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

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.

Author(s):  
Jonathan Price

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.


2008 ◽  
Vol 36 (5) ◽  
pp. 867-874 ◽  
Author(s):  
R Chen ◽  
FX Liang ◽  
J Moriya ◽  
J Yamakawa ◽  
H Sumino ◽  
...  

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.


2004 ◽  
Vol 115 (10) ◽  
pp. 2372-2381 ◽  
Author(s):  
Vlodek Siemionow ◽  
Yin Fang ◽  
Leonard Calabrese ◽  
Vinod Sahgal ◽  
Guang H. Yue

2021 ◽  
Vol 15 ◽  
Author(s):  
Adonis Sfera ◽  
Carolina Osorio ◽  
Carlos M. Zapata Martín del Campo ◽  
Shaniah Pereida ◽  
Steve Maurer ◽  
...  

Myalgic encephalomyelitis/chronic fatigue syndrome is a serious illness of unknown etiology, characterized by debilitating exhaustion, memory impairment, pain and sleep abnormalities. Viral infections are believed to initiate the pathogenesis of this syndrome although the definite proof remains elusive. With the unfolding of COVID-19 pandemic, the interest in this condition has resurfaced as excessive tiredness, a major complaint of patients infected with the SARS-CoV-2 virus, often lingers for a long time, resulting in disability, and poor life quality. In a previous article, we hypothesized that COVID-19-upregulated angiotensin II triggered premature endothelial cell senescence, disrupting the intestinal and blood brain barriers. Here, we hypothesize further that post-viral sequelae, including myalgic encephalomyelitis/chronic fatigue syndrome, are promoted by the gut microbes or toxin translocation from the gastrointestinal tract into other tissues, including the brain. This model is supported by the SARS-CoV-2 interaction with host proteins and bacterial lipopolysaccharide. Conversely, targeting microbial translocation and cellular senescence may ameliorate the symptoms of this disabling illness.


2012 ◽  
Vol 5 ◽  
pp. IJTR.S10085 ◽  
Author(s):  
Adele Blankfield

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).


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