"whining about neurologists"

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

Postby Cece » Fri Jan 14, 2011 8:07 am

marcstck wrote:The entire section of that post devoted to Zivadinov's presentations at ECTRIMS was presented to Dr. Z for his approval and to ensure accuracy before it was posted on my blog. All of the verbiage in the post regarding Dr. Z and his conclusions were okayed by the man himself.

I remember that now, I knew it was solid, that's why I brought it up here.

In your assessment, Marc, and I know this is simplifying things, but would you say Zivadinov is or isn't "behind" CCSVI?

Not sure if that can be answered, it's such an oversimplification.
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Postby cheerleader » Fri Jan 14, 2011 8:26 am

Sorry, Cece...you really got his blood boiling. Tell him that cortisol is not good for his endothelium...he should be careful! :-)
1. Zivadinov is addressing the insufficiency of MRV in detecting CCSVI in a few new publications. This is an inside argument between the doctors regarding MRV vs. doppler. Zamboni asserts the same thing. The Haacke protocol is very different than stagnant MRV, it shows flow, not just architecture. These doctors will need to battle it out, and they will in the ISNVD.
2. Jeff had no brain atrophy, yet slowed perfusion. He did have over 20 lesions, which are now shrinking. (I might suggest that Jeff's large amount of lesions and immune response actually protected his brain from axonal death and atrophy, as asserted by the Weizmann Institute's study on the protective autoimmune response in MS, but that's another thread) Perfusion deficit has not been linked to specific atrophy in MS. It is being linked to slowed blood flow thru the Haacke protocol.
3. Bee stings, scorpion stings, HBOT, Swank diet, prokarin, and all of the treatments neurologists love to mock are effective at symptom relief because they address MS from the vascular side. Every one of these treatments enhances NO, endothelial function, creates vasodilation and helps heal the BBB. But angioplasty for CCSVI is attempting to address the cause.
more to come at the ISNVD meeting that's been linked on this thread.
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Postby 1eye » Fri Jan 14, 2011 10:48 pm

It seems to be the opposite of ad-hominem; whether Dr. Zivadinov approved some text doesn't make it true or false. Does anybody have an answer to my question about genetics?

From your blog:
If CCSVI were the cause of MS, the researchers would expect that a constant level of vascular abnormalities would be seen across the entire spectrum of disability levels and duration of disease among patients studied, which is not what their studies demonstrated.


I still don't see how that follows. How does a constant level of abnormalities predict variation in disability and duration anyway? Certainly I don't see anything in that to prove, support, or even hint whether or not "CCSVI were the cause of MS."
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Postby marcstck » Sat Jan 15, 2011 12:59 am

1eye wrote:It seems to be the opposite of ad-hominem; whether Dr. Zivadinov approved some text doesn't make it true or false. Does anybody have an answer to my question about genetics?

From your blog:
If CCSVI were the cause of MS, the researchers would expect that a constant level of vascular abnormalities would be seen across the entire spectrum of disability levels and duration of disease among patients studied, which is not what their studies demonstrated.


I still don't see how that follows. How does a constant level of abnormalities predict variation in disability and duration anyway? Certainly I don't see anything in that to prove, support, or even hint whether or not "CCSVI were the cause of MS."


The assumption is that if the venous abnormalities were congenital, they would not vary in severity in accordance with the severity of the patient's disease profile. In other words, the severity of venous abnormality would be expected to remain the same, if these abnormalities were congenital, throughout the course of a patient's disease progression.

Instead, it was found that the severity of vascular abnormality increased with the severity of disease progression, indicating that either worsening stenosis created worsening disease, or worsening disease created worsening stenosis. Congenital abnormalities wouldn't be expected to behave in such a manner.

