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It's a sign of how far we've come that no one even mentions that buffalo is finally finding 80% ccsvi in MS parents.

"CSVI criteria were fulfilled in 79.7% of MS patients and 18.2% of HC"

cheerleader wrote:Thanks, Squeaky---
it's a great paper for many reasons....especially the fact that BNAC researchers are now finding CCSVI in 80% of pwMS and 18% of HC....which is closer to Dr. Zamboni's results.

Oh, it's been noticed and mentioned, Bill
Also exciting is the Case Western/Cleveland Clinic study, which is also finding CCSVI in 85% of pwMS. The connection between all of these studies is the fact that the doppler technicians actually trained with Dr. Zamboni's team and utilized the full protocol. Imagine if researchers had done that in the first place, two years ago...before they devised their own studies....we'd be so much further along in understanding truncular venous malformations and MS.
cheer

the acceptance of the relationship between MS and CCSVI by the Neurology field will happen more or less .... like this :

For example .... people who work in offices will understand how this works. Somewhere out there is an office. The carpeting is shaggy and wornout. The workers are always complaining to the management. They trip ... they fall. Nothing is done about it. You are told to just be more careful . Or you are just clumsey . The carpet's just fine as is.

Until one day .... the Boss's wife visits the office ..... catch's her heel .... and does a serious face plant in front of everyone.

I GUARANTEE you ... the next week ... the whole damn office will have NEW carpeting from wall to wall.

I hate to say it .... but until someone " up the ladder " in the Neurology world get's MS , or one of their loved ones get's MS ....... the shitty old carpet ........ stays.

Life works like that ........ whether we like it or not.


Mr.Success

Billmeik wrote:It's a sign of how far we've come that no one even mentions that buffalo is finally finding 80% ccsvi in MS parents.

"CSVI criteria were fulfilled in 79.7% of MS patients and 18.2% of HC"

If new research supplants older research, we should be hearing these numbers instead of the lower percentage from earlier!

Back when there was Zamboni's original work and the one Buffalo study coming in as replication, it held a lot of weight. But since then, we've become a little numb from the many different studies with many different percentages. But Buffalo is a well-respected institution and they are looking at large numbers of patients, so the high numbers coming in for CCSVI in MS is a very good thing.

Can we call the 18.2% healthy controls anymore since they have CCSVI? Just because there isn't a 1:1 relationship between CCSVI and MS, doesn't mean that having CCSVI without MS is benign. For instance, would treating CCSVI in these so-called healthy controls make them smarter or faster or stronger?

You have to test the "healthy controls" with CCSVI against the healthy controls without CCSVI. What are the specific, not-MS symptoms that may be CCSVI symptoms? Cogfog, weakness, fatigue, vision issues. You could do a neuro exam on the healthy controls with CCSVI vs the healthy controls without CCSVI. Wouldn't that be something if the healthy controls with CCSVI turned up with neurological signs. It can be minor differences, as long as it's statistically signficant. Look at the vascular fundus of the healthy controls with CCSVI, see if there are signs of congestion.

If one wants to do CCSVI research, there are opportunities upon opportunities.

Asking if these so-called healthy controls have a sub-clinical malady besides CCSVI may not even be the right question. The right question might be better stated as to whether they are living up to their full potential? I asked Dr. Arata if my valvular issues were congenital. He thought they were. I asked if he thought that it would have affected me even before my MS diagnosis. He thought it would. Perhaps I would have sucked less at sports, or had even better marks in school. Food for thought anyway.

At a conference here in Ottawa yesterday we heard of three patients, of an enviromental doctor, who were treated for CCSVI. None of them had an MS diagnosis but had many of our symptoms and had not responded to the normal treatments.
Two of them are doing very well and the third was found to have a clotting disease so has not done as well.

..

I have read that inflammation causes venous anamolies through Venous Growth Factor. It is created as a repair operation in the body. Are the venous anomolies noted by ccsvi not supposed to be caused by inflamation? Does that make them genetic anamolies? Do any other venous disease show organ specific immune responses?

MSBOB wrote:I have read that inflammation causes venous anamolies through Venous Growth Factor. It is created as a repair operation in the body. Are the venous anomolies noted by ccsvi not supposed to be caused by inflamation? Does that make them genetic anamolies? Do any other venous disease show organ specific immune responses?

Hi Bob-
The types of anomolies created by inflammation would be stenosis and thrombosis. What the researchers are finding in CCSVI are truncular malformations, formed in uetero. These include inverted valves, malformed valves, webs, atresia (missing veins) and hypoplasia (unformed or small veins)
Here's a paper on the differentiation, written by a vascular expert, which shows these same malformations in Budd Chiari disease
http://fondazionehilarescere.org/pdf/03-2518-ANGY.pdf

The response of the liver in Budd Chiari disease is different, because there is not a blood brain barrier in the liver, and the immune system is not kept out, as it is in the brain and spine....so the appearance of an "auto immune" reaction won't be found in other organs. However, there is an immune activation and fibrin cuffs found in venous ulcers of the legs, when flow is impeded by damaged valves, which is what started Dr. Zamboni on this exploration of venous disease and MS.
http://jrsm.rsmjournals.com/content/99/11/589.full

hope this helps!
cheer

Interesting. I think the inflammation does play a role in the venous anomlies. I have to see more about the other side. Thanks for posting the links. I meant to say VEGF, vascular endothelial growth factor. I was trying to go by memory in the last post.

http://en.m.wikipedia.org/wiki/Vascular ... wth_factor

In case you are not familiar, wiki covers is well enough.

http://www.ncbi.nlm.nih.gov/m/pubmed/14624758/

It has been long known that inflammation is associated with VEGF and angiogenesis. I do wonder if this is part of the reasoning why other neurological disease have high association with ccsvi as we know it.

I can't see how inflammation within the brain would cause issues with the valves at the base of the jugulars at the base of the neck. That's a fair distance away. Personally I have low inflammatory MS, to the extent that I had one relapse in five years and no oligoclonal bands in my spinal tap, but had severe bilateral jugular stenoses (and the cogfog and fatigue and vision issues to go with it). There are also patients with low-inflammatory progressive disease who have stenoses.

The vascular researchers have enough expertise to recognise intraluminal abnormalities that are truncular malformation for what they are.

Sure. I am not arguing. I thought it was interesting. Inflammation can come and go. It doesn't need to be constant to do it's Thing. I am just saying ccsvi and MS could possibly be independently triggered by inflammation. Either that or you were just born with ccsvi.

It would be interesting to imagine an autoimmune condition of the valves, similar to the autoimmune theory of the brain and eyes. But such an autoimmune condition would strike not just the valves of the jugulars but all valves throughout the body, including the heart. If it were an autoimmune condition against the collagen of the valves, that would have even further targets throughout the body. I know someone who suffers from lupus, which attacks throughout the body but not the brain/spinal cord. And here I am, with MS which attacks the brain/spinalcord/eyes and leaves the rest of the body alone.

My body only attacks things that are locked securely away, like the inner fluid of the eye and the brain behind the blood brain barrier. That indicate, imo, a failure of the barriers; the brain is locked away for a reason. Delicate tissue. There never was a good explanation for me before for my eye issues (optic neuritis and pars planitis) when there is no myelin on the optic nerve or in the vitreous inside the eye. Dr. Diana's presentation on venous congestion of the fundus explains a lot, as well as explaining the relief I've had in my eyes since my procedure.