CCSVI - Pride and Prejudice

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby robbie » Wed May 12, 2010 7:46 am

Malden seems like you know alot about CCSVI can you tell me how with blockage in the jugulars the opposite to Hypo-perfusion can happen thanks for any explanation
Had ms for over 19 years now.
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Postby cheerleader » Wed May 12, 2010 7:55 am

Chronic Cerebrospinal Venous Insufficiency is a chronic, ongoing event. As Budd-Chiari sometimes takes 30 years to show damage to the liver, CCSVI takes a long time to show damage to brain and spine- This correlation was made by Dr. B.B. Lee, vascular surgeon in 2009. Much has happened in vascular studies since the 1920s. The reality of hypoperfusion is being defined now that we have better methods of imaging.

This has happened with the portal vein--
The literal definition of portal hypoplasia is underdevelopment, incomplete or arrested development of the portal vein. Portal venous hypoperfusion, is a more appropriate descriptive term.

Definitive Imaging: Until recently, the definitive gold standard for PSVA diagnosis was portovenous venography, with portography completed in right and left lateral and ventrodorsal recumbency. PSVA have been missed when only a single lateral or VD image was recorded.

Ultrasonography: Ultrasonography can detect "classic" features: small liver, hypovascular intrahepatic portal system, large kidneys, uroliths, and in 60 to 90% of cases (depending on ultrasonographer skill) identification of an aberrant shunting vessel. Doppler color flow interrogation identifies PSVA associated turbulence in the vena cava. Otherwise, a slow, tedious, systematic search of the portal vasculature is required.

link to portal venous hypoperfusion

We know MUCH more about hypoperfusion today, in 2010- thanks to BOLD and SWIM MRI technology and Dr. Haacke. (we have also spoken about hypoperfusion, and he understands it better than I. Look for papers from him in the coming months.) We also have doppler ultrasound which identifies turbulence in veins. This is new research, and we know it is linked to MS. Study of the venous system has been woefully inadequate. Any vascular doctor or imager will admit to that.

Anecdotally, my husband did have small, tortured curly collateral veins when supine. Dr. Dake explained that they were insufficient (thus the I in CCSVI) to take blood back to the heart. Collateral veins are the sign of venous insufficiency. If he didn't have collaterals, he'd be dead. Instead, he had inefficient collaterals, and he had MS. After his jugular occlusions were opened, the collaterals disappeared, and the rate of return was better.

I am not a vascular doctor, but I speak and correspond with some of the best, and they understand hypoperfusion better than I ever will. I try to share some of the research and that understanding in layman's terms. There is a language barrier here with Alan Malden, and I think that's a large part of our problem....but if he does not read the current research that I and others have linked on hypoperfusion, we really are speaking two different languages...
hope that helps-
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby 1eye » Wed May 12, 2010 9:31 am

I have been reading this thread. I have not read Krogh, but I see nothing to contradict what he said above. The limiting factors in perfusion are the number of capillaries that can open, the oxygenation of the arterial blood, the availability of matching vein and artery capacity, as well as pressure on either side of the capillary, viscosity of the blood, compliance of the artery and vein walls, and availability of alternate venous and arterial routes. I think in the most common cases of CCSVI, vein area is limiting.

As far as pressure goes, the arterial side is high pressure compared to the venous side. The vein pressure hovers about a balanced level, and sometimes goes positive. It is balanced by muscular pumping downwards, and by gravity, so that the net effect should be that there is enough transit time, for enough oxygen and food, for the current activity, to be absorbed. Since the venous pressure can go temporarily above zero, it has to remain negative for long enough to result in a net flow down, There has to be enough flow through both total vein area available, and enough open capillary area, or we will never get back to the heart and lungs. Capillaries open and close, veins not a lot. Some become constricted, and that can only be corrected by corollary growth. The growth of corollaries may be why there is remission, just as restenosis may cause relapse.

The blood can slow down, if the vein area is too small. The result will be a pressure increase above the stricture, as blood is still passing through, and gravity, plus pumping still occur (sometimes with not much pumping). When prone, there is likely to be far less downward force (it's now mostly sideways), so pressure from the heart will more easily result in a momentary positive pressure, especially if it occurs when there is less instantaneous arterial pressure because your heart has relaxed, and less average arterial pressure, because you are asleep. Like many things, timing can be important.

