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Query: UMLS:C0015674 (chronic fatigue syndrome)
 2,978 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Considerable knowledge has accumulated in recent decades concerning the significance of physical activity in the treatment of a number of diseases, including diseases that do not primarily manifest as disorders of the locomotive apparatus. In this review we present the evidence for prescribing exercise therapy in the treatment of metabolic syndrome-related disorders (insulin resistance, type 2 diabetes, dyslipidemia, hypertension, obesity), heart and pulmonary diseases (chronic obstructive pulmonary disease, coronary heart disease, chronic heart failure, intermittent claudication), muscle, bone and joint diseases (osteoarthritis, rheumatoid arthritis, osteoporosis, fibromyalgia, chronic fatigue syndrome) and cancer, depression, asthma and type 1 diabetes. For each disease, we review the effect of exercise therapy on disease pathogenesis, on symptoms specific to the diagnosis, on physical fitness or strength and on quality of life. The possible mechanisms of action are briefly examined and the principles for prescribing exercise therapy are discussed, focusing on the type and amount of exercise and possible contraindications.
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PMID:Evidence for prescribing exercise as therapy in chronic disease. 1664 91

The intensity of acute and chronic pain depends on interactions between peripheral impulse input and CNS pain mechanisms, including facilitation and inhibition. Whereas tonic pain inhibition is a characteristic of most pain-free individuals, pain facilitation can be detected in many chronic pain patients. The capability to inhibit pain is normally distributed along a wide continuum in the general population and can be used to predict chronic pain. Accumulating evidence suggests that endogenous pain inhibition depends on activation of the prefrontal cortex, periaqueductal gray and rostral ventral medulla. Quantitative sensory test paradigms have been designed to acquire detailed information regarding each individual's endogenous pain inhibition and facilitation. Such tests include: temporal summation of pain, which is mostly used to assess facilitatory pain modulation by measuring the change in pain perception during a series of identical nociceptive stimuli; and conditioned pain modulation, which tests pain inhibition by utilizing two simultaneously applied painful stimuli (the 'pain inhibits pain' paradigm). Considerable indirect evidence seems to indicate that not only increased pain facilitation but also ineffective pain inhibition represents a predisposition for chronic pain. This view is supported by the fact that many chronic pain syndromes (e.g., fibromyalgia, temporomandibular joint disorder, irritable bowel syndrome, headache and chronic fatigue syndrome) are associated with hypersensitivity to painful stimuli and reduced endogenous pain inhibition. However, future prospective studies will be necessary to provide definitive evidence for this relationship. Such research would not only provide important information about mechanisms relevant to chronic pain but would also permit identification of individuals at high risk for future chronic pain.
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PMID:Abnormal endogenous pain modulation is a shared characteristic of many chronic pain conditions. 2255 Sep 86

Central sensitivity syndromes are characterized by distressing symptoms, such as pain and fatigue, in the absence of clinically obvious pathology. The scientific underpinnings of these disorders are not currently known. Modern neuroimaging techniques promise new insights into mechanisms mediating these postulated syndromes. We review the results of neuroimaging applied to five central sensitivity syndromes: fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, temporomandibular joint disorder, and vulvodynia syndrome. Neuroimaging studies of basal metabolism, anatomic constitution, molecular constituents, evoked neural activity, and treatment effect are compared across all of these syndromes. Evoked sensory paradigms reveal sensory augmentation to both painful and nonpainful stimulation. This is a transformative observation for these syndromes, which were historically considered to be completely of hysterical or feigned in origin. However, whether sensory augmentation represents the cause of these syndromes, a predisposing factor, an endophenotype, or an epiphenomenon cannot be discerned from the current literature. Further, the result from cross-sectional neuroimaging studies of basal activity, anatomy, and molecular constituency are extremely heterogeneous within and between the syndromes. A defining neuroimaging "signature" cannot be discerned for any of the particular syndromes or for an over-arching central sensitization mechanism common to all of the syndromes. Several issues confound initial attempts to meaningfully measure treatment effects in these syndromes. At this time, the existence of "central sensitivity syndromes" is based more soundly on clinical and epidemiological evidence. A coherent picture of a "central sensitization" mechanism that bridges across all of these syndromes does not emerge from the existing scientific evidence.
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PMID:Neuroimaging of Central Sensitivity Syndromes: Key Insights from the Scientific Literature. 2671 48