This Is MS Multiple Sclerosis Community: Knowledge & Support

The following is designed to promote discussion by patients and specialists alike. Please feel free to comment on the subject:-


What if CCSVI is actually a symptom not a cause? Has this actually been explored?

My partner underwent treatment for CCSVI in December 2010, like many other patients showed very promising real world physical results most of which gradually faded away again. We have decided to undertake an alternative form of treatment which I am documenting on this forum.

Why? How can a procedure produce such great results for them only to slip away again? Well maybe, just maybe we're treating another symptom.

CCSVI has raced forward in the two years since I've been aware of the theory, mostly caused by the freedom of information that the world wide web allows us. But what if we've all missed the obvious?

Think of the following:-

CCSVI is increasingly being attributed to congenitally malformed valves. The thing is, why would something you were born with not effect you for 20, 30, 40, 50 sometimes 60 years before becoming a problem? Surely there would be many more cases of children being diagnosed with MS or the condition would appear in far more younger people than it does.

Malformed valves is not a new problem - it's what causes varicose veins (Copy and paste from www.womenshealth.gov) :-

What causes varicose veins?
Varicose veins can be caused by weak or damaged valves in the veins. The heart pumps blood filled with oxygen and nutrients to the whole body through the arteries. Veins then carry the blood from the body back to the heart. As your leg muscles squeeze, they push blood back to the heart from your lower body against the flow of gravity. Veins have valves that act as one-way flaps to prevent blood from flowing backwards as it moves up your legs. If the valves become weak, blood can leak back into the veins and collect there. (This problem is called venous insufficiency.) When backed-up blood makes the veins bigger, they can become varicose.

The part I'm interested in here is "As your leg muscles squeeze, they push blood back to the heart". Consider the valve operation. What if they actually require external muscle activity to keep them healthy and operating? What would actually happen if the muscles surrounding the veins froze or ceased to operate or even simply started operating at a reduced level of functionality.Would the blood flow start to suffer due to muscle weakness/loss. Would the valves then start to suffer atrophy? Would there be a slow degradation in their operation that would lead them to cause what we currently understand as CCSVI?

Logically this would explain "restenosis", treating a symptom rather than a cause would explain initial good results that over a period of months regress.

From everything I've read published by the many centers now offering CCSVI treatment, there is a direct link with the severity and length of time a patient has had symptoms and the result they are getting. Therefore the reoccurrence will take longer for those patients that were less "unhealthy" beforehand. It wouldn't be beyond the realms of possibility that a patient with an EDSS like Emma of 6.5 will regress in 3 to 6 months and a patient with an EDSS of say 3 or 4 might take 3 to 6 years to regress. Seeing as we're only 2 to 3 years into this we don't have the data on the longevity in these cases.

Venous leg diseases are often congenital.
First symptoms / problems start in many cases in the age of 20-30.
MS has the same “timing”. This is a strong argument pro CCSVI as a major risk factor for triggering MS but clearly no proof.

Perhaps CCSVI may be caused by MS and the treatment only optimizes the functions of the damaged brain.

With the results of this link

http://www.ccsvi-tracking.com/index.php

there seems to be the tendency of slowing down (stopping?) the disease with a treatment of CCSVI.

For me in some(?) cases of MS there seems to be another origin for MS: some sort of liver dysfunction. Because there are a few anecdotal reports, that after a liver transplant the disease completely disappeared. I think there should be a small liver transplant trial, to get more insight if there really is some sort of a distorted liver metabolism.

R.

