A neuro-inflammatory model can explain the onset, symptoms and flare-ups of myalgic encephalomyelitis/chronic fatigue syndrome
Angus Mackay 1
+ Author Affiliations
- Author Affiliations
Biochemistry Department, University of Otago, 710 Cumberland Street, Dunedin 9016, New Zealand. Email: angus1mackay@hotmail.com
Journal of Primary Health Care 11(4) 300-307 https://doi.org/10.1071/HC19041
Published: 29 November 2019
Journal Compilation © Royal New Zealand College of General Practitioners 2019 This is an open access article licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License
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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