Chronic Fatigue Syndrome: An Immunological Perspective

1998 ◽  
Vol 32 (4) ◽  
pp. 523-527 ◽  
Author(s):  
Uté Vollmer-Conna ◽  
Andrew Lloyd ◽  
Ian Hickie ◽  
Denis Wakefield
Keyword(s):  
Central Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Cytokine Production ◽  
Neuropsychiatric Symptoms ◽  
Chronic Fatigue ◽  
Cytokine Release ◽  
Fatigue Syndrome ◽  
Cytokine Levels ◽  
The Brain ◽  
Neural Dysfunction

Objective: The aim of this study is to review research examining an immunological basis for chronic fatigue syndrome (CFS) and to discuss how a disturbance in immunity could produce central nervous system (CNS)-mediated symptoms. Method: Data relevant to the hypothesis that abnormal cytokine release plays a role in the pathogenesis of CFS are reviewed as well as recent evidence relating to potential mechanisms by which immune products may enter the brain and produce a disturbance in CNS processes. Results: Examinations of cytokine levels in patients with CFS have produced inconclusive results. Recent evidence suggests that abnormal release of cytokines within the CNS may cause neural dysfunction by a variety of complex mechanisms. Conclusion: Neuropsychiatric symptoms in patients with CFS may be more closely related to disordered cytokine production by glial cells within the CNS than to circulating cytokines. This possibility is discussed in the context of unresolved issues in the pathogenesis of CFS.

Chronic Fatigue Syndrome and the Central Nervous System

2008 ◽  
Vol 36 (5) ◽  
pp. 867-874 ◽  
Author(s):  
R Chen ◽  
FX Liang ◽  
J Moriya ◽  
J Yamakawa ◽  
H Sumino ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Neurotrophic Factors ◽  
Focal Point ◽  
Chronic Fatigue ◽  
Fatigue Syndrome ◽  
The Central Nervous System ◽  
The Brain

An increasing amount of neuroimaging evidence supports the hypothesis that chronic fatigue syndrome patients have structural or functional abnormalities within the brain. Moreover, some neurotrophic factors, neurotransmitters and cytokines have also been evaluated in order to elucidate the mechanism of abnormal neuropsychic findings in chronic fatigue syndrome. In this review, we suggest that the focal point of chronic fatigue syndrome research should be transferred to the central nervous system.

scholarly journals Causes of extreme fatigue in underperforming athletes - a synthesis of recent hypotheses and reviews

2006 ◽  
Vol 18 (4) ◽  
pp. 108 ◽  
Author(s):  
PJ Robson-Ansley ◽  
L Lakier Smith
Keyword(s):  
Chronic Fatigue Syndrome ◽  
South African ◽  
Athletic Performance ◽  
Sports Medicine ◽  
Chronic Fatigue ◽  
Cytokine Release ◽  
South African Journal ◽  
Fatigue Syndrome ◽  
Inflammatory State ◽  
African Journal

The underperformance syndrome (UPS), previously known as the overtraining syndrome (OTS), has been defined as a persistent decrement in athletic performance capacity despite 2 weeks of relative rest. Clinical research has suggested that cytokines play a key role in fatigue in disease and chronic fatigue syndrome. Furthermore, it has recently been demonstrated that exogenous administration of interleukin-6 (IL-6) increases the sensation of fatigue during exercise. In light of current cytokine and chronic fatigue syndrome research, this article reviews and updates the cytokine theories that attempt to explain the aetiology of the debilitating fatigue experienced in OTS/UPS. Initially, it was proposed that UPS may be caused by excessive cytokine release during and following exercise, causing a chronic inflammatory state and ‘cytokine sickness'. More recently, the hypothesis was extended and it was proposed that time-dependent sensitisation could provide a model through which the aetiology of UPS may be explained. According to this model, the principal abnormal factor in UPS is an intolerance/heightened sensitivity to IL-6 during exercise. South African Journal of Sports Medicine Vol. 18 (4) 2006: pp. 108-114

Treatment of fibromyalgia (chronic widespread pain) and chronic fatigue syndrome

2020 ◽  
pp. 1330-1341
Author(s):  
Jonathan Price
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Chronic Widespread Pain ◽  
Widespread Pain ◽  
Fatigue Syndrome ◽  
System P ◽  
The Central Nervous System ◽  
Key Aspects

Fibromyalgia (FM), one of the chronic widespread pain syndromes, and chronic fatigue syndrome (CFS) are important and common conditions. They are considered together here because they are commonly comorbid and because of their similarities—they are long-term conditions with a relatively poor prognosis; central nervous system mechanisms and deconditioning play an important role in aetiology; graded exercise and psychological treatments have an important role in management; and comorbid mental disorders are common and have an adverse impact on important outcomes, including disability and chronicity. The prevalence of FM is rising, while that of CFS is declining. There is increased acceptance of the pivotal role of central nervous system factors in FM, while in CFS, the positions of different aetiological ‘movements’ appear bitterly entrenched. The main focus of this chapter is on FM and, in particular, key aspects of aetiology and treatment, especially those relating to the central nervous system.

