No need for CCSVI reseach

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

No need for CCSVI reseach

Postby Nunzio » Fri Mar 19, 2010 5:45 am

If we had to set up a research project on CCSVI we would choose an animal model in which we would restrict the blood flow to the brain.
Naturally the best animal to use would be a human model but that would be unethical. Fortunately there is already a model: please look at the abstract below.

"The antiphospholipid antibody syndrome, frequently seen in young individuals, is often associated with transient ischemic attacks or strokes. In some cases, this syndrome may be difficult to distinguish from exacerbating and remitting multiple sclerosis. We report four such cases. In addition, the finding of hyperintense signals on magnetic resonance imaging in multiple sclerosis may also be seen in the antiphospholipid antibody syndrome, as demonstrated in these cases. Small strokes that affect the white matter in the antiphospholipid antibody syndrome may be misdiagnosed as multiple sclerosis.

(Arch Intern Med. 1994;154:917-920)"

This syndrome is part of the hypercoagulability syndrome which slow down the blood circulation everywhere including the brain with symptoms identical to MS and with MRI also identical to MS.
Of course when the syndrome is treated with blood thinner then the MS symptoms disappear.
Now try to explain this using the autoimmune theory
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Postby weegie1 » Fri Mar 19, 2010 5:59 am

Really interesting post Nunzio
Great find
Let it be a reason but never an excuse
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Postby thisisalex » Fri Mar 19, 2010 6:10 am

Its interesting Nunzio what you say...
Especially because my first SM symptom was a mini stroke (already spoke about it in a separate thread here). I had a coagulation test and everyíthing was fine.

The problem is that APS IS an autoimmune disorder, and as far as this article describes, it has definitely nothing to do with MS:

http://rheumatology.oxfordjournals.org/ ... l/44/4/434

APS can be resolved by using anticoagulants, but not MS

just my 2 cents...
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Postby cheerleader » Fri Mar 19, 2010 7:47 am

APS is a differential...one of the diseases they test for to make an MS diagnosis. Docs rule it out before giving a dx of MS. Not the same mechanism. Can be tested for, and blood is anti-coagulated. CCSVI is a stenosis (physical narrowing) of the veins. Maybe CCSVI will be determined to be a differential diagnosis, maybe it will be the cause of MS-- we'll see.
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Postby ozarkcanoer » Fri Mar 19, 2010 11:02 am

No matter what, there IS need for CCSVI research. We want to know as much as we can about MS and about CCSVI so we can unravel this mystery step by step. It may take years, but we should be able to be liberated before all those years go by !!! I can't wait to get my hands on the book :"The MSterys of MS Unraveled". But before anyone can write the book we need the research !!

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Postby Nunzio » Sat Mar 20, 2010 10:08 am

I agree with you, my title was meant to be provocative.
In the past I worked at the NIH, National Cancer Institute studying changes of Blood Brain Barrier and Blood Flow secondary to brain cancer in an animal model so I am perfectly aware of the importance of research.
I know APS is not MS and it is in the differential diagnosis.
What I am saying is that the common tread is decrease blood flow to the brain. By narrowing blood vessel for CCSVI and by thickened blood by APS.
The result is the same both in symptoms and MRI finding.
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Postby mangio » Sat Mar 20, 2010 10:25 am

What is known about autoimmunity is almost NOTHING. I have
spent almost 5 years researching autoantibodies and disease
because so many of my near and dear have been devasted
by so my different conditions. You should see what lupus
does to the brain well after it's destruction of the heart,
kidneys and many other comparts of the body. I could go forever
on this subject.

Just a little rant for the 25 million people plus that suffer from 100 or so
autoimmunity conditions in north america alone.
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Postby cheerleader » Sat Mar 20, 2010 10:27 am

Nunzio, I agree- and get your ironic post. The problem is, making provocative thread titles is confusing to new people here. All of this APS research seems to corroborate what we see in MS brains, but if it is not the exact mechanism, neurologists will not give up the Dr. Rivers/EAE model.

Fortunately, researchers are working on the CCSVI animal model- which looks alot like what Dr. Tracy Putnam did with his beagles some 60 years ago, only it involves extracerebral jugular vein restriction rather than intracerebral blockage of veins with liquids.

Will it be enough to encourage neurologists to finally abandon the EAE model? I fear only if drugs can be found to treat the new model. But vascular doctors understand cerebrospinal venous insufficiency already.
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby ozarkcanoer » Sat Mar 20, 2010 10:56 am

mangio, it is clear to me that very little is known about "autoimmunity". Autoimmunity with respect to MS should be called a hypothesis as much as CCSVI. I know about research going on now under the title of MS research where they are trying to understand some molecular pathway (the signaling, etc) in the immune response in the brain. That is where neurology is at with the autoimmune theory of MS. I truly hope that these researchers are considering the possibility of CCSVI and taking that into account now. As Dr Zamboni says "We know MS is an autoimmune disease". But do we know the mechanism that leads to autoimmunity ? NO.

