My take on all this, for whatever's worth...
The study results released today were really not surprising from a blinded study of CCSVI. The results previously found (upwards of 95% correlation between CCSVI and MS) were from completely unblinded studies, meaning that the researchers conducting the studies as well as the technicians doing imaging were aware of which subjects had MS and which didn't. Though I don't think any intentional bias was present, unintentional bias could very well have played a part, and results such as those reported are the very reason that scientific scrutiny demands blinded studies.
I find the results of the buffalo study very encouraging. They discovered a 2:1 ratio of CCSVI found in MS patients vs. healthy subjects. This is a very significant finding, and only seems dim in comparison to the hard to fathom universal correlation that was previously reported. The high level of MS misdiagnosis alone cast immediate doubt on such high figures of correlation, and led many researchers (such as those at the NIH) to look at Zamboni's reports with skepticism. These new numbers should lend some scientific credibility to CCSVI theory, and I think they'll spark further interest from the "mainstream" research community.
As for the rather high level of CCSVI found in healthy subjects, the reason for this is most likely that CNS venous anatomy has very rarely been studied in depth. There is no actual definition of what "normal" looks like in venous anatomy, unlike that of arterial anatomy, which has been scrutinized for decades.
Venous anatomy varies widely from patient to patient, and even within an individual patient. Very often, the venous structure in individual patients is different in their left and right appendages. This normally is not true of arterial anatomy, which shows much greater conformity.
What the buffalo study suggests is that CCSVI is a component of the wider MS picture, not the panacea that we'd hoped for. What we call multiple sclerosis is most likely a collection of several different diseases that share some common symptoms and markers. This explains the heterogeneity seem from patient to patient, as well as the difference in efficacy levels of current MS therapies from patient to patient. There is very likely a subset for whom CCSVI is THE single most important factor in their disease etiology. There is also very likely a cohort for whom CCSVI plays no role at all. That said, it's vital that CCSVI research continues vigorously and expeditiously.
Of course, we are only at the very beginning of research into an area that has been largely unexplored. I'm sure that many more surprises await.
For those of you who would like to read more of my blather, I'd posted a rather long article on the buffalo results in my blog:
http://www.wheelchairkamikaze.com/2010/ ... ealed.html
I hope my words have not upset anybody here, as that certainly is not my intention. One of the hard life lessons I've learned through the years is that when something seems too good to be true, it probably is. It sucks, but it is what it is...