scholarly journals Diagnostic and Pharmacological Potency of Creatine in Post-Viral Fatigue Syndrome

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 503
Author(s):  
Sergej M. Ostojic
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Neurological Disease ◽  
Chronic Fatigue ◽  
Guanidino Compounds ◽  
Fatigue Syndrome ◽  
Open Questions ◽  
Phosphocreatine Resynthesis ◽  
The Brain ◽  
Creatine Metabolism

Post-viral fatigue syndrome (PVFS) is a widespread chronic neurological disease with no definite etiological factor(s), no actual diagnostic test, and no approved pharmacological treatment, therapy, or cure. Among other features, PVFS could be accompanied by various irregularities in creatine metabolism, perturbing either tissue levels of creatine in the brain, the rates of phosphocreatine resynthesis in the skeletal muscle, or the concentrations of the enzyme creatine kinase in the blood. Furthermore, supplemental creatine and related guanidino compounds appear to impact both patient- and clinician-reported outcomes in syndromes and maladies with chronic fatigue. This paper critically overviews the most common disturbances in creatine metabolism in various PVFS populations, summarizes human trials on dietary creatine and creatine analogs in the syndrome, and discusses new frontiers and open questions for using creatine in a post-COVID-19 world.

Unusual pattern of mitochondrial DNA deletions in skeletal muscle of an adult human with chronic fatigue syndrome

1995 ◽  
Vol 4 (4) ◽  
pp. 751-754 ◽  
Author(s):  
Chunfang Zhang ◽  
Alessandra Baumer ◽  
Ian R. Mackay ◽  
Anthony W. Linnane ◽  
Phillip Nagley
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Dna ◽  
Chronic Fatigue Syndrome ◽  
Chronic Fatigue ◽  
Unusual Pattern ◽  
Adult Human ◽  
Fatigue Syndrome ◽  
Dna Deletions

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 A Paradigm for Post-Covid-19 Fatigue Syndrome Analogous to ME/CFS

2021 ◽  
Vol 12 ◽  
Author(s):  
Angus Mackay
Keyword(s):  
Critical Evaluation ◽  
Significant Proportion ◽  
Chronic Fatigue ◽  
Neural Pathways ◽  
Fatigue Syndrome ◽  
Chronic Neuroinflammation ◽  
Stress Threshold ◽  
Wide Range ◽  
Stress Signals ◽  
The Brain

A significant proportion of COVID-19 patients are suffering from prolonged Post-COVID-19 Fatigue Syndrome, with characteristics typically found in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). However, no clear pathophysiological explanation, as yet, has been provided. A novel paradigm for a Post-COVID-19 Fatigue Syndrome is developed here from a recent unifying model for ME/CFS. Central to its rationale, SARS-CoV-2, in common with the triggers (viral and non-viral) of ME/CFS, is proposed to be a physiologically severe stressor, which could be targeting a stress-integrator, within the brain: the hypothalamic paraventricular nucleus (PVN). It is proposed that inflammatory mediators, released at the site of COVID-19 infection, would be transmitted as stress-signals, via humoral and neural pathways, which overwhelm this stress-center. In genetically susceptible people, an intrinsic stress-threshold is suggested to be exceeded causing ongoing dysfunction to the hypothalamic PVN's complex neurological circuitry. In this compromised state, the hypothalamic PVN might then be hyper-sensitive to a wide range of life's ongoing physiological stressors. This could result in the reported post-exertional malaise episodes and more severe relapses, in common with ME/CFS, that perpetuate an ongoing disease state. When a certain stress-tolerance-level is exceeded, the hypothalamic PVN can become an epicenter for microglia-induced activation and neuroinflammation, affecting the hypothalamus and its proximal limbic system, which would account for the range of reported ME/CFS-like symptoms. A model for Post-COVID-19 Fatigue Syndrome is provided to stimulate discussion and critical evaluation. Brain-scanning studies, incorporating increasingly sophisticated imaging technology should enable chronic neuroinflammation to be detected, even at a low level, in the finite detail required, thus helping to test this model, while advancing our understanding of Post-COVID-19 Fatigue Syndrome pathophysiology.