Heterogeneity of serum tryptophan concentration and availability to the brain in patients with the chronic fatigue syndrome

2005 ◽  
Vol 19 (4) ◽  
pp. 385-391 ◽  
Author(s):  
Abdulla A.-B. Badawy ◽  
Christopher J. Morgan ◽  
Meirion B. Llewelyn ◽  
Selwyn R.J. Albuquerque ◽  
Anne Farmer
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Fatigue Syndrome ◽  
Tryptophan Concentration ◽  
The Brain

scholarly journals Oxygen-ozone therapy in meningoencephalitis and chronic fatigue syndrome. Treatment in the field of competitive sports: case report

Ozone Therapy ◽  
2019 ◽  
Vol 4 (1) ◽  
Author(s):  
Luca Morelli ◽  
Simona Carla Bramani ◽  
Federico Carlo Morelli
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Nuclear Antigen ◽  
Weekly Basis ◽  
Serological Tests ◽  
Barr Virus ◽  
Fatigue Syndrome ◽  
Epstein Barr ◽  
The Brain ◽  
Post Infectious

Our study was born from the observation of a clinical case of a boy who arrived in the Emergency Room of our hospital for persistent hyperpyrexia, headache and prolonged emetic episodes and complaining of objective photophobia and dizziness. The patient underwent haematochemical tests, chemical-physical examination of Chronic Fatigue Syndrome (CFS), negative for bacteria, negative for Neisseria Meningitidis, Escherichia Coli 121, Haemophilus Influenzae, Stafilococcus Pneumoniae, Stafilococcus Agalactiae and with slightly positive reaction to Pandy’s test; he was subjected to neurological examination, to Nuclear Magnetic Resonance of the brain and encephalic trunk with contrast agent which resulted negative, and to EEG that showed a slightly slowed-down brain electrical activity, in right occipital region, and frontal irritative abnormalities. Given these clinical and instrumental investigations, an acute meningoencephalitis was diagnosed. During his hospitalization, the patient was treated with intravenous antibiotic therapy and intravenous antiviral therapy for 12 days. At discharge, in the absence of specific therapy, and considering the protraction of the cephalic, dizzying, asthenic and myalgic symptoms and in relation to hematochemical and serological tests (positive for antibodies to Herpes 1 IgG), Epstein Barr Virus antibodies (positive for Viral Capsid Antigen IgG and IgGE BNA, for Extractable Nuclear Antigen and IgG Cytomegalovirus) he was diagnosed a Post-infectious CFS. The patient was treated with Oxygen Ozone Rectal Insufflative Therapy on a bi-weekly basis for 4 weeks, associated with Micetrin, a dietary supplement with sweetener based on Vitamin C, Shitake, Reishi, Maitake, Cordyceps, Magnesium and SOD, continued the treatment on a weekly basis for a further 4 weeks until the complete remission of the symptoms of asthenic, neurological and clinical parameters.

scholarly journals Article Commentary: Kynurenine Pathway Pathologies: Do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM)

2013 ◽  
Vol 6s1 ◽  
pp. IJTR.S11193 ◽  
Author(s):  
Adele Blankfield
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Neuropsychiatric Symptoms ◽  
Protein Energy Malnutrition ◽  
Chronic Fatigue ◽  
Kynurenine Pathway ◽  
Metabolic Dysfunction ◽  
Fatigue Syndrome ◽  
Inflammatory Conditions ◽  
Protein Energy ◽  
Definition Of

Chronic fatigue syndrome (CFS) and fibromyalgia (FM) appear to meet the criteria of a tryptophan-kynurenine pathway disorder with potential neuroimmunological sequelae. Aspects of some of the putative precipitating factors have been previously outlined. 2 , 3 An analysis of the areas of metabolic dysfunction will focus on future directions for research and management. The definition of dual tryptophan pathways has increased the understanding of the mind-body, body-mind dichotomy. The serotonergic pathway highlights the primary (endogenous) psychiatric disorders. The up-regulation of the kynurenine pathway by physical illnesses can cause neuropathic and immunological disorders 1 associated with secondary neuropsychiatric symptoms. Tryptophan and nicotinamide deficiencies fall within the protein energy malnutrition (PEM) spectrum. They can arise if the kynurenine pathway is stressed by primary or secondary inflammatory conditions and the consequent imbalance of available catabolic/anabolic substrates may adversely influence convalescent phase efficiency. The replacement of depleted or reduced NAD+ levels and other cofactors can perhaps improve the clinical management of these disorders.

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