Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016053 (fibromyalgia)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association between migraine and functional gastrointestinal disorders has been confirmed by many clinical observations and epidemiological studies. In most patients during the attacks of migraine, apart from various neurological and vascular symptoms, gastrointestinal disturbances occur including nausea, vomiting, abdominal pain or diarrhea. Functional gastrointestinal disorders, such as irritable bowel syndrome (IBS), are reported in migraine patients in periods between the attacks as well. On the other hand 23-53% of IBS patients have frequent headaches. Migraine and IBS often coexist with fibromyalgia and other chronic pain syndromes and functional disorders. Migraine and IBS affect approximately 10-20% of the general population, usually young adults. Both diseases are more prevalent in women, perhaps due to the role of estrogen in their pathogenesis. Looking for the common pathogenetic mechanisms of IBS and migraine the role of the brain-gut axis, neuroimmune and neuroendocrine interactions are being considered. The influence of stress on symptom occurrence and severity seems to be associated with hyperactivity of the hypothalamic-pituitary-adrenal axis. The enteric nervous system as a source of numerous neurotransmitters and visceral reflexes is a plausible common pathogenic link between IBS and migraine. In particular serotonin being the main neurotransmitter of the gastrointestinal tract plays a relevant role in the pathogenesis of IBS as well as migraine. Nowadays, agonists and antagonists of serotoninergic receptors are the most efficacious drugs for IBS and migraine therapy. Some side effects of triptans, 5-HT(1B/D) agonists, used in migraine treatment may be connected with the influence of triptans on the gastrointestinal functions. A better understanding of the relationship between migraine and IBS may result in more effective treatment of both diseases.
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PMID:[Migraine and irritable bowel syndrome]. 1641 71

Chronic pain is one of the frequently encountered clinical problems that is difficult to cure. Hyperbaric oxygen (HBO) therapy has been reported in chronic pain syndromes with promising results. In this review, we focus on the effectiveness of HBO in fibromyalgia syndrome, complex regional pain syndrome, myofascial pain syndrome, migraine, and cluster headaches. HBO may be beneficial if appropriate patients are selected. HBO is a reliable method of treatment. However, physicians performing HBO must be aware of oxygen toxicity. Another problem regarding HBO is the scarcity of centers administering it. Further research is required focusing on the optimal treatment protocol, the cost/benefit ratio, and the safety of HBO in chronic pain management.
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PMID:Hyperbaric oxygen therapy in chronic pain management. 1653 61

The aim of the present study was to verify cerebrospinal fluid (CSF) levels of glial cell line-derived neurotrophic factor (GDNF) and somatostatin, both measured by sensitive immunoassay, in: 16 chronic migraine (CM) patients, 15 patients with an antecedent history of migraine without aura diagnosed as having probable chronic migraine (PCM) and probable analgesic-abuse headache (PAAH), 20 patients affected by primary fibromyalgia syndrome (PFMS), and 20 control subjects. Significantly lower levels of GDNF and somatostatin were found in the CSF of both CM and PCM + PAAH patients compared with controls (GDNF =P < 0.001, P < 0.002; somatostatin = P < 0.002, P < 0.0003), without significant difference between the two groups. PFMS patients, with and without analgesic abuse, also had significantly lower levels of both somatostatin and GDNF (P < 0.0002, P < 0.001), which did not differ from those of CM and PCM + PAAH patients. A significant positive correlation emerged between CSF values of GDNF and those of somatostatin in CM (r = 0.70, P < 0.02), PCM + PAAH (r = 0.78, P < 0.004), and PFMS patients (r = 0.68, P < 0.008). Based on experimental findings, it can be postulated that reduced CSF levels of GDNF and somatostatin in both CM and PCM + PAAH patients can contribute to sustained central sensitization underlying chronic head pain. The abuse of simple or combination analgesics does not seem to influence the biochemical changes investigated, which appear to be more strictly related to the chronic pain state, as demonstrated also for fibromyalgia.
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PMID:Glial cell line-derived neurotrophic factor and somatostatin levels in cerebrospinal fluid of patients affected by chronic migraine and fibromyalgia. 1655 41

Fibromyalgia syndrome (FMS) is a chronic pain syndrome of unknown aetiology characterized by diffuse pain over more than 3 months and tenderness in specific sites named tender points. The aim of this study was to assess the prevalence and severity of FMS among patients suffering from episodic migraine. Ninety-two consecutive patients (20 male, 72 female) fulfilling the International Headache Society criteria for migraine with and without aura from a tertiary headache clinic were evaluated. A headache and generalized pain history was recorded, tender points were evaluated by thumb palpation. The diagnosis of FMS was made based on the 1990 American College of Rheumatology classification criteria for FMS. Sixteen (22.2%) of the female patients and none of the male patients were diagnosed as suffering from FMS. Migraine severity and characteristics were similar to other female migraine patients. Patients suffering from migraine-FMS had lower quality of life scores and higher levels of mental distress. A high incidence of FMS was found among female migraine patients but not in males. The coexistence of FMS should be considered when choosing a prophylactic migraine therapy.
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PMID:Prevalence of fibromyalgia syndrome in migraine patients. 1655 47