If this average brain/neck vein pressure gets too far positive, the result will be slowing down of the blood volume passing through, even if by whatever mechanism all capillaries are open. Veins being all open will help, in this situation, which is why venoplasty works most of the time. It is much more likely to happen when you are prone. Positive pressure occurs, either by regurgitation from the heart, or by thoracic pumping, or both. This is otherwise known as reflux.
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'MS' is over - if you want it
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Postby BooBear » Wed May 12, 2010 11:26 am

I am open to debate on this topic, as we all are, because we all want to be better. We all want to be cured.

I have 36- THIRTY SIX- lesions in my brain. Two new ones in the past six months in the anterior body/genu of the corpus callosum and left middle cerebeller pendacle. The new lesions did not come with any relapse; the asymptomatic progression of the disease seems to indicate the onset of SPMS.

I am participating in a clinical trial for oral cladribine with Avonex weekly therapy. No results.

I have been on IV steroids a total of 14 times. Two of those times were for 5 day stretches; the other for three. No benefit; coming off of the drugs was excrutiating. I even obtained some hairline fractures in my spinal vertebrae from the leeching of calcium that Solu-medrol can do.

I was diagnosed in 2004. And I am done gambling on pharmaceutical theories.

An antigen for the auto-immune response has never been identified, yet we subject ourselves to needles, drugs (and their side-effects) while our disease progresses. Even the medical community refers to the drugs as "disease modifying", yet offer no explanations when the drugs do not modify the disease. All I have seen the neuros do is up the ante to another, or stronger, drug.

Enough.

Has it occurred to you that the autoimmune response may be warranted? That if excess iron is in my brain, cozying up in the myelin, that my immune system is doing its job by eating away at the iron to get it out?

Look at it this way. RevImmune, which destroys the white blood cells through high doses of chemo, also proved to have positive responses. Yet there are still recurrences of the disease with RevImmune- perhaps because the problem has not yet been fixed.

If the veins are the issue, then why not unclog them? What could it hurt to have the same free-flowing blood in our veins as everyone else? Why not allow those of us that have the issue to get resolution? If the worry is truely recurrence, then how are we getting treated at all?? Is there any therapy out there that guarantees no more relapses? No- because if such a therapy existed, we would all already be on it.
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Postby ndwannabe » Wed May 12, 2010 11:31 am

Oh, and bumble bee is NOT supposed to be able to fly.

According to our immense knowledge, logic and calculation.
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Postby vivavie » Wed May 12, 2010 11:58 am

Aside from "Mine is bigger than yours!" part, I don't understand the WHY part! I am right there with Johnson. If all this talk about capillary is preventing you to take action either you're really scare or you don't have ms or it is not bad enough yet.

I tried Rebiff, Copaxone, Tisabri and chemo (Mito) for 2 years each and it did not work. Before the chemo I was having 3 to 5 attacks per year. I would take 2 cancers in exchange for my ms (I'm allow to say that because I almost did not make it 15y ago) On Feb 15 they stop looking for a 2nd cancer, I took 2 weeks vacation then started looking into CCSVI. I was lucky, everything went really really fast.

I was liberated (1 stent) in Poland on April 25. I did not have a WOW liberation but it is still much better than before .

For some of us life with ms is not a life. You are definitely not there yet...

You sound like those really small dog that barks real loud (red green blue letters) because there are soooo scared.
Happy mother'93, cancer survivor'95, angry ms'er'00 and... neuro daughter'63
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Postby AMcG » Wed May 12, 2010 1:14 pm

Hi Malden

Seems like you have stirred up a bit of a hornet’s nest.

My point 4. Venous blood can easily open a capillary is based on this statement from Krogh’s Nobel Lecture:

“very low venous pressure is sufficient to fill capillaries whose walls are flaccid, while the high arterial pressure cannot force entry into a contracted capillary.”

Alan
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Postby malden » Thu May 13, 2010 12:05 am

AMcG wrote:Hi Malden

Seems like you have stirred up a bit of a hornet’s nest.

My point 4. Venous blood can easily open a capillary is based on this statement from Krogh’s Nobel Lecture:

“very low venous pressure is sufficient to fill capillaries whose walls are flaccid, while the high arterial pressure cannot force entry into a contracted capillary.”