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Autoimmunity

Postby Nunzio » Sun Mar 21, 2010 1:12 am

I think autoimmunity is when we are not smart enough to figure out what is damaging a tissue and we only see the attempt to clean up the mess that our immune system does and therefore call the condition an "autoimmune" disease. The immune system is much smarter than that.
In case of MS there has been a recent paper on Dec. 2009 that showed that the initial insult to the tissue in MS is oligodendrocyte apoptosis(death) without the presence of immune cells. Their conclusion is: "The findings suggest that plaque formation has some basis other than destructive cell-mediated immunity directed against a myelin or oligodendrocyte antigen."
http://www.ncbi.nlm.nih.gov/pubmed/20035511.

I always had a problem with MS being autoimmune because Myelin cover our nerves throughout our entire body except the inside of the eye but in MS the attack is only against the brain which is protected by the Blood Brain Barrier(BBB). It would make more sense if MS would attach our nerve in other parts of our body and spare our brain because of the BBB.
CCSVI cause damage to the nerves by accumulation of toxins or possibly iron and then the immune system comes in to clean up the mess.
Just a thought
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Re: Autoimmunity

Postby NHE » Sun Mar 21, 2010 2:26 am

Nunzio wrote:I always had a problem with MS being autoimmune because Myelin cover our nerves throughout our entire body except the inside of the eye but in MS the attack is only against the brain which is protected by the Blood Brain Barrier(BBB). It would make more sense if MS would attach our nerve in other parts of our body and spare our brain because of the BBB.
CCSVI cause damage to the nerves by accumulation of toxins or possibly iron and then the immune system comes in to clean up the mess.
Just a thought


It's a different cell type. The myelin of the peripheral nervous system is composed of Schwann cells while the myelin in the central nervous system is composed of oligodendrocytes. Myelin oligodendrocyte glycoprotein (MOG) is one of the immune targets in MS.

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Postby sou » Sun Mar 21, 2010 3:26 am

Primary autoimmunity is a theory that can not explain even itself.

What is the autoantigen? Why do newly forming lesions contain no adaptive immunity cells at all? And why so many super-hyper-powerful drugs have shown little benefit in the long term while the very same drugs completely halt other autoimmune conditions?

The list could grow veeery long, but we have to stop somewhere. In the last 2 years we have understood more about MS than what we had the previous century as a whole. That's a HUGE step forward.

Autoimmunity was and is a hypothesis. CCSVI is a real condition supported by real concrete evidence. Why stick to an hypothesis and try to make the evidence compatible with it instead of changing the hypothesis to make it compatible with the evidence? CCSVI and autoimmunity are not religions that can not undergo criticism. If CCSVI proves inexistent we should not waste out time on it. Until then, we will first have to PROVE that it has nothing to do with the pathogenesis of MS. Can anyone of the MS specialists do it? We need an official scientifically based answer, negative or positive.

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Postby Nunzio » Sun Mar 21, 2010 3:38 am

Good point; it is possible that because the cells that produce the myelin are different the attack is against the protein associated with myelin that are specific from those cells and different.
Try this then: MS is associated with an inflammation inside the eye called Uveitis, specially a type called Snow bank Uveitis; one problem: there is no myelin in the eye.
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Postby sou » Sun Mar 21, 2010 5:05 am

Indeed, there is no myelin inside the eye. Nor along the endothelium.

Myelin oligodendrocyte glycoprotein (MOG) is one of the immune targets in MS.


A more accurate statement could be:

Myelin oligodendrocyte glycoprotein (MOG) is thought to be one of the immune targets in MS.


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Postby Nunzio » Sun Mar 21, 2010 10:54 am

In fact the paper I mentioned before titled
Multiple sclerosis: distribution of inflammatory cells in newly forming lesions.

disproof the autoimmune theory by showing that the initial insult is cell death and only later the immune system comes in for cleanup as it is supposed to do. My previous URL did not work because there was an extra dot at the end.
this one should: http://www.ncbi.nlm.nih.gov/pubmed/20035511
The conclusion was:
INTERPRETATION: Early loss of oligodendrocytes is a prominent feature in tissue bordering rapidly expanding MS lesions. Macrophage activity is largely an innate scavenging response to the presence of degenerate and dead myelin. Adaptive immune activity involving T and B cells is conspicuous chiefly in recently demyelinated tissue, which may show signs of oligodendrocyte regeneration. The findings suggest that plaque formation has some basis other than destructive cell-mediated immunity directed against a myelin or oligodendrocyte antigen.
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