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- W2103928848 abstract "The aetiological and pathophysiological basis of chronic fatigue syndrome (CFS) remains a controversial field of inquiry in the research community. While CFS and similar disease conditions such as fibromyalgia (FM) and post-infectious encephalopathy have been the focus of intense scrutiny for the past 20 years, results of research were often contradictory and a cohesive pathological model has remained elusive. However, recent developments in understanding the unique immunophysiology of the brain may provide important clues for the development of a truly comprehensive explanation of the pathology of CFS. We argue that CFS pathogenesis lies in the influence of peripheral inflammatory events on the brain and the unique immunophysiology of the central nervous system. There is also evidence that CFS patients have a relative immunodeficiency that predisposes to poor early control of infection that leads to chronic inflammatory responses to infectious insults. The neurological and endocrine changes have been described in CFS patients support the view that CFS has an inflammatory pathogenesis when considered as a whole. An inflammatory model of disease also provides an explanation for the marked female sex bias associated with CFS. This review therefore posits the hypothesis that CFS as a disease of long-term inflammatory processes of the brain. We will also provide an investigative framework that could be used to justify the use of anti-TNF biological agents as a reliable and effective treatment approach to CFS, a syndrome that to date remains frustratingly difficult for both patients and health care professionals to manage." @default.
- W2103928848 created "2016-06-24" @default.
- W2103928848 creator A5021675138 @default.
- W2103928848 creator A5030264676 @default.
- W2103928848 creator A5051504430 @default.
- W2103928848 creator A5084713074 @default.
- W2103928848 date "2011-07-01" @default.
- W2103928848 modified "2023-09-27" @default.
- W2103928848 title "Chronic fatigue syndrome – A neuroimmunological model" @default.
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- W2103928848 doi "https://doi.org/10.1016/j.mehy.2011.03.030" @default.
- W2103928848 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21474251" @default.