This Is MS Multiple Sclerosis Community: Knowledge & Support

Also I think it's more reasonable to conclude that these abnormalities cause MS than that MS causes the abnormalities.

Sure is, David. Especially since these same malformations cause Budd Chiari disease (which takes decades to manifest in liver failure.) Here's Dr. B.B. Lee's paper on this----it has pictures of these malformations and explains how they are formed in utero, and can create CCSVI. Note---it's from 2009.

http://fondazionehilarescere.org/pdf/03-2518-ANGY.pdf

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Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

i think that it's more reasonable to conclude that ccsvi is associated with ms. whether either causes the other is more speculative. Since treatment sometimes results in near immediate recovery of function one can more likely conclude that ccsvi causes symptoms

this is all moot for the moment. the question will take ten years to answer.

right now we have an opportunity to improve the livers of PwMS regardless of which causes which

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Salvatore JA Sclafani MD
Patient contact: ccsviliberation@gmail.com

This study seems to show a correlation between MS and CCSVI. When studies show a correlation between A and B there are in general 4 possibilities.
Either
-A causes B or
-B causes A or
-Something else causes both or
-In the case of a fairly weak correlation it may be that there is in fact no correlation and that the results of the study are just dumb luck.

I think a number of people have put forth plausible theories of how CCSVI might cause MS, although none are proven. But I haven't seen any theories of how MS might cause CCSVI. And it seems unlikely to me that the noted CCSVI conditions which look like birth defects could be caused by MS.

It is possible that something else causes both. That can't be ruled out.

The article says: "Marked valvular and other intraluminal abnormalities with potential hemodynamic consequences were identified in 5 of 7 MS patients (7 abnormalities) and in 1 of 6 controls (1 abnormality)." According to my handy dandy stats calculator there is a 2% chance that the result was dumb luck so that is possible but unlikely.



15 years of MS has taken a toll on me. I can hardly wait to see what it will do to me in the next ten years.



I think that either means CCSVI causes MS, or CCSVI is a separate disease that causes our problems rather than MS. Then what is MS?

I don't mean to be argumentative but like everyone else here I have a personal stake in this and I want to find answers.

Specificity and sensitivity are important when considering if CCSVI is causal to MS. Does everyone with CCSVI get MS? Does no one without CCSVI get MS? Does everyone with MS have CCSVI? Does no one without MS have CCSVI? Right now we can't answer these questions affirmatively based on the data collected so far.

Is there any reason we are not mentioning the placebo effect?

Placebo effect is something for the controlled trials to determine....

I suspect that MS is the complicated end result of damage to the brain caused by the weakened blood-brain barrier, cross-over of leukocytes that may be genetically partial to autoimmune attack, and hypoxic unhealthy conditions in the brain, all caused by the blood flow situation caused by CCSVI blockages.

So fixing that goes in reverse: fix the blockages, which if successful will fix the blood flow situation, which if successful will fix some but not necessarily all of the unhealthy conditions in the brain (which will directly relieve some CCSVI symptoms previously considered to be MS symptoms), which if successful should set the brain up for healing if healing is possible. (Hypoxia should be gone, focal points of blood flow hypertension should be gone, better glucose supply should be available, waste removal should be improved, CSF should be better, blood-brain barrier may strengthen but maybe not to normal, leukocytes sensitized to myelin may still be present in the brain, and the scars, atrophy, prior white and gray matter damage, enlargened ventricles, and reduced oligodendrocytes of MS will still be present.)

But this is all theory.

Wow, Cece! ! !
What a fantastic write-up!
In thanks, I have to say this yet again...
TIMS-CCSVI is extremely lucky you're its leader
In thanks, I have to say this yet again...
What a fantastic write-up!
Wow, Cece! ! !

Thank you, although we have many leaders here, and you've shown your leadership in the Daflon thread, the Dr. Flanagan thread and the Dr. Sclafani thread, to think of a few.

Going by what Dr. Sclafani said a few posts up, all this speculation is just speculation, and what matters is this smaller portion:

Nice consolidation of the sequence Cece. I will be expanding on this sequence at the presentation here in Ottawa on Nov 5 and then extend it into a discussion of the modulating effects of factors such as gender, genetics, vitamin d, cigarette smoking, viral infection etc. I end up the presentation talking about integrating all these effects using computational fluid dynamics - in fluid dynamics velocity profiles determine pressure profiles with the inclusion of appropriate boundary conditions, (like percentage obstruction, position of obstruction, vein compliance snf gravity. I am little more optomistic than Dr. S.S. - I predict that the origins of MS will be relatively well known within four years. BUT, there would need to be more scientific emphasis put into understanding why the effects occur, not simply focusing on clinical measurements of what occurs. If two or three bio-engineers stepped forward who had an interest in venous flow and fluid dynamics, two or three bio-chemists who had an interest in the impact of cerebral hypoxia on endothelium health and compliance, some IRs to carry out measurements and some neurologists to describe the impact of leukocytes on deteriorating myelin, most of the threads could be tied up. I am anticipating perhaps 8 or 10 good PhD theses in the next 4 years.

Trev. Tucker

sorry: snf = and

Trev. Tucker

Cece, there might be different leaders of different threads, but you're the LEADER of TIMS-CCSVI.

Dr. Tucker, it's wonderful that you're a part of the CCSVI paradigm--you're giving hope to lots of pwMS/CCSVI.

Edit: Cece, I dispute that I am a leader on any thread, except, perhaps, for a couple of threads that mysteriously disappeared

Dr. Tucker---Hope you'll be looking at those factors as related to endothelial dysfunction, vasoconstriction, c-reactive protein and nitric oxide. All of those factors (and many more) change the lumen and blood viscousity, affecting flow.
http://www.ccsvi.org/index.php/helping- ... ial-health
look forward to all the new research!
cheer

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

Yes I agree with you 100% that the trials are the place to determine how much is placebo, but we should not be blind to the fact and give recognition to the fact that all trials have shown us there IS a placebo effect. The placebo effect is the one thing that most would agree is NOT just theory.

It sounds like a very interesting talk, and I wish that I were able to attend.

Dr. J. Steven Alexander of LSU is our first biochemist, who will be publishing on cerebral endothelial disruption in CCSVI. That still leaves us short a few specialties, but we will get there.