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 ◽  
...  

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.

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.


Author(s):  
Ariel Y. Deutch ◽  
Robert H. Roth

Chapter 2 describes the neurochemical organization of the brain. It summarizes the diverse types of molecules that neurons in the brain use as neurotransmitters and neurotrophic factors, and how these molecules are synthesized and metabolized. The chapter also presents the array of receptor proteins through which these molecules regulate target neuron functioning and the reuptake proteins that generally terminate the neurotransmitter signal. Today a large majority of all drugs used to treat psychiatric disorders, as well as most drugs of abuse, still have as their initial targets proteins involved directly in neurotransmitter function.


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

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Le-wei Tang ◽  
Hui Zheng ◽  
Liang Chen ◽  
Si-yuan Zhou ◽  
Wen-jing Huang ◽  
...  

Chronic fatigue syndrome (CFS) is a debilitating and complex disorder characterized by profound fatigue with uncertain pathologic mechanism. Neuroimage may be an important key to unveil the central nervous system (CNS) mechanism in CFS. Although most of the studies found gray matter (GM) volumes reduced in some brain regions in CFS, there are many factors that could affect GM volumes in CFS, including chronic pain, stress, psychiatric disorder, physical activity, and insomnia, which may bias the results. In this paper, through reviewing recent literatures, we discussed these interferential factors, which overlap with the symptoms of CFS.


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).


1998 ◽  
Vol 32 (4) ◽  
pp. 523-527 ◽  
Author(s):  
Uté Vollmer-Conna ◽  
Andrew Lloyd ◽  
Ian Hickie ◽  
Denis Wakefield

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.


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.


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