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

Fibromyalgia is a chronic functional illness that presents with widespread musculoskeletal pain as well as a constellation of symptoms including fatigue, cognitive dysfunction, sleep difficulties, stiffness, anxiety, and depressed mood. The diagnosis of fibromyalgia, similar to other functional disorders, requires that organic diseases are not causing the symptoms. Systemic and rheumatic diseases can be ruled out by a patient history, physical examination, and laboratory investigations. Because there are no specific laboratory tests for fibromyalgia, the 1990 American College of Rheumatology (ACR) classification criteria have been used in clinical settings; however, they are not ideal for individual patient diagnosis. Clinicians should be aware of limitations inherent in using tender points in the diagnosis of fibromyalgia. The multiple symptoms of fibromyalgia often overlap with those of related disorders and may further complicate the diagnosis. One of the most challenging diagnostic dilemmas that clinicians face is distinguishing fibromyalgia from other central pain disorders (e.g., irritable bowel syndrome, chronic fatigue syndrome, migraine). Screening questions based on published criteria can be used as a first approach in diagnosing functional illnesses. Numerous studies report a higher prevalence of psychiatric disorders in patients with fibromyalgia. Therefore, a careful history and evaluation should be taken for the presence of primary mood disturbances. To date, there is no "gold standard" for diagnosing fibromyalgia. Until a better clinical case definition of fibromyalgia exists, all diagnostic criteria should be interpreted with caution, considered rudimentary, and subject to modification.
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PMID:Diagnosis and differential diagnosis of fibromyalgia. 1996 92

During the last 20 years, numerous clinical trials have examined the therapeutic usefulness of melatonin in different fields of medicine. The objective of this article is to review, in depth, the science regarding clinical trials performed to date. The efficacy of melatonin has been assessed as a treatment of ocular diseases, blood diseases, gastrointestinal tract diseases, cardiovascular diseases, diabetes, rheumatoid arthritis, fibromyalgia, chronic fatigue syndrome, infectious diseases, neurological diseases, sleep disturbances, aging and depression. Melatonin has been also used as a complementary treatment in anaesthesia, hemodialysis, in vitro fertilization and neonatal care. The conclusion of the current review is that the use of melatonin as an adjuvant therapy seems to be well funded for macular degeneration, glaucoma, protection of the gastric mucosa, irritable bowel syndrome, arterial hypertension, diabetes, side effects of chemotherapy and radiation in cancer patients or hemodialysis in patients with renal insufficiency and, especially, for sleep disorders of circadian etiology (jet lag, delayed sleep phase syndrome, sleep deterioration associated with aging, etc.) as well as in those related with neurological degenerative diseases (Alzheimer, etc.,) or Smith-Magenis syndrome. The utility of melatonin in anesthetic procedures has been also confirmed. More clinical studies are required to clarify whether, as the preliminary data suggest, melatonin is useful for treatment of fibromyalgia, chronic fatigue syndrome, infectious diseases, neoplasias or neonatal care. Preliminary data regarding the utility of melatonin in the treatment of ulcerative colitis, Crohn's disease, rheumatoid arthritis are either ambiguous or negative. Although in a few cases melatonin seems to aggravate some conditions, the vast majority of studies document the very low toxicity of melatonin over a wide range of doses.
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PMID:Clinical uses of melatonin: evaluation of human trials. 2042 9

The irritable bowel syndrome (IBS) is the best known of the functional gastrointestinal tract disorders. Many IBS patients have at least one co-morbid somatic complaint and many meet diagnostic criteria for other functional disorders. Patients with IBS and another functional disorder, in comparison with patients with IBS only, have more severe IBS symptoms, a higher rate of psychopathology, greater impairment of quality of life, and more illness-related work absenteeism. Estimates of the prevalence of IBS in patients with fibromyalgia range from 30-35% to as high as 70%. Studies of IBS among patients with chronic fatigue syndrome have reported a prevalence ranging from 35-92%. The prevalence of IBS among patients with chronic fatigue syndrome is reported to be 14%. IBS patients with other co-morbid functional disorders appear to manifest a greater degree of somatization. It has been suggested that the presence of multiple co-morbid disorders may be a marker for psychological influences on etiology. This raises the question of whether the functional syndromes represent the same pathophysiological process, i.e., are the same entity that has been separated into different clinical entities because of medical sub-specialization, or are indeed separate disorders. While the answer to this question awaits further research, it would appear that most functional patients who meet formal diagnostic criteria for more than one functional disorder manifest one disorder clinically more that the others and seek consultation differentially for that set of symptoms.
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PMID:Irritable Bowel Syndrome and Co-morbid Gastrointestinal and Extra-gastrointestinal Functional Syndromes. 2053 41

