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Chronic fatigue syndrome is a heterogeneous disorder with unknown pathogenesis and etiology, characterized by disabling fatigue, difficulty in concentration and memory, and concomitant skeletal and muscular pain. Several mechanisms have been suggested to play a role in CFS, such as excessive oxidative stress following exertion, immune imbalance characterized by decreased natural killer cell and macrophage activity, immunoglobulin G subclass deficiencies (IgG1, IgG3) and decreased serum concentrations of complement component. Autoantibodies were also suggested as a possible factor in the pathogenesis of CFS. Recent studies indicate that anti-serotonin, anti-microtubule-associated protein 2 and anti-muscarinic cholinergic receptor 1 may play a role in the pathogenesis of CFS. It has been demonstrated that impairment in vasoactive neuropeptide metabolism may explain the symptoms of CFS.
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PMID:Chronic fatigue syndrome: characteristics and possible causes for its pathogenesis. 1830 May 82

Individuals with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) have little stamina and endurance, and pose a challenge for nursing professionals. The Energy Envelope Theory, which posits that maintaining expended energy levels consistent with available energy levels may reduce the frequency and severity of symptoms, is particularly useful when working with clients with ME/CFS. Anecdotal support from the client community for this theory supports its use as a management tool for ME/CFS, but little formal research has been done in this area. In this study, a daily energy quotient was established by dividing the expended energy level by the perceived energy level and multiplying by 100. It was predicted that those participants who expended energy beyond their level of perceived energy would have more severe fatigue and symptoms and lower levels of physical and mental functioning. Findings are congruent with the Energy Envelope Theory as they indicated that the daily energy quotient was related to several indices of functioning including depression, anxiety, fatigue, pain, quality of life, and disability. The overall results provide support for a strategy health care professionals can use when working with clients with ME/CFS.
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PMID:The Energy Envelope Theory and myalgic encephalomyelitis/chronic fatigue syndrome. 1857 85

Anxiety symptoms are commonly described in children with chronic fatigue syndrome or myalgic encephalopathy (CFS/ME) but to date there has been little information on the type of anxiety children experience or the relationship between anxiety and school attendance, disability or fatigue. The aim of this study was to first describe the prevalence and type of anxiety symptoms in children with CFS/ME compared with a normal European population, and secondly to investigate the association of anxiety symptoms with age, gender, school attendance, fatigue, and physical function in paediatric CFS/ME. Data were prospectively collected on children and young people with CFS/ME referred to a large specialist CFS/ME service. One hundred and sixty-four children with CFS/ME had complete data for the Spence Children's Anxiety Scale. Teenage girls had the highest rates of total anxiety symptoms with 38% (95% CI 27-49) over the cut off (top 10% of normal European population) and significantly higher rates of symptoms in each subscale. Younger girls were more likely to score over the cut off in separation anxiety (37%, 19-40) and social phobia (39%, 25-47). There was no evidence of association between total anxiety symptoms and: time at school, time to assessment, pain or age. Associations with fatigue and physical function were attenuated when adjusted for other variables. Although anxiety symptoms are high in CFS/ME, particularly in teenage girls, it does not appear to be associated with school attendance or other measures of disability. Separation anxiety and social phobia were the most clearly elevated in paediatric CFS/ME.
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PMID:Anxiety in children with CFS/ME. 1945 95

The new diagnostic criteria for pediatric ME/CFS are structurally based on the Canadian Clinical Adult case definition, and have more required specific symptoms than the (Fukuda et al. Ann Intern Med 121:953-959, 1994) adult case definition. Physicians specializing in pediatric ME/CFS referred thirty-three pediatric patients with ME/CFS and 21 youth without the illness. Those who met ME/CFS criteria were separated into Severe and Moderate categories. Significant differences were found for symptoms within each of the six major categories: fatigue, post-exertional malaise, sleep, pain, neurocognitive difficulties, and autonomic/neuroendocrine/immune manifestations. In general, the results showed participants who met the Severe ME/CFS criteria reported the highest scores, the Moderate ME/CFS group show scores that were a little lower, and the control group evidenced the lowest scores. Findings indicate that the Pediatric Case Definition for ME/CFS can distinguish between those with this illness and controls, and between those with Severe versus Moderate manifestations of the illness.
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PMID:Severe versus Moderate criteria for the new pediatric case definition for ME/CFS. 1951 26