The congenital model of CCSVI states that over the course of decades, vascular abnormalities present at the time of birth lead to an ever increasing amount of central nervous system damage, which remains subclinical for several decades until becoming symptomatic and consequently diagnosed as MS. Such abnormalities would not be expected to worsen with disease progression, as they'd be genetically hardwired into the anatomy.
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Postby Cece » Sat Jan 15, 2011 11:16 am

In contrast, vascular malformations have a quiescent endothelium and are considered to be localized defects of vascular morphogenesis, likely caused by dysfunction in pathways regulating embryogenesis and vasculogenesis (Table 1). Vascular tumors can regress or persist depending on their type. Vascular malformations never regress, they persist throughout life. Most of them have commensurate growth during childhood, and some worsen over time if not treated (11, 17). Differentiating between vascular tumors and malformations is essential as not only their clinical, radiological and pathologic features and their morbidity, but also their management are quite different.
http://assets.cambridge.org/97805218/48 ... xcerpt.htm

It's yet to be shown but it seems reasonable that CCSVI may be among the category of vascular malformations that worsen over time. Cheer has discussed the effects of hormones, such as at puberty, on vascular malformations.

cheerleader wrote:Sorry, Cece...you really got his blood boiling. Tell him that cortisol is not good for his endothelium...he should be careful! :-)

He got my blood boiling too.... :wink:

We'll see how the next appointment goes. After that I won't see him for another year, it'll be interesting to see how he progresses in his thoughts on CCSVI, if he does progress.

I started off with a different neurologist, who I didn't really care for one way or the other; when I moved onto my current MS specialist, I liked him a lot better. He put up with a few years of me telling him I did not have MS (since some of my symptoms stretch back to childhood, since I am so stable) with kindness, despite his own (correct) opinion being that I had MS. He diagnosed my pars planitis which had previously been missed. He encouraged me when I had to choose between nursing my third child or going back on Copaxone; I ended up nursing for a full year. So just talking about this one appointment that went badly doesn't account for all those earlier things that have gone well. I am getting good care from him for my MS but will have to keep on top of CCSVI developments on my own...and of course revisit this choice if I end up stressed after every appointment with him.
Last edited by Cece on Sat Jan 15, 2011 12:22 pm, edited 1 time in total.
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Postby cheerleader » Sat Jan 15, 2011 12:21 pm

marcstck wrote:
Instead, it was found that the severity of vascular abnormality increased with the severity of disease progression, indicating that either worsening stenosis created worsening disease, or worsening disease created worsening stenosis. Congenital abnormalities wouldn't be expected to behave in such a manner.

The congenital model of CCSVI states that over the course of decades, vascular abnormalities present at the time of birth lead to an ever increasing amount of central nervous system damage, which remains subclinical for several decades until becoming symptomatic and consequently diagnosed as MS. Such abnormalities would not be expected to worsen with disease progression, as they'd be genetically hardwired into the anatomy.


Marc,
I love you....but you are wrong about this, and it's confusing people. Cece's right. I've referred to the BB Lee paper over a dozen times on this site. PLEASE read it. Truncular venous malformations are present at birth and worsen as the body ages. They grow as the body grows and have a growth spurt at puberty. DISTURBED BLOOD FLOW makes them worse. ENDOTHELIAL DYSFUNCTION makes them worse. This happens with age. Dr. Lee likens CCSVI to BUDD CHIARI disease, where the damage to the liver doesn't show up until the third or fourth decade even though the malformation is CONGENITAL. And the liver disease progresses with age, until the liver fails. Further studies need to be done....but IT MAKES SENSE to Dr. B.B. Lee, Dr. Laredo, Dr. Neville and the venous experts at Georgetown University.

CCSVI and venous malformations will get worse as the body ages and MS progresses.

HERE IS THE PAPER again. Sorry to yell, but we have to be careful about making medical pronouncements WITHOUT linking to RESEARCH. I've discussed this with the doctors, listened to them speak at conferences....I don't make stuff up or write bold pronouncements. I am not an "expert." I just collect information and put it online. If you find RESEARCH that refutes this, please post it.

http://www.fondazionehilarescere.org/pd ... 8-ANGY.pdf

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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby cheerleader » Sat Jan 15, 2011 12:37 pm

Again, here is the program for the 1st ISNVD meeting. I'm invited and hoping to go and report back. Being at the first conference in Bologna, Sept. '09 was a mind-opening experience.
The doctors will be discussing Dr. Zivadinov and Dr. Haacke's very different MRV protocols.
http://www.isnvdannualmeeting.org/

ISNVD ANNUAL MEETING // 1ST ANNOUNCEMENT //

// WHERE+WHEN
Ferrara, march 13, 2011 Italy
Vascular Diseases Center University of Ferrara - corso Giovecca 203

Bologna, march 14-15, 2011 Italy
CNR National Research Council of Bologna - via Gobetti 101