Alan


Seems like you extract one sentence from context. Its part of experiment on frog tongue. Totaly different context than you implied.

Whole paragraph is:

First, I have attempted to solve the question as to whether capillary changes in the tongue of the frog are independent of the arteries. When the tongue of a frog is spread across a glass slide, it is a particularly suitable specimen for investigation. It is translucent and, on one side, a smooth mucous membrane is found, with a widely distributed capillary network, in which the individual capillaries are readily responsive to excitation, and where both the small arteries and veins can be observed directly. So long as the tongue is not excited, the great majority of these capillaries are closed, and the tongue is extremely pale and bloodless. It is well known that mechanical irritation of human skin by, for example, a scratch from a needle, produces a red streak, because the vessels fill with blood. A corresponding reaction can be produced very easily on the tongue of the frog, and under the microscope one can show that this depends, in the first instance, on capillary dilation, and one can bring about dilation of a single capillary, or part of a capillary. Fig. 8 shows such a capillary, part in uninfluenced condition, part after it has been lightly scratched in the middle. Fig.9 shows how it is further possible to find a completely closed capillary by careful scratching along a tiny venous branch (v). Blood passes out from the vein, and fills a part of the capillary, but does not flow through. By further scratching, one can obtain the capillary filled bit by bit, until it makes connection with an open capillary or artery, when flow suddenly commences. This experiment is important because it shows that the very low venous pressure is sufficient to fill capillaries whose walls are flaccid, while the high arterial pressure cannot force entry into a contracted capillary.


Image
Fig. 9. Effect of repeated mechanical irritation on the tongue of the frog (v = tiny venous branch).

...conclusion:

This behaviour is of great theoretical and practical importance. One can conclude from this and from many other analogous facts that, when appreciable capillary dilation occurs, it cannot be because of a simple rise in arterial blood pressure but must depend on change in condition of the capillary walls - a relaxation of their contractile elements. Widening of the arteries, on its own, only leads to a higher pressure in the capillaries, and a more rapid flow of blood through them. The greater or lesser red colouration of an organ depends, in the first instance, on the blood content of the capillaries, and one is therefore justified in concluding that, in all such cases, where there is marked redness, we are dealing with widened capillaries. However, only closer examination can give information as to whether, at the same time, the arteries are widened, and capillary pressure is also high. The capillaries in human skin become, for example, widened with strong heat and by excitation with strong light, and with different emotions, while cooling to a certain level and psychological depression results in contracted capillaries. The detailed mechanism of these reactions has not yet been studied. By various chemical agents, the capillaries can be made to dilate, and urethane, for example, in fairly strong solution, causes very great dilation of the capillaries of the frog's tongue, while it has no effect on the arteries. With urethane, one can produce the situation depicted in Fig. 10, where blood is pumped out from a very narrow artery into a capillary, which widens more and more, and retains all the blood corpuscles it receives. The capillary walls widen so forcefully that they become permeable to blood plasma, so that the capillary is at last filled by a solid mass of corpuscles. This observation is not irrelevant to the problem of oedema, and is at the moment being more closely investigated by my colleague, Dr. Harrop, along the lines of a determination of the size of openings which appear in the walls of the capillaries. Suitable substances are introduced into the blood through a vein. A group of capillaries in the tongue of the frog can be caused to dilate themselves, and observations made on the substance passing out through the capillary walls. If the colloidal dye "vital red" was administered, followed by application of urethane, a fine red stripe appeared alongside the widened capillary. If Indian ink, whose particles are on the borderline of the microscopically visible, was administered, the widened capillaries showed themselves closed towards that substance. We have similarly ascertained that molecules of starch can pass through.


....So, your point:

My point 4. Venous blood can easily open a capillary

can be:

My point 4. Venous blood can easily open a capillary after it has been lightly scratched (with a needle).

But we don't stratch our brain with a needle, aren't we?

M.
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Postby HappyPoet » Thu May 13, 2010 12:44 am

Malden,

Unfortunately for you, I was an English professor in my pre-MS life, and since I easily pegged you as a fraud, I owe it to the TIMS' community to expose you for the fraud that you are.

Your lame attempts at pretending not to be a native user of American English give us a clearer picture of your real personality and your possible motivations.