Chronic fatigue syndrome and/or fibromyalgia (CFS/FM) consists of highly overlapping, medically unexplained symptoms, including long-lasting fatigue, effort intolerance, cognitive dysfunction, and widespread pain and tenderness. CFS/FM often seems to be triggered by infections and physical trauma, but depression, sleep disturbances, and personality may also be involved. Moreover, dysregulation of the stress system, the immune system, and central pain mechanisms may determine the pathophysiology of the illness, leading to a loss of capacity to adapt to all kind of stressors. CFS/FM patients can be best helped by a pragmatic and individualized approach aimed at adjusting lifestyle and optimizing self-care, which in the long run may contribute to a restoration of physical and mental adaptability. Future psychiatric research into CFS/FM should focus on the complex interrelationships among pain/fatigue, stress/depression, and personality, as well as on processes of therapeutic change and the advantages of customized treatment.
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PMID:Psychiatric aspects of chronic fatigue syndrome and fibromyalgia. 2042 82

There is a significant 'comorbidity' between depression and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Depressive symptoms frequently occur during the course of ME/CFS. Fatigue and somatic symptoms (F&S), like pain, muscle tension, and a flu-like malaise, are key components of depression. At the same time, depression and ME/CFS show major clinical differences, which allow to discriminate them with a 100% accuracy. This paper aims to review the shared pathways that underpin both disorders and the pathways that discriminate them. Numerous studies have shown that depression and ME/CFS are characterized by shared aberrations in inflammatory, oxidative and nitrosative (IO&NS) pathways, like systemic inflammation and its long-term sequels, including O&NS-induced damage to fatty acids, proteins and DNA; dysfunctional mitochondria; lowered antioxidant levels, like zinc and coenzyme Q10; autoimmune responses to neoepitopes formed by O&NS; lowered omega-3 polyunsaturated fatty acid levels; and increased translocation of gram-negative bacteria. Some IO&NS-related pathways, like the induction of indoleamine 2-3-dioxygenase, neurodegeneration and decreased neurogenesis, are more specific to depression, whereas other pathways, like the 2'-5' oligoadenylate synthetase/RNase L pathway, are specific to ME/CFS. Most current animal models of depression, e.g. those induced by cytokines, are not reminiscent of human depression but reflect a mixture of depressive and F&S symptoms. The latter symptoms, sometimes called sickness behavior, differ from depression and ME/CFS because the former is a (sub)acute response to infection-induced pro-inflammatory cytokines that aims to enhance recovery, whereas the latter are characterized by long-term sequels in multiple IO&NS pathways. Depression and ME/CFS are not 'comorbid' disorders, but should be regarded as 'co-associated disorders' that are clinical manifestations of shared pathways.
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PMID:An intriguing and hitherto unexplained co-occurrence: Depression and chronic fatigue syndrome are manifestations of shared inflammatory, oxidative and nitrosative (IO&NS) pathways. 2060 77

Frequency of active human herpesvirus-6, -7 (HHV-6, HHV-7) and parvovirus B19 (B19) infection/coinfection and its association with clinical course of ME/CFS was evaluated. 108 ME/CFS patients and 90 practically healthy persons were enrolled in the study. Viral genomic sequences were detected by PCR, virus-specific antibodies and cytokine levels-by ELISA, HHV-6 variants-by restriction analysis. Active viral infection including concurrent infection was found in 64.8% (70/108) of patients and in 13.3% (12/90) of practically healthy persons. Increase in peripheral blood leukocyte DNA HHV-6 load as well as in proinflammatory cytokines' levels was detected in patients during active viral infection. Definite relationship was observed between active betaherpesvirus infection and subfebrility, lymphadenopathy and malaise after exertion, and between active B19 infection and multijoint pain. Neuropsychological disturbances were detected in all patients. The manifestation of symptoms was of more frequent occurrence in patients with concurrent infection. The high rate of active HHV-6, HHV-7 and B19 infection/coinfection with the simultaneous increase in plasma proinflammatory cytokines' level as well as the association between active viral infection and distinctive types of clinical symptoms shows necessity of simultaneous study of these viral infections for identification of possible subsets of ME/CFS.
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PMID:Association of active human herpesvirus-6, -7 and parvovirus b19 infection with clinical outcomes in patients with myalgic encephalomyelitis/chronic fatigue syndrome. 2292 50

