Chronic Cerebrospinal Venous Insufficiency (CCSVI)-

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

Postby jimmylegs » Thu Jan 08, 2009 4:38 pm

oo, cheer, how recently? i'd missed that tidbit about the azygous having a valve. so now, on to how to make those valves behave. i think it would be much like other problems of venous insufficiency then.

Phlebology 2008;23:85-98
doi:10.1258/phleb.2007.007027
© 2008 Royal Society of Medicine Press

Mechanisms of varicose vein formation: valve dysfunction and wall dilation
J D Raffetto* and R A Khalil
Varicose veins are a common venous disease of the lower extremity. Although the mechanisms and determinants ... are not clearly defined, recent clinical studies and basic science research have cast some light on possible mechanisms ... reflux and incompetent valves as well as vein wall dilation. Primary structural changes in the valves may make them ‘leaky’, with progressive reflux causing secondary changes in the vein wall. Alternatively, or concurrently, the valves may become incompetent secondary to structural abnormalities and focal dilation in vein wall segments near the valve junctions, and the reflux ensues as an epiphenomenon. The increase in venous pressure causes structural and functional changes in the vein wall that leads to further venous dilation. Increase in vein wall tension augments the expression/activity of matrix metalloproteinases (MMPs), which induces degradation of the extracellular matrix proteins and affect the structural integrity of the vein wall. ... effect of MMPs on the endothelium and smooth muscle components of the vein wall and thereby causing changes in the venous constriction/relaxation properties. Endothelial cell injury also triggers leukocyte infiltration, activation and inflammation, which lead to further vein wall damage. ...vein wall dilation appears to precede valve dysfunction, and the MMP activation and superimposed inflammation and fibrosis would then lead to chronic and progressive venous insufficiency and varicose vein formation.


http://www.ncbi.nlm.nih.gov/pubmed/10725813
...Venous ulcers manifest as a breakdown of the collagenous stromal tissue and are highly associated to chronic venous insufficiency.


http://www.ecureme.com/emyhealth/data/C ... ciency.asp
* Chronic venous insufficiency means that blood and fluid in the veins of the legs [JL: or brain?] do not drain out properly. Because of the buildup of fluid, the legs become swollen...
* Usually the first sign is swelling of the leg -- most often around the ankle. [JL: MaggieMae? you on this?]...
* Some patients complain of aching or discomfort in the leg after standing for long periods...

[JL: sounds familiar don't it]

if you didn't catch the post from last may on zinc in ms, this 1992 study found men averaging 13 (range 11-15) and women averaging even lower at 12 (10-14)

Code: Select all
             Males(n=21)       Me(n=1)Females(n=21)
             MS       Ctrls    MS     MS       Ctrls
Zn(µmol/l)   13.0±1.9 14.8±1.6 8.6    12.1±2.1 13.2±1.6
Cu(µmol/l)   14.7±3.7 15.3±1.6        15.7±3.3 16.8±2.1
Albumin(g/l) 42 ±3    43 ±4           41 ±4    41 ±3

adapted from: Palm and Hallmans. (1992). Zinc and copper in multiple sclerosis. Journal of Neurology, Neurosurgery, and Psychiatry45:691-698

an interesting update... my lab says normal for zinc is 11-18. this 2006 study of 1113 thai healthy controls finds an AVERAGE zinc level of 18 µmol/l.

http://cat.inist.fr/?aModele=afficheN&cpsidt=18101339
The average serum zinc level of the population (n = 1113) was 18.20 μmol/l (95% CI = 18.05–18.36). There was no significant difference in the zinc levels between males and females, i.e. 18.20 μmol/l (95% CI = 17.90–18.36) vs. 18.36 μmol/l (95% CI = 18.05–18.66). The zinc level tended to decrease significantly as age increased, particularly in the male population (p < 0.05).

test yer zinc ppl, fix up those veins.
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Postby mrhodes40 » Thu Jan 08, 2009 5:54 pm

Cool JL, the venous insufficiency papers read like the MS hit parade don't they?

I find it fascinating that these venous ulcer cellular changes appear to be such a dead on match for MS; and it is not autoimmune at all; ALL of this stuff is known to be present in venous ulcers, a phenomenon that is well described and understood and most definitely NOT autoimmune.

MS would be considered a primarily degenerative issue then if this is correct in the brain and MS is in actuality a venous ulcer type damage, but in the brain upstream from the azygous or jugular rather than in the leg upstream from the femoral.

But I have been thinking all day about the fact that in venous ulcers inflammatory cells cause part of the damage. BOOM! There's your logic for campth etc helping MS at least while it is still inflammatory and not completely degenerative as it is in SPMS, which is exactly how the immune suppressives like revimmune etc work: they help people who are still in the inflammatory phase of the disease but do not help later on. (Dr Kerr told me after I sent my MRI that I was a no go-he already knew revimmune would not help because I have no inflammation)

We have been told that the reason suppression does help early but not late MS is that it is the inflammation that causes the degeneration and later MS is pure degeneration; a consequence of the early inflammation. All we have to do is stop the inflammation and that second phase will never happen. or so it is assumed....

