Posted: Sun Sep 06, 2009 8:47 am
Hi Cure,
I'd like to comment on the idea that maybe the veins collapse because of low flow. I am sorry but that idea makes no sense, because a stenosis is not an area of low flow. It is an area of restricted flow.
Imagine a hose made out of a soft flexible stretchy latex or something. Imagine that you have a pump pulsing fluid continuously through it so you can see it swell as the pulse of fluid travels down it now imagine in one area you put hard metal sheath over the hose that was the same size as the empty hose.
As the water flows through it gets stopped up in that area because it is not flexing as it should, the pressure builds up behind the sheath area and in fact on the other side of it when the blood DOES get through it makes turbulence.
Stenosis in the veins is like that.
This IS the way it is rather than a low flow situation because we have the pressure readings from the venograms. There is high pressure behind it and turbulence on the other side. If it were low flow the readings would be low.
As for the idea that maybe collaterals form first that Terry had, what causes them is hypertension in a localized area. The research into that is not "proven" but what it appears to happen is that the blockage in the vein results in local hypertension and a variety of cytokines etc are up-regulated as a result, and this allows smaller veins nearby to change so they can take the over load. Ordinarily these smaller veins are not visible because they are tiny small things, but when they take the extra load they suddenly become visible on venogram and they look like a spider web of veins going around the stenosis.
The proof that this does not happen first is that when the stent is put in the collaterals disappear immediately--while you are on the operating table. The pressure differential changes immediately also.
It happens because the blood is taking the path of least resistance--the stent. Because of that, the collaterals suddenly have the normal amount of blood in them and they no longer appear on the venogram.
This is one way the stenting doctor knows he was successful and Dr Dake considers it the most important evidence that the operation was successful even though he also has evidence of reduced pressure across the stenosis. We do love our numbers and something like "pressure behind the stenosis before surgery was 8 and after it was 3" sounds good (they were checking that while I was on the table), but when I asked Dr Dake for the details on that stuff he was like "Oh I know we were successful because the collaterals collapsed, that is really the most important evidence."
So it is what it seems to be at least with regards to the stenosis, although what exactly is causing the stenosis is still up for research.
Obviously there is an immense amount of work to still be done, I am just grateful that they have a new direction to look and can spend their energy on these important findings rather than spending all the time looking at autoimmunity.
My personal belief is that many things can cause the stenosis in an individual but the reason it is MS and not, say, May-Thurner is the location of the stenosis, NOT something special about the stenosis.
We have Cat now with a cyst, Lew with double jugs, me and Jeff with tight jaw, Mark with pigs tail twist in his vein, the varaitions are NOT the same thing, but the common thread is blocking drainage from the brain.
I honestly think it is too narrow to say that because of these findings MS is now going to be some weird disease that causes a particular kind of stenosis. It may be, but it also may be that there are a half dozen ways a person can have a stenosis that could cause this.
Obviously as research goes forward we will learn so much about these things that are speculative at this point. I think it is natural to speculate about what causes the stenosis and it will be interesting as some answers start to come in on that aspect of this
I'd like to comment on the idea that maybe the veins collapse because of low flow. I am sorry but that idea makes no sense, because a stenosis is not an area of low flow. It is an area of restricted flow.
Imagine a hose made out of a soft flexible stretchy latex or something. Imagine that you have a pump pulsing fluid continuously through it so you can see it swell as the pulse of fluid travels down it now imagine in one area you put hard metal sheath over the hose that was the same size as the empty hose.
As the water flows through it gets stopped up in that area because it is not flexing as it should, the pressure builds up behind the sheath area and in fact on the other side of it when the blood DOES get through it makes turbulence.
Stenosis in the veins is like that.
This IS the way it is rather than a low flow situation because we have the pressure readings from the venograms. There is high pressure behind it and turbulence on the other side. If it were low flow the readings would be low.
As for the idea that maybe collaterals form first that Terry had, what causes them is hypertension in a localized area. The research into that is not "proven" but what it appears to happen is that the blockage in the vein results in local hypertension and a variety of cytokines etc are up-regulated as a result, and this allows smaller veins nearby to change so they can take the over load. Ordinarily these smaller veins are not visible because they are tiny small things, but when they take the extra load they suddenly become visible on venogram and they look like a spider web of veins going around the stenosis.
The proof that this does not happen first is that when the stent is put in the collaterals disappear immediately--while you are on the operating table. The pressure differential changes immediately also.
It happens because the blood is taking the path of least resistance--the stent. Because of that, the collaterals suddenly have the normal amount of blood in them and they no longer appear on the venogram.
This is one way the stenting doctor knows he was successful and Dr Dake considers it the most important evidence that the operation was successful even though he also has evidence of reduced pressure across the stenosis. We do love our numbers and something like "pressure behind the stenosis before surgery was 8 and after it was 3" sounds good (they were checking that while I was on the table), but when I asked Dr Dake for the details on that stuff he was like "Oh I know we were successful because the collaterals collapsed, that is really the most important evidence."
So it is what it seems to be at least with regards to the stenosis, although what exactly is causing the stenosis is still up for research.
Obviously there is an immense amount of work to still be done, I am just grateful that they have a new direction to look and can spend their energy on these important findings rather than spending all the time looking at autoimmunity.
My personal belief is that many things can cause the stenosis in an individual but the reason it is MS and not, say, May-Thurner is the location of the stenosis, NOT something special about the stenosis.
We have Cat now with a cyst, Lew with double jugs, me and Jeff with tight jaw, Mark with pigs tail twist in his vein, the varaitions are NOT the same thing, but the common thread is blocking drainage from the brain.
I honestly think it is too narrow to say that because of these findings MS is now going to be some weird disease that causes a particular kind of stenosis. It may be, but it also may be that there are a half dozen ways a person can have a stenosis that could cause this.
Obviously as research goes forward we will learn so much about these things that are speculative at this point. I think it is natural to speculate about what causes the stenosis and it will be interesting as some answers start to come in on that aspect of this