This Is MS Multiple Sclerosis Community: Knowledge & Support

Direct-MS has posted an article which analyses the new results from the University of Buffalo and Georgetown University and recommends appropriate actions on the basis of this scientific analysis.

http://www.direct-ms.org/magazines/Embr ... 2%2010.pdf

Thanks, Ashton, for being prepared to stick your neck out!

May I suggest a correction that I noticed in a brief skim of the paper? You say:
Although I agree with you that CCSVI isn't likely the sole cause of MS, the 40% you talk about is almost certainly too high given that it was 20% for people that were clinically diagnosed, according to the BNAC study (and much lower in Zamboni's and Simka's clinical experiences).

Also, I never realized that 80+% of CIS patients go on to develop clinically diagnosed MS. But then, I guess it depends on how CIS is defined.
...Ted

_________________
Dx SPMS in 2004.  Liberated 29/04/2010.
My blog: www.my-darn-ms.blogspot.com

Interesting...

ozarkcanoer

Dr. Embry, thanks for one more selfless article and keeping MS patients in mind ...

Do pwMS who have a negative result for CCSVI still have Dawson’s fingers or lesions around veins or iron deposits occurring around veins? If so, then perhaps a blood flow problem of some sort could be still associated with their MS.
The full Buffalo results in which iron deposits are imaged may be interesting in this respect.

Also, people with PPMS have less immune activity (that is why current drugs targeted at the immune system don't work on PPMS) but they had the worst outcomes from having their stenosis or blockage cleared in Dr Zamboni's study.
Direct MS says "... On the other extreme, CCSVI might be by far the main causal factor in some cases and these would have only a little, if any, autoimmune involvement.[/quote]

There are going to be a lot of studies and trials on CCSVI and it's relationship to MS over the next several years. If nothing else it will be interesting to observe. What is true or not true at this point I am unwilling to speculate. But I am willing to be tested for CCSVI. I guess I have such an emotional involvement in the CCSVI idea right now I just have to know. I'm going to Buffalo (not scheduled yet) and pay serious $$$$ to find out. It's better than throwing money away gambling, LOL. Now gambling is something that I just can't comprehend !!!

ozarkcanoer

I don't understand how the 80% number for CDMS holds up mathematically given the rest of the study numbers.

If CIS patients did indeed display CCSVI 38% of the time, and the combination of CDMS and CIS cases displayed CCSVI approximately 56% of the time, then the 80% CDMS number would only hold up mathematically if the tested CDMS and CIS populations were equal in number.

Instead, we know that the CDMS:CIS ratio was more than 4:1. Given that ratio, the CIS incidence of CCSVI it would have to be much lower, somewhere in the neighborhood of 8%, to make an 80% number for the clinically definite multiple sclerosis population stand up mathematically.

Am I missing something?

_________________
Marc
www.wheelchairkamikaze.com

Many people are not reading the Buffalo results properly. There were 4 separate groups - CDMS, healthy controls, persons with other diseases and CIS. THe 55% with CCSVI refers to CDMS and NOT CDMS and CIS. The 80% with CCSVI referred to a subgroup in the CDMS who had more severe disease. Many people seem to be thinking the 80% refers to the entire CDMS group which it does not. CIS had 38% CCSVI.

But Zivadinov said (in answer to Billmeik):



So, unless Zivadinov misunderstood the question, CDMS (not "severe MS patients") have 80% CCSVI.

See:
http://www.thisisms.com/ftopic-10255-days0-orderasc-75.html
...Ted

_________________
Dx SPMS in 2004.  Liberated 29/04/2010.
My blog: www.my-darn-ms.blogspot.com

I'm with you, the buffalo numbers don't make a lot of sense mathematically.
Also why wouldn't buffalo release this 80% number?? it also makes sense to me that if its a sub group they wouldn't release that number. They would include it within the 55% which covers the majority of the ms population.

I'm very curious to see if CCSVI is the reason behind why the current crab drugs only work in 30% of the ms population.

I think the current crab drugs target the immune system. The fact that they often don't have any impact on the course of the disease would suggest to a person who knows nothing such as myself, that while the immune system may be involved, suppressing it doesn't alter the disease course. You would think that if MS was autoimmune, and you suppressed the immune system, it would get better. But it doesn't!!
CCSVI has to be involved there somewhere.

The immune response in MS has been identified simply cause of t and b cells attacking myelin thus causing the formation of lesions and the clinical manifestations we all know by the name relapse. It is only natural to suffer a "relapse" when inflammation takes place in the cns.
So, drugs altering the immiune response may have some effect on relapses but the degenarative proccess of the disease (when axons and neurons simply die) have never been found to have an obvious reason. Until maybe now...
Campath for instance (which i have had) leaves the body with no immune system so to speak, by targeting and destroying a t cell population for good. This is why it is known to have such a dramatic effects on relapse rate. On the other hand, MS continue to progress no matter what simply because the underlying cause of MS still exists.
Drugs treat some symptoms and if i knew that i would still feel like shit after campath even if i changed my body's chemistry for ever i d never do it.

That is Zamboni's findings are so promising. They dictate that immune response in MS is due to a "mechanical" malfunction.

One more note worth point Dr Embry makes - one must investigate if CCSVI is the underlying cause of other neurological diseases.
I once made this point and get battered like hell (for rumour mongering) ...

Of course they will look into that too eventually. Once it is proved for MS...

Does anyone know whether the pattern of iron deposition in other neurological diseases, is centred on veins like MS or whether there are other patterns?