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

A large group of patients (236) was examined for myofascial pain dysfunction syndrome. The parameters used for diagnosis of the syndrome were pain and tenderness in the head and neck muscles and temporomandibular joint, joint sounds, and limited function. It was found that the demographic profile of our patient population did not vary greatly from those reported previously in other studies. However, we did examine more details of the patients' backgrounds than any other single study. The relationships of age, sex, occupation, marital status, emotional stress, and head trauma were discussed.
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PMID:Statistical analysis of an urban population of 236 patients with head and neck pain. Part I. Patient profile. 28 13

The fibrositis syndrome represents a clinically definable entity, which is characterised by spontaneous pain, especially in the lumbar and cervical region, and more rarely in other movable parts, multiple tendomyosis, tendinitis and insertion tendinitis, as well as a wide variety of functional syndromes, vegetative symptoms and psychological disturbances. The course of the illness is rather variable; its commencement can be slow to develop or acute, initially presenting a localised clinical picture similar to a lumbar or cervical condition, and gradually, or in jumps, showing a deterioration accompanied by a generalisation of complaints. Various factors are probably instrumental in triggering off the fibrositis syndrome. The most important ones are emotional stress whereby symptoms of fear, depression, etc. lead to muscle tension and insertion tendinitis. Somatic factors such as malposition of the spinal column, may also contribute towards the manifestation of the clinical picture. The so-called secondary fibrositis syndromes should be defined from the point of view of differential diagnosis; they can develop within the framework of inflammatory rheumatic conditions, through infections and endocrinopathy. Differential diagnosis is very difficult considering depression alongside pain in the movable parts and "psychogenic rheumatism". Smooth transitions are in existence. Polymyalgia rheumatica and polymyositis, which produce similar clinical pictures, must be differentiated from the fibrositis syndrome.
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PMID:The fibrositis syndrome: diagnosis, differential diagnosis and pathogenesis. 331 8

Neurogenic switching is proposed as a hypothesis for a mechanism by which a stimulus at one site can lead to inflammation at a distant site. Neurogenic inflammation occurs when substance P and other neuropeptides released from sensory neurons produce an inflammatory response, whereas immunogenic inflammation results from the binding of antigen to antibody or leukocyte receptors. There is a crossover mechanism between these two forms of inflammation. Neurogenic switching is proposed to result when a sensory impulse from a site of activation is rerouted via the central nervous system to a distant location to produce neurogenic inflammation at the second location. Neurogenic switching is a possible explanation for systemic anaphylaxis, in which inoculation of the skin or gut with antigen produces systemic symptoms involving the respiratory and circulatory systems, and an experimental model of anaphylaxis is consistent with this hypothesis. Food-allergy-iducing asthma, urticaria, arthritis, and fibromyalgia are other possible examples of neurogenic switching. Neurogenic switching provides a mechanism to explain how allergens, infectious agents, irritants, and possibly emotional stress can exacerbate conditions such as migraine, asthma, and arthritis. Because neurogenic inflammation is known to be triggered by chemical exposures, it may play a role in the sick building syndrome and the multiple chemical sensitivity syndrome. Thus neurogenic switching would explain how the respiratory irritants lead to symptoms at other sites in these disorders.
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PMID:Neurogenic switching: a hypothesis for a mechanism for shifting the site of inflammation in allergy and chemical sensitivity. 762 26

Fibromyalgia (FM) is a chronic pain disorder that afflicts predominantly middle-aged women with cardinal symptoms of diffuse musculoskeletal pain, defined tender points, deprived sleep, and fatigue. The etiology and pathological mechanisms are poorly understood, and treatment approaches are largely ineffective. The clinical features of the syndrome are presented, and the relevance of muscle dysfunction in the etiopathogenesis of the disorder is explored. The evidence for involvement of muscle pathophysiology as a primary mechanism mediating the onset of symptoms is not compelling. Musculoskeletal dysfunction can be considered secondary to central abnormalities of pain modulation and altered sleep physiology precipitated by emotional stress in genetically predisposed individuals. Contemporary evidence favors treatment strategies that emphasize pain control, sleep enhancement, and a program of conditioning.
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PMID:The fibromyalgia syndrome: musculoskeletal pathophysiology. 803 24

Fibromyalgia (FM) and chronic fatigue syndrome (CFS) fall into the spectrum of what might be termed stress-associated syndromes by virtue of frequent onset after acute or chronic stressors and apparent exacerbation of symptoms during periods of physical or emotional stress. These illnesses also share perturbation of the hypothalamic-pituitary-adrenal axis and sympathetic stress response systems. In this article, the authors discuss the specific neurohormonal abnormalities found in FM and CFS and potential mechanisms by which dysfunction of neurohormonal stress-response systems could contribute to vulnerability to stress-associated syndromes and to the symptoms of FM and CFS.
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PMID:Evidence that abnormalities of central neurohormonal systems are key to understanding fibromyalgia and chronic fatigue syndrome. 886 Jul 99

