This Is MS Multiple Sclerosis Community: Knowledge & Support

I am starting this thread in the hope that it can become a summary of evidence we have for the i) venous malformations and ii) venous flow anomalies being congenital on one side, as well as of arguments for CCSVI starting later in life on the other side. There's been some discussion over in the antibiotics forum of the stenosis being caused by Cpn, etc:

http://www.thisisms.com/ftopic-6670-day ... asc-0.html

On the other side it seems to be widespread opinion in the CCSVI forum that the stenoses and resulting blood flow issues are mostly congenital.
This is clearly a very important question so I thought it would be worthwhile collecting arguments on both sides.

I recall two arguments in favor of the stenoses being *often* congenital. One is that some of the patients treated by Dr. Dake had twisted jugulars or jugulars squeezed by surrounding material, like jawbone, which are clearly not caused by ulcers. Another is Zamboni re-visiting people (as far as I know it is not clear how many?) in Sardinia after 20 or so years, who he had diagnosed with (some form of?) venous malformations in their childhood to find that now 90% of them had MS.

As far as I understand Dr. Lee's talk (conference notes) he specializes in venous malformations on a more general scale, and states that many of them are congenital, but has not looked at IJV stenosis in particular. There's mention of association with Caucasian race, but MS is not limited to Caucasians.

One thing that puzzles me is that (as I read it) azygos *reflux* is seen more often in secondary progressive patients than in relapsing-remittent ones. Azygos *malformations* on the other side are (as I understand) not seen often by Dr. Dake. This would mean that at least the azygos reflux is not congenital (except for, maybe, in primary progressive people), and caused by something else.

Thanks for thoughts and hints to articles by anybody!

_________________
RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap

Actually this would mean that azygous is blocked when you go from RR to SP! .

As far as I understand Zamboni says that RR and SP MS types have related patterns of obstructions and they are different from PP. This is logical as SP is the second phase of a RR course.

From Zamboni's paper:



As far as I remember only one patient operated by Dake needed stenting in her azygous and she was PP.

Radeck,
Just to clear it up, Dr Dake has treated some azygos issues. Not 86% of patients as did Dr Zamboni ....

and he has seen some other venous anomalies as well, including at least one congential brachiocephalic anomaly which I heard about that he did not fix, but later after venogram review decided it could/should have been repaired. Every patient represents a new opportunity to learn about the venous system as it relates to the brain and head.

Learning !!!

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I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
http://www.ccsvibook.com Read my book published by McFarland Health topics

I'm bumping this thread up, as I think this is an absolutely important question. For if we don't have enough evidence for CCSVI being congenital, there is something going on in MS bodies that will sooner or later lead to re-stenosis, and should be fixed itself.

Do any of those on this forum who have medical knowledge, read into CCSVI theory more than the majority of users on this forum, or been to the Bologna conference any thoughts on this?

Or do we conclude that the jury is out on this, and that we simply don't know?

Thanks for taking your time to read and think about this together!

While I don't have anything substantive to contribute at this time, I do agree with your point (and logic) and hope that a great exploration ensues.

_________________
diagnosed RR in spring '04
1 stent placed in left jugular vein 7/15/09
on and off Copaxone
allergric to interferons and Tysabri

radeck-
You ask many questions that are not answerable today. The truth of the matter is we are just beginning the years and years of research it is going to take to completely understand CCSVI. Dr. Zivadinov from Jacobs says he expect 20,000 research papers to be written in the next 10 years on CCSVI in MS.

I reported what Dr. B.B. Lee said at the conference,(which hasn't changed in one month.) He says that CCSVI in the jugulars looks like congenital truncular venous malformations. But he has not undertaken any official studies on this. I also reported that Dr. Zamboni saw children in Sardinia with these jugular venous malformations over 20 years ago, and 90% of these individuals now have MS. This is what we have today. It's looks like this is a congenital condition. I also reported that Dr. Zamboni said that "endothelial disrupters" such as EBV, low vitamin D, Cpn, heavy metals, toxins, etc" can exacerbate the stenosis and cause even worse reflux. For anyone that wants to read my notes from Bologna, they are on the 2nd post of the "Research Sticky."

Dr. Lee made one comment over and over again in Bologna, "We do not know what we do not know." He's right.

We can theorize and guess and come up with all sorts of questions, but the research will have to be done in labs, and this is going to take time.
cheer

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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

Thanks cheer for reminding us of these three pieces of knowledge we have (I think I did mention the first two earlier, but not as clearly as you). I think if we can find out more about just these three, we're in a good position to make an educated guess as to whether the stenosis are often/mostly congenital.

