Since I saw his video presentation at the MS Society Ontario General Meeting I have been doing a bit of digging on the work her is doing and have found a few extracts on different websites and forums. I have put them together for my own benefit but maybe others would like to read them too. It is encouraging that some scientists are not stuck in the auto-immune theory and are beginning to break out of the straight jacket which has contained research for the past 60 years or so, thanks to Joan Beal for posting some extracts, the rest of the information comes from a number of different websites:

Dr. Stys is a neurologist/neuroscientist and a world leader in the detailed study of pathophysiological mechanisms of white matter injury in stroke and trauma. He has extensive expertise in electrophysiological recording methods in myelinated axons and his team has recently developed confocal, multiphoton and coherent anti-Stokes Raman scattering (CARS) imaging techniques for both fixed immune-stained and live myelinated axons and glial cells.

Will the real multiple sclerosis please stand up?

Stys PK, Zamponi GW, van Minnen J, Geurts JJ.

Source

Department of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta T2N 4N1, Canada. pstys@ucalgary.ca

Abstract

Multiple sclerosis (MS) is considered to be an autoimmune, inflammatory disease of the CNS. In most patients, the disease follows a relapsing-remitting course and is characterized by dynamic inflammatory demyelinating lesions in the CNS. Although on the surface MS may appear consistent with a primary autoimmune disease, questions have been raised as to whether inflammation and/or autoimmunity are really at the root of the disease, and it has been proposed that MS might in fact be a degenerative disorder. We argue that MS may be an 'immunological convolution' between an underlying primary degenerative disorder and the host's aberrant immune response. To better understand this disease, we might need to consider non-inflammatory primary progressive MS as the 'real' MS, with inflammatory forms reflecting secondary, albeit very important, reactions.

Here is an extract from the paper which is not available without subscription:

One might reasonably ask why other common neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease, do not also result in relapsing–remitting neuro-inflammation. In fact, both diseases do exhibit inflammation in pathologically vulnerable regions 83,84. Indeed, in these research fields there is also an on-going debate about whether inflammation is a reaction to, or cause of, on-going degeneration. For example, post-mortem examination of human and primate brains after exposure to MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a neurotoxin that induces parkinsonian features by killing dopaminergic neurons, reveals a sustained inflammatory response that continues for years after exposure to the toxin. Clearly, in this example the initiating insult was a monophasic degenerative one (toxin-induced death of a specific neuronal population), which secondarily entrained a protracted inflammatory reaction and, interestingly, continued neuro-degeneration that long outlasts the toxic insult. The reasonable question that was raised was whether such secondary inflammation could now feed back and promote further degeneration, completing an analogous ‘inside-out’ cycle as we propose for multiple sclerosis (MS). Because diseases such as Alzheimer’s and Parkinson’s have a much more prominent degenerative rather than inflammatory phenotype, the initial assumption was that a degenerative mechanism (or mechanisms) was primarily responsible, with inflammation perhaps a secondary, but possibly important, consequence of the degeneration. In MS, the situation is reversed: inflammation occurs early and is very prominent in many patients, so it was naturally assumed that autoimmunity might be causal; but, as we argue throughout this Perspective, such an assumption may be incorrect. If MS is primarily a degenerative disorder in line with an inside-out mechanism, why would this disease be unique in engendering such prominent and cyclic inflammation? The differences may be related to age: Alzheimer’s disease and Parkinson’s disease present decades later than MS, and immune responsiveness wanes with age through a process of ‘immune senescence’ . Indeed, the responsiveness of T cells, which are known to be centrally involved in the immune-pathogenesis of MS, appears to be particularly altered with age. Moreover, it is conceivable that the putative cyto-degeneration involving the myelinating unit (oligodendroglia, their processes and myelin) in MS releases debris that is more antigenic than the debris that is shed from the mainly synaptic and neuronal degeneration in Alzheimer’s disease and other traditional neurodegenerative disorders.

In an article in Nature Reviews Neurosciences (Nature Reviews Neuroscience 13, 507-514 (July 2012) Peter K. Stys, Gerald W. Zamponi, and Jan van Minnen (University of Calgary, Canada) and Jeroen J.G. Geurts (VUmc) state that MS might start in the brain and not in the immune system.

It is quite well possible that multiple sclerosis (MS) starts in the brain and not in the immune system as is now generally accepted. On basis of recent research findings, a group of Dutch and Canadian researchers published this research hypothesis in Nature Reviews Neuroscience.
"In medical science MS is considered to be a disease of the immune system that turns against the brain (autoimmunity). In our opinion article we reverse this. Something is wrong within the brain. The disruption of the immune system could be a mere consequence of this primary pathology in the brain”, says Jeroen Geurts. “It is obvious that in MS something is wrong with the immune system as well, but we think that is a consequence, not the cause.”
If this is true, it means a radical change of thought about multiple sclerosis pathogenesis. "MS research has been done for more than 150 years now. A great deal has been achieved in the field of treatment of the disease, by looking at the immune system, but we still have no definitive solution to the disease”, says Geurts. To improve the treatment of the disease, it is important to discover what causes MS. It is undeniably true that the immune system plays an important role in MS. Treatment of the disrupted immune system therefore remains necessary, but if our hypothesis turns out to be true, it might offer possibilities to specify the search for additional treatment methods that may directly affect the pathological process in the brain.