But in venous ulcers, inflammation is part of the damage; the injury to the tissues occur, then the inflammation makes it worse.

But the cause of the primary injury is NOT the inflammation; it is the mechanical injury that sets it in motion.

SO if you stop the inflammation it will reduce the injury, at least a little bit, though the mechanical damage will continue and eventually people would notice the antiinflammatory approach was not helping and progression is happening anyway.

This matches my personal experience with CRABs. My MRI's are so inflammation free and have been for years that I was told I'd never get bad, but I use a rollator now and I am only 48. After 6 years of MS, I could still jog when I started copaxone 11 years ago and I jogged a couple of miles several times a week. From that to a rollator with no apparent inflammation happening in 11 years on cop.

But if this is right and I have this venous issue that makes sense. The copaxone reduced inflammaiton right enough, but the mechanical damage went on anyway and I slowly progressed over years even though I did not have inflammation. Bingo, perfect fit.

I am lightheaded too and also drag a plastic lawn chair around to sit instead of trying to bend over Lew. And let's get eough magnesium to keep from straining in the bathroom....
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Postby CureOrBust » Thu Jan 08, 2009 6:52 pm

I found out from my third "back-up" doppler lab, that they are not prepared / skilled to do the tests.

That leaves my original choice, which I will find out further info on next week, when the vascular dr's are back in the office. They are also the ones for which my referral is actually too. I am starting to think that maybe it would of been best to first get a referral to a vascular doc, who would know where and who could of performed the tests. However, at this stage, I don't think it would of made it any faster. All my delays appear to be based around individuals x-mas / new-years vacations.

I feel pretty comfortable that I can get these done (except test 2 may be difficult), now that I have spoken to the sonographer in the hospital, yesterday. She may not know it yet, but she is now part of my medical team. :P
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Postby jimmylegs » Thu Jan 08, 2009 7:27 pm

RIGHT marie. if the drugs stop the inflammation but don't stop that damage that's causing it, why would it keep working. meanwhile, zinc is anti-inflammatory AND it helps heal permeable veins. keeping in mind of course, that zinc is only one piece of the puzzle, as usual.
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Postby jimmylegs » Thu Jan 08, 2009 7:45 pm

an interesting crossover between vascular issues, ms, and zinc status
- small n, but whatever:
Williams and colleagues16 compared the nutritional status of a group of 10 women with multiple sclerosis and pressure ulcers with 10 women free from any chronic wound. While the women had low normal values of several vitamins and trace elements suggesting very mild deficits, serum zinc levels were considerably less than normal ranges, suggesting a more significant
deficiency. Balaji and Mosley17 treated a group of 50 patients with large vascular ulcers of the lower extremities and associated both zinc and vitamin
C deficiency with delayed wound healing.

the following was posted on p.3 of this thread but i thought it was a good time to come back to it:

more on zinc Smile

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 defi ciency 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.
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Postby jimmylegs » Thu Jan 08, 2009 8:08 pm

on p. 1 of this thread ww wondered why pregnancy would be protective yet women get varicose veins in late pregnancy. i suggested that the zinc gets depleted throughout pregnancy resulting in the vascular damage but that in the third trimester the levels of highly elevated anti-inflammatory 1,25dihydroxycholecalciferol protect against ms patients feeling the low zinc effect, sort of as a band-aid measure. post partum, no zinc, and no band-aid. if someone had such low vitamin d3 status that they couldn't even boost their 1,25 d3 to a protective level they might relapse during pregnancy.
the point here is that i had run across a link to uric acid, the liver, ammonia, and urea. this sparked an interest in the possible connection between vascular issues, zinc status, and the typically low uric acid in ms patients. i have been hypothesizing that correcting my zinc deficiency will have restored my nice antioxidant uric acid to a healthy control ballpark. i haven't had the bloodwork done, but i have been trying to find research to support the idea that zinc and uric acid are correlated, so that we could maybe address low uric acid in ms patients through correcting zinc deficiency. i finally found some rats who have cooperated somewhat:

Effect of Zinc Deficiency on Urinary Excretion of Nitrogenous Compounds and Liver Amino Acid-catabolizing Enzymes in Rats
Jeng M. Hsu and William L. Anthony

The effect of dietary zinc deficiency in rats on the levels of urinary nitrogen, urea, uric acid, and creatinine was studied. Zinc deficiency substantially increased urinary excretion of total nitrogen. The amount of urea excretion of zinc-deficient rats was approximately 42 and 87% more than that of zinc-supplemented pair-fed and ad libitum-fed rats, respectively. Zinc-deficient rats also showed significantly higher excretion of uric acid. No difference was observed in creatinine excretion between zinc-deficient and zinc-supplemented groups. Further studies demonstrated that zinc-deficient rats had increased activities of liver tryptophan pyrrolase and arginase. The activities of liver threonine dehydratase and serine dehydratase were unaffected by zinc deficiency. Overall findings support in principle the concept that zinc deficiency results in an increased protein catabolism and also indicate that the hepatic amino aciddegrading enzymes may be one of the possible regulating sites involved in the protein metabolism of rats.


