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

1. Chronic fatigue syndrome is characterized by muscle fatigue and pain at rest, symptoms which are usually exacerbated with exercise. Although various studies have shown minor, non-specific morphological and biochemical changes in muscle of patients with chronic fatigue syndrome, no consistent defect has been identified. Some have suggested that an enteroviral infection in muscle may cause the chronic muscle fatigue seen in patients with chronic fatigue syndrome, with acute infection directly and irreversibly impairing mitochondrial function, and persistent infection depressing muscle protein synthesis and metabolism. 2. To clarify the involvement of enterovirus infection in chronic fatigue syndrome, muscle biopsies from a group of patients with chronic fatigue syndrome were examined for the presence of enteroviral RNA by reverse transcriptase-polymerase chain reaction techniques in relation to functional studies of muscle mitochondria and the muscle RNA/DNA ratio. 3. Fifty-eight percent of patients reported an uncharacterized 'viral infection' before the onset of their illness, but none of the muscle samples from 34 patients contained detectable amounts of enteroviral RNA. Muscle tissue had a general reduction in the RNA/DNA ratio and mitochondrial enzyme activities with no specific abnormality in the activity of enzymes encoded partially on the mitochondrial genome (cytochrome-c oxidase) or nuclear genome (citrate synthase, succinate reductase). 4. These data provide no evidence of an enteroviral infection in muscle of patients with chronic fatigue syndrome, although this does not exclude a role of enterovirus in initiating the disease process. The general reduction in RNA/DNA ratio and mitochondrial enzyme activities is consistent with a general reduction in habitual activity.
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PMID:Investigation by polymerase chain reaction of enteroviral infection in patients with chronic fatigue syndrome. 877 36

Chronic fatigue syndrome (CFS) is often preceded by a viral illness and has recurrent "flu-like" symptoms. We compared demographic, clinical, and laboratory features (markers of inflammation and viral infection) among 717 patients with chronic fatigue (CF) with and without a self-reported postinfectious onset to identify associated clinical and biologic findings and to examine the subset of patients with CFS. Only subjective fever, chills, sore throat, lymphadenopathy, poorer functional status, and attribution of illness to a physical condition were significantly associated with a postinfectious onset. The features of patients with CFS were virtually identical to those of the broader category of patients with CF. We conclude that a postinfectious onset was not associated with a pattern of abnormalities across multiple psychosocial and biologic parameters.
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PMID:Postinfectious chronic fatigue: a distinct syndrome? 884 79

Traditional aetiological models in neuropsychiatry have placed little emphasis on the abnormal behavioural responses (decreased psychomotor activity, anorexia, weight loss, decreased social exploration and sexual behaviour, impaired cognitive function and increased somnolence) that are common to both psychiatric syndromes, notably depression, and the illness behaviour of sick animals. In recent years, the possible role of cytokines, as mediators of not only the immunological and metabolic responses to infection and inflammation but also a co-ordinated behavioural response, has been described. Further, a range of possible mechanisms for these effects has been postulated, notably involving corticotropin releasing factor (CRF) and prostaglandins of the E series (PgE) with the central nervous system (CNS). Here we outline a series of human clinical conditions where neuropsychiatric syndromes co-occur with a host response to infection or inflammation. These may be characterized by cytokine production (e.g. acute, recurrent and chronic viral illness, systemic autoimmune diseases and chronic fatigue syndrome). Other clinical situations characterized by exposure to or in vivo production of cytokines (e.g. treatment of chronic infections and malignancies, progression and/or recurrence of malignancies) are also discussed. We postulate that the stereotyped behavioural repertoire observed is mediated by cytokine-dependent mechanisms within the CNS. Systematic studies of the behavioural responses of such patient groups are suggested, noting specifically correlations between the time course and severity of immune and neuroendocrine and behavioural responses and dose-response effects.
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PMID:Are cytokines associated with neuropsychiatric syndromes in humans? 884 62

