“As encephalomyelitis describes an unproven pathological process - namely inflammation in the brain and spinal cord - many doctors have become reluctant to use this term. Some, including the author, have suggested that encephalopathy is a more acceptable way of describing the various neurological abnormalities and symptoms.“ - Charles Shepherd, 2006.



ME patients deal with a great many misconceptions about their disease from not only family members and friends, but also medics. The name itself, specifically encephalomyelitis, is arguably one of the most contentious issues. Amongst those medics, researchers and scientists who deal directly with the disease or chronic fatigue syndrome, it has long been debated whether the name is appropriate to the actual disease. The answer is an unequivocal yes. 

To be an encephalomyelitis, ME patients would have inflammation of the brain and spinal cord. Advances in scientific measurements and understanding of causes of encephalomyelitis have revealed that specifically in the brain this is neuroinflammation, which is indicated by the presence of activated microglia (immune cells in the brain).


“Activated microglia secrete a variety of inflammatory mediators including cytokines (TNF, and interleukins IL-1β and IL-6) and chemokines (macrophage inflammatory protein MIP-1α, monocyte chemoattractant protein MCP-1 and interferon (IFN) inducible protein IP-10) that promote the inflammatory state.”



Microglia are activated by the adaptive immune response due to various triggers, producing various proinflammatory cytokines and immune mediators. This response can then become chronic due to sustained activation and as a result lead to neuronal dysfunction and eventually neurodegeneration.  

The presence of activated microglia in the brain and spinal cord is thus a hallmark of all neuroimmune diseases, such as Alzheimer's, Parkinson's, ALS, MS, and so on.

In ME, autopsies have already demonstrated that dorsal root ganglionitis, which is the result of inflammatory processes targeting the sensory ganglia, is present in patients. Dorsal root ganglionitis is an alternative name for sensory ganglionitis, which may occur as a result on inflammation caused by HIV.

In view of these findings and sciences understanding of the mechanism underlying encephalomyelitis and the availability of tools such as PET scanners to determine the presence of a biological process that is absolutely required for a diagnosis of ME, we must ask why there is a complete absence of any such research within the field? Why ignore such a simple diagnostic method that defies crackpot beliefs and would surely open a more fruitful area of investigation for treatments then the study of downstream symptoms? 


ME Advocacy
9 November 2012
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