My thoughts about the Beirut study

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

My thoughts about the Beirut study

Postby frodo » Mon Oct 18, 2010 1:45 pm

Probably the paper that I find more interesting from ECTRIMS is the Beirut study. This study confirms one of the early findings of Zivadinov (stenosis are more likely to appear in advanced cases of MS, 24% in early MS and 92% in long time MS)

But they forget that CCSVI is not only about stenosis, but about reflux (valves, webs, etc). Probably they are looking for CCSVI without invasives phlebographies, and they focus in stenosis.

My question is, Could an early problem such as a defective valve produce a stenosis in a vein? This would explain perfectly the result of Zivadinov and the Beirut researches, and at the same time, it would be in line with the main theory of Zamboni.

I think this explanation (a small defect in a vein increases with time and produces stenosis) is more logical than to state that an autoimmune problem causes both multiple sclerosis and stenosis in the IJVs.

What do you think? Could this be plausible?
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Re: My thoughts about the Beirut study

Postby David1949 » Tue Oct 19, 2010 3:19 pm

frodo wrote:Probably the paper that I find more interesting from ECTRIMS is the Beirut study. This study confirms one of the early findings of Zivadinov (stenosis are more likely to appear in advanced cases of MS, 24% in early MS and 92% in long time MS)


I'm not sure what conclusions they draw from that. I don't see how this would establish that MS causes CCSVI rather than the other way around. The only conclusion I could draw is that perhaps stenoses are not entirely congenital. Maybe they develop or worsen over time and result in worsening MS symptoms.
So I tend to agree with your conclusion.

frodo wrote: Could an early problem such as a defective valve produce a stenosis in a vein? This would explain perfectly the result of Zivadinov and the Beirut researches, and at the same time, it would be in line with the main theory of Zamboni.

I think this explanation (a small defect in a vein increases with time and produces stenosis) is more logical than to state that an autoimmune problem causes both multiple sclerosis and stenosis in the IJVs.

What do you think? Could this be plausible?
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CCSVI and DMDs ???

Postby Shayk » Thu Oct 21, 2010 3:15 pm

Frodo
This study confirms one of the early findings of Zivadinov (stenosis are more likely to appear in advanced cases of MS, 24% in early MS and 92% in long time MS)

I think there may be a big (? significant) difference between the Zivadinov and Beirut data. The Beirut data found stenosis occurred in 92% of people with RRMS (of 10 or more years duration) and I believe Zivadinov found 92% in SPMS.

Since the Beirut reseachers found stenosis associated with disease duration in people with RRMS, I think another question that needs to be addressed (especially if they're going to pursue the idea that MS causes CCSVI) is whether or not the stenosis is due to CRABS. If one assumes that many people with RRMS in the study were on a DMD for 10 years, that is a variable that will need to be examined and ruled out as the cause of the stenosis.

Now, I didn't know whether or not they used DMDs in Lebanon, so I tried to find out and here's what popped up from the lead author in the Beirut study :roll:

Bone marrow mesenchymal stem cell transplantation in patients with multiple sclerosis: a pilot study

Anyway, it does appear they do use DMDs in Lebanon.

Lastly, I don't have a clue as to whether a defective valve could cause stenosis in a vein.

For those who haven't seen it yet, here's a link to the Beirut study.

Chronic cerebrospinal venous insufficiency is an unlikely cause of multiple sclerosis

Take care all

Sharon
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Postby sou » Fri Oct 22, 2010 3:42 am

A shot in the dark:

I was a typical "Zamboni Type A", left IJV's and azygos' obstructions. The left IJV was somehow atrophic and narrow. 1 month after removing the web at the junction with the brachiocephalic vein, its width and flow was restored to 100% normal.

Thus, what could be seen as stenosis, was a collapse, because there was no flow in it. The force moving the blood down to the heart was equal to the opposite force originating from the obstruction, giving 0 flow when upright.

Unlike Zamboni's studies, my radiologist insisted on performing a Valsalva test just to see if its venous walls were still elastic. Luckily, they were and the vein was opening during the test. That was a good sign that it would restore to normal when the flow came back to normal.

On a follow up check, he spotted a tiny membrane on the healthy right IJV. Perhaps, there was the very same problem in the left, but it grew with me, because the left clavicle is a little malformed and pressed the vein enough to stick the membrane to the opposite wall, when I was a fetus, and make it grow.
Shortest joke: "We may not be able to cure MS but we can manage its symptoms."
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