Impaired oxygen delivery to muscle in chronic fatigue syndrome.
(9/626)
The purpose of this study was to determine if chronic fatigue syndrome (CFS) is associated with reduced oxygen delivery to muscles. Patients with CFS according to CDC (Center for Disease Control) criteria (n=20) were compared with normal sedentary subjects (n=12). Muscle oxygen delivery was measured as the rate of post-exercise and post-ischaemia oxygen-haem resaturation. Oxygen-haem resaturation was measured in the medial gastrocnemius muscle using continuous-wavelength near-IR spectroscopy. Phosphocreatine resynthesis was measured simultaneously using (31)P magnetic resonance spectroscopy. The time constant of oxygen delivery was significantly reduced in CFS patients after exercise (46.5+/-16 s; mean+/-S.D.) compared with that in controls (29.4+/-6.9 s). The time constant of oxygen delivery was also reduced (20.0+/-12 s) compared with controls (12.0+/-2.8 s) after cuff ischaemia. Oxidative metabolism was also reduced by 20% in CFS patients, and a significant correlation was found between oxidative metabolism and recovery of oxygen delivery. In conclusion, oxygen delivery was reduced in CFS patients compared with that in sedentary controls. This result is consistent with previous studies showing abnormal autonomic control of blood flow. Reduced oxidative delivery in CFS patients could be specifically related to CFS, or could be a non-specific effect of reduced activity levels in these patients. While these results suggest that reduced oxygen delivery could result in reduced oxidative metabolism and muscle fatigue, further studies will be needed to address this issue. (+info)
Chronic Fatigue Syndrome and Primary Fibromyalgia Syndrome as recognized by GPs.
(10/626)
BACKGROUND: Prevalence studies on Chronic Fatigue Syndrome (CFS) are rare. Because of the similarity in symptoms, the prevalence of Primary Fibromyalgia Syndrome (PFS) was investigated at the same time. OBJECTIVES: To determine the prevalence of CFS and PFS as recognized by GPs in The Netherlands and to inform them of the existence of CFS. METHODS: A postal questionnaire was sent to all GPs. RESULTS: The questionnaire was returned by 60% of the GPs. Seventy-three per cent reported one or more CFS patients and 83% one or more PFS patients in their practice. CONCLUSION: The estimated prevalence of CFS as recognized by GPs of 112 (PFS 157) patients per 100,000 is a minimum estimate. (+info)
The course of severe chronic fatigue syndrome in childhood.
(11/626)
Little has been reported on prognostic indicators in children with chronic fatigue syndrome (CFS). We used interviews with children and parents, a mean of 45.5 months after illness onset, to follow up 25 cases of CFS referred to tertiary paediatric psychiatric clinics. At its worst, the illness had been markedly handicapping (prolonged bed-rest and school absence in two-thirds); mean time out of school was one academic year. Two-thirds, however, had recovered and resumed normal activities--mean duration of illness to recovery/assessment 38 months--and none had developed other medical conditions. Recovery was associated with specific physical triggers to the illness, with start of illness in the autumn school term and with higher socioeconomic status. Severe fatigue states in children can cause serious and longlasting handicap but most children recover. (+info)
Nutritional strategies for treating chronic fatigue syndrome.
(12/626)
Despite considerable worldwide efforts, no single etiology has been identified to explain the development of chronic fatigue syndrome (CFS). It is likely that multiple factors promote its development, sometimes with the same factors both causing and being caused by the syndrome. A detailed review of the literature suggests a number of marginal nutritional deficiencies may have etiologic relevance. These include deficiencies of various B vitamins, vitamin C, magnesium, sodium, zinc, L-tryptophan, L-carnitine, coenzyme Q10, and essential fatty acids. Any of these nutrients could be marginally deficient in CFS patients, a finding that appears to be primarily due to the illness process rather than to inadequate diets. It is likely that marginal deficiencies not only contribute to the clinical manifestations of the syndrome, but also are detrimental to the healing processes. Therefore, when feasible, objective testing should identify them and their resolution should be assured by repeat testing following initiation of treatment. Moreover, because of the rarity of serious adverse reactions, the difficulty in ruling out marginal deficiencies, and because some of the therapeutic benefits of nutritional supplements appear to be due to pharmacologic effects, it seems rational to consider supplementing CFS patients with the nutrients discussed above, along with a general high-potency vitamin/mineral supplement, at least for a trial period. (+info)
Diagnosis of psychiatric disorder in clinical evaluation of chronic fatigue syndrome.