Partial sequencing was performed on cloned DNA obtained from cultures of a stealth virus isolated from a patient with the chronic fatigue syndrome. The results extend earlier findings showing regions of homology to cytomegalovirus (CMV). Although the virus is much more closely related to simian CMV than to human CMV, many of the cloned viral segments could be aligned with the human CMV genome. The aggregate size of the aligned segments exceeds 100 kilobase pairs (kbp). Undigested viral DNA has a mobility in agarose gel electrophoresis corresponding to approximately 20 kbp. The virus, therefore, apparently exists in multiple fragments. Considerable sequence variation exists between individual clones which overlap to similar regions of the human CMV genome. The fragmented genome and sequence microheterogeneity suggest that both the processivity and the fidelity of replication of the viral genome are defective. An unstable viral genome may provide a potential mechanism of recovery from stealth viral illness.
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PMID:Genetic instability and fragmentation of a stealth viral genome. 885 90

This study investigated psychosocial morbidity, coping styles and health locus of control in 64 cases with and without chronic fatigue identified from a cohort of primary care patients recruited 6 months previously with a presumed, clinically diagnosed viral illness. A significant association between chronic fatigue and psychosocial morbidity, somatic symptoms and escape-avoidance coping styles was shown. Chronic fatigue cases were significantly more likely to have a past psychiatric history and a current psychiatric diagnosis based on a standardized clinical interview. Twenty-three of the cases fulfilled criteria for chronic fatigue syndrome (CFS). Such cases were significantly more fatigued than those not fulfilling criteria, but had little excess psychiatric disorder. A principal components analysis provided some evidence for chronic fatigue being separable from general psychosocial morbidity but not from the tendency to have other somatic complaints. Past psychiatric history and psychological distress at the time of the viral illness were risk factors for psychiatric 'caseness' 6 months later, while presence of fatigue, psychologising attributional style and sick certification were significant risk factors for CFS. These findings extend a previous questionnaire study of predictors of chronic 'post-viral' fatigue.
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PMID:Psychosocial risk factors for chronic fatigue and chronic fatigue syndrome following presumed viral illness: a case-control study. 893 Nov 66

A group of 222 patients suffering from cellular immunodeficiency (CID), frequently combined with chronic fatigue syndrome (CFS) and/or chronic viral infections by Epstein-Barr virus (EBV) and/or cytomegalovirus (CMV), were immunologically investigated and treated with transfer factor (TF). The age range was 17-77 years. In order to elucidate the influence of aging on the course of the disease and on treatment, 3 subgroups were formed: 17-43 years, 44-53 years, and 54-77 years. Six injections of Immodin (commercial preparation of TF by SEVAC, Prague) were given in the course of 8 weeks. When active viral infection was present, IgG injections and vitamins were added. Immunological investigation was performed before the start of therapy, and subsequently according to need, but not later than after 3 months. The percentages of failures to improve clinical status of patients were in the individual subgroups, respectively: 10.6%, 11.5% and 28.9%. The influence of increasing age on the percentage of failures to normalize low numbers of T cells was very evident: 10.6%, 21.2% and 59.6%. In individuals uneffected by therapy, persistent absolute lymphocyte numbers below 1,200 cells were found in 23.1%, 54.5% and 89.3% in the oldest group. Statistical analysis by Pearson's Chi-square test, and the test for linear trend proved that the differences among the individual age groups were significant. Neither sex, nor other factors seemed to influence the results. The results of this pilot study show that age substantially influences the failure rate of CID treatment using TF. In older people, it is easier to improve the clinical condition than CID: this may be related to the diminished number of lymphocytes, however, a placebo effect cannot be totally excluded.
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PMID:The influence of age on transfer factor treatment of cellular immunodeficiency, chronic fatigue syndrome and/or chronic viral infections. 899 65

The chronic fatigue syndrome (CFS) has been intensively studied over the last 40 years, but no conclusions have yet been agreed as to its cause. Most cases nowadays are sporadic. In the established chronic condition there are no consistently abnormal physical signs or abnormalities on laboratory investigation. Many physicians remain convinced that the symptoms are psychological rather than physical in origin. This view is reinforced by the emotional way in which many patients present themselves. The overlap of symptoms between CFS and depression remains a source of confusion and difficulty. But even if all CFS patients were rediagnosed as depressives, this would not negate the possibility of an underlying organic cause for the condition, in view of the growing evidence that depression itself has a physical cause and responds best to physical treatments. There is some evidence both for active viral infection and for an immunological disorder in the CFS. Many observations suggest that the syndrome could derive from residual damage to the reticular activating system (RAS) of the upper brain stem and/or to its cortical projections. Such damage could be produced by a previous viral infection, leaving functional defects unaccompanied by any gross histological changes. In animal experiments activation of the RAS can change sleep state and activate or stimulate cortical functions. RAS lesions can produce somnolence and apathy. Studies by modern imaging techniques have not been entirely consistent, but many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis--in both of which conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present. A number of logical approaches to treatment can already be envisaged.
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PMID:Chronic fatigue syndrome--aetiological aspects. 946 37

