Neuroimmune model

The neuroimmune model or neuro immune hypothesis of ME/CFS proposes that an initial infection and immune activation, which can be caused by a number of different pathogens results in "a state of chronic peripheral immune activation driven by activated O&NS pathways that lead to progressive damage of self epitopes even when the initial infection has been cleared".

The ATP deficiency, inflammation and oxidative and nitrosative stress are proposed to result from this, and to be the cause of the symptoms characteristic of ME/CFS.

Notable studies and publications

• 2011, Chronic fatigue syndrome – A neuroimmunological model (Full text)

• 2013, A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome (Full text)

• 2017, The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) (Full text)

See also

• O&NS pathway
• Gerwyn Morris
• Michael Maes
• Medical hypotheses (category)

Learn more

• A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome

See myalgic encephalomyelitis.

See chronic fatigue syndrome.

myalgic encephalomyelitis (M.E.) - A disease often marked by neurological symptoms, but fatigue is sometimes a symptom as well. Some diagnostic criteria distinguish it from chronic fatigue syndrome, while other diagnostic criteria consider it to be a synonym for chronic fatigue syndrome. A defining characteristic of ME is post-exertional malaise (PEM), or post-exertional neuroimmune exhaustion (PENE), which is a notable exacerbation of symptoms brought on by small exertions. PEM can last for days or weeks. Symptoms can include cognitive impairments, muscle pain (myalgia), trouble remaining upright (orthostatic intolerance), sleep abnormalities, and gastro-intestinal impairments, among others. An estimated 25% of those suffering from ME are housebound or bedbound. The World Health Organization (WHO) classifies ME as a neurological disease.