If CCSVI is congenital...

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

If CCSVI is congenital...

Postby Shannon » Fri Feb 04, 2011 7:47 am

...then how about if we start trying to create the condition in mice using the different theories behind how it occurs. What would you start with? I would start by depriving impregnated mice of certain vitamins such as folic acid, vitamin D, etc., or perhaps just malnourishment during pregnancy, in general. Is it possible to get a pregnant mouse to smoke cigarettes? ;)

It seems like an obvious course in the research, if it ever gets going. Then, when the mouse progeny starts showing signs of CCSVI, a cause can be pinpointed and perhaps CCSVI can be avoided for some. However, I guess it really does nothing for those of us who already have the condition.
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Postby pairOdime » Fri Feb 04, 2011 8:02 am

Shannon,

The International Society for Neurovascular Disease (ISNVD) will discuss new evidence of CCSVI in animal models at their March meeting in Italy. We are very interested in this new evidence. As you mentioned, this is a big step.

This is linked on TIMS...
http://www.thisisms.com/ftopict-15423-isnvd.html

See this link for topics....
http://www.isnvd.org/2010/11/annual-meeting-italy/
It's a paradigm shift
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Postby cheerleader » Fri Feb 04, 2011 8:30 am

Shannon---the specific truncular venous malformation (like a web) won't be created in mice. The affect this web has on the jugular vein can be created by crimping, pinching and closing off jugular veins in mice. That is how animal models are created.
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Postby Cece » Fri Feb 04, 2011 8:38 am

I think they may have simply ligated the veins in the mice.

How does the cerebral drainage in a mouse differ from in a human?

Does a mouse have an azygous vein?
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Postby cah » Fri Feb 04, 2011 10:02 am

This was one of the first things I investigated after I heard of CCSVI: How is the situation in animals? I found out that the neck vessel anatomy is very different in any other mammal because of the upright gait of humans.

Btw: Usually Vit D doesn't play a big role in animals with a natural habit beneath the surface ;)
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Postby Billmeik » Fri Feb 04, 2011 10:40 am

a bit off topic but where are the animal studies?I hoped the stanford ones would be either positive or negative by now. I dont see any mention of it in the march conference. How hard would it be to replicate putnam?(maybe very hard?)
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Postby pairOdime » Fri Feb 04, 2011 10:51 am

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 relationships to CCSVI
New evidence of CCSVI in animal models
Related vascular problems: venous embriology, idiopathic intracranial hypertension, normotensive hydrocephalus, carotid surgery in stroke
CCSVI treatment: procedure and neurological outcomes
Genetic studies
Plethysmography
Flow dynamics: modeling the cerebral venous system

http://www.isnvd.org/2010/11/annual-meeting-italy/
It's a paradigm shift
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Postby cheerleader » Fri Feb 04, 2011 11:07 am

Billmeik wrote:a bit off topic but where are the animal studies?I hoped the stanford ones would be either positive or negative by now. I dont see any mention of it in the march conference. How hard would it be to replicate putnam?(maybe very hard?)


The INSVD will have pre-publication models in Bologna in March. Dr. Dake explained to me that non-human primate studies (apes, chimps etc...better models for humans circulatory system) would be the best model, but these studies are too expensive.
The Animal Welfare Act prohibit experimentation on animals, unless they receive anesthesia...so Putnam's experiment would be too expensive, too. Mice are not protected under this law...which is why they are used.
http://www.nal.usda.gov/awic/pubs/AWA2007/1980s.shtml

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Postby Billmeik » Fri Feb 04, 2011 3:02 pm

New evidence of CCSVI in animal models



thanks I hoped I missed it. I can also look in the fridge and not see what I am looking for right in front of me.
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Postby David1949 » Fri Feb 04, 2011 3:09 pm

At least one study shows CCSVI to be more common among more advanced cases of MS and less common among early cases. That doesn't fit with the theory that CCSVI is congenital. Also if we are born with these defects then why does MS not manifest itself until we are in our thirties? (or 44 in my case?) I remain open to the idea that CCSVI is not congenital or at least not entirely congenital.
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Postby 1eye » Fri Feb 04, 2011 3:19 pm

cheerleader wrote:Shannon---the specific truncular venous malformation (like a web) won't be created in mice. The affect this web has on the jugular vein can be created by crimping, pinching and closing off jugular veins in mice. That is how animal models are created.
cheer


Animal models are also created using genetic modification. I think to get things very close, an animal which walks upright may be needed. Experiments have been done on macaques, but I want to go on record as being against this. For CCSVI, animal experiments are in my opinion cruel and unnecessary. I certainly wouldn't want to get into a pithing contest over it.
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Postby cheerleader » Fri Feb 04, 2011 3:36 pm

David1949 wrote:At least one study shows CCSVI to be more common among more advanced cases of MS and less common among early cases. That doesn't fit with the theory that CCSVI is congenital. Also if we are born with these defects then why does MS not manifest itself until we are in our thirties? (or 44 in my case?) I remain open to the idea that CCSVI is not congenital or at least not entirely congenital.


We've been down this path a few times, David. Dr. Simka says he found CCSVI in all ages of pwMS. So has Dr. Zamboni and Dr. Dake and Siskin, and all of those looking at CCSVI with venography. The venous experts are the ones who say CCSVI looks like truncular venous malformations. Dr. B.B. Lee explains it this way---it takes years of collateral circulation and venous congestion to create Budd Chiari disease (venous disease of the liver) Most are not diagnosed with this disease until their 30s or 40s, when the liver begins to fail. This would make sense with the later diagnosis in MS, when the brain begins to fail. Here's his paper, comparing the truncular venous malformations of CCSVI with Budd Chiari and other congenital defects:
http://www.fondazionehilarescere.org/pd ... 8-ANGY.pdf

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Postby Cece » Fri Feb 04, 2011 3:53 pm

In the paper from Germany that Colin Rose linked to today, the researchers asked why we don't see MS in patients who have radical neck dissections with bilateral jugular ligations. It's because of the 30 years it takes for this to chronically result in neurological damage. With bilateral jugular ligation, there can be acute immediate venous congestion and issues of that sort, with possible fatal consequences, but there isn't MS.
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Postby Lyon » Fri Feb 04, 2011 3:58 pm

..
Last edited by Lyon on Sun Jun 26, 2011 7:07 am, edited 1 time in total.
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Postby Cece » Fri Feb 04, 2011 4:05 pm

thanks Lyon
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