Chronic fatigue and chronic fatigue syndrome (CFS) have become increasingly recognized as a common clinical problem, yet one that physicians often find difficult to manage. In this review we suggest a practical, pragmatic, evidence-based approach to the assessment and initial management of the patient whose presentation suggests this diagnosis. The basic principles are simple and for each aspect of management we point out both potential pitfalls and strategies to overcome them. The first, and most important task is to develop mutual trust and collaboration. The second is to complete an adequate assessment, the aim of which is either to make a diagnosis of CFS or to identify an alternative cause for the patient's symptoms. The history is most important and should include a detailed account of the symptoms, the associated disability, the choice of coping strategies, and importantly, the patient's own understanding of his/her illness. The assessment of possible comorbid psychiatric disorders such as depression or anxiety is mandatory. When the physician is satisfied that no alternative physical or psychiatric disorder can be found to explain symptoms, we suggest that a firm and positive diagnosis of CFS be made. The treatment of CFS requires that the patient is given a positive explanation of the cause of his symptoms, emphasizing the distinction among factors that may have predisposed them to develop the illness (lifestyle, work stress, personality), triggered the illness (viral infection, life events) and perpetuated the illness (cerebral dysfunction, sleep disorder, depression, inconsistent activity, and misunderstanding of the illness and fear of making it worse). Interventions are then aimed to overcoming these illness-perpetuating factors. The role of antidepressants remains uncertain but may be tried on a pragmatic basis. Other medications should be avoided. The only treatment strategies of proven efficacy are cognitive behavioral ones. The most important starting point is to promote a consistent pattern of activity, rest, and sleep, followed by a gradual return to normal activity; ongoing review of any 'catastrophic' misinterpretation of symptoms and the problem solving of current life difficulties. We regard chronic fatigue syndrome as important not only because it represents potentially treatable disability and suffering but also because it provides an example for the positive management of medically unexplained illness in general.
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PMID:Chronic fatigue syndrome. A practical guide to assessment and management. 921 87

Chronic fatigue syndrome (CFS), a recently named heterogeneous disorder, is an illness of unknown etiology. The association between CFS and several viral infection has been suggested. Here, we centered on the possible link between CFS and Borna disease virus (BDV) infection. BDV is a neurotropic, nonsegmented negative-strand (NNS) RNA virus. Recent epidemiological data have suggested that BDV may be closely associated with depression and schizophrenia in humans. In Japanese patients with CFS, the prevalence of BDV infection was 34% (30/89) and 12% (7/57) by immunoblotting and PCR analysis, respectively. Furthermore, anti-BDV antibodies and BDV RNA were detected in a family cluster with CFS. These results suggested that this virus contributes to or initiates CFS, although the single etiologic role of BDV is unlikely.
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PMID:[Demonstration on Borna disease virus in patients with chronic fatigue syndrome]. 939 13

The frequent association of an active viral infection with the symptoms of CFS led researchers to hypothesize that chronic fatigue syndrome (CFS) is induced by a virus. Results of these studies indicated that despite clinical support for this hypothesis, there were no clear data linking viruses to CFS. In this overview, we will explore the interrelation of the immune, endocrine, and central nervous systems, and the possibility that stress and/or the reactivation/replication of a latent virus (such as Epstein Barr virus) could modulate the immune system to induce CFS. Relevant research conducted in the developing field of psychoneuroimmunology will be reviewed, with a particular focus on cytokine synthesis, natural killer (NK) cell activity, and T-lymphocyte function, as they relate to CFS.
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PMID:Stress-associated immune modulation: relevance to viral infections and chronic fatigue syndrome. 979 Apr 80


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