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating condition characterised by diverse symptoms such as fatigue, pain, sleep disturbance and autonomic dysfunction. There remains to be a singular biomarker identified for this illness, hence numerous theories about its development and perpetuation have been posited in the literature. This brief report presents the model of 'allostasis' as a framework for understanding ME/CFS, specifically the notion that the physiological mechanisms employed in the body to deal with stress termed here as 'allostatic states' (e.g. elevation of inflammatory cytokines), may in and of themselves contribute to the perpetuation of the disorder. This theoretical assertion has important consequences for the understanding of ME/CFS and treatment; rather than searching for a singular pathogen responsible for this condition, ME/CFS can be conceptualised as a maladaptive stress disorder and interventions aimed at addressing the allostatic states may be incorporated into current symptom management programmes.
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PMID:Allostatic overload in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). 2385 Mar 95

This review was written from the viewpoint of the treating clinician to educate health care professionals and the public about Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). It includes: the clinical definition of ME/CFS with emphasis on how to diagnose ME/CFS; the etiology, pathophysiology, management approach, long-term prognosis and economic cost of ME/CFS. After reading this review, you will be better able to diagnose and treat your patients with ME/CFS using the tools and information provided. Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex, chronic medical condition characterized by symptom clusters that include: pathological fatigue and malaise that is worse after exertion, cognitive dysfunction, immune dysfunction, unrefreshing sleep, pain, autonomic dysfunction, neuroendocrine and immune symptoms. ME/CFS is common, often severely disabling and costly. The Institute of Medicine (IOM) reviewed the ME/CFS literature and estimates that between 836,000 and 2.5 million Americans have ME/CFS at a cost of between 17 and 24 billion dollars annually in the US. The IOM suggested a new name for ME/CFS and called it Systemic Exertion Intolerance Disease (SEID). SEID's diagnostic criteria are less specific and do not exclude psychiatric disorders in the criteria. The 2010 Canadian Community Health Survey discovered that 29% of patients with ME/CFS had unmet health care needs and 20% had food insecurity--lack of access to sufficient healthy foods. ME/CFS can be severely disabling and cause patients to be bedridden. Yet most patients (80%) struggle to get a diagnosis because doctors have not been taught how to diagnose or treat ME/CFS in medical schools or in their post-graduate educational training. Consequently, the patients with ME/CFS suffer. They are not diagnosed with ME/CFS and are not treated accordingly. Instead of compassionate care from their doctors, they are often ridiculed by the very people from whom they seek help. The precise etiology of ME/CFS remains unknown, but recent advances and research discoveries are beginning to shed light on the enigma of this disease including the following contributors: infectious, genetic, immune, cognitive including sleep, metabolic and biochemical abnormalities. Management of patients with ME/CFS is supportive symptomatic treatment with a patient centered care approach that begins with the symptoms that are most troublesome for the patient. Pacing of activities with strategic rest periods is, in our opinion, the most important coping strategy patients can learn to better manage their illness and stop their post-exertional fatigue and malaise. Pacing allows patients to regain the ability to plan activities and begin to make slow incremental improvements in functionality.
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PMID:Review of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: an evidence-based approach to diagnosis and management by clinicians. 2661 25

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a severe acquired illness characterized by a profound sensation of fatigue, not ameliorated by rest and resulting in a substantial decrease in the amount and quality of occupational, social and recreational activities. Despite intense research, the aetiology and pathogenesis of ME/CFS is still unknown and no conclusive biological markers have been found. As a consequence, an accepted curative treatment is still lacking and rehabilitation programmes are not very effective, as few patients recover. Increased knowledge of the mechanisms leading to the emergence and maintenance of the illness is called for. In this study, I will put forth an alternative hypothesis to explain some of the pathologies associated with ME/CFS, by concentrating on one of the major strategic organs of the brain, the hippocampus. I will show that the ME/CFS triggering factors also impact the hippocampus, leading to neurocognitive deficits and disturbances in the regulation of the stress system and pain perception. These deficits lead to a substantial decrease in activity and to sleep disorders, which, in turn, impact the hippocampus and initiate a vicious circle of increased disability.
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PMID:The role of the hippocampus in the pathogenesis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). 2680 93


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