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NAWM (normal appearing white matter) is the name for abnormal white matter areas that look normal in MRI, but under special MRIs are abnormal. They are important because MS lesions appear inside these NAWM areas, and therefore they represent an early problem before developing the lesions.

As anybody here would have bet, they are connected with blood flow, more exactly, with cerebral small vessel disease (SVD) :

Diffusion tensor imaging and cognition in cerebral small vessel disease
http://www.ncbi.nlm.nih.gov/pubmed/21549191

CONCLUSION: DTI parameters in both WML and NAWM correlate with cognitive performance, independent of SVD. DTI may be a promising tool in exploring the mechanisms of cognitive decline and could function as a surrogate marker for disease progression in therapeutic trials. This article is part of a Special Issue entitled: Imaging Brain Aging and Neurodegenerative disease.

Edit: There is also a relationship to the condition known as "Leukoaraiosis"

http://www.thisisms.com/forum/chronic-c ... 22309.html

In EAE, the mice do not develop NAWM, so this is unexplained by autoimmune theory but explained by CCSVI theory.

Very interesting!

I do not think EAE is a very good or comprehensive model of all autoimmune disease or theory. In fact I don't even know much about why it's thought to model autoimmunity at all.

Dateline: Vancouver
March 1993

Today, at the offices of Western Canada's pre-eminent neurologist, a young man of 31 years had the audacity to refuse the new, experimental betaSerone injections; stating "I don't believe that my immune system is attacking my central nervous system (CNS)", "You don't know what causes it ("Multiple Sclerosis"), have never cured anyone, don't know the long-term benefits or risks of the drugs..."

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18 years later, congenital venous malformations of the IJVs and azygous vein are identified by IVUS, and treated. These CVMs were not caused by the immune system, and are not treatable by any known DMDs (disease modifying drugs).

Conclusion: "MS" is not an auto-immune disease, in my experience. I believe that it is congenitally compromised cerebral venous outflow in conjunction with exogenous factors - such as; bacterial infection, environmental insult, iatrogenic insult (vaccines, etc.).

Bottom line: no one knows still, what causes "MS", but there is a lot more pointing toward vasculature than a rogue immune system.

By the way, related to this, NAWM also presents hypoperfusion, and that is previous to axonal loss and BBB breakdown.

Hypoperfusion of the cerebral white matter in multiple sclerosis: possible mechanisms and pathophysiological significance

http://www.ncbi.nlm.nih.gov/pubmed/18594554

And it would be funny to hear the supporters of the "only-autoimmune" theory explaining this.