Fibromyalgia is a complex condition that is characterized by chronic widespread pain and multiple other symptoms, including fatigue, sleep disturbances, cognitive dysfunction, stiffness, and depressive episodes. Fibromyalgia may coexist and/or overlap with other conditions that may involve central sensitivity, including chronic fatigue syndrome, irritable bowel syndrome, irritable bladder syndrome or interstitial cystitis, and temporomandibular disorder. The pathophysiology of fibromyalgia remains uncertain but is believed to be partly the result of central systems affecting afferent processing as well as impaired endogenous pain-inhibitory systems. Abnormal central nociceptive processing may contribute to fibromyalgia, producing heightened responses to various noxious stimuli with resulting mechanical hyperalgesia. Fibromyalgia remains a clinical diagnosis. There has been a recent paradigm shift away from requiring 11 or more out of 18 tender points and instead focusing on the presence of chronic widespread pain as well as symptoms of fatigue, unrefreshed sleep, and other somatic complaints. Although there is no known cure for fibromyalgia, multidisciplinary team efforts using combined treatment approaches, including patient education, aerobic exercise, cognitive behavioral therapy, and pharmacologic therapies (serotonin norepinephrine reuptake inhibitors [eg, duloxetine, milnacipran] and alpha 2-delta receptor ligands [eg, pregabalin]) may improve symptoms as well as function of patients with fibromyalgia.
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PMID:Fibromyalgia syndrome: a discussion of the syndrome and pharmacotherapy. 2056 96

Functional somatic symptoms are prevalent in all medical settings, but their management is hampered by an obsolete theoretical framework and inadequate classification systems. Epidemiological and neurobiological studies suggest that the functional somatic syndromes, e.g. fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome and somatoform disorders belong to the same family of disorders. An empirically based diagnosis including different subtypes and severities is proposed as a unifying diagnostic construct: bodily distress syndrome. This construct provides a common language for functional disorders across medical specialties.
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PMID:[New unifying diagnosis of functional diseases]. 2080 86

New information about the pathophysiology of idiopathic nonallergic rhinopathy indicates a high prevalence in chronic fatigue syndrome (CFS). This article shows the relevance of CFS and allied disorders to allergy practice. CFS has significant overlap with systemic hyperalgesia (fibromyalgia), autonomic dysfunction (irritable bowel syndrome and migraine headaches), sensory hypersensitivity (dyspnea; congestion; rhinorrhea; and appreciation of visceral nociception in the esophagus, gastrointestinal tract, bladder, and other organs), and central nervous system maladaptations (central sensitization) recorded by functional magnetic resonance imaging (fMRI). Neurological dysfunction may account for the overlap of CFS with idiopathic nonallergic rhinopathy. Scientific advances are in fMRI, nociceptive sensor expression, and, potentially, infection with xenotropic murine leukemia-related virus provide additional insights to novel pathophysiological mechanisms of the "functional" complaints of these patients that are mistakenly interpreted as allergic syndromes. As allergists, we must accept the clinical challenges posed by these complex patients and provide proper diagnoses, assurance, and optimum care even though current treatment algorithms are lacking.
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PMID:Relationships among rhinitis, fibromyalgia, and chronic fatigue. 2061 18

Fatigue is a symptom whose causes are protean and whose phenotype includes physical, mood, and behavioral components. Chronic fatigue syndrome (CFS) is an illness that has strong biological underpinnings and no definite etiology. Diagnostic criteria established by the Centers for Disease Control and Prevention have helped classify CFS as an overlap of mood, behavioral, and biological components. These include the presence of fatigue for more than 6 months associated with a diminution of functional activity and somatic symptoms, and pain not attributable to a specific diagnosis or disease. Four of the following criteria need to be present: sore throat, impaired memory or cognition, unrefreshing sleep, postexertional fatigue, tender glands, aching stiff muscles, joint pain, and headaches. Many researchers have observed that CFS shares features in common with other somatic syndromes, including irritable bowel syndrome, fibromyalgia, and temporomandibular joint dysfunction. Correlations between inflammation and infection, augmented sensory processing, abnormalities of neurotransmitters, nerve growth factors, low levels of serotonin and norepinephrine, abnormalities of homeostasis of the stress system, and autonomic dysfunction may be hallmarks of CFS. The relative contributions of each of these abnormalities to the profound fatigue associated with CFS need to be explored further to better evaluate and treat the syndrome.
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PMID:Perspectives on fatigue from the study of chronic fatigue syndrome and related conditions. 2065 23

