Theory “CCSVI leads to the term ‘MS’”

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

Theory “CCSVI leads to the term ‘MS’”

Postby NZer1 » Sun May 02, 2010 4:07 pm

My thoughts on the brilliant work done to create CCSVI awareness and the knowledge progression that is unfolding.

What if CCSVI was the primary aspect of what has been nicknamed ‘MS’ (because of its visible later stages of disease damage).
CCSVI primary symptoms are specific to poor drainage of the brain, for example cog fog, heat intolerance, balance issues, cold extremities, vision changes, these symptoms are improved by rectifying the blood flow issues. Drainage improvement from angioplasty treatment can sometimes, in a short time frame, improve the initial symptoms and they can continue to improve over time depending on the flow improvement and amount of nerve conduction damage. These symptoms appear to be related to flow pressure or reflux rather than iron deposition.
CCSVI over time allows iron deposits to build up which then damages and crosses the blood brain barrier which causes direct iron damage to the central nervous system. At this time for some people the disability is more variable and has a relapse remit cycle as the body creates collateral vein flow to bypass the restrictions within main veins (jugular and azygous system).
During this time iron deposits that are crossing the blood brain barrier cause more direct damage to the central nervous system. At this time in the progression the disease course can be classified using the old terminology Begnin, RRMS, SPMS, and PPMS.
The possibilities are:
Benign meaning that the body has developed collaterals that cope with the flow restrictions which has very slow, sometimes stagnant progression of disability, although MRI may show activity of disease.
Relapse remitting form being the process of collaterals improving the flow temporarily, in a repeating fashion, and over time collateral flow will not be able to cope with the deteriorating blood flow that leads to a secondary progression stage that becomes continuous progression because the iron deposition and blood flow issues are getting worse with time.
Primary progressive disability, the growth of collateral and disability are happening at the same time, and disability progresses faster. This is where the stop start nature of the relapse remitting form is balanced out by the timing of collateral flow increases and goes directly to the progressive disease because the blood flow decreases and iron deposition damage increases.
There have been red herrings that have been used as bridge in the lack of research historically with the disease known as MS. Two examples are thinking that inflammation was a primary symptom and using EAE as a research tool have delayed progress in finding the disease origin and treatments for the cause of what became known as ‘MS’.
The signs of inflammation are tertiary symptoms and should not be confused with the primary cause, CCSVI, although one cannot happen without the other.
The mouse model EAE has recently been proven to be a different disease process to the human process.
I think at times the research has to be redirected regularly and reviewed to keep the focus of researchers on track with finding relevant data that will benefit the MS population rather than creating a career in research. Its about us not them!!!!!!!
Enjoy your day!
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Postby jackiejay » Sun May 02, 2010 8:08 pm

I'm intrigued by your theory....makes a lot of sense. It explains the difference between the primary symptoms of flow issues and the symptoms of iron deposition on the CNS. I was wondering if only the people with primary symptoms have CCSVI because of their immediate relief in many instances after treatment.....but the way you explain it I now understand the role iron deposition could play in RRMS....and how the venous routes could reroute for a time till the next flareup. A person getting the angioplasty treatment with the iron problem would however not find immediate relief from symptoms but it undoubtedly would prevent further damage from the iron deposits....Bingo!!
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Postby sbr487 » Sun May 02, 2010 8:30 pm

I would like to add one more thing which I have been thinking about a lot:
People whose blood circulation has been restored have reported lot of improvements immediately. This means that most of the symptoms we see are not due to sclerosis, destruction of white matter, inflammation, but rather temporary response to bad blood flow.
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Postby jackiejay » Sun May 02, 2010 8:55 pm

would the lesions that show up on MRI tests actually be iron deposits then?
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Postby mshusband » Mon May 03, 2010 5:03 am

Yes. Doctors have found that lesions are heavy in iron.

You're exactly right.
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Re: Theory “CCSVI leads to the term ‘MS’”

Postby Cece » Mon May 03, 2010 9:02 am

NZer1 wrote:The signs of inflammation are tertiary symptoms and should not be confused with the primary cause, CCSVI, although one cannot happen without the other.


exactly...which also explains why all our drugs that are somewhat effective at controlling inflammation or reducing the number of relapses do nothing to halt long term progression...when the hypothesis or expectation about that was just the opposite, a decade ago...
"However, the truth in science ultimately emerges, although sometimes it takes a very long time," Arthur Silverstein, Autoimmunity: A History of the Early Struggle for Recognition
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Postby magoo » Mon May 03, 2010 1:53 pm

This is my exact thought process when trying to understand CCSVI's relationship to MS. It makes sense to me.
Rhonda~
Treated by Dake 10/19/09, McGuckin 4/25/11 and 3/9/12- blockages in both IJVs, azy, L-iliac, L-renal veins. CCSVI changed my life and disease.
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Postby Badger » Tue May 04, 2010 8:55 am

I have been thinking along the same lines!!

I have had MS for over six year so my improvements will be gradual and some may not ever recover to the way that they were before.

My friend, however, was diagnosed around 8-9 months ago and after her initial dose of steroids, shows no signs of having MS. So in theory she has the early stages of CCSVI and if she is liberated soon will not develop MS.

It is all so simple!!!

:D
<em>Badger
RRMS 2004</em>
Appt Katowice 23/24th March
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Postby jackiejay » Tue May 04, 2010 9:49 am

but if someone has had MS for 6 years and has only had 1 relapse which subsided over time....can I assume that they have CCSVI but perhaps is having the iron deposit issue....
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Postby NZer1 » Fri May 14, 2010 1:24 pm

Jackiejay I think that the timing of all of the symptoms and being able to measure progression varies in everyone. The veins that are effected may be from birth or earlier and the effect that has, will be compounding.
There are environment/diet/lifestyle and a host of other determinants that will dictate the course of observable symptoms. The indications from another thread on symptom wish lists for changes "Survey Wish lists for treatment outcomes of CCSVI" leads me to think that some symptoms are resolved quickly by improving blood flow. That is to say on the theater table.
There are other symptoms that appear to have been created by prolonged lack of blood flow. These symptoms appear to improve with blood flow improvement, and require time to heal lessions or flush iron. My guess is that at this stage there is repairable axon type damage through possibly remyelination.
The most serve and more permanent residual symptoms I would guess to be where the nerve is damaged beyond the bodies ability to repair. At a guess this is where stem cell research would be important if it is proven to work.
Please note this is my theory as a layman.
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