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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cognitive approach to the treatment of chronic fatigue syndrome (CSF) is based on a multifactor etiological hypothesis, i.e. inaccurate beliefs and attitudes to the illness interact with pathophysiological processes, ineffective coping behaviours, negative states of mood, social problem, to perpetuate the illness. Patients suffering from CFS are supposed to be hypervigilant to somatic sensations and to interpret them as signs of impending physical catastrophe. The aim of the this paper is to describe the clinical implementation of principles of cognitive therapy in the treatment of CFS. Basic to the treatment approach is a collaborative, listening and empathic attitude, sensitive to the patient's personal beliefs and potential threats to self-esteem. The aim is to develop more useful, functional, formulations of the illness. The patient and the therapist work together to look at how the patient thinks about herself/himself and the illness, detect unhelpful attitudes, thoughts and mental images about the illness, and to make them accessible to Socratic reasoning. Graded behavioural interventions are planned in order to disconfirm unhelpful beliefs and reverse the spiral of tiredness, demoralization and reduced activity. The treatment is structured according to the general principles of cognitive therapy.
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PMID:[Chronic fatigue syndrome in a cognitive perspective. A therapeutic model]. 1498 43

Chronic fatigue syndrome is a disorder characterised by prolonged fatigue and debility and is mostly associated with post-infection sequelae although ongoing infection is unproven. Immunological aberration is likely and this may prove to be associated with an expanding group of vasoactive neuropeptides in the context of molecular mimicry and inappropriate immunological memory. Vasoactive neuropeptides including vasoactive intestinal peptide (VIP) and pituitary adenylate activating polypeptide (PACAP) belong to the secretin/glucagon superfamily and act as hormones, neurotransmitters, immune modulators and neurotrophes. They are readily catalysed to smaller peptide fragments by antibody hydrolysis. They and their binding sites are immunogenic and are known to be associated with a range of autoimmune conditions. Vasoactive neuropeptides are widely distributed in the body particularly in the central, autonomic and peripheral nervous systems and have been identified in the gut, adrenal gland, reproductive organs, vasculature, blood cells and other tissues. They have a vital role in maintaining vascular flow in organs, and in thermoregulation, memory and concentration. They are co-transmitters for acetylcholine, nitric oxide, endogenous opioids and insulin, are potent immune regulators with primarily anti-inflammatory activity, and have a significant role in protection of the nervous system to toxic assault, promotion of neural development and the maintenance of homeostasis. This paper describes a biologically plausible mechanism for the development of CFS based on loss of immunological tolerance to the vasoactive neuropeptides following infection, significant physical exercise or de novo. It is proposed that release of these substances is accompanied by a loss of tolerance either to them or their receptor binding sites in CFS. Such an occurrence would have predictably serious consequences resulting from compromised function of the key roles these substances perform. All documented symptoms of CFS are explained by vasoactive neuropeptide compromise, namely fatigue and nervous system dysfunction through impaired acetylcholine activity, myalgia through nitric oxide and endogenous opioid dysfunction, chemical sensitivity through peroxynitrite and adenosine dysfunction, and immunological disturbance through changes in immune modulation. Perverse immunological memory established against these substances or their receptors may be the reason for the protracted nature of this condition. The novel status of these substances together with their extremely small concentrations in blood and tissues means that clinical research into them is still in its infancy. A biologically plausible theory of CFS causation associated with vasoactive neuropeptide dysfunction would promote a coherent and systematic approach to research into this and other possibly associated disabling conditions.
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PMID:Is chronic fatigue syndrome an autoimmune disorder of endogenous neuropeptides, exogenous infection and molecular mimicry? 1508 83

The syndrome of chronic fatigue is a rather new pathology, included in ADS 10. There is no specific treatment. Vitamins and microelements are very important for the prevention and treatment of CFS. Of special significance are BAA on the basis of yarsts, which are universal in their biological chemical composition and contain high amounts of vitamins B, K and essential aminoacids. The aim this work is clinical diagnostic of "Nagipol" use, made on the basis of beer yeasts, for the prevention and treatment of CFS. Clinical-dietologic study showed that "Nagipol" biologically active additive, useful in CFS, prodvecins clinical status improvement in CFS, positively influencing cognitive CNS functions, symptoms of psychoemtional instability, normalizing blood biochemical parameters, can be recommended as one of the addition element in diet-therapy of patients with excessive body mass and otesitg with the associated CFS. Recommended "Nagipol" as preventive-medical dietetic means for this pathology.
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PMID:[Biologically active food additives for correction of the chronic fatigue syndrome]. 1515 66

