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

Pain related to fibromyalgia may consist of a complex interaction of nociceptive, neuropathic, dysregulatory central nervous system and psychosomatic mechanisms. Nociceptor pain is based on the excitation of nervous sensors specialized to signal potentially harmful stimuli, i.e., the nociceptors. Metabolic deficiencies in muscle and neurogenic inflammation induced by the release of substance P and other neuropeptides from the peripheral nerve endings may result in chemical sensitization of nociceptors and an ensuing hyperalgesia particularly present in tender points. Neuropathic pain is due to pathological mechanisms within nerve cells and fibers in the peripheral and central nervous system. Pathophysiology may be related to compression (such as in the carpal tunnel syndrome or a vertebral disk herniation) or regeneration of nerves, resulting in ectopic impulse discharges and disturbances of axonal transport. The ensuing neuronal hyperexcitability and trophic changes induced by a disturbed axonal transport system may be major factors of pain in fibromyalgia. Dysregulatory pain denotes pain maintained by dysfunction of efferent control loops. Thus, if spinal motoneuron output results in excessive tension of postural muscle, nociceptors in muscles, tendons and joints might become more excited. Persistent abnormal spinal reflex transmission due to, e.g., peripheral trauma or inappropriate postural habits may result in a vicious circle between muscle hypertension and pain. Similarly, a defective sympathetic control may result in disturbed microcirculation and nociceptor excitation (e.g., in sympathetic algodystrophy). Many symptoms of pain in fibromyalgia (trigger points, pain referral, pain associated with muscle spasm or neurogenic joint immobilization) can be attributed to abnormal control mechanisms in a complex cybernetic system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiological mechanisms of fibromyalgia. 181 May 27

Botulinum toxin (BTX) injection is being increasingly used 'off label' in the management of chronic pain. Data support the hypothesis of a direct analgesic effect of BTX, different to that exerted on muscle. Although the pain-reducing effect of BTX is mainly due to its ability to block acetylcholine release at the synapse, other effects on the nervous system are also thought to be involved. BTX affects cholinergic transmission in both the somatic and the autonomic nervous systems. Proposed mechanisms of action of BTX for pain relief of trigger points, muscular spasms, fibromyalgia and myofascial pain include direct action on muscle and indirect effects via action at the neuromuscular junction. Invitro and invivo data have shown that BTX has specific antinociceptive activity relating to its effects on inflammation, axonal transport, ganglion inhibition, and spinal and suprasegmental level inhibition. Our review of the mechanisms of action, efficacy, administration techniques and therapeutic dosage of BTX for the management of chronic pain in a variety of conditions shows that although muscular tone and movement disorders remain the most important therapeutic applications for BTX, research suggests that BTX can also provide benefits related to effects on cholinergic control of the vascular system, autonomic function, and cholinergic control of nociceptive and antinociceptive systems. Furthermore, it appears that BTX may influence the peripheral and central nervous systems. The therapeutic potential of BTX depends mainly on the ability to deliver the toxin to the target structures, cholinergic or otherwise. Evidence suggests that BTX can be administered at standard dosages in pain disorders, where the objective is alteration of muscle tone. For conditions requiring an analgesic effect, the optimal therapeutic dosage of BTX remains to be defined.
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PMID:Botulinum toxin for pain. 1809 50

The authors report a case of a 52-year old female previously followed at the Outpatient Rheumatology Clinic with the diagnosis of Fibromyalgia (FM). Approximately 2 years after this diagnosis, she presents with a 2nd degree burn in a hand, as a result of thermal hypoesthesia. The patient described hipostesia of the distal upper and lower limbs, incontinence of the anal sphincter and chronic diarrhoea with progressive worsening. The electromiography showed sensory-motor axonal polyneuropathy, chronic, moderate to severe. The muscle and nerve biopsy showed deposition of amyloid substance. The search for TTR Met 30 was positive, confirming the diagnosis of familial amyloidotic polyneuropathy. This is the first reported case of familial amyloidotic polyneuropathy as part of the differential diagnosis of fibromyalgia.
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PMID:[An unusual case of generalized pain: paramyloidosis simulating fibromyalgia]. 1972 56

Fibromyalgia (FM) syndrome is a chronic condition causing pain, affecting approximately 0.5%-6% of the developed countries' population, and on average, 2% of the worldwide population. Despite the large amount of scientific literature available, the FM etiology is still uncertain. The diagnosis is based on the clinical presentation and the severity of the symptomatology. Several studies pointed out pathological alterations within the central nervous system, suggesting that FM could originate from a central sensitization of the pain processing centers. Research supports the thesis of a peripheral neuropathic component, with the finding of axonal damages. The fibromyalgia patient has many myofascial system abnormalities, such as pain and fatigue, impairing the symptomatic profile. This paper revises the myopathic compensations, highlighting the possible role of the fascia in generating symptoms, being aware of the new information about the fascia's activity in stimulating inflammation and fat cell production.
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PMID:Fascial preadipocytes: another missing piece of the puzzle to understand fibromyalgia? 2975 60