Journal of Chronic Fatigue Syndrome: Volume 4, Issue 2, 1998

Volume 4, Issue 2, 1998

 * Editorial by Roberto Patarca
 * The Role of Glutamine in the Aetiology of the Chronic Fatigue Syndrome: A Prospective Study"Abstract - 'Background: Recent studies have observed low plasma glutamine concentrations in chronic fatigue syndrome (CFS) subjects. Glutamine has been shown to be essential for immune function and a key substrate in brain neurochemistry. A dysfunctional immune response to infection and/or neurotransmitter dysfunction may be associated with CFS. Objective: To compare the glutamine status of CFS subjects to matched controls and to test the effect of L-glutamine supplementation on the symptoms associated with CFS. Design: A 26-week, randomised, double-blind, placebo-controlled trial. Patients: Sixteen subjects diagnosed with CFS and 16 age- and sex-matched, healthy controls. Intervention: L-glutamine or placebo (2000 mg/day for 26 weeks).Measurements: Plasma and muscle glutamine concentrations, complete haematology counts, lymphocyte surface marker analysis, serum cortisol and testosterone concentrations, and self-reported symptomatic status. Results: Plasma and muscle glutamine concentrations were lower in CFS subjects than controls (P < 0.001 and P = 0.027, respectively). Significant increases in plasma (P = 0.020) and muscle (P = 0.037) glutamine concentration were observed following L-glutamine, but not placebo (P > 0.05), supplementation. However, improvements in symptomatic status were not observed in the L-glutamine group. Although six subjects showed clinical improvements during the trial, there was no change in their plasma or muscle glutamine concentrations. Conclusions: These data suggest that while low plasma glutamine concentrations may occur coincident with CFS, they may not be directly causative of fatigue or other symptoms.'"
 * Prolongation of Central Motor Conduction Time in Chronic Fatigue Syndrome"Abstract - 'We compared the central motor conduction time (CMCT) obtained by magnetic stimulation of the central nervous system (CNS) of 181 patients who fulfilled the criteria (see Fukuda 1994) for CFS with those of 27 healthy control subjects. A cortical and a cervical stimulation was performed on each person under standardised conditions, and the motor evoked potentials (MEP) either from Musculus Abductor Pollicis Brevis (M. APB) or from Musculus Abductor Digiti Minimi (M. ADM) was recorded. For the CFS patients a significant prolongation of the central motor conduction time (M. APB right: p < 0.0001; M. A DP left: p < 0.00005; M. ADM right: p < 0.00005; M. ADM left: p < 0.005) was observed compared to controls. The results presented in this study suggest a central nervous system dysfunction in CFS.'"
 * The Physiological Response to Exercise in Chronic Fatigue Syndrome"Abstract - 'Background: The chronic fatigue syndrome (CFS) is characterised by a limited exercise capacity. Studies have reported reduced muscle oxidative capacity in CFS, evidenced by abnormal acidosis during exercise and reduced aerobic capacity and exercise endurance. Objective: To compare physiological responses to walking exercise in CFS subjects, sedentary controls, and clinically improved CFS subjects. Design: Age- and sex-matched pairs, with repeated measures. Subjects: Sixteen subjects diagnosed with CFS and 16 age- and sex-matched sedentary controls. Measurements: Heart rate (HR), oxygen uptake (V02) ventilation (VE) and relative perceived exertion (RPE) responses to incremental walking exercise to volitional exhaustion. Results: CFS subjects reached significantly lower HRpeak (P = 0.023) and achieved nonsignificantly (P > 0.05) lower TO2penk than control subjects. Despite no differences in submaximal exercise responses, CFS subjects reported higher RPE scores than controls (P = 0,003) at submaximal workloads. RPE scores correlated with symptomatic scores for emotionality (r = 0.642) and general fatigue (r = 0.568). Symptomatic recovery in six CFS subjects was associated with nonsignificant increases in HRpeak, VO2peak and VEpeak and nonsignificant decreases in RPE scores at submaximal workloads. Conclusions: These data suggested that the limited exercise capacity in CFS subjects may be explained by deconditioning due to the sedentary lifestyle necessitated by the condition, coupled with an increased perception of exertion, potentially linked to psychological symptoms associated with CFS.'"