The authors' purpose in this study was to compare the perception of fatigue severity as measured by different fatigue questionnaires. The authors evaluated 3 groups of patients in a cross-sectional study: chronic fatigue syndrome (CFS, n = 20), non-CFS fatigue (n = 20), and familial Mediterranean fever (FMF n = 25). In addition, the authors tracked 7 patients with CFS longitudinally for severity of fatigue. The severity of fatigue-related symptoms was assessed with 2 questionnaires: the unidimensional Chalder's Fatigue Severity Scale (CH) and the composite Fatigue Impact Scale (FI) which has 3 subscales--cognitive, physical, and social--and a total score. In the cross-sectional study, correlations between CH and FI cognitive scores were r = .78 (p < .0001), CH versus FI physical scores r = .603 (p < .0001), CH versus FI social scores r = .66 (p < .0001), and CH versus FI total scores r = .74 (p < .0001). In the longitudinal survey of CFS patients, the authors compared 30 questionnaires revealing correlations of CH versus FI cognitive scores r = .64 (p = .0004), CH versus FI physical r = .68 (p = .0001), CH versus FI social r = .87 (p < .0001), and CH versus FI total r = .90 (p < .0001). Fatigue severity as assessed by the unidimensional CH scale and the composite FI scale is comparable. The simple CH scale may be adequate for the assessment of the feeling of fatigue, in general, and for monitoring the severity of fatigue in CFS, in particular.
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PMID:The feeling of fatigue--fatigue severity by unidimensional versus composite questionnaires. 1536 97

Spreading of fatigue-related effects from active to inactive parts in the cat gastrocnemius muscle was studied. Fatiguing contractions of a part of gastrocnemius muscle were evoked through stimulation of the cut ventral root (VR) S1 with rate 50 s(-1) during 20 s followed by 10 s of rest, over 10-30 min (CFS). To test activation of a non-active part of this muscle the distributed stimulation of dissected VR L7 with rate of 10 s(-1) per filament was applied. After achieving by the muscle a steady-state level of isometric contraction, a quick transition to isotonic condition was produced. Transient responses of shortening and lengthening were analyzed in terms of the two-component model including the fast inertialess and slow aperiodic components. Test duration was 12 s, time intervals between tests consisted of 3 min. CFS reduced isometric force of the tested part of muscle as well as the velocity of shortening and lengthening. The muscle lengthening had been slowing down with development of the fatigue effects; the final steady value of the muscle length in transients was reduced, while weight of the inertialess component increased. Slowing of shortening was accompanied by reduction of the final length amplitude and the time constants of aperiodic component were increased. We suppose that diffusion of metabolites from active to inactive muscle fibers was the major reason for contractility deterioration.
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PMID:[Effects of fatigue on the characteristics of cat gastrocnemius muscle contraction and elongation in response to changes of the controlled load]. 1569 97

Previous work by others have suggested the occurrence of one or more chemical or metabolic 'markers' for ME/CFS including specific amino acids and organic acids and a number of unidentified compounds (CFSUM1, CFSUM2). We have shown elsewhere that CFSUM1 is partially derivatised pyroglutamic acid and CFSUM2 partially derivatised serine and have suggested and demonstrated that the analytical methods used were unsuitable to identify or to accurately quantify urinary metabolites. We have now made a detailed analysis of plasma and urinary amino acids and of urinary organic acids from patients with ME/CFS and from three control groups. Fasting blood plasma and timed urine samples were obtained from 31 patients with CFS, 31 age and sex-matched healthy controls, 15 patients with depression and 22 patients with rheumatoid arthritis. Plasma and urinary amino acids and urinary organic acids were determined using established and validated methods and data compared by statistical analysis. None of the previously reported abnormalities in urinary amino acids or of organic acids could be confirmed. Results however provide some evidence in patients with ME/CFS for underlying inflammatory disease and for reduced intramuscular collagen with a lowered threshold for muscle micro-injury. These factors in combination may provide a basis for the fatigue and muscle pain that are the major symptoms in these patients.
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PMID:Urinary and plasma organic acids and amino acids in chronic fatigue syndrome. 1599 88

We aimed to determine how menopausal transition symptoms cluster across 216 midlife women with fibromyalgia, chronic fatigue syndromes (FMS/CFS), or both and subsequently to compare symptom factor severity scores by menopausal status among these women and compare symptom reporting with prior community-based samples of women without obvious illness. We designed a cross-sectional telephone survey of 216 women aged 35 to 55, diagnosed with FMS/CFS, symptomatic in the prior 6 months, and without hysterectomy. Thirty-six of 61 symptoms loaded on five factors: aroused/anxious mood, depressed mood/withdrawal, musculoskeletal, gastrointestinal (GI), and vasomotor. Peri- and postmenopausal women had higher symptom severity scores for musculoskeletal, GI, and vasomotor factors but not mood factors. Symptoms for the women we studied who had FMS/CFS clustered similar to those in previous community-based samples of midlife women without major illness; however, the number of women experiencing symptoms was much higher among our sample.
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PMID:Menopausal transition symptoms in midlife women living with fibromyalgia and chronic fatigue. 1684 73