Fibromyalgia (FM) falls into the spectrum of what might be termed 'stress-associated syndromes' by virtue of frequent onset after acute or chronic stressors and apparent exacerbation of symptoms during periods of physical or emotional stress. Patients with FM exhibit disturbances of the major stress-response systems, the HPA axis and the sympathetic nervous system. Integrated basal cortisol levels measured by 24-hour urine-free cortisol are low. FM patients display a unique pattern of HPA axis perturbation characterized by exaggerated ACTH response to exogenous CRH or to endogenous activators of CRH such as insulin-induced hypoglycaemia. The cortisol response to increased ACTH in these stress paradigms is blunted, as is the the cortisol response to exercise. Functional analysis suggests that FM patients may also exhibit disturbed autonomic system activity. For example, plasma NPY, a peptide co-localized with norepinephrine in the sympathetic nervous system, is low in patients with FM. Abnormalities of related neuronal systems, particularly decreased serotonergic activity, may contribute to the observed neuroendocrine perturbations in FM. Finally, other neuroendocrine systems, including the growth hormone axis, are also abnormal in FM patients. Many clinical features of FM and related disorders, such as widespread pain and fatigue, could be related to the observed neuroendocrine perturbations. This hypothesis is supported by the observation that many useful treatments for FM affect the function of these central nervous system centres. Further clarification of the role of neuroendocrine abnormalities in patients with FM, and the relationship of these disturbances with particular symptoms, may lead to improved therapeutic strategies.
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PMID:Neurohormonal perturbations in fibromyalgia. 891 54

Physical and emotional stress and altered reactivity of the autonomic nervous system have been implicated in the development and maintenance of fibromyalgia syndrome (FMS). This study investigated blood pressure, heart rate (HR), skin conductance levels (SCL), and surface electromyograms (EMG) from the trapezius muscle in 30 FMS patients and 30 age- and sex-matched healthy controls (HCs). All measures were continuously recorded during baseline (BL), social conflict, mental arithmetic, and relaxation tasks. The FMS patients showed significantly higher stress ratings and self-reported stress responses. Baseline EMG levels were significantly lower, and BL HR was significantly elevated. During both stress tasks, HR reactivity was significantly lower, and SCL reactivity was significantly higher in the FMS group. This pattern of low BL muscle tension and high BL HR, along with low HR and high SCL reactivity to stress, is discrepant to other chronic pain syndromes and suggests unique psychophysiological features associated with FMS. Several potential mechanisms for these psychophysiological responses are discussed.
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PMID:Psychophysiological responses in patients with fibromyalgia syndrome. 1708 46

Elevated catecholamine levels are a well-recognized cause of various types of cardiomyopathy. Causes of catecholamine elevation include tumors, toxins, drugs, emotional stress, and sepsis. Milnacipran is a dual and equipotent inhibitor of norepinephrine and serotonin uptake. It is frequently prescribed as therapy for fibromyalgia, and the drug has a good safety profile. Herein, we report the case of a 42-year-old woman with undefined connective-tissue disease and fibromyalgia who developed a severe and reversible cardiomyopathy while taking recommended doses of milnacipran. The cardiomyopathy was associated with a hyperadrenergic state manifested by tachycardia, hypertension, and elevated plasma catecholamine levels. The discontinuation of milnacipran and the initiation of anti-failure therapy resulted in complete resolution of the cardiomyopathy in 6 months. To our knowledge, this is the first report of milnacipran as a possible cause of catecholamine-induced cardiomyopathy.
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PMID:Hypertension, tachycardia, and reversible cardiomyopathy temporally associated with milnacipran use. 2219 46

In this manuscript we summarize the role of chronic stress as a potential trigger factor for Parkinson's disease. Underlying mechanisms and stress-induced changes to the neuronal networks have been highlighted. Examples of stress induced reversible symptoms that resemble parkinsonism in humans and in animal models raise the question whether emotional stress can cause striatal degeneration in susceptible patients. A Pubmed literature review searching for the terms 'Stress', 'Distress and Parkinson's disease', 'Emotional Distress and Parkinson's disease', 'Stress and Parkinson's disease', 'Prodromal Parkinson's disease', 'Non motor symptoms and Parkinson's disease', 'Paradoxical kinesia', 'Psychogenic parkinsonism', 'Functional somatic syndromes', 'Chronic fatigue syndrome', 'Irritable bowel syndrome', 'Fibromyalgia', 'Dopamine and fibromyalgia', 'Dopamine and chronic fatigue syndrome' and 'Dopamine and irritable bowel syndrome' was carried out until April 2013. Articles were also identified through searches of the authors' own files. Only papers published in English were reviewed. The final reference list was generated on the basis of originality and relevance to the broad scope of this viewpoint.
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PMID:Can stress trigger Parkinson's disease? 2425 93

Fibromyalgia Syndrome (FMS) is a condition considered to represent a prototype of central sensitization syndrome, characterized by chronic widespread pain and along with symptoms of fatigue, non-restorative sleep and cognitive difficulties. FMS can be induced by trauma, infection or emotional stress with cumulative evidence that dissociation is relatively frequent in FMS patients. Two randomized controlled trials have shown that hyperbaric oxygen therapy (HBOT) can induce neuroplasticity and be effective in patients suffering from FMS. In this paper we present, for the first time, case series of female fibromyalgia patients who, in the course of HBOT, suddenly recalled repressed traumatic memories of childhood sexual abuse (CSA). The surfacing of the repressed (dissociative) memories decades after the sexual abuse events was sudden and utterly surprising. No psychological intervention was involved. As the memories surfaced, the physical pain related to FMS subsided. In one patient who had brain single photon emission CT (SPECT) before and after HBOT, the prefrontal cortex appeared suppressed before and reactivated after. The 3 cases reported in this article are representative of a total of nine fibromyalgia patients who experienced a retrieval of repressed memory during HBOT. These cases provide insights on dissociative amnesia and suggested mechanism hypothesis that is further discussed in the article. Obviously, prospective studies cannot be planned since patients are not aware of their repressed memories. However, it is very important to keep in mind the possibility of surfacing memories when treating fibromyalgia patients with HBOT or other interventions capable of awakening dormant brain regions.
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PMID:Recovery of Repressed Memories in Fibromyalgia Patients Treated With Hyperbaric Oxygen - Case Series Presentation and Suggested Bio-Psycho-Social Mechanism. 2989 50


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