Chronic Cerebrospinal Venous Insufficiency (CCSVI)-

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

Postby jimmylegs » Fri Dec 19, 2008 5:18 am

now i'm totally confused! the abstract i read doesn't mention nutrition at all :S is it a different paper dignanlegs?
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Postby gibbledygook » Fri Dec 19, 2008 8:22 am

The Schelling paper seems fairly emphatic that the lesion results from mechanical injury and develops from the veins rather than the other way around.

On page 79 begins a section "Impacting Veins, the Real Agents of Brain Injury". It seems that the distension which arises from venous backflow which in turn probably arises from stenoses is the cause of the lesions. At least that's my rather cursory reading so far.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby cheerleader » Fri Dec 19, 2008 8:31 am

gibbledygook wrote:The Schelling paper seems fairly emphatic that the lesion results from mechanical injury and develops from the veins rather than the other way around.
.

I've e-mailed Schelling, and he visited Zamboni's lab in Dec. 2007 and watched some of the doppler testing. He believes it proves his observations from over 30 years ago. He believes cerebral lesions are created "up river" where the pressure builds up from venous back flow- above the blocked jugular vein.

JL...Dignan's (swoon) post was from a previous Zamboni study on iron deposits in the brain. It's a different paper. He posted it earlier in our iron thread.
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby dignan » Fri Dec 19, 2008 9:15 am

Aw shucks Cheer...jimmy, the paper I posted the link for is from 2006 and predates his two clinical studies. The older paper is more about his theories. Maybe he has changed his mind about iron since then.
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Postby gibbledygook » Fri Dec 19, 2008 10:24 am

I can't believe that researchers have sat on information for nigh on a century which is so important. How easily they have been side-tracked by non-issues. I was feeling my way to exactly this conclusion (that it is a vascular rupture problem) in less than a year, hence my use of horsechestnut which is used for chronic venous insufficiency. It must once again be dismally observed that large organisations/social structures encourage nothing but slavish following of orders and lack of imagination. The human race will never learn and is doomed to repeat the errors of its forefathers. Just look as Depression II unfolds. A world war in a decade? Probably.

That being the case we had better work out a strategy to undo these venous stenoses for ourselves.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby gibbledygook » Fri Dec 19, 2008 10:39 am

I guess that surgical intervention like angioplasty or stent insertion might do the job nicely. I will discuss with a neurosurgeon as soon as possible.

I reckon in the interim that a little bit of vasodilation/anti-coagulation might be helpful although not too much as we must try to keep the distended vein away from the spinal cord/cerebellum whilst trying to keep the blood flowing through the venous obstruction.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby jimmylegs » Fri Dec 19, 2008 11:08 am

more on zinc :)

http://www.rowett.ac.uk/newsletter/Reso ... ticle4.pdf
In this article, John Beattie describes how dietary zinc intake may influence vascular health and disease. He demonstrates that the development of vascular disease is accelerated in marginal zinc deficiency and investigates a mechanistic basis for this influence, possibly involving vascular smooth muscle structural proteins...

http://grande.nal.usda.gov/ibids/index. ... row=361901
Our data indicate that zinc is vital to vascular endothelial cell integrity, possibly by regulating signaling events to inhibit apoptotic cell death.
Last edited by jimmylegs on Sat Sep 11, 2010 8:11 am, edited 1 time in total.
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Postby cheerleader » Fri Dec 19, 2008 7:24 pm

Cerebral venous outflow impairment is known to produce cerebral dysfunction in many clinical and animal studies. However, knowledge and understanding of the cerebral venous system is far less than that of the arterial system. The internal jugular vein, which is easily
observed by color-coded Doppler sonography, is one of the main tracts for cerebral venous drainage. Recently, internal jugular venous reflux has been found to be related to several neurologic disorders. These associations suggest that the mechanism of these dis- orders is related to cerebral venous outflow impairment. In this article, we will briefly
introduce the cerebral venous system and extracranial venous drainage pathway, then specifically review the characteristics of the internal jugular vein, its branches, and the hemodynamic factors involved in internal jugular venous reflux.

Cerebral circulation encompasses both the arterial and venous system (CVS). The venous system con- tains approximately 70% of the blood volume, with approximately three-quarters contained within small veins and venules [1,2]. An alteration in cerebral venous volume would influence cerebral hydro- kinetics and intracranial pressure [2,3]. In addition to cerebral venous drainage impairment, an alteration in cerebral venous volume would produce brain edema and/or decreased cerebral perfusion, leading to cerebral dysfunction [3–8]. Despite its significance in cerebral circulation, in contrast to the cerebral arterial system, the CVS is far less described and studied.

Jean-Martin Charcot (1825–1893), a great teacher and physician, created the foundations for neurology as an independent discipline and has had a phenomenal influence on contemporary neu- rology [9–11].
Charcot proposed a topographic distribution of brain diseases according to the distribution of cerebral arteries, but paid little attention to the CVS. In the first half of the 20thcentury, his students, also very celebrated neurologists, established the principle of neuropathology. Since then, extensive studies and observations have been carried out on the cerebral arterial system compared with those on the CVS. Insufficient description makes for a poor understanding of the physiology and pathology of the CVS, which might lead to the underestimation of cerebral venous disorders
[3].


