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I just hope those lesions are not hard as nails because of my age and are reversible. I will consider myself hitting the jackpot if I have no further disability though.

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?

chrishasms wrote: It was wild hearing him say that the lesions could be edemas from the backflow.

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.

123

patientx wrote:

chrishasms wrote: It was wild hearing him say that the lesions could be edemas from the backflow.

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.

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

1234

chrishasms wrote:Yes you are right on there and I was way off. I am so glad someone can correct my bassackwardness

I actually understand what and why this is going on and happening now! Thanks Cheer!

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

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.

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

robbie wrote:

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.

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

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

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....

neuropathologists have sometimes proposed that any edema in fact any intense vascular seepage or leakage into some part of the brain or spinal coord preferentialy damages the myelin sheaths. One researcher even posited that there is no demyelination other than that attributed to perivascular edema.

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?

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?

LR1234 wrote: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?

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.

Perhaps the most striking maternal phisiologic alteration occurring during pregnancy is the increase in the blood volume. The magnitude of the increases varies according to the size of woman, the number of pregnancies she has had, the number of infants she has delivered, and whether there is one or multiple fetuses.The increases in blood volume progress until term;the average increase in volume at term is 45-50%. The increase is needed for extra blood flow to the uterus, extra metabolic needs of fetus, and increased perfusion of others organs, especially kidneys. Extra volume also compensate for maternal bllod loss delivery. The average blood loss with vaginal delivery is 500-600ml, and with cesarean section is 1000ml.

Red Blood Cells The increase in red blood cell mass is about 33%. Since plasma volume increases early in pregnancy and faster than red blood cell volume, the hematocrit falls until the end of the second trimester, when the increase in the red blood cells is synchronized with the plasma volume increase. The hematocrit then stabilizes or may increase slightly near term.
Fibrinolytic activity is depressed during pregnancy and labor, although the precise mechanism is unkown. The placenta may be partially responsible for this alteration in fibrinolytic status.Plasminogen levels increase concomitantly with fibrinogens levels, causing an equilibrationof clotting and lysing activity.

Clearly, coagulation and fibrinolytic systems undergo major alterations during pregnancy. Understanding these physiologic changes is necessary to manange two of the more serious problems of pregnancy: hemorrage and thromboembolic desease, both caused by disorders in the mechanism of hemostasis.

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