic vasoconstriction, to establish painful muscular ischemia. FMS pain, with or without a coexistent regional pain condition, is stressful, setting up a vicious circle of reciprocal interaction. Also, stress interacts reciprocally with systems of control over depression, mentation, and sleep, establishing FMS as a multiple-system disorder. Thus, stress and the ischemic pain it generates are fundamental to the multiple disorders of FMS, and a therapeutic procedure that attenuates stress and peripheral vasoconstriction should be highly beneficial for FMS. Physical exercise has been shown to counteract peripheral vasoconstriction and to attenuate stress, depression, and fatigue and improve mentation and sleep quality. Thus, exercise can interrupt the reciprocal interactions between psychological stress and each of the multiple-system disorders of FMS. The large literature supporting these conclusions indicates that exercise should be considered strongly as a first-line approach to FMS therapy.
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PMID:A mechanism-based approach to prevention of and therapy for fibromyalgia. 2211 Sep 47


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