A study on Jugular Venous Reflux from Neurological Institute, Veterans General Hospital-Taipei, and National Yang-Ming University, Taipei, Taiwan, April 2008

http://health.elsevier.com/ajws_archive ... 3A4703.pdf

A wonderful paper for those who want to understand the importance of the entire cerebral venous system.

These researchers go back to Charcot's hyper-focusing on cerebral arteries inside the brain (as opposed to the entire cerebral venous system and drainage of blood) as the reason neurologists do not consider the importance of the jugular vein in brain health. Neurologists haven't see the forest for the trees...or the brain in relation to its drainage system.

Now, thanks to doppler...those days are over.
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby mrhodes40 » Fri Dec 19, 2008 8:14 pm

Great find Cheer!
Man I can't wait until some of us get these tests and share the results.
I am absolutely fascinated by this material.
I can't wait until people have discussed this with a few specialists and we start getting some feedback.

marie
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Postby gibbledygook » Sat Dec 20, 2008 11:18 am

I reckon women suffer disproportionately from MS is the same reason that they suffer disproportionately from varicose veins.

Personally, I think we've hit the JACKPOT!!! Hoooray!
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby mrhodes40 » Sun Dec 21, 2008 7:07 pm

Many more links to Schelling's work on this forum thread found here
http://answers.google.com/answers/threadview?id=271074

I think there are likely other factors that go into play though on reflection.

Example if a pregnant lady has MS she does well with pretty stable MS until a few months after the birth then bingo, exacerbations. pregnancy itself results in dramatically increased blood volume, and often increased pressure there should be issues during pregnancy, not mainly after. This seems illogical and needs looking into. If it is a venous issue causing the lesions it should get worse during pregnancy. :?:

Also Zamboni mentioned that treatment had no efect whatsoever on the vascular pproblem, you have the problem whether you are on treatment or not.

But if you get a bad lesion and go get steroids the effects of the worsening clear up. Why? It can't have removed the vascular issue or lesion, is it just that the inflammation related to your body trying to deal with the damage is less and thus the symptoms less? Because inflammation is causing standby damage but not the actual cause of MS?

Or is there an inflammatory component, like maybe the distended areas with back jets force some things through the BBB--say CPn-- and THAT causes inflammation..... If so it is a multi faceted problem

Also, why would known MS triggers like a UTI cause a venous issue to suddenly worsen?

how about a virus causing an exacerbation? How would that relate to a venous cause of MS? The flu?

Maybe you could make a case that a hard, hacking cough is the problem in the last two.

I am really excited to find out what kind of things others interested in this find out and post once they've had a consult with someone.

The bottom line is this thing seems to exist as described and it needs to be thoroughly investigated! Last year! :wink:

I cannot BELIEVE there is a thing exclusive to MS and it has been ignored
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Postby mrhodes40 » Sun Dec 21, 2008 7:37 pm

An earlier Zamboni paper this one on 89 patients with matched controls.

http://www.ms-info.net/Intracranial_Ven ... erosis.pdf

This paper outlines how the backjets and anomalies related thereto are assoicated with MMP9 adhesion mlecules and other factors already known to be common in MS........answered my question above!

Therefore, venous reflux overloads microcirculation (Bergan et
al., 2006) and increases trans-mural pressure (Zamboni et al.,
2007); in MS, changes of microcirculatory MRI perfusional parameters,
have been shown to precede plaque formation in a longitudinal
study (Wuerfel et al., 2004). Furthermore venous reflux,
with consequent microcirculatory overload and increased transmural
pressure, facilitates erytrocyte diapedesis (Zamboni, 2006;
Bergan et al., 2006; Zamboni et al., 2007) resulting in increased
perivenous iron deposits demonstrated histologically also in MS
lesions (Adams, 1989; Adams 1988) and confirmed by advanced
MRI techniques (Haacke et al., 2005; Tjoa et al., 2005; Brass et al.,
2006). Moreover, the excess of stored iron in the brain triggers a
series of deleterious events that lead to neurodegeneration, possibly
involving mechanisms of iron-driven free radicals generation and
oxidative stress (Ke et al., 2003,
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Postby gibbledygook » Mon Dec 22, 2008 2:18 am

Hi Marie!

Just wondering what treatment Zamboni was discussing when you wrote the following.

Also Zamboni mentioned that treatment had no efect whatsoever on the vascular pproblem, you have the problem whether you are on treatment or not.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby Terry » Mon Dec 22, 2008 5:15 am

Also, what about the Faroe Islands and the issue of where you live in adolescence? Were these incorrect studies or do these show that the venous issues are "just" a symptom of something else?

Terry
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Postby gibbledygook » Mon Dec 22, 2008 8:00 am

It's quite possible that an infection and low vitamin d status contribute to a major dysfunction of the central nervous system venous system. The Faroe island and teenage findings don't in any way contradict the primary cause of our disabilities; the obstructed venous outflow and contraflow derived venous distensions.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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