Abstract:
Despite its new name, chronic fatigue syndrome is not a new disease. This chapter reviews current definitions, emphasizing that chronic fatigue syndrome is a diagnosis of exclusion. The author also discusses viral infections that are associated with CFS, including Epstein-Barr virus, cytomegalovirus, herpesvirus type 6, enteroviruses, and retroviruses.
Source: Glover DM. Chronic Fatigue Syndrome. Adolesc Med. 1995 Feb;6(1):101-114. http://www.ncbi.nlm.nih.gov/pubmed/10358305
Abstract:
Increased fatigability necessarily occurs in every patient with muscle weakness, regardless of whether the latter is due to a central or peripheral neurological disorder. The tendency for disuse to increase fatigability, as a secondary phenomenon, must also be considered; disuse affects both motoneuron recruitment and the biochemical and physiological properties of the muscle fibers. In recent studies impaired recruitment has been observed in postpolio patients, while patients with multiple sclerosis or spinal cord injury have shown, in addition, altered neuromuscular function. Findings are also presented in ALS and the chronic fatigue syndrome. In general, the most dramatic increases in fatigability take place in disorders of the peripheral nervous system and almost any cell component can be incriminated. There is a need to study fatigability systematically in neurology and rehabilitation.
Source: McComas AJ, Miller RG, Gandevia SC. Fatigue brought on by malfunction of the central and peripheral nervous systems. Adv Exp Med Biol. 1995;384:495-512. http://www.ncbi.nlm.nih.gov/pubmed/8585475
Abstract:
The justification for disordered chronobiology for fibromyalgia and chronic fatigue syndrome (CFS) is based on the following evidence: The studies on disordered sleep physiology and the symptoms of fibromyalgia and CFS; the experimental studies that draw a link between interleukin-1 (IL-1), immune-neuroendocrine-thermal systems and the sleep-wake cycle; studies and preliminary data of the inter-relationships of sleep-wakefulness, IL-1, and aspects of peripheral immune and neuroendocrine functions in healthy men and in women during differing phases of the menstrual cycle; and the observations of alterations in the immune-neuroendocrine functions of patients with fibromyalgia and CFS (Moldofsky, 1993b, d). Time series analyses of measures of the circadian pattern of the sleep-wake behavioural system, immune, neuroendocrine and temperature functions in patients with fibromyalgia and CFS should determine whether alterations of aspects of the neuro-immune-endocrine systems that accompany disordered sleep physiology result in nonrestorative sleep, pain, fatigue, cognitive and mood symptoms in patients with fibromyalgia and CFS.
Source: Moldofsky H. Sleep, neuroimmune and neuroendocrine functions in fibromyalgia and chronic fatigue syndrome. Adv Neuroimmunol. 1995;5(1):39-56. http://www.ncbi.nlm.nih.gov/pubmed/7795892
Abstract:
Chronic fatigue syndrome (CFS) is a disorder of unknown etiology characterized by debilitating fatigue and other somatic and neuropsychiatric symptoms. A range of heterogeneous clinical and laboratory findings have been reported in patients with CFS. Various theories have been proposed to explain the underlying pathophysiologic processes but none has been proved.
Research findings of immunologic dysfunction and neuroendocrine changes suggest the possible dysregulation of interactions between the nervous system and the immune system. Without a clear understanding of its etiopathogenesis, CFS has no definitive treatment.
Management approaches have been necessarily speculative, and they have evolved separately in a number of medical and nonmedical disciplines. The results of several controlled treatment studies have been inconclusive. An accurate case definition identifying homogeneous subtypes of CFS is needed. The integration of medical and psychologic treatment modalities and the use of both biologic and psychologic markers to evaluate treatment response will enhance future treatment strategies.
Source: Farrar DJ, Locke SE, Kantrowitz FG. Chronic fatigue syndrome. 1: Etiology and pathogenesis. Behav Med. 1995 Spring;21(1):5-16. http://www.ncbi.nlm.nih.gov/pubmed/7579775
Abstract:
Diagnosis and management of chronic fatigue syndrome (CFS) is a difficult challenge for nurse practitioners. The syndrome is widespread, poorly-defined, and problematic. Despite extensive etiologic research, no cause has been identified. Each case should be carefully evaluated for possible organic, psychiatric, and other factors reported as potential causes. Clinical manifestations, possible causes, and options for management are reviewed.
Source: Fox DS. Chronic fatigue syndrome: a review and practical guide. J Am Acad Nurse Pract. 1994 Dec;6(12):565-70. http://www.ncbi.nlm.nih.gov/pubmed/7848743
Abstract:
Chronic fatigue syndrome (CFS) is characterized by a sudden onset of an influenza-like illness followed by marked chronic fatigue and abnormal exercise-induced exhaustion. The precise pathogenesis of this disorder is unknown, but viral infection triggering immune imbalance has been suggested. The literature on CFS is reviewed. We find no consistent support for chronic viral infection or immunological dysfunction. The data in the published studies are rather conflicting, and further research in order to identify parameters that differentiate CFS from other disorders is necessary.
