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

In Sweden, several studies have been performed in patients with fibromyalgia to study muscle morphology, chemistry and physiology in order to understand the origin of the most prominent symptoms in fibromyalgia: muscle pain, muscle fatigue and muscle stiffness. These studies have shown changes indicating disturbed microcirculation, mitochondrial damage and a reduced content of high energy phosphates. Thus, there may be an energy deficiency state in the resting painful muscle in fibromyalgia. Pain analysis has supported the idea that there is a nociceptive origin of the pain. Our hypothesis is that any condition that could lead to constant muscle hypoxia, e.g., through establishment of abnormal motor patterns, might be a possible cause of fibromyalgic pain.
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PMID:The muscle in fibromyalgia--a review of Swedish studies. 269 74

Muscle fiber degeneration and regeneration, inflammation in the intramuscular connective tissue and hypoxia in resting muscle are not necessarily associated with pain. However, when sustained or dynamic muscle contractions are performed in an ischaemic muscle, severe pain develops. In the chronic muscle pain syndrome called fibromyalgia (or fibrositis) the most likely cause of the pain is a combination of muscle tension and muscle hypoxia. This conclusion is supported by the finding of a pathological distribution of tissue oxygen pressure in painful muscles and a subjective feeling of muscle tension and muscle stiffness in the majority of patients. A decrease of high energy phosphates is found in biopsies from painful muscle. The most characteristic morphological finding is the so-called ragged red fiber, a finding that can be seen in mitochondrial disorders. The morphological and chemical findings are possibly a consequence of a long standing hypoxia. The possibility that sympathetic nerve activity is important for the development of chronic muscle pain is discussed.
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PMID:Muscle pain in neuromuscular disorders and primary fibromyalgia. 270 25

This new name for an old and common disease has introduced fresh criteria and initiated clinical and basic research. The present clinical knowledge of the diagnosis and treatment is reviewed. Morphological and biochemical findings in the muscle of fibromyalgia patients have shown an unevenly distributed reduction of the oxygen tension. Hypoxia in the muscle sensitizes nociceptors, resulting in hyperalgesia with a diffuse distribution of pain symptoms. These are difficult for the individual to localize and are often combined with muscle stiffness and increased fatigability. These symptoms correspond to complaints received from fibromyalgia patients.
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PMID:[Fibromyalgia--a new name for a syndrome with diffuse muscular disorders]. 291 89

Muscle fibre degeneration and regeneration, inflammation in intramuscular connective tissue and hypoxia in resting muscle are not necessarily associated with pain. However, when sustained or dynamic muscle contractions are performed in an ischaemic muscle, severe pain develops. In the chronic muscle pain syndrome called fibromyalgia (or fibrositis) the most likely cause of the pain is a combination of muscle tension and muscle hypoxia. This conclusion is supported by the finding of a pathological distribution of tissue oxygen tension in painful muscles and a subjective feeling of muscle tension and muscle stiffness in the majority of patients. A decrease in high energy phosphates is found in biopsies from painful muscle. The most characteristic morphological finding is the so called ragged red fibre, which is a finding that can been seen in mitochondrial disorders. The morphological and chemical findings are possibly a consequence of a long standing hypoxia. The possibility that activity in muscle sympathetic nerves is important for the development of chronic muscle pain is discussed.
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PMID:Muscle pain in neuromuscular disorders and primary fibromyalgia. 316 51

Muscle fatigue is the most disabling symptom in primary fibromyalgia (PF), which in addition is characterized by generalised pain and muscle stiffness. In order to assess whether the fatigue is of central and/or peripheral origin, skeletal muscle function was studied by measuring maximum voluntary hand grip strength, and by measuring various contraction characteristics in the adductor pollicis muscle after electrical stimulation of the ulnar nerve. The PF-patients were also studied after a regional sympathetic blockade of the forearm with guanethidine. A lower hand grip strength was found in the PF-patients compared to the controls, before as well as during the sympathetic blockade. The developed force, measured during electrical stimulation, did not differ between patients and controls. A lower muscle relaxation rate was found in the PF-patients. The relaxation rate increased in the PF-patients during the sympathetic blockade. The results indicate both a central and a peripheral cause of muscle dysfunction. Activity in the muscle sympathetic system may be one link in the chain of events that leads to muscular symptoms in PF.
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PMID:Skeletal muscle function in primary fibromyalgia. Effect of regional sympathetic blockade with guanethidine. 337 44

A 43-year-old woman presented at the age of 38 with joint pains and muscle stiffness. Tender points were found fulfilling ACR criteria (1) for fibromyalgia. She had well developed muscles and decreasing muscle power since the age of 35. Muscle pains increased after exercise. Her 10-year-old son had similar symptoms and one paralytic attack. Muscle pain and fatigue increasing with age were found by history in three close relatives. Forearm cold water test produced myotonia in both mother and son. Electromyography was normal and muscle biopsy showed minor unspecific changes. Biochemical investigation of muscle mitochondrial function was normal. Peroral potassium load test produced complete muscle paralysis at a potassium serum level of 5.0 mmol/l. Autosomal dominant hyperkalemic periodic paralysis was diagnosed. Frequent carbohydrate enriched meals, peroral bendroflumethiazide and restriction to submaximal exercise improved muscle and joint pain. Salbutamol peroral spray relieved the periodic weakness.
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PMID:Fibromyalgia in hyperkalemic periodic paralysis. 980 5