// MAJOR TOPICS COVERED
Ultrasound and MR imaging in treatment planning
The role of iron in MS and neurodegenerative disease
Perfusion deficits and hypoxia and possible relaitonships to CCSVI
Related vascular problems: venous embriology. idiopathic intracranial hypertension, normotensive hydrocephalus, carotid surgery in stroke
New evidence of CCSVI in animal models
CCSVI treatment: procedure and neurological outcomes
Genetic studies
Plethysmography
Flow dynamics: modeling the cerebral venous system
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby Cece » Sat Jan 15, 2011 12:54 pm

While I still think it is possible that CCSVI malformations or the veins affected by them may worsen over time, I couldn't find support for it in that paper, Cheer. When it talks about extratruncular venous malformations, these are affected by hormones or trauma and can grow, but it specifically states CCSVI as being in the truncular category which is a malformation of the already formed veins, with the malformation having occurred later embrologically and therefore the 'grow' switch/mesenchymal nature being turned off.

It could be that the CCSVI malformations are able to grow because the hypoxia of the underlying tissue of the malformation itself stimulates growth.

Or it could be that the malformations do not grow but that collaterals grow, which divert the blood flow and create the appearance on MRVs that there are worse IJVs as one ages but it's actually better compensatory routes.
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Postby marcstck » Sat Jan 15, 2011 1:21 pm

cheerleader wrote:
marcstck wrote:
Instead, it was found that the severity of vascular abnormality increased with the severity of disease progression, indicating that either worsening stenosis created worsening disease, or worsening disease created worsening stenosis. Congenital abnormalities wouldn't be expected to behave in such a manner.

The congenital model of CCSVI states that over the course of decades, vascular abnormalities present at the time of birth lead to an ever increasing amount of central nervous system damage, which remains subclinical for several decades until becoming symptomatic and consequently diagnosed as MS. Such abnormalities would not be expected to worsen with disease progression, as they'd be genetically hardwired into the anatomy.


Marc,
I love you....but you are wrong about this, and it's confusing people. Cece's right. I've referred to the BB Lee paper over a dozen times on this site. PLEASE read it. Truncular venous malformations are present at birth and worsen as the body ages. They grow as the body grows and have a growth spurt at puberty. DISTURBED BLOOD FLOW makes them worse. ENDOTHELIAL DYSFUNCTION makes them worse. This happens with age. Dr. Lee likens CCSVI to BUDD CHIARI disease, where the damage to the liver doesn't show up until the third or fourth decade even though the malformation is CONGENITAL. And the liver disease progresses with age, until the liver fails. Further studies need to be done....but IT MAKES SENSE to Dr. B.B. Lee, Dr. Laredo, Dr. Neville and the venous experts at Georgetown University.

CCSVI and venous malformations will get worse as the body ages and MS progresses.

HERE IS THE PAPER again. Sorry to yell, but we have to be careful about making medical pronouncements WITHOUT linking to RESEARCH. I've discussed this with the doctors, listened to them speak at conferences....I don't make stuff up or write bold pronouncements. I am not an "expert." I just collect information and put it online. If you find RESEARCH that refutes this, please post it.

http://www.fondazionehilarescere.org/pd ... 8-ANGY.pdf

cheer


Joan, I love you too, and I'm not being facetious about that. But to accuse me of making statements without medical backup is just plain wrong. I referred people back the my original post on WK, which links to the many abstracts at ECTRIMS that dispute CCSVI as a cause of MS. It also links to several that contradict this finding.

You refer time and time again to the same pieces of research, all conducted by a limited number of physicians, most of whom fall under Zamboni's umbrella. I have read the Lee paper, and believe it has merit, but it represents the opinions of one group. You have a large emotional investment in CCSVI, which I completely understand, but it seems clear that you tend to denigrate any research that contradicts your beliefs and venerate research findings that supports them. Given the weight of your influence among the CCSVI community, accusing me of confusing the issue is a bit of the pot calling the kettle black.

You're not the only one who has spoken to a variety of well-respected doctors about these issues. I've done my due diligence as well, and stand by any statements I've made. I've consistently presented as balanced a view of the evolution of the CCSVI hypothesis as I possibly can, and have striven to not let emotion cloud perception. I'd love the hypothesis to prove absolutely correct, and completely revolutionize the perception and treatment of MS. I can't let that desire, though, cloud my take on the ever-expanding CCSVI knowledgebase.

