Society Logo
ME/CFS Australia Ltd
Please click here to donate ME/CFS South Australia Inc

Registered Charity 3104


Mailing address:

PO Box 322,
Modbury North,
South Australia 5092

1300 128 339

Office Hours:
Monday - Friday,
10am - 4pm

ME/CFS South Australia Inc supports the needs of sufferers of Myalgic Encephalomyelitis, Chronic Fatigue Syndrome and related illnesses. We do this by providing services and information to members.


ME/CFS South Australia Inc aims to keep members informed of various research projects, diets, medications, therapies, news items, etc. All communication, both verbal and written, is merely to disseminate information and not to make recommendations or directives.

Unless otherwise stated, the views expressed on this Web site are not necessarily the official views of the Society or its Committee and are not simply an endorsement of products or services.

Become a Member
DOCX Application Form (Word, 198 KB)
Why become a member?

A Compromised Paraventricular Nucleus Within A Dysfunctional Hypothalamus: A Novel Neuroinflammatory Paradigm For ME/CFS

Friday 14 December 2018


From the International Journal of Immunopathology and Pharmacology:



A compromised paraventricular nucleus within a dysfunctional hypothalamus: A novel neuroinflammatory paradigm for ME/CFS

Authors: Angus Mackay, Warren P Tate
First Published: December 6, 2018


A neuroinflammatory paradigm is presented to help explain the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).

The hypothalamic paraventricular nucleus (PVN) is responsible for absorbing and processing multiple, incoming and convergent ‘stress’ signals, and if this cluster of neurons were affected (by neuroinflammation), the ongoing hypersensitivity of ME/CFS patients to a wide range of ‘stressors’ could be explained.

Neuroinflammation that was chronic and fluctuating, as ‘inflammatory-marker’ studies support, could reflect a dynamic change in the hypothalamic PVN’s threshold for managing incoming ‘stress’ signals.

This may not only be a mechanism underpinning the characteristic feature of ME/CFS, post-exertional malaise, and its associated debilitating relapses, but could also be responsible for mediating the long-term perpetuation of the disease.

Triggers (sustained physiological ‘stressors’) of ME/CFS, such as a particular viral infection, toxin exposure, or a traumatic event, could also target the hypothalamic PVN, a potentially vulnerable site in the brains of ME/CFS susceptible people, and disruption of its complex neural circuitry could account for the onset of ME/CFS.

In common with the different ‘endogenous factors’ identified in the early ‘neuroinflammatory’ stages of the ‘neurodegenerative’ diseases, an as yet, unidentified factor within the brains and central nervous system (CNS) of ME/CFS patients might induce both an initial and then sustained ‘neuroinflammatory’ response by its ‘innate immune system’.

Positron emission tomography/magnetic resonance imaging has reinforced evidence of glial cell activation centred on the brain’s limbic system of ME/CFS patients.

Neuroinflammation causing dysfunction of the limbic system and its hypothalamus together with a consequently disrupted autonomic nervous system could account for the diverse range of symptoms in ME/CFS relating, in particular to fatigue, mood, cognitive function, sleep, thermostatic control, gastrointestinal disturbance, and hypotension.

Keywords dysfunctional paraventricular nucleus, hypothalamus, limbic system, myalgic encephalomyelitis/chronic fatigue syndrome, neuroinflammation, stress


Full article…


Arrow right

More Fibromyalgia News



blog comments powered by Disqus
Previous Previous Page