Myofascial pain syndrome (MPS) is a common illness, characterised by acute or chronic focal pain, muscle stiffness and fatigue. The pathophysiology of MPS remains unclear. Previous preliminary studies have demonstrated therapeutic efficacy of the muscle relaxant botulinum toxin type A (BTX-A) in the treatment of MPS. A single-centre, randomised trial compared the effects of BTX-A with the steroid methylprednisolone (both administered intramuscularly with 0.5% bupivacaine), in 40 patients suffering from chronic myofascial pain in the piriformis, iliopsoas or scalenus anterior muscles. Thirty days after receiving an injection of either BTX-A or steroid followed by post-injection physiotherapy, pain severity had decreased significantly from baseline in both treatment groups, with no significant difference between the two treatment groups. However, the baseline pain score was significantly higher in the BTX-A treatment group compared with the steroid group (7.9 vs. 7.3), and the reduction in pain score between baseline and 30 days post-injection was greater in the BTX-A group compared with the steroid group (-3.9 vs. -3.5; P=0.06). At 60 days post-injection, the pain severity score for the BTX-A-treated patients was statistically significantly lower than the pain score for the steroid-treated population (2.3 vs. 4.9). Furthermore, the reduction in pain score in the BTX-A group at 60 days post-injection was greater than at 30 days (-5.5 vs. -3.9), whereas the effect of the steroid had begun to wane. These results indicate the superior efficacy of BTX-A over conventional steroid treatment in patients suffering from MPS, when combined with appropriate physiotherapy.
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PMID:A comparative trial of botulinum toxin type A and methylprednisolone for the treatment of myofascial pain syndrome and pain from chronic muscle spasm. 1069 8

Fibromyalgia is a common disorder occurring in approximately 2-5% of most populations, with female patients outnumbering males by up to nine to one. The two essential components of fibromyalgia, experienced in conjunction, are widespread pain and widespread abnormal bodily tenderness, although other common features of the syndrome include fatigue, muscle stiffness, poor-quality sleep and emotional distress. The clinical features result from complex changes of pain-related neurophysiological function in the brain and spinal cord, particularly through the neurophysiological process of sensitization. Management of fibromyalgia is directed to the inputs to this process, through a combination of education, exercise and psychological strategies. A number of drugs can also target this mechanism. With use of selected combinations of these strategies, the prognosis of fibromyalgia is now much improved.
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PMID:Fibromyalgia: current diagnosis and management. 2047 65

Fibromyalgia (FM) is a condition of chronic generalized musculoskeletal pain that is thought to be a disorder of central pain sensitization. A number of neurotransmitters in the ascending and descending pain pathways have been implicated in FM including glutamate and GABA. Glutamic acid decarboxylase (GAD) is the rate-limiting enzyme in the conversion of glutamate to GABA and decreased expression or activity of this enzyme could result in an imbalance of excitatory and inhibitory neurotransmission in the ascending and descending pain pathways. Specifically, the expression and activity of the predominant isoform of GAD (GAD65) is influenced by several factors that are associated with FM such as female sex, poor diet, obesity, sedentary lifestyle, and stress. We hypothesize that decreased GAD expression and/or activity plays a role in the development and exacerbation of FM leading to impairments in the three common domains of FM symptomatology: increased pain (hyperalgesia and allodynia), disrupted sleep, and disturbances in mood (anxiety and depression). There are several lines of evidence that appear to support a role of GAD in FM. First, the defining symptom of FM is pain and GAD65 knockout mice have been shown to exhibit supraspinal hyperalgesia. Second, GAD has been implicated in disorders of muscle stiffness and rigidity and morning stiffness is a common symptom of FM. Third, stress, depression, and anxiety, which are often comorbid with FM, decrease GAD activity. Fourth, FM is associated with poor sleep, specifically disrupted non-rapid eye movement (NREM) sleep, and the pharmacological induction of NREM sleep is associated with the activation of GAD-containing neurons in the preoptic hypothalamus. Fifth, FM is more commonly diagnosed in women than men and the activity of GAD is reduced by low levels of its cofactor pyroxidine, which is less well-absorbed by women and can be further lowered by diet, tobacco, and alcohol intake. Sixth, FM patients tend to be overweight or obese and caloric restriction and exercise have been shown to increase GAD expression and activity. These six general lines of evidence suggest that GAD expression and/or activity might underlie the pathophysiology of FM. If this hypothesis is supported by future empirical studies, our understanding of the etiology of FM could be greatly improved. Moreover, behavioral and pharmacological therapies that modulate or mimic the effects of GAD might hold promise for the treatment of this debilitating and poorly understood disorder.
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PMID:Possible role for glutamic acid decarboxylase in fibromyalgia symptoms: a conceptual model for chronic pain. 2168 92

Fibromyalgia is a common condition characterised by widespread musculoskeletal pain, muscle stiffness, unrefreshed sleep and fatigue. The condition is associated with several physical and psychological manifestations, including irritable bowel syndrome and anxiety. The efficacy of drug therapy is limited, therefore the nurse has an important role in providing advice and guidance on symptom management to optimise functioning for patients.
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PMID:Care of patients with fibromyalgia: assessment and management. 2427 70


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