This my question though. Maybe all these "congential" venous diseases aren't congenital, maybe they are being casued by muscular or nerve related problems. It's just no one has ever had casue to investigate as we've all assumed it was congenital.

the bones surrounding a section of her left jug grew so small, even a fully expanded balloon could only get the vein to 4 mm. (verified by IVUS)

a valve in her azygos vein was completely grown shut. (verified by IVUS)

as a result of the two conditions above, sections of her right jug grew to over 20mm. (verified by IVUS)

unfortunately, 20mm was not enough. each time little baby Donna's heart pumped blood, her right jug had to carry the load. (a side note. her doctors always told her she had a very strong heart).

but her right jug couldn't handle all that blood. thus, since birth, she was introduced to "reflux caused by CCSVI". blood was pooling inside her brain, slowly attacking the BBB.(God's perfect poison. Slow and untraceable)

for over 20 years, she was a happy girl.

then one day, CCSVI won the battle and finally broke thru the BBB. Donna woke up blind.(another note. for the doctors. why is Optic Neuritis a very common first sympton? is it the first place attacked once the barrier is broken?)

again for over 20 years (Slow and untraceable), drugs were pumped into Donna and she recovered from each attack. but sadly, the reflux was still there and the BBB was still under attack. she slowly went from RRMS to SPMS.

now, i am no doctor and i certainly would not admit to being a neurologist. i am just a guy who learned about a disease called MS less than a year ago. just my simple opinion, but what i wrote above is the first thing i have read that MIGHT explain how MS developed in Donna.

again only my opinion, but the CCSVI surgery Donna got is the first thing i have read that gives HOPE that maybe the damage can be stopped and even reversed.

Has she had any imaging tests done since the improvements slipped away? Doppler or MRV? The first way to answer that question would be to see if the veins are no longer open.

We've known from the beginning, with Dr. Zamboni's research showing 50% restenosis of the veins visible on imaging as having closed up again, that this is a significant problem in CCSVI. It would be more easily managed (balloon them open again, just as is done for dialysis patients) if we weren't in a crazy-making situation where people are self-paying for these procedures and can sometimes only afford once.

My own emissary veins, which are a fetal drainage vein that are no longer needed once the jugulars develop and take over, are visible on flouroscopy and much larger than average. These veins go through little channels through the skull, which necessitate that the skull had to grow around them, so any enlargement of these veins took place during fetal development, prior to birth. In me, it is likely that CCSVI was a congenital condition.

As for why it takes so long for MS to appear, I think I have one tough brain and one strong blood-brain barrier to have held up pretty well against 36 years of the effects of slow drainage. I am however quite happy to have the siege ended, nutrients restored, focal points of hypertension no longer battering away at the bbb wall....

Emma had a re scan at 7 months post procedure. The valves had returned to the condition they were pre procedure.

Last month I called the Edinburgh Clinic where we had the procedure and had a chat with them about where we go from here. They then mentioned about their theoris of Jaw Misalignment, which independently I'd been researching also.

Emma is now going down this route and I have to say it's completely left field but an eye opener.

It is this treatment and conversations with Amir that are making me question the cause of CCSVI. I am staring to think it is symptom and the casue is a step further back.

Don't get me wrong, I think CCSVI is a big part of MS, but I'm starting to wonder if in all the excitement, everyone has assumed CCSVI is THE cause and no one has actually checked if there is something more fundamental that is causing CCSVI.

On Tuesday this week when I sat in a dentist surgery and watch a dental specialist fit a brace and move Emmas teeth and jaw into a position which completely stopped neuralgic pain. The previous week, after only seven days of having a simple lower brace fitted Emma's wandering left eye and resulting motion sickness was gone.

I'm simply starting to question some assumptions that we all have. Has anyone actually asked the question "What causes CCSVI?" as opposed to "Does CCSVI cause MS?".

Such a good question. I have asked myself the same thing. What is the starting point to MS/CCSVI? I am afraid it will be a long time before there is an answer.

There was the consortium of the international union of phebologists paper:
http://www.fondazionehilarescere.org/pd ... s-ANGY.pdf

And there's this one:
http://fondazionehilarescere.org/pdf/03-2518-ANGY.pdf
“Embryological background of truncular venous malformation in the extracranial venous pathways as the cause of chronic cerebrospinal venous insufficiency” by B.B. Lee, J. Laredo, R. Neville in International Angiology, 29(2), pp.95-108.