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.

Tetramethoxyluteolin for the Treatment of Neurodegenerative Diseases

2019 ◽  
Vol 18 (21) ◽  
pp. 1872-1882 ◽  
Author(s):  
Theoharis C. Theoharides ◽  
Irene Tsilioni
Keyword(s):  
Mast Cells ◽  
Substance P ◽  
Neurodegenerative Diseases ◽  
Oral Absorption ◽  
Chronic Fatigue ◽  
Autism Spectrum ◽  
Medline Search ◽  
Fatigue Syndrome ◽  
The Brain

Background: Most neurodegenerative and other brain disorders, especially Myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS) and autism spectrum disorder (ASD) continue to elude objective biomarkers and effective treatments. Increasing evidence indicates that such diseases involve focal inflammation of the brain. Objective: To review the role of cytokine-neuropeptide interactions in the pathogenesis of inflammation of the brain and the beneficial role of natural flavonoids. Methods: Medline search was conducted (2000-2017) for articles using the terms allergy, amygdala, atopy, autism, brain, chemokines, cytokines, hypothalamus, immunity, inflammation, mast cells, microglia, neurotensin, peptides, substance P, and TNF. Results: Neuropeptides and cytokine stimulation of mast cells and microglia can result in focal inflammation in the hypothalamus and amygdala, thus explaining most of the symptoms at least in ME/CFS and ASD. Some of the triggers may be corticotropin-releasing hormone (CRH), neurotensin (NT), and substance P (SP), which have synergistic action on IL-33. The natural flavonoids luteolin and tetramethoxyluteolin inhibit these processes and have neuroprotective actions. Tetramethoxyluteolin is also more metabolically stable and has greater oral absorption. Conclusion: Inhibition of inflammatory processes unique to the brain with intranasal formulations of tetramethoxyluteolin could provide new possibilities for the understanding and treatment of neurodegenerative diseases.

scholarly journals Pathophysiology of skeletal muscle disturbances in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Klaus J. Wirth ◽  
Carmen Scheibenbogen
Keyword(s):  
Skeletal Muscle ◽  
Chronic Fatigue Syndrome ◽  
Skeletal Muscles ◽  
Vascular Dysfunction ◽  
Ischemia Reperfusion ◽  
Chronic Fatigue ◽  
Exercise Intolerance ◽  
Fatigue Syndrome ◽  
Sodium Loading ◽  
Sodium Overload

AbstractChronic Fatigue Syndrome or Myalgic Encephaloymelitis (ME/CFS) is a frequent debilitating disease with an enigmatic etiology. The finding of autoantibodies against ß2-adrenergic receptors (ß2AdR) prompted us to hypothesize that ß2AdR dysfunction is of critical importance in the pathophysiology of ME/CFS. Our hypothesis published previously considers ME/CFS as a disease caused by a dysfunctional autonomic nervous system (ANS) system: sympathetic overactivity in the presence of vascular dysregulation by ß2AdR dysfunction causes predominance of vasoconstrictor influences in brain and skeletal muscles, which in the latter is opposed by the metabolically stimulated release of endogenous vasodilators (functional sympatholysis). An enigmatic bioenergetic disturbance in skeletal muscle strongly contributes to this release. Excessive generation of these vasodilators with algesic properties and spillover into the systemic circulation could explain hypovolemia, suppression of renin (paradoxon) and the enigmatic symptoms. In this hypothesis paper the mechanisms underlying the energetic disturbance in muscles will be explained and merged with the first hypothesis. The key information is that ß2AdR also stimulates the Na+/K+-ATPase in skeletal muscles. Appropriate muscular perfusion as well as function of the Na+/K+-ATPase determine muscle fatigability. We presume that dysfunction of the ß2AdR also leads to an insufficient stimulation of the Na+/K+-ATPase causing sodium overload which reverses the transport direction of the sodium-calcium exchanger (NCX) to import calcium instead of exporting it as is also known from the ischemia–reperfusion paradigm. The ensuing calcium overload affects the mitochondria, cytoplasmatic metabolism and the endothelium which further worsens the energetic situation (vicious circle) to explain postexertional malaise, exercise intolerance and chronification. Reduced Na+/K+-ATPase activity is not the only cause for cellular sodium loading. In poor energetic situations increased proton production raises intracellular sodium via sodium-proton-exchanger subtype-1 (NHE1), the most important proton-extruder in skeletal muscle. Finally, sodium overload is due to diminished sodium outward transport and enhanced cellular sodium loading. As soon as this disturbance would have occurred in a severe manner the threshold for re-induction would be strongly lowered, mainly due to an upregulated NHE1, so that it could repeat at low levels of exercise, even by activities of everyday life, re-inducing mitochondrial, metabolic and vascular dysfunction to perpetuate the disease.

