An abstract that mentions that myelin basci protein is targeted after stroke, so not only is oligoclonal bands a non specific finding, MBP antibodies are too:
Immune mechanisms contribute to cerebral ischemic injury. Therapeutic immunosuppressive options are limited due to systemic side effects. We attempted to achieve immunosuppression in the brain through oral tolerance to myelin basic protein (MBP). Lewis rats were fed low-dose bovine MBP or ovalbumin (1 mg, five times) before 3 h of middle cerebral artery occlusion (MCAO). A third group of animals was sensitized to MBP but did not survive the post-stroke period. Infarct size at 24 and 96 h after ischemia was significantly less in tolerized animals. Tolerance to MBP was confirmed in vivo by a decrease in delayed-type hypersensitivity to MBP. Systemic immune responses, characterized in vitro by spleen cell proliferation to Con A, lipopolysaccharide, and MBP, again confirmed antigen-specific immunologic tolerance. Immunohistochemistry revealed transforming growth factor β1 production by T cells in the brains of tolerized but not control animals. Systemic transforming growth factor β1 levels were equivalent in both groups. Corticosterone levels 24 h after surgery were elevated in all sham-operated animals and ischemic control animals but not in ischemic tolerized animals. These results demonstrate that antigen-specific modulation of the immune response decreases infarct size after focal cerebral ischemia and that sensitization to the same antigen may actually worsen outcome. FOUND HERE
ANOTHER ONE HERE
So this paper is discussing how a stroke's size (infarct size) is reduced by treating ahead of time to make sure the animal tolerates myelin basic protein rather than having the immune system attack it.
This would be your tovaxin type approach: make it so the body does not attack myelin=better stroke outcomes.
It is also known that if you give steroids or even the kind of immune suppressive drugs we give MS after stroke it improves outcomes. Again it is seen that the overactive immune system causes damage of its own by simply being there and responding to the stroke.
Of course it goes without saying that autoimmunity does not cause stroke.
If Dr Zamboni had not done his studies yet but the theory was out there as a hypothetical idea, it would still be a compelling theory just based on this other material.
In other words: this "story" about what causes MS is at least
equal to the autoimmune "story" that they have been treating us with. Add to that the strong evidence in these large well blinded and controlled studies that it is actually there and it becomes very compelling.
It is a little specious to claim that this CCSVI is "unproven" when autoimmunity has NEVER been proven in MS either. As this thread highlights, a lot of the so called proof of autoimmunity is actually this kind of non specific material that does not actually mean "autoimmunity" at all even though they have been pretending that it does and using it to support the argument that they are justified to give immune suppressives so strong that we can actually get immune deficiency diseases.
There is no scientific moral high ground in the autoimmune model. The emperor has no clothes there.