Comment in:
[Chronic fatigue syndrome and angiotensin-converting enzyme]. [Ugeskr Laeger. 1995]
[Chronic fatigue syndrome–a psychosocial syndrome?]. [Ugeskr Laeger. 1995]
Source: Rasmussen AK, Andersen V, Nielsen H, Wiik A. Chronic fatigue syndrome–a defined unity?Ugeskr Laeger. 1994 Nov 14;156(46):6832-6. [Article in Danish] http://www.ncbi.nlm.nih.gov/pubmed/7839497
Abstract:
Neither Epstein-Barr virus nor human herpesvirus 6 appears to play a causative role in chronic fatigue syndrome. The possibility that a novel human retrovirus may be present in patients with the syndrome needs further study. A number of abnormalities found in patients with chronic fatigue syndrome point to central nervous system (CNS) involvement. These include immunologic abnormalities, indications of pituitary and hypothalamic involvement, abnormal basal plasma levels of certain neurotransmitter metabolites, and cerebral perfusion abnormalities. The symptom pattern of chronic fatigue syndrome may eventually be explainable in terms of CNS dysfunction.
Source: Bell DS. Chronic fatigue syndrome update. Findings now point to CNS involvement. Postgrad Med. 1994 Nov 1;96(6):73-6, 79-81. http://www.ncbi.nlm.nih.gov/pubmed/7971614
Abstract:
The author reported the works of the “Fatigue Studies Group” founded 20 years ago to explore the different dimensions of “fatigue” complaint. The emphasis is placed on the asthenic syndromes evaluation instrument created by the group, which takes into account the socio-demographic data of the patient, clinical signs and their severity as well as the potential etiological factors. Its first version (GEF-3) enabled to isolate 4 groups of asthenia (overworking, somatic, psychosomatic and psychic), each of them requesting a specific treatment. An ulterior version (GEF-4) has been elaborated to describe better the psychiatric semeiology. Finally, a simplified version (GEF-10) was used as an evaluation instrument in different therapeutic researches. At the same time, the group continued its researches on the fatigue psychosocial dimensions and its nosographic status, especially in comparison with dysthymic disorders.
Source: Crocq L. Research about fatigue in France over the past 20 years. Encephale. 1994 Nov;20 Spec No 3:615-8. [Article in French] http://www.ncbi.nlm.nih.gov/pubmed/7843059
Abstract:
Fatigue chronic syndrome (SFC) is the heir-at-law of neurasthenia. Both are seen like physical diseases and share certain therapeutic measures, such as sleep; they have the same symbolic function and enable patients as well as doctors reluctant to psychological dimensions of pathology, to get and express sympathy and attention. A strong controversy developed these last years concerning the SFC physiopathology particularly concerning the responsibility of viral infectious agents or psychiatric troubles.
The SFC fatigue is unlikely hysterical or neuromuscular but it probably depends on several associated factors; cerebral neurobiochemistry anomalies (possibly induced by an infection or immune reactions), effort perception trouble, affective trouble, lack of physical activity. The handicap seems to be worse on account of unsuitable care and inefficacious treatment. Especially sleep, which is often beneficial in a short term, is source of ulterior chronicisation. Antidepressants are the only justified pharmacological treatment for SFC at the moment. Referring to the existence and the nature of cognitive distortions, the author suggests a cognitive-behavioural therapy, whose aim is a progressive activity resumption.
Source: Wessely S. Chronic fatigue syndrome. Clinical, social psychological problems and management. Encephale. 1994 Nov;20 Spec No 3:581-95. [Article in French] http://www.ncbi.nlm.nih.gov/pubmed/7843055
Abstract:
OBJECTIVE: To review the literature and current research about the causes of chronic fatigue syndrome (CFS).
DATA SOURCES: Recent research articles about CFS and data gathered by the author.
STUDY SELECTION: Performed by the author.
DATA EXTRACTION: Performed by the author.
DATA SYNTHESIS: Chronic fatigue syndrome (CFS) is a disease of pain, excessive fatigue after minor exertion, cognitive difficulties, and other symptoms-all occurring in cycles. While its etiology is unclear, CFS is associated with abnormal results of immune system tests. There is no specific marker for the illness. Treatment is symptomatic, and the long-term outlook for recovery is good.
CONCLUSION: A rational, symptomatic approach to treating CFS patients can be made using the model developed at the author’s institution. Research into the causes of CFS must continue.
Source: Lanham RJ. Chronic fatigue syndrome: a diagnostic challenge for the laboratory. Clin Lab Sci. 1994 Sep-Oct;7(5):279-82. http://www.ncbi.nlm.nih.gov/pubmed/10150382