scholarly journals A Brief Historic Overview of Clinical Disorders Associated with Tryptophan: The Relevance to Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM).

2012 ◽  
Vol 5 ◽  
pp. IJTR.S10085 ◽  
Author(s):  
Adele Blankfield
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Cognitive Dysfunction ◽  
Chronic Fatigue ◽  
Fatigue Syndrome ◽  
Skin Hyperpigmentation ◽  
Clinical Disorders ◽  
Dietary Deficiency

Last century there was a short burst of interest in the tryptophan related disorders of pellagra and related abnormalities that are usually presented in infancy. 1 , 2 Nutritional physiologists recognized that a severe human dietary deficiency of either tryptophan or the B group vitamins could result in central nervous system (CNS) sequelae such as ataxia, cognitive dysfunction and dysphoria, accompanied by skin hyperpigmentation. 3 , 4 The current paper will focus on the emerging role of tryptophan in chronic fatigue syndrome (CFS) and fibromyalgia (FM).

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.

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.

Altered central nervous system signal during motor performance in chronic fatigue syndrome

2004 ◽  
Vol 115 (10) ◽  
pp. 2372-2381 ◽  
Author(s):  
Vlodek Siemionow ◽  
Yin Fang ◽  
Leonard Calabrese ◽  
Vinod Sahgal ◽  
Guang H. Yue
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Motor Performance ◽  
Chronic Fatigue ◽  
Fatigue Syndrome

scholarly journals A neuro-inflammatory model can explain the onset, symptoms and flare-ups of myalgic encephalomyelitis/chronic fatigue syndrome

2019 ◽  
Vol 11 (4) ◽  
pp. 300
Author(s):  
Angus Mackay
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Viral Infections ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Diverse Range ◽  
Variable Threshold ◽  
Fatigue Syndrome ◽  
Neuro Inflammation

Abstract A neuro-inflammatory model is proposed to explain the onset, symptoms and perpetuation of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) via characteristic flare-ups (relapses). In this article, I explore the proposition that a range of triggers (intense physiological stressors such as severe viral infections, chemical toxin exposure or emotional trauma) in ME/CFS-predisposed people causes disruption in the neural circuitry of the hypothalamus (paraventricular nucleus), which induces a neuro-inflammatory reaction in the brain and central nervous system of ME/CFS patients, via over-active innate immune (glial) cells. Resulting dysfunction of the limbic system, the hypothalamus and consequently of the autonomic nervous system can then account for the diverse range of ME/CFS symptoms. Ongoing stressors feed into a compromised (inflamed) hypothalamus and if a certain (but variable) threshold is exceeded, a flare-up will ensue, inducing further ongoing neuro-inflammation in the central nervous system, thus perpetuating the disease indefinitely.

scholarly journals Post-Exertional Malaise May Be Related to Central Blood Pressure, Sympathetic Activity and Mental Fatigue in Chronic Fatigue Syndrome Patients

2021 ◽  
Vol 10 (11) ◽  
pp. 2327
Author(s):  
Sławomir Kujawski ◽  
Joanna Słomko ◽  
Lynette Hodges ◽  
Derek F. H. Pheby ◽  
Modra Murovska ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Chronic Fatigue Syndrome ◽  
Systolic Blood Pressure ◽  
Sympathetic Activity ◽  
Chronic Fatigue ◽  
Mental Fatigue ◽  
Fatigue Syndrome ◽  
Central Systolic Blood Pressure

Post-exertional malaise (PEM) is regarded as the hallmark symptom in chronic fatigue syndrome (CFS). The aim of the current study is to explore differences in CFS patients with and without PEM in indicators of aortic stiffness, autonomic nervous system function, and severity of fatigue. One-hundred and one patients met the Fukuda criteria. A Chronic Fatigue Questionnaire (CFQ) and Fatigue Impact Scale (FIS) were used to assess the level of mental and physical fatigue. Aortic systolic blood pressure (sBPaortic) and the autonomic nervous system were measured with the arteriograph and Task Force Monitor, respectively. Eighty-two patients suffered prolonged PEM according to the Fukuda criteria, while 19 did not. Patients with PEM had higher FIS scores (p = 0.02), lower central systolic blood pressure (p = 0.02) and higher mental fatigue (p = 0.03). For a one-point increase in the mental fatigue component of the CFQ scale, the risk of PEM increases by 34%. For an sBPaortic increase of 1 mmHg, the risk of PEM decreases by 5%. For a one unit increase in sympathovagal balance, the risk of PEM increases by 330%. Higher mental fatigue and sympathetic activity in rest are related to an increased risk of PEM, while higher central systolic blood pressure is related to a reduced risk of PEM. However, none of the between group differences were significant after FDR correction, and therefore conclusions should be treated with caution and replicated in further studies.

scholarly journals Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: The Human Herpesviruses Are Back!

Biomolecules ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 185
Author(s):  
Maria Eugenia Ariza
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Disease Process ◽  
Chronic Fatigue ◽  
Myalgic Encephalomyelitis ◽  
Barr Virus ◽  
Fatigue Syndrome ◽  
Specific Proteins ◽  
Epstein Barr ◽  
Human Herpesviruses

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) or Systemic Exertion Intolerance Disease (SEID) is a chronic multisystem illness of unconfirmed etiology. There are currently no biomarkers and/or signatures available to assist in the diagnosis of the syndrome and while numerous mechanisms have been hypothesized to explain the pathology of ME/CFS, the triggers and/or drivers remain unknown. Initial studies suggested a potential role of the human herpesviruses especially Epstein-Barr virus (EBV) in the disease process but inconsistent and conflicting data led to the erroneous suggestion that these viruses had no role in the syndrome. New studies using more advanced approaches have now demonstrated that specific proteins encoded by EBV could contribute to the immune and neurological abnormalities exhibited by a subgroup of patients with ME/CFS. Elucidating the role of these herpesvirus proteins in ME/CFS may lead to the identification of specific biomarkers and the development of novel therapeutics.

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