Bioelectric activity of the women’s brain with vulvar lichen sclerosus

GYNECOLOGY ◽  
2020 ◽  
Vol 22 (6) ◽  
pp. 68-73
Author(s):  
Victor V. Loginov ◽  
Alexander V. Vartanov ◽  
Semyon A. Feigin ◽  
Anastasiia V. Sokolova ◽  
Inna A. Apolikhina
Keyword(s):  
Brain Activity ◽  
Lichen Sclerosus ◽  
External Genitalia ◽  
Chronic Fatigue ◽  
Acute Stage ◽  
Average Score ◽  
Bioelectric Activity ◽  
Fatigue Syndrome ◽  
The Brain ◽  
Vulvar Lichen Sclerosus

Aim. To study the characteristics of bioelectric activity of the brain in patients with vulvar lichen sclerosus (VLS), as well as the interaction between certain structures of the brain and their relationship with the manifestations of VLS. Materials and methods. 102 patients aged 21 to 78 years (average age 50.5713.92 years) were questioned about the VLS symptoms, the quality of sleep and presence of phobias, of which 30 patients aged 21 to 72 years (average age 46.0715.42 years) after signing informed consent underwent electroencephalographic (EEG) study. Inclusion criteria were patients aged 18 and older, vulvar lichen sclerosus in the acute stage, confirmed by histological examination. Results. The common complaint was itching in external genitalia (73.3%), which was statistically evident in the analysis of brain activity. Itching of external genitalia in patients with VLS could account for systemic changes in the activity and interactions of such structures as the brain stem and globus pallidus, ventral striatum, islet, parietal cortex, field 40 according to Broadman (supramarginal gyrus), as well as areas of the primary visual cortex (field 17 according to Broadman). Conclusion. VLS is often accompanied by itching in the external genitalia (73.3%), and has an average score of 5.6 on a ten-point scale. EEG is recommended with a disease duration of more than 6 years and an itch level of 56 points or more. The main feature of brain bioelectric activity in patients with VLS is evident signs of organic brain damage. The disease is accompanied by impairment of the visceral regulatory mechanisms of the brain, which leads to the formation of a low-complementary viscerom and neurodegenerative signs in the EEG. A frequent combination of disorders in the central nervous system and immune system gives reason to consider VLS associated with chronic fatigue syndrome.

Skeletal Muscle Metabolism in the Chronic Fatigue Syndrome

CHEST Journal ◽  
1992 ◽  
Vol 102 (6) ◽  
pp. 1716-1722 ◽  
Author(s):  
Roger Wong ◽  
Gary Lopaschuk ◽  
Gang Zhu ◽  
Dorothy Walker ◽  
Dianne Catellier ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Chronic Fatigue Syndrome ◽  
Muscle Metabolism ◽  
Chronic Fatigue ◽  
Skeletal Muscle Metabolism ◽  
Fatigue Syndrome

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.

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