Studies of pediatric MS have the advantage of determining the factors which cause MS onset because of the small amount of time between the onset of the disease process and its diagnosis. In most cases of MS, the time between disease onset and clinical diagnosis is often 10-20 years whereas in pediatric MS it can be only a few years.

Past studies have shown that an Epstein Barr infection is a key factor in MS development as less than half of healthy controls had an EBV infection whereas almost everyone with pediatric MS had been infected by EBV. Notably, no other childhood virus showed any difference. Vitamin D has also been shown to be a factor in pediatric MS and it was found that those with pediatric MS and juvenile arthritis (RA) had significant T cell responses to multiple milk proteins. Those with MS reacted to different proteins than those with RA suggesting specific milk proteins are an important factor in MS as had been previously suspected from studies in adult MS.

The latest study on pediatric MS was recently put online at the Annals of Neurology  and to me it contained a most important discovery which provides understanding as to what is causing MS. The title of the paper is “Implication of perturbed axoglial apparatus in early pediatric Multiple Sclerosis” and the lead author is A. Dhaunchak.

The researchers looked at proteins in the spinal fluid of children with MS as well as those with another inflammatory brain disease, ADEM. They did not find myelin proteins in the spinal fluid as they had been expecting but found proteins related to the mechanism to how myelin is attached to axons. These proteins were from the axoglial apparatus which interacts with oligodendrocytes which manufacture the myelin for the axons. Notably these proteins were not there for ADEM.

As the authors discuss, this finding strongly suggests that MS is an “inside-out” disease. This means that something causes a problem in myelination and that intact myelin is not being attacked from the outside as in the autoimmune model. As the authors also note, the inflammatory response to myelin comes afterwards because of the lack of proper myelination. These findings match very well with the detailed pathological studies of John Prineas and colleagues who examined early lesions. They too found that myelin disintegration preceded inflammation.

In summary, this latest finding in pediatric MS strongly supports the concept that MS is primarily a neurodegenerative disease and that inflammation is secondary. Of course, this leaves the question of what causes the initial faulty myelination which leads to degeneration and eventual inflammation. Currently, the only reasonable explanation is that the consequences of CCSVI cause such an effect. We await the results of a study of CCSVI and pediatric MS from the same researchers.