Since you're probably dying to know how I discovered the truth about you: Inattention to details (highlighted by your overconfident, sophomoric efforts) and over-kill (highlighted by your unsophisticated, soporific efforts) blew your cover.

You go beyond the definition of "outlier" which puts you into the category of "fraud." Why, with over ten years of participation on MS forums and with having read an estimated 20,000 posts (10 posts/day for 200 days/yr for 10 yrs) from hundreds of real MSers, you're the very first fraud of this type that I've had the pleasure to "out," so to speak.

You might find this tidbit interesting . . .

Oddly enough, two days ago, I "outed" another fraud, and now for the really interesting part: You fake that you do have MS and hide that you can write English well, and he fakes that he does not have MS and shows that he does write well. You two are opposite frauds -- I'd introduce you to him, but I just can't shake off the feeling that you two might be the very same person.

Have a nice day, Malden!

~HappyPoet
.
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Postby costumenastional » Thu May 13, 2010 12:48 am

HappyPoet love when you are doing this man...

check out my blog to SEE something more interesting rather than frogs and drawings haha
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Postby sbr487 » Thu May 13, 2010 1:20 am

HappyPoet wrote:Malden,

Unfortunately for you, I was an English professor in my pre-MS life, and since I easily pegged you as a fraud, I owe it to the TIMS' community to expose you for the fraud that you are.

Your lame attempts at pretending not to be a native user of American English give us a clearer picture of your real personality and your possible motivations.

Since you're probably dying to know how I discovered the truth about you: Inattention to details (highlighted by your overconfident, sophomoric efforts) and over-kill (highlighted by your unsophisticated, soporific efforts) blew your cover.

You go beyond the definition of "outlier" which puts you into the category of "fraud." Why, with over ten years of participation on MS forums and with having read an estimated 20,000 posts (10 posts/day for 200 days/yr for 10 yrs) from hundreds of real MSers, you're the very first fraud of this type that I've had the pleasure to "out," so to speak.

You might find this tidbit interesting . . .

Oddly enough, two days ago, I "outed" another fraud, and now for the really interesting part: You fake that you do have MS and hide that you can write English well, and he fakes that he does not have MS and shows that he does write well. You two are opposite frauds -- I'd introduce you to him, but I just can't shake off the feeling that you two might be the very same person.

Have a nice day, Malden!

~HappyPoet
.


it was pretty obvious from the beginning that Malden was masquerading, sprinkling his response with spelling errors to cloud his real face ...
The sentences, punctuations were perfect but only spell errors. I have not come across such non native people ...
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Postby Johnson » Thu May 13, 2010 1:33 am

It won't engage you when it knows you can see it, HappyPoet. It's wasting the energies of real people. Nice call-out. The lexical loping is a lie.

vivavie - it was a joke that begged to be expressed. But you knew that. Grin
My name is not really Johnson. MSed up since 1993
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Postby malden » Thu May 13, 2010 1:39 am

HappyPoet, (are you a realy happy poet?)

you can join your efforts to discovery my real indentity with Gordon, he is also curious who I working for. He send me Private Message:

From: Gordon
To: Malden
Posted: Tue May 11, 2010 11:41 pm
Subject: Hi
Malden, you joined just a few days ago, who do you work for by the way??


You two can be nucleus of the TIMS secret branch "Frod Slayers"

Keep looking, there are many of us here and there....

M.
malden
 

Postby sbr487 » Thu May 13, 2010 1:52 am

Malden wrote:HappyPoet, (are you a realy happy poet?)

you can join your efforts to discovery my real indentity with Gordon, he is also curious who I working for. He send me Private Message:

From: Gordon
To: Malden
Posted: Tue May 11, 2010 11:41 pm
Subject: Hi
Malden, you joined just a few days ago, who do you work for by the way??


You two can be nucleus of the TIMS secret branch "Frod Slayers"

Keep looking, there are many of us here and there....

M.


WOW look at the english ... what a transformation in just a few weeks ...
Reminds me of K-PAX movie ...
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Postby malden » Thu May 13, 2010 2:01 am

Johnson,

Unfortunately for you, I discovered the truth about you: Your name is not really Johnson.

I will report my discovery emediatly to Frod Slayer Sqad.

M.
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