This Is MS Multiple Sclerosis Community: Knowledge & Support

gee, me too. 18 years of MS is nothing to sneeze at, and since Dr Zamboni has not released his information just an interview in which he commented that people who are early in the disease do better, we'll be the first to talk about how we are doing in this paradigm out front and free of censure. poor wobbly is stuck with small cryptic notes only or jeopardise the project, but I bet he would like to talk a bunch about it just like we do. I wonder if he found our new home?

I don't mean to be a wet blanket, but it bothers me a little that conflicting ideas are being thrown around. Edemas are swelling; as the lesions seen with MS are demyelinating plaques (this has been observed on autopsies of MS patients), I don't see how the lesions could be edemas. And, if I understand Zamboni's papers, this isn't what he is claiming.

And, as it was explained to me, the stenoses in the veins are not causing an actual backflow, but an increase in venous pressure.

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No wet blanket needed, there is no disagreement, there's consensus here, it's just there is a misunderstanding and misuse in the medicalese- Chris, you're a bit off on what Dr. Dake has stated-

Just to clarify...it's NOT about venous pressure in the brain and spine, it IS about backflow, or "reflux." The stenosis block the flow of blood back to the heart and created reflux. The demyelinating lesions are not "edema", (which is swelling), but are created due to edema and reflux causing a break of the blood brain barrier and deposition of all kinds of things into the brain that shouldn't be there. This is what activates the demyelinating process.

The language is confusing, but the imagery is not. Like I said regarding our flooded house without drains...the brain and spine need release of the pressure of blood. "Perfusion" (which is transit time of blood in the brain), is slowed in MSers because there is not adequate drainage. Stenosis of the veins causes reflux which causes edema and slowed perfusion, which creates axonal degeneration and demyelination.

I hope that clarifies some of the language....
There is no disagreement, just some misuse of medical words.
I'm sure Dr. Dake did not say the lesions were edema....but they were created, in part, by edema. That's what we talked about last week.
AC

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

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no worries, Chris...I still get slammed by the medical words. Just picture my poor, flooded house without drainage- me cursing the wet vac while the water keeps pouring in. 10 grand later, some cool new french drains, no more flooded house
cheer

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

so where ever there is an edema there will be a lesion ?

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Had ms for over 19 years now.

No, Robbie...
Edema (swelling due to fluid accumulation) is only part of the picture of CCSVI. Slowed perfusion time, reflux, inflammation and a break in the BBB are all part of the scenario of lesion creation. I believe the lesions are only forming because axons are dying in the brain and spine, and the immune system is trying to clean up. (But the last part isn't fact in CCSVI, that's just my feeling)
AC

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

The oligodendrocytes are fragile they are separate cells that wrap the myelin around the axons. See it here:

CLICK FOR OLIGO

because of the thin connections between the axon and the oligo the oligodendrocyte is more vulnerable to damage. When the endothelium becomes leaky and the fluids and cells from the congested veins slips into the brain tissue, it is the oligodendrocytes that get hurt first, it is even possible that congestion, or edema and inflammation in the area can break the bonds between the oligo and the axon of the nerve.

From Schelling page 30. see research thread....



It is also known that in spinal cord injury there is demyelination.
FROM HERE
Spinal cord injury has an immense amount of inflammation/swelling/fluid in the area.

So even though we have not been taught to think in terms of edema or fluid or congestion as being the START of the MS process by causing demyelination, it is absolutely true that it can do that.

Go back to the picture of the oligodendrocyte and then imagine a lot of fluid gets in the area, pushing the structures apart. It is easy to see that the thin fragile threads connecting the oligo to the nerve could be the thing that breaks first, then the myelin dies because it is not attached to the oligo any more then the macrophages come and clean it up...... and all the stuff that was thought to be proof of an attack by the immune system is suddenly explained: the myelin filled macrophages, the dead myelin and the demyelinated nerve which functions poorly, the activated miroglia and the inflammation cascade.

This even explains why Prineas and Barnett, who looked at a young girl who died 17 hours into her MS attack found that the oligodendrocytes were dead but the immune system was NOT there yet. In fact the microglia were only starting to respond to the dead oligo. They concluded that MS is not autoimmune but something else is killing the oligos first.

this new model of CCSVI explains all that very nicely it seems.

I hope I made that easy enough and plain enough. marie

Great post Marie - you answered some of my questions,

When ms progresses is this just the CCSVI getting worse?

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Had ms for over 19 years now.

Sharon, oh Good! you're most welcome I enjoy figuring out answer to questions like that. It gives me a chance to challenge the model, since it is as yet unproven, no one should take it on faith.

I have a tough question....Why in some pregnant women does the MS seem to subside? The current theory is because of the hormones suppressing the nervous system. Surely CCSVI would get worse during pregnancy with all the extra strain of carrying a baby....also why do relapses tend to happen in the 3-6 months after birth if CCSVI is the cause and not the result of something else?

Marie should answer this -


But, I will try to answer ----
During pregancy the immune system is less active ( natural response to keep the body from rejecting the fetus). Soon after delivery the immune system starts to get active again. The immune system is going to act the same in any woman during pregnancy. If a woman has MS, her immune system is going to be less active just like anyone else.

This really would not relate to anything with CCSVI

Comments Marie?

IMHO, the pregnancy situation has less to do with the immune system in MS than the blood...I actually looked into this a bit when studying circulation....by the third trimester- check out how the blood changes in pregnancy. Volume is up by 50%! Fibrinolytic activity is depressed...more, thinner blood going thru the veins.


http://www.medstudents.com.br/ginob/ginob5.htm

These changes to the blood last until delivery, then blood levels return and relapses are more likely.

Marie...any thoughts?
AC

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