 * Pilot Study of a Multidisciplinary Inpatient Rehabilitation of Severely Incapacitated Patients with the Chronic Fatigue Syndrome"Abstract - 'The outcome of severely incapacitated patients with the chronic fatigue syndrome is poor. We examined the outcome of the first 19 such patients admitted to a psychiatric ward in a general hospital for a multidisciplinary rehabilitation programme. Seventeen (89%) patients had functionally improved by discharge, the median Kamofsky score improvement being 15 points in all 19 patients. All fourteen patients who were followed up had maintained or exceeded their improvement by one year, with a median Karnofsky score improvement of 25 in all 16 followed up patients, compared to admission. Only two patients had not improved by discharge and they were the same or worse at one year. A randomised controlled trial is necessary to confirm the efficacy and acceptability of this form of rehabilitation.'"
 * Elevated Plasma Prolactin and EEG Slow Wave Power in Post-Polio Fatigue: Implications for a Dopamine Deficiency Underlying Post-Viral Fatigue Syndromes"Abstract - 'To test the hypothesis that plasma prolactin and clcc-troencephalographic (EEG) slow wave activity are correlated with fatigue, 33 polio survivors without medical or psychologic comorbid-ities were studied. Subjects were administered the Post-Polio Fatigue Questionnaire (PFQ) and had resting measurement of both plasma prolactin and bilateral temporal-occipital power across the EEG frequency spectrum. Typical daily fatigue severity on the PFQ was significantly correlated with daily difficulty with attention, staying awake and motivation, but not with measures of acute polio severity or the number of limbs affected by laie-onset Post-Polio Sequelae symptoms. Prolactin was significantly correlated with daily fatigue severity on the PFQ (r = .39; p < .05). EEG power was equal between the two hemispheres across all frequency bands. However, EEG slow wave power in the right hemisphere was significantly correlated with daily fatigue severity and prolactin level (r = .37; p < .05). Using multiple linear regression, age at acute polio, frequency of difficulty with attention on the PFQ, prolactin and right hemisphere slow wave power predicted 72% of the variance of the daily fatigue severity rating (r = .85; p < .0001). These data suggest that increased prolactin secretion and EEG slowing are related to the severity of post-polio fatigue, findings similar to those in patients with acute paralytic and non-paralytic poliomyelitis and with chronic fatigue syndrome. A primary role is suggested for a dopamine deficiency (versus serotonergic receptor supersensitivity) underlying impaired cortical activation and the symptoms associated with putative post-viral fatigue syndromes.'"
 * Review and Hypothesis: Might Patients with the Chronic Fatigue Syndrome Have Latent Tetany of Magnesium Deficiency"Abstract - 'The latent tetany syndrome (LTS) parallels CFS in its neuromuscular and psychiatric manifestations, as well as in inner ear disturbances: vestibular in CFS and FM, as well as in LTS, and increased vulnerability to noise-induced deafness in LTS. Microvascular damage to the cochlea is seen in Mg deficiency, noise-induced deafness, and might be a factor in migraine and other severe headaches in both LTS and in CFS and FM. Abnormal sleep patterns occur in both LTS and CFS; impaired cognition more in CFS than in LTS. However, some brain and neurotransmitter dysfunctions seen with Mg deficiency might be contributory to cognitive disorders of CFS. Mg loss caused by enhanced catecholamine release produced by stress may well be contributory to stress-induced acute episodes of CFS. Malfunctions of the cellular and humoral immunological systems are caused by experimental Mg deficiency. Whether allergies in CFS patients and abnormal response to antigenic challenge are results of low Mg remains to be proven. Mitral valve prolapse is seen in many LTS and CFS patients; whether a putative Mg deficiency predisposes to this abnormality is not known. Clinical improvement with Mg treatment has been proven in LTS, and seemed helpful in the rare cases of CFS and FM in whom it has been tried. The Mg status should be determined in patient with CFS and FM, but methodology is a handicap. Serum Mg is an inaccurate index. Three methods show promise. Percentage retention of a Mg load is accurate but requires patient's cooperation. Free ionic Mg measurement requires ion-selective electrodes. Blood cell Mg is reliable in a little more than half the patients; sublingual cell Mg seems more accurate. More intensive, and controlled studies of the Mg status of CFS and FM patients, and of their response to Mg therapy is desirable.'"