As I wrote above I have been wondering if we can find out more about the children in Sardegna Zamboni looked at. I think there's paper written about his original findings but can't find it. Once we knew more about the methods that went into the study, the kinds of stenoses reported, and in particular the number of patients followed up, that would be really good. Do you (or anybody else) know if this is discussed in a paper and do you have access to it?

The third point you mention, that "endothelial disrupters" such as EBV, low vitamin D, Cpn, heavy metals, toxins, etc" can exacerbate the stenosis and cause more reflux, is very interesting and I indeed missed it. Now I wonder how Zamboni meant this, isn't the endothelial lining at the area of the stenosis relatively normal? I thought the problem with endothelial disruption occurred upstream from the stenosis, i.e. in the CNS, where endothelial disruption caused micro-bleeding, iron deposition, immune-system activation and so on. Have any of the researchers at the conference found signs of endothelial disruption at the place of the stenosis?

I appreciate your notes from the conference, but think this topic deserves its own thread, since it's often assumed here that the stenoses are congenital.

radeck...
apologies. I've been writing about the endothelium for over a year now, so I forget that folks new here may not have read all of our discussions. Endothelial dystruption is systemic, and not related to location. We have 60,000 miles of blood vessels, and a change in nitric oxide can affect the whole body. Endothelial disruption has been found in every autoimmune disease, as well as cardiovascular disease.

It was the endothelial health program I wrote up last year and sent to Dr. Cooke that put me in touch with Stanford. Dr. Cooke is an endothelial researcher and author of The Cardiovascular Cure. This was a trail I followed since Jeff's diagnosis-

Here are some links regarding endothelial disruption and healing-
http://www.thisisms.com/ftopict-6318.html

Here's the program I made for Jeff-
http://www.facebook.com/note.php?note_id=123456602210
cheer

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

Thank you, to clarify, Zamboni does think that endothelial disruption happens AT the site of the stenosis? Has this been analyzed by taking samples from these sites?

It seems that you and Marie have read more than anybody here on CCSVI, have you come across a paper where Zamboni describes his experience with the patients in Sardegna?

Finally a question to everyone, cheer wrote that Dr. Lee reports the truncular malformations to occur more often in Causasians than others. Does MS affect a larger proportion of Caucasians in, say North America, than people with different ancestry?

OK, as this discussion of whether CCSVI is congenital or now isn't exactly an active one, I thought I'd summarize what I think we have now, before the thread gets buried down the list. It is my understanding that until we have more research results, the effect of endothelial disruption on stenosis itself is only speculation, the children in Sardinia Zamboni looked at may have had different kinds of venous problems than the ones we're interested in, and Lee's truncular malformations might have no relation to CCSVI, in particular because they're more common in Caucasians, while MS may not be (?).

While an unknown percentage of IJV stenoses MAY be congenital, some MAY hence be not, and this might explain, e.g.

*the fact that identical twins don't always both develop MS,

*the correlation between EBV antibodies and MS occurrence, and

*the fact that antibiotics work in some in stopping progression, through attacking Cpn or other bacteria.

One speculation is that inflamed lymph knots in the neck could cause the IJV's to become inflamed due to their vicinity. This is something Dr. Dake finds possible as well. Since inflamed lymphs are a hallmark of EBV infection, perhaps repeated outbreaks of EBV during adolescence can lead to stenosis such as the ones seen in Z's and D's patients. Another speculation is that jugular vein TWISTS could be caused by traumatic events to the head/neck area.

Fernando, one thing I'd like to re-iterate in response to your posting and in the context of Marie's clarification is that as far as I could tell Zamboni did not find more STENOSIS in the azygos in SPMS patients than in RRMS patients, just more REFLUX. It seems from the "The value of cerebral Doppler haemodynamics in the assessment of MS" paper, that there's a trend toward more reflux issues in both a second jugular and the azygos happening during the later stages of RRMS in conversion to SPMS. As far as I can tell Zamboni doesn't quote numbers on the number of azygos STENOSIS reported. This means that there may not be a disagreement between Zamboni and Dake, in that Dake doesn't look for azygos reflux issues.

However it still means that it has to be explained (and this is what puzzles me a lot) why for some reason reflux in the azygos is increased toward later stages of RRMS in conversion to SPMS, if the only connection between azygos and the (possibly congenital) jugular malformation is through the cerebrospinal fluid (CSF)? Something appears to be happening to the CSF that leads to extra reflux, in a second jugular, and in the azygos, without there being any congenital issues in these systems. One can only hope that this misterious process is stopped by fixing the original jugular stenosis.