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The overlap of symptoms in chronic fatigue syndrome (CFS) and psychiatric disorders such as depression can complicate diagnosis. Patients often complain that they are wrongly given a psychiatric label. We compared psychiatric diagnoses made by general practitioners and hospital doctors with diagnoses established according to research diagnostic criteria. 68 CFS patients referred to a hospital fatigue clinic were assessed, and psychiatric diagnoses were established by use of a standardized interview schedule designed to provide current and lifetime diagnoses. These were compared with psychiatric diagnoses previously given to patients. Of the 31 patients who had previously received a psychiatric diagnosis 21 (68%) had been misdiagnosed: in most cases there was no evidence of any past or current psychiatric disorder. Of the 37 patients who had not previously received a psychiatric diagnosis 13 (35%) had a treatable psychiatric disorder in addition to CFS. These findings highlight the difficulties of routine clinical evaluation of psychiatric disorder in CFS patients. We advise doctors to focus on subtle features that discriminate between disorders and to use a brief screening instrument such as the Hospital Anxiety and Depression Scale. (+info)
Human herpesviruses 6 and 7 in chronic fatigue syndrome: a case-control study.
(14/626)
We conducted this study to determine whether infection with human herpesvirus (HHV) 6A, HHV-6B, or HHV-7 differed between patients with chronic fatigue syndrome and control subjects. We recruited 26 patients and 52 nonfatigued matched control subjects from Atlanta. Serum samples were tested by enzyme immunoassay for seroreactivity to HHV-6, and all were seropositive. Lymphocyte specimens were cocultivated with cord blood lymphocytes and assayed for HHV-6 and HHV-7; neither virus was isolated. Finally, lymphocytes were tested by use of 3 polymerase chain reaction methods for HHV-6A, HHV-6B, and HHV-7 DNA. HHV-6A or HHV-6B DNA was detected in 17 (22.4%) of 76 samples, and there were no significant differences (by matched analyses) between patients (3 [11.5%] of 26) and control subjects (14 [28%] of 50). HHV-7 DNA was detected in 14 subjects, and although control subjects (12 [24%]) were more likely than patients (2 [7.7%]) to be positive, the difference was not statistically significant. We found no evidence that active or latent infection with HHV-6A, HHV-6B, HHV-7, or any combination these 3 HHVs is associated with chronic fatigue syndrome. (+info)
Strength and physiological response to exercise in patients with chronic fatigue syndrome.
(15/626)
OBJECTIVE: To measure strength, aerobic exercise capacity and efficiency, and functional incapacity in patients with chronic fatigue syndrome (CFS) who do not have a current psychiatric disorder. METHODS: Sixty six patients with CFS without a current psychiatric disorder, 30 healthy but sedentary controls, and 15 patients with a current major depressive disorder were recruited into the study. Exercise capacity and efficiency were assessed by monitoring peak and submaximal oxygen uptake, heart rate, blood lactate, duration of exercise, and perceived exertion during a treadmill walking test. Strength was measured using twitch interpolated voluntary isometric quadriceps contractions. Symptomatic measures included physical and mental fatigue, mood, sleep, somatic amplification, and functional incapacity. RESULTS: Compared with sedentary controls, patients with CFS were physically weaker, had a significantly reduced exercise capacity, and perceived greater effort during exercise, but were equally unfit. Compared with depressed controls, patients with CFS had significantly higher submaximal oxygen uptakes during exercise, were weaker, and perceived greater physical fatigue and incapacity. Multiple regression models suggested that exercise incapacity in CFS was related to quadriceps muscle weakness, increased cardiovascular response to exercise, and body mass index. The best model of the increased exercise capacity found after graded exercise therapy consisted of a reduction in submaximal heart rate response to exercise. CONCLUSIONS: Patients with CFS were weaker than sedentary and depressed controls and as unfit as sedentary controls. Low exercise capacity in patients with CFS was related to quadriceps muscle weakness, low physical fitness, and a high body mass ratio. Improved physical fitness after treatment was associated with increased exercise capacity. These data imply that physical deconditioning helps to maintain physical disability in CFS and that a treatment designed to reverse deconditioning helps to improve physical function. (+info)
Cerebral perfusion in chronic fatigue syndrome and depression.
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BACKGROUND: Patients with chronic fatigue syndrome (CFS) and depressive illness share many, but not all, features. AIMS: To test the hypothesis that patients with CFS have abnormal cerebral perfusion, that differs from that in patients with depressive illness. METHOD: We recruited 30 patients with CFS who were not depressed, 12 depressed patients and 15 healthy volunteers. Regional cerebral perfusion at rest was assessed using region of interest (ROI) and voxel-based statistical parametric mapping (SPM) techniques. RESULTS: On SPM analysis there was increased perfusion in the right thalamus, pallidum and putamen in patients with CFS and in those with depressive illness. CFS patients also had increased perfusion in the left thalamus. Depressed patients differed from those with CFS in having relatively less perfusion of the left prefrontal cortex. The results were similar on ROI analysis. CONCLUSIONS: Abnormal cerebral perfusion patterns in CFS subjects who are not depressed are similar but not identical to those in patients with depressive illness. Thalamic overactivity may be a correlate of increased attention to activity in CFS and depression; reduced prefrontal perfusion in depression may be associated with the greater neuropsychological deficits in that disorder. (+info)