We also have the cleveland clinic autopsy study, which found equal numbers of venous stenosis (vein wall narrowing) in MS and nonMS cadavers but found a large number of intraluminal abnormalities almost exclusively in the MS cadavers. Specifically valves and septums were mentioned. More septums were found than I'd have expected, making me wonder if septums are underdiagnosed in us living patients. A septum is definitely a truncular venous malformation.

It's good to discuss. I think that CCSVI begets more CCSVI; the very conditions of CCSVI cause worsened blood flow that leads to further thickening. We have abnormal collagen in our jugulars.

Thats a bit of Light reading there Cece ,

You can see where I'm coming from though can't you. I've seen some things this week that have made me question things that I previously took as fact.

I've now realised they were assumed fact.

What if, and bear with me here, the causes of CCSVI are malformations of muscles and skeletal structures either from birth, or as a result of an accident or as a result of surgical intervention or as a result of something as simple as a wisdom tooth extraction. What we haven't considered is how the muscles and nerves act on the valves and viens.

I'm wondering if medicine has advanced to such a degree and spilt down into such minutia that we can't now see the wood for the trees.

I'm taking a completely sideways look at MS with the help of Amir and we're documenting where we get with this.

I'd like to encourage others to ask questions. It's the questions that lead to solutions.

Interesting comment about liver transplantation:

"How is organ rejection prevented? To keep your body from rejecting the new liver, you will take anti-rejection medicines, also called Immunosuppressive medicines. You will need to take anti-rejection medicines for the rest of your life."

supposition is fun, but research is best.

http://fondazionehilarescere.org/pdf/03-2518-ANGY.pdf
http://www.avidsymposium.com/pdf/vei/4772.pdf
http://ms.about.com/b/2011/10/25/a-ccsv ... ink-so.htm

the chicken and egg debate is being elucidated by Dr. B.B. Lee, Dr. Zamboni, Dr. Fox and many others.
truncular venous malformations, such as the ones found upon autopsy, are congenital.
cheer

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

interestingly, my mind continues to wander toward some oral surgery my wife had.

Oral surgery to have wisdom teeth removed in 2003. After this dental work she started suffering from tmj and now has tinitus pretty bad on that side where she has the tmj problems (we've always attributed the tinnitus to MS) Officially diagnosed with MS in 2006, yet after her diagnosis we realized the signs started around 2004 (weakness in legs, dizziness).

We went to NY earlier this year where she underwent CCSVI testing and treatment, had some small improvements but nothing lasting or major.

When she does any kind of physical exertion she said there is a 'whooshing' type sound on the same side as her tinitus.

I think we should take a closer look at the tmj/tinnitus from another specialist.....her wisdom teeth surgery was an ordeal, 2 dry sockets, bad infection and tons of pain. There may be something to this.

Thanks for the links Cheer. I read each one all the way through.

These are all postulations, in fact one of the documents even uses the word postulate. Or best guess if you like.

I'm asking, are they barking up the wrong tree? Which is actually quite a reasonable question to ask.

http://www.jvascsurg.org/article/S0741- ... 9/abstract

An article on the prevalence of congenital vascular malformations: 1.5% in the general population.
You would agree that these are all congenital conditions? Hypoplasia, aplasia, phlebectasia, aneurysms, and avalvulia? That last one sounds like it means absence of valves. Hypoplasia is sometimes seen in CCSVI. Phlebectasia can occur in the jugulars, and I have heard that pediatric jugular phlebectasia was treated by Dr. Zamboni in his early career by ligating jugulars. (!)

We agree that there is such a thing as a congenital vascular malformation, whether or not CCSVI is known to fall into that category?

It's a topic worth discussing, because if CCSVI is congenital, then it might be possible to treat it and be done. If CCSVI is not congenital, then there would possibly be ongoing conditions that would recreate the condition of CCSVI.

But I think the phlebologists have it right on this one.

Our stubborn veins seem to like to recreate the condition of CCSVI all on their own, through elastic recoil, returning to the positions that they are used to.

Or are there actual outside (physical) influences that cause the initial occurance and reoccurance rather than congenital deformation and elastic recoil post treatment?