Inflammation of the brain causing a dysfunctional hypothalamus can explain Myalgic Encephalomyeltis

What is it about?

A neuro-inflammatory model to explain the onset, symptoms and perpetuation of ME/CFS. A range of triggers (intense physiological stressors) e.g. particular viral infections, chemical toxin exposure, emotional trauma, in ME/CFS predisposed people causes a significant disruption within the neural circuitry of the hypothalamic paraventricular nucleus (PVN), which induces a neuro-inflammatory reaction within the brains of ME/CFS patients, via over-active innate immune (glial) cells. Resulting dysfunction of the limbic system, its 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) hypothalamic PVN and if a certain (but variable) threshold is exceeded a flare-up (relapse) will ensue, inducing further neuro-inflammation, thus perpetuating the disease indefinitely.

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Why is it important?

The model is a simple, coherent and unifying as it can account for all triggers of the disease, when each viewed as a different form of intense stressor results in the same disease outcomes. It can explain symptoms and flare-ups. It is particularly important as hopefully it will influence researchers to not only refocus their thoughts towardss ME/CFs as a neurological/ neuro-inflammatory disease, but also to change there apprach from researching it by moving away from blood-biomarker studies towards brain/ CNS studies by in particular using developing/ evolving MRI technologies.

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