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Has anyone seen any theories as to why stenoses occur? Are we born with them? If so, why doesn't MS start at birth rather than in the mid 30's.

CCSVI seems to be congenital, we are born with it and it gets worse over time because of aging and probably not good vascular diet/excercise.

I've read some theories on vascular congenital conditions and it seems that the diet of our parents before our conception matter, including vitaminD sunshine exposure during pregnancy.

My mum had plenty of sunshine and good diet when she was pregnant with me. So in addition to diet I think genes play an important role in CCSVI.

We are born with them, but there can also be injury to the veins from car accidents or gunshot wounds (the former more likely than the latter, at least in the circles I run in) or neck surgery or a few other things that will worsen the underlying condition. Simka has asserted that CCSVI slowly progresses over time, but it's hard to know why that is.

There was a genetic connection found in a paper released in April that showed a link between people with MS and a specific gene abnormality linked to venous malformations. This supports the "born with it" theory, as does the fact that these are often abnormalities like all-sorts-of-wrongness valves that can only result from being formed that way prenatally.

It takes thirty years, on average, before diagnosis because it's chronic slow damage. In Budd Chiari, a liver condition caused by insufficient venous drainage, it takes thirty years before diagnosis but by that time the liver is wrecked and needs a transplant.

Also anything that strengthens the veins (exercise, vitamin D, good diet) is good; anything that weakens them (EBV virus, etc) is bad, but these will only help or hurt to the extent possible dependent on how bad the underlying stenosis is.

At least that's how I understand it! Another significant point is the idea that it requires more than one stenosis to cause this sort of health issues. With just one, the body has alternate routes and can compensate. With 2 or 3 or 4 stenoses or valve abnormalities, including MT syndrome, the body's ability to compensate is overwhelmed.

Thank you for your replys.

another model is that ms causes ccsvi. In this case the 'clenching' that scarr cells do to close wounds would be acting wrongly on veins. Sure there are lots of scar cells washing down from the brain, but why would they stop in the jugulars?

Perhaps some incite into why we see more venous insuffiency in the 3rd decade and later has some similarities with the leg veins and the venous insufficiency seen in them ? We see the deposition of iron in leg veins during peripheral venous insufficiency-just like in CCSVI-
the cellular damage has a similar look under a microscope ( Zamboni mentions this in his first paper)

As for why its later rather than from birth- it perhaps has to do with how severe it is and I believe its multifaceted- a bit genetic- look at the patterns and structure of your veins and your same sex parent.......hhmmm see any similarity? My hands look just like my moms! When did that happen?

Then add in diet, amount of exercise,smoking, environmental exposures, general activity and weight, etc.

There is vein structure and vein health and both contribute I am sure.

theoretically impeded veins then can cause, flow impairment, decreased wash out of deoxygenated blood( which has increased CO2), increase in deposition of iron and other solutes, decreased brain glucose, etc.

the brain is designed to have efficient receipt of oxygen and glucose, and wash out of wastes and carbon dioxide- CCSVI is INSUFFICIENT-

during youth there is not the build up of the iron either over time it builds up?----

our bodies are designed to try to overcome inefficiencies-ie development of collateral circulation but sometimes over time the diseased state wins

The severity of the blockage and the location probably have a big influence in when the bad effects are experienced and they coincide with the location and severity of the MS symptoms AND disease course.

I wonder if in the future they screen with dopplers for risks.......just like screening for high lipids or high BP?

MegansMom wrote:I wonder if in the future they screen with dopplers for risks.......just like screening for high lipids or high BP?

Particularly for those who are high risk, i.e. with a parent or close relative with MS.

First I want to thank everyone who provided thoughtful answers to the question; why do stenoses occur. I don’t mean to beat a dead horse but this question is becoming even more perplexing to me. It isn’t just a question of why do we get stenoses, but why do they restenose even after they’ve been forced opened by angioplasty? Some forum participants even report restenosis after stents were installed. In this case it seems the vein beyond the stent closes up. Apparently this is an area that was not closed before. So now I have to wonder why our veins are so determined to engage in such a self destructive behavior. What force drives them to do this? And were we really born with closed veins or is there some mechanism that forces them to close later in life? Maybe whatever caused them to restenose also caused the original stenosis.

Elastic recoil and intimal hyperplasia. The first is the vein retaking its former shape, because it's spent 30+ years in it; think of a garden hose that pops back to how it was. The second is the response of a vein wall to an injury; it regrows like a wound on your arm or a scab might.

A lot of the 're-stenosis' could possibly be caused by the procedure itself. I've read that catheterization is the number one cause of IJV thrombosis, which can result in swelling of the neck and face. Has there been any cases of this yet??

Cece wrote:Elastic recoil and intimal hyperplasia. The first is the vein retaking its former shape, because it's spent 30+ years in it; think of a garden hose that pops back to how it was. The second is the response of a vein wall to an injury; it regrows like a wound on your arm or a scab might.

Elastic recoil I understand, but the intimal hyperplasia was a new one on me. After I looked it up, it sounds like you're probably right. Good find Cece! How did you know that ?

Thanks, David. Check out Dr. Sclafani's thread, it's all in there, including intimal hyperplasia. There's an index too maintained by AlmostClever if you want to jump to certain topics.

Billmeik wrote:another model is that ms causes ccsvi. In this case the 'clenching' that scarr cells do to close wounds would be acting wrongly on veins. Sure there are lots of scar cells washing down from the brain, but why would they stop in the jugulars?

I seriously disagree with this model, i've NEVER been able to tip my head back or upside down without passing out...