As it now stands, nothing definitive can be said about CCSVI, and we can only go where the science leads us. In Dr. Zivadinov's case, the science is leading him away from believing that CCSVI is the cause of MS, as can be gleaned from the steady stream of research, and Dr. Z's conclusions of that research, coming out of BNAC.

As for links to research, here are a few. Their conclusions are open to debate, as are the conclusions of any scientific research, but to dismiss them outright is folly.

http://registration.akm.ch/einsicht.php ... KEN_ID=900

http://registration.akm.ch/einsicht.php ... KEN_ID=900

http://registration.akm.ch/einsicht.php ... KEN_ID=900
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Postby Cece » Sat Jan 15, 2011 1:31 pm

On the facebook site, it was just said that in a personal email with Dr. Zivadinov, he has said that he believes CCSVI is central to the pathogenesis of MS.

Marc, when you say nothing definitive can be said about CCSVI...even my neurologist thought that a definitive association has been shown between CCSVI and MS.
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Postby MrSuccess » Sat Jan 15, 2011 2:00 pm

marc - I don't love you ..... but I sure in hell like you ... :wink:

I think Ringleader knows her stuff.

And we do not exchange Christmas cards ....... :P




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Postby zanne10000 » Sat Jan 15, 2011 4:02 pm

"I had brought up CCSVI a year ago and he blew it off, said it was way too soon, made some dismissive comments"

Same story here! This week, I had another f/u, told my neuro I was scheduled for Hubbard ("some guy in San Diego", lol) and was promptly told we were at a "philosophical impasse". But, at least my neuro (protecting the gender in case s/he happens to be a lurker) agreed to follow-up with me even though s/he doesn't agree with what I'm doing.
:(
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Postby cheerleader » Sat Jan 15, 2011 4:13 pm

Marc--
You said congenital venous malformations wouldn't worsen with age.
I showed research that says they do.
Truncular venous malformations can become worse with age and duration of disease and disturbed blood flow.
All of the reseach you linked shows CCSVI is worse in those with more with disease progression--which makes sense.
I made no argument as to causation in CCSVI (which is still being researched and further illucidated).

Dr. Lee is not under anyone's umbrella. He was the most vocal skeptic at the Bologna conference. He is a vascular doctor, as is Dr. Zamboni. Their research into venous malformations comes from a lifetime of vascular practice, not neurology, not imaging. But looking at actual veins. Seeing the webs, the septi, the aneurysms. Here is another paper he wrote on Budd-Chiari.
http://www.jvascsurg.org/article/S0741-5214(05)01420-5/abstract

The doctors who are researching and publishing in Phlebology and other vascular publications are independent experts in their fields. Again, there is no Zamboni umbrella. The fact that they are are not consulted or are denigrated in the ongoing neurological studies of CCSVI is a sad fact. Phlebology hasn't been considered an important medical field....but that may change.

cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby 1eye » Sat Jan 15, 2011 4:37 pm

Instead, it was found that the severity of vascular abnormality increased with the severity of disease progression, indicating that either worsening stenosis created worsening disease, or worsening disease created worsening stenosis. Congenital abnormalities wouldn't be expected to behave in such a manner.

The congenital model of CCSVI states that over the course of decades, vascular abnormalities present at the time of birth lead to an ever increasing amount of central nervous system damage, which remains subclinical for several decades until becoming symptomatic and consequently diagnosed as MS. Such abnormalities would not be expected to worsen with disease progression, as they'd be genetically hardwired into the anatomy.


On the contrary, I and a few others believe just that. I think it quite reasonable to think that vascular abnormalities will worsen over time, and we already know 'MS' does. Certainly a change that happened during development will not appear elsewhere after development is done, but as damage from the malformation occurs, the body will try to make thing better. That is one of the reasons collateral veins appear, and are expected. The remediation coming from the biological response to a malformation, increasing over time especially if the malformation causes more damage over time, will have varying success. The level of success is hard-wired.
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Postby Cece » Sat Jan 15, 2011 4:40 pm

cheerleader wrote:Marc--
You said congenital venous malformations wouldn't worsen with age.
I showed research that says they do.
Truncular venous malformations can become worse with age and duration of disease and disturbed blood flow.

Cheer, will you help me find where it says this, in this research or elsewhere? Do aplasia-type truncular vascular malformations worsen with age and/or duration of disease, would be the question.
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