The use of sustained release tri-iodothyronine (SR-T3) in clinical practice, has gained popularity in the complementary and alternative medical community in the treatment of chronic fatigue with a protocol (WT3) pioneered by Dr. Denis Wilson. The WT3 protocol involves the use of SR-T3 taken orally by the patient every 12 hours according to a cyclic dose schedule determined by patient response. The patient is then weaned once a body temperature of 98.6 degrees F has been maintained for 3 consecutive weeks. The symptoms associated with this protocol have been given the name Wilson's Temperature Syndrome (WTS). There have been clinical studies using T3 in patients who are euthyroid based on normal TSH values. However, this treatment has created a controversy in the conventional medical community, especially with the American Thyroid Association, because it is not based on a measured deficiency of thyroid hormone. However, just as estrogen and progesterone are prescribed to regulate menstrual cycles in patients who have normal serum hormone levels, the WT3 therapy can be used to regulate metabolism despite normal serum thyroid hormone levels. SR-T3 prescription is based exclusively on low body temperature and presentation of symptoms. Decreased T3 function exerts widespread effects throughout the body. It can decrease serotonin and growth hormone levels and increase the number of adrenal hormone receptor sites. These effects may explain some of the symptoms observed in WTS. The dysregulation of neuroendocrine function may begin to explain such symptoms as alpha intrusion into slow wave sleep, decrease in blood flow to the brain, alterations in carbohydrate metabolism, fatigue, myalgia and arthralgia, depression and cognitive dysfunction. Despite all thermoregulatory control mechanisms of the body and the complex metabolic processes involved, WT3 therapy seems a valuable tool to re-establish normal body functions. We report the results of 11 patients who underwent the WT3 protocol for the treatment of CFS. All the patients improved in the five symptoms measured. All patients increased their basal temperature. The recovery time varied from 3 weeks to 12 months.
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PMID:Supraphysiological cyclic dosing of sustained release T3 in order to reset low basal body temperature. 1688 75

In addition to chronic hepatitis, many individuals infected with hepatitis C virus (HCV) suffer from fatigue, which may compromise their health-related quality of life (HRQL). To assess systematically health-related quality of life (HRQL) in patients with chronic hepatitis C and to determine if any clinical, biochemical, virologic, demographic, and histologic features are associated with HRQL status. In this cross-sectional observational study, one hundred thirty patients with chronic HCV infection (HCV RNA positive by PCR) and 61 healthy controls were enrolled from a tertiary care teaching medical center. All patients and controls completed one generic HRQL questionnaire (MOS SF-36) and one liver-disease specific instrument (Chronic Liver Disease Questionnaire, CLDQ). Ninety-five HCV patients and all the controls also completed a fatigue questionnaire (Chronic Fatigue Screener, CFS) and had immunologic markers determined (Cryoglobulin, Soluble IL-2 receptors, Rheumatoid Factor). We compared the HRQL of HCV-infected patients to the controls and, using data from other studies, to the general population, patients with diabetes, and patients with chronic low back pain. Patients with chronic HCV had greater HRQL impairment than healthy controls and those with type II diabetes. Fatigue was the most important symptom with negative impact on HRQL. Sixty-one percent of HCV-infected patients reported fatigue-related loss of activity. Additionally, other factors associated with HRQL were gender and histologic cirrhosis. Chronic HCV infection has a profound negative impact on patients' HRQL. Disabling fatigue is the most important factor that contributes to loss of well-being in this relatively young group of patients.
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PMID:Fatigue and health-related quality of life (HRQL) in chronic hepatitis C virus infection. 1740 28

Chronic fatigue syndrome in childhood and adolescents(CCFS) is a complex and debilitation with severe morbidity and confusion. It is common condition with up to 3-5% of children and adolescents showing strange fatigue and confusion for more than 30 days. In this condition, four major symptoms are important: sleep disorders, easy fatigability, disturbed learning and memorization and immunological problems. Routine laboratory studies are similar to adult CFS, although abnormalities can be seen on serum pyruvic acid level, OGTT pattern, deep body temperature rhythm, hormonal secretion rhythm, and cerebral blood flow. For a diagnosis of CCFS, a research group supported by Japanese ministry of health, labor and welfare developed CCFS case definition on 2004. Treatment focused to correct disrupted circadian rhythms and supply of energy.
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PMID:[Childhood chronic fatigue syndrome]. 1756 4


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