For many years, a deficiency of monoamines including serotonin has been the prevailing hypothesis on depression, yet research has failed to confirm consistent relations between brain serotonin and depression. High degrees of overlapping comorbidities and common drug efficacies suggest that depression is one of a family of related conditions sometimes referred to as the "affective spectrum disorders", and variably including migraine, irritable bowel syndrome, chronic fatigue syndrome, fibromyalgia and generalized anxiety disorder, among many others. Herein, we present data from many different experimental modalities that strongly suggest components of mitochondrial dysfunction and inflammation in the pathogenesis of depression and other affective spectrum disorders. The three concepts of monoamines, energy metabolism and inflammatory pathways are inter-related in many complex manners. For example, the major categories of drugs used to treat depression have been demonstrated to exert effects on mitochondria and inflammation, as well as on monoamines. Furthermore, commonly-used mitochondrial-targeted treatments exert effects on mitochondria and inflammation, and are increasingly being shown to demonstrate efficacy in the affective spectrum disorders. We propose that interactions among monoamines, mitochondrial dysfunction and inflammation can inspire explanatory, rather than mere descriptive, models of these disorders.
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PMID:Beyond the serotonin hypothesis: mitochondria, inflammation and neurodegeneration in major depression and affective spectrum disorders. 2069 44

The relationship between corticosteroids (endogenous and exogenous) and stress is well known, as is the use of steroids as concomitant treatment in pain management during acute inflammation. In the past, steroids have not been considered the first line of treatment in pain management. In this review, we examine new scientific and clinical evidence that demonstrates the direct role that steroids play in the generation and clinical management of chronic pain. We will discuss the new findings demonstrating the fact that steroids and related mediators produce paradoxical effects on pain such as analgesia, hyperalgesia, and even placebo analgesia. In addition, we will examine the physiologic effect of stress, high allostatic load, and idiopathic disease states such as chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, and burnout. The recently observed positive relationship between glutaminergic activity in the insula and clinical pain will be examined in the context of understanding the central role of steroids in chronic pain. The complex role of the hypothalamic-pituitary-adrenal axis in pain will be discussed as well as other heterogeneous forms of chronic pain that involve many components of the central nervous system. Components of the hypothalamic-pituitary-adrenal axis have paradoxical effects on certain types of pain that are dependent on dose and on site (whether peripheral or central) and mode of application. Recent studies on glia have shown that they prolong a state of neuronal hypersensitization in the dorsal root ganglia by releasing growth factors and other substances that act on the immune system. We will discuss the implication of these new findings directly linking pain to steroids, stress, and key higher brain regions in the context of future therapeutic targets.
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PMID:The role of corticosteroids and stress in chronic pain conditions. 2083 96

Chronic fatigue syndrome (CFS) is a debilitating disease characterized by unexplained disabling fatigue and a combination of accompanying symptoms the pathology of which is incompletely understood. Many CFS patients complain of gut dysfunction. In fact, patients with CFS are more likely to report a previous diagnosis of irritable bowel syndrome (IBS), a common functional disorder of the gut, and experience IBS-related symptoms. Recently, evidence for interactions between the intestinal microbiota, mucosal barrier function, and the immune system have been shown to play a role in the disorder's pathogenesis.Studies examining the microecology of the gastrointestinal (GI) tract have identified specific microorganisms whose presence appears related to disease; in CFS, a role for altered intestinal microbiota in the pathogenesis of the disease has recently been suggested. Mucosal barrier dysfunction promoting bacterial translocation has also been observed. Finally, an altered mucosal immune system has been associated with the disease. In this article, we discuss the interplay between these factors in CFS and how they could play a significant role in GI dysfunction by modulating the activity of the enteric nervous system, the intrinsic innervation of the gut.If an altered intestinal microbiota, mucosal barrier dysfunction, and aberrant intestinal immunity contribute to the pathogenesis of CFS, therapeutic efforts to modify gut microbiota could be a means to modulate the development and/or progression of this disorder. For example, the administration of probiotics could alter the gut microbiota, improve mucosal barrier function, decrease pro-inflammatory cytokines, and have the potential to positively influence mood in patients where both emotional symptoms and inflammatory immune signals are elevated. Probiotics also have the potential to improve gut motility, which is dysfunctional in many CFS patients.
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PMID:Gut inflammation in chronic fatigue syndrome. 2093 23


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