Fibromyalgia (FMS) is a debilitating disorder characterized by chronic diffuse muscle pain, fatigue, sleep disturbance, depression and skin sensitivity. There are no genetic or biochemical markers and patients often present with other comorbid diseases, such as migraines, interstitial cystitis and irritable bowel syndrome. Diagnosis includes the presence of 11/18 trigger points, but many patients with early symptoms might not fit this definition. Pathogenesis is still unknown, but there has been evidence of increased corticotropin-releasing hormone (CRH) and substance P (SP) in the CSF of FMS patients, as well as increased SP, IL-6 and IL-8 in their serum. Increased numbers of activated mast cells were also noted in skin biopsies. The hypothesis is put forward that FMS is a neuro-immunoendocrine disorder where increased release of CRH and SP from neurons in specific muscle sites triggers local mast cells to release proinflammatory and neurosensitizing molecules. There is no curative treatment although low doses of tricyclic antidepressants and the serotonin-3 receptor antagonist tropisetron, are helpful. Recent nutraceutical formulations containing the natural anti-inflammatory and mast cell inhibitory flavonoid quercetin hold promise since they can be used together with other treatment modalities.
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PMID:Fibromyalgia--new concepts of pathogenesis and treatment. 1656 42

Fibromyalgia (FM) pain is frequent in the general population but its pathogenesis is only poorly understood. Many recent studies have emphasized the role of central nervous system pain processing abnormalities in FM, including central sensitization and inadequate pain inhibition. However, increasing evidence points towards peripheral tissues as relevant contributors of painful impulse input that might either initiate or maintain central sensitization, or both. It is well known that persistent or intense nociception can lead to neuroplastic changes in the spinal cord and brain, resulting in central sensitization and pain. This mechanism represents a hallmark of FM and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established only minimal nociceptive input is required for the maintenance of the chronic pain state. Additional factors, including pain related negative affect and poor sleep have been shown to significantly contribute to clinical FM pain. Better understanding of these mechanisms and their relationship to central sensitization and clinical pain will provide new approaches for the prevention and treatment of FM and other chronic pain syndromes.
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PMID:Biology and therapy of fibromyalgia: pain in fibromyalgia syndrome. 1909 Sep 66

Milnacipran is a serotonin (5-HT) and norepinephrine (NE) reuptake inhibitor currently available for use as an antidepressant in several countries. Phase III clinical trials are currently underway to assess its potential role in the treatment of fibromyalgia syndrome, and in pursuit of US Food and Drug Administration approval for this indication. Evidence has accumulated suggesting that in animal models, milnacipran may exert pain-mitigating influences involving NE- and 5-HT-related processes at supraspinal, spinal and peripheral levels of pain transmission. Preliminary evidence suggests that milnacipran may be useful in mitigating pain and fatigue associated with fibromyalgia. However, its role in addressing comorbidities associated with fibromyalgia, including visceral pain and migraine, has yet to be investigated.
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PMID:Clinical potential of milnacipran, a serotonin and norepinephrine reuptake inhibitor, in pain. 1686 17

Despite extensive research, the pathogenesis of pain in fibromyalgia syndrome is incompletely understood. Fibromyalgia pain is consistently felt in deep tissues including ligaments, joints and muscles. Increasing evidence points towards these tissues as relevant contributors of nociceptive input that might either initiate or maintain central sensitization, or both. Persistent or intense nociception can lead to transcriptional and translational changes in the spinal cord and brain resulting in central sensitization and pain. This mechanism represents a hallmark of fibromyalgia and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established, only minimal nociceptive input is required for the maintenance of the chronic pain state. Other factors, including pain-related negative affect, have been shown to significantly contribute to clinical fibromyalgia pain. An improved understanding of the mechanisms that characterize central sensitization and clinical pain will provide new approaches for the prevention and treatment of fibromyalgia and other chronic pain syndromes.
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PMID:Mechanisms of disease: pain in fibromyalgia syndrome. 1693 62

Since the first mitochondrial dysfunction was described in the 1960s, the medicine has advanced in its understanding the role mitochondria play in health, disease, and aging. A wide range of seemingly unrelated disorders, such as schizophrenia, bipolar disease, dementia, Alzheimer's disease, epilepsy, migraine headaches, strokes, neuropathic pain, Parkinson's disease, ataxia, transient ischemic attack, cardiomyopathy, coronary artery disease, chronic fatigue syndrome, fibromyalgia, retinitis pigmentosa, diabetes, hepatitis C, and primary biliary cirrhosis, have underlying pathophysiological mechanisms in common, namely reactive oxygen species (ROS) production, the accumulation of mitochondrial DNA (mtDNA) damage, resulting in mitochondrial dysfunction. Antioxidant therapies hold promise for improving mitochondrial performance. Physicians seeking systematic treatments for their patients might consider testing urinary organic acids to determine how best to treat them. If in the next 50 years advances in mitochondrial treatments match the immense increase in knowledge about mitochondrial function that has occurred in the last 50 years, mitochondrial diseases and dysfunction will largely be a medical triumph.
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PMID:Mitochondrial dysfunction and molecular pathways of disease. 1723 70

Sleep disorders have been described in migraine patients. Among sleep disorders RLS has been reported in up to one-third of migraineurs. Adverse effects of anti migraine therapy by dopamine antagonists can not fully explain this association. Therefore we present the hypothesis that RLS and migraine may have a joint origin. The hypothesis is supported by: (1) the same genetic origin for migraine without aura and RLS in single Italian family on chromosome 14q21; this gene codes survival motor neuron-interacting protein 1 (SIP1) which can play role in both diseases. (2) Correlation of both RLS and migraine with fibromyalgia. (3) Alteration of cortical excitability in both migraine and RLS.
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PMID:Possible joint origin of restless leg syndrome (RLS) and migraine. 1725 1


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