Chuck, CCSVI might be the reason for MS. But we shouldn't ignore the evidence for auto-immune involvement, so we can get as complete and unbiased a picture as possible, you know?
So, I personally have not seen convincing evidence for Interferons and Copaxone slowing disability progression. There's evidence of them reducing annualized brain shrinkage by 30% or so, but in my humble opinion this is on shaky grounds, because it is based on the assumption that the trials were truly placebo controlled. In reality the drugs in those trials had significant side effects and could be distinguished from the placebo by most participants, so that true placebo control is missing, and AFAIK placebo itself can easily yield 30% improvement.
I think it gets more interesting when you look at more intense immune suppressers like Alemtuzumab, which is currently in phase III trials for MS. In phase II trials it has shown *no* brain shrinkage and *no* disability progression in *early* MS patients (on average less than a year from diagnosis at trial entry) over two years. See this <shortened url
Again one could be skeptical and say this could be placebo effect in action because Alemtuzumab has more side effects than the Rebif it was tested against, but I think a complete average stop of progression in 100 patients seems unlikely to be caused that way.
The reason I find this interesting is because I want to understand why in the beginning the immune-system causes most of the damage, while later it doesn't contribute much anymore.
(PS: Alemtuzumab makes your immune system destroy your T and B cells, and it's hard to imagine how that would improve the CCSVI itself.)