on to try finding the same thing in people studies :S
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Postby jimmylegs » Thu Jan 08, 2009 8:50 pm

oh and i went looking to see what kind of numbers might cause zinc excess issues, in case any one wants to address the zinc facet of their vascular health and ms, but is concerned about supplementing.

at first i couldn't seem to find any involving excess supplementation, just weird metabolic problems in 5 patients, one a man who did not supplement and had zinc up over 28 µmol/L (http://archneur.ama-assn.org/cgi/reprint/60/9/1303.pdf), and another with an 11-yr old whose levels were at 200 µmol/L (http://cat.inist.fr/?aModele=afficheN&cpsidt=2747383), and another 3 adults looking as though just having a copper deficiency made their zinc go high, with there being no evidence of excess zinc intake to explain the imbalance.

and then:
http://www.medscape.com/viewarticle/497023_2
...He sought care at the emergency department complaining of a 2- to 3-week history of fatigue and new onset fever (40.6°C). At the time of admission, the patient was taking approximately 600 mg/d of zinc, which was several times the dosage prescribed by his physician.
Laboratory testing revealed moderate normocytic anemia, leukopenia with severe neutropenia, and a normal platelet count (Table 1). Based on the morphologic examination of a bone marrow specimen, serum ceruloplasmin, copper, and zinc levels were obtained. The serum copper and ceruloplasmin were found to be extremely low, and the zinc level was high normal. (JL: from table 1, zinc level was 22.2 µmol/L; ref range for their lab is 8.4-23) ...second patient... His symptoms continued to progress, and by January 2004, he had difficulty walking with a steady gait and holding objects in his hands owing to the lack of sensation. Nerve conduction studies revealed evidence of sensory neuropathy. However, the patient was noted at this time to be anemic and neutropenic (JL: from table 1, zinc level was 65 µmol/L) and a bone marrow evaluation was performed in March 2004... Based on our review of the bone marrow biopsy specimen, additional laboratory testing was obtained, which revealed serum copper levels below the detectable range, extremely low ceruloplasmin levels, and high zinc levels (Table 1). The patient was asked further about possible zinc ingestion, and it was determined that he had been consuming an entire tube (68 g) of PoliGrip denture cream (containing polymethyvinylether maleic acid calcium-zinc salt) daily for the past 4 to 5 years.

there. so provided that we don't have copper deficiency or a genetic or surgically caused metabolic copper-zinc problem, i think we're good aiming for that ~18.5 µmol/L healthy thai sweet spot. i don't feel so bad about my 20µmol/L 'excess' finding last trip to the lab now.
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Postby DIM » Fri Jan 09, 2009 1:03 am

Wife takes daily for more than a year 50mg Zinc and her last blood test came at 15,76µmol/L Zinc (103µg/dL) so it's obvious she has had some kind of zinc defficiency before!
What I found in my wife the first few months after diagnosis:

Low vitamin B12
Low vitamin D
Low Zinc
Low Uric Acid
Elevated liver enzymes (about 2X the normal values)
Low normal T3-T4 with high normal TSH (thyroid tests)
High normal Iron, TIBC (waiting ferritin and sTfR results and I am sure there are also high)

We fix through supplementation, diet, LDN and lifestyle changes all the above except iron abnormalities but just read about them from your reasearch so we add in her daily regimen 700mg EGCG, 1000mg quercetin and double the dose of pycnogenol (120mg), ginkgo (240mg) and resveratrol (120mg)!


PS: For those that take IP6, EGCG, quercetin and other iron chelators (usualy they are also copper chelators) DON'T take them with food as they reduce absorption of other minerals say calcium, magnesium, zinc and often fatty acids and they directly bind with the iron from foods so they don't chelate it from brain and other affected areas.
PS1: LDN boosts pituitary and other glands function and I believe she has had hormone imbalances before but except thyroid tests we haven't test her hormones the pre-LDN period.
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Postby gibbledygook » Fri Jan 09, 2009 6:02 am

This is hilarious, my doctor told me there were no valves in the jugular and azygos but a quick check via google shows he is wrong!

I may dust down the horsechestnut and butcher's broom once again as these are used for varicose veins. My previous experiments with these herbs have been mixed, however.
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 Jan 09, 2009 8:16 am

PubMed seems to have very little on what causes varicose veins beyond valvular incompetence. But what causes the valves to fail? Still no further on what causes the stenoses... :cry:
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 Jan 09, 2009 8:30 am

calcification?
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Postby cheerleader » Fri Jan 09, 2009 8:54 am

So many culprits could cause venous blockage or valve failure. Calcification, chronic infection, hypertension in the vein, and a congenital lack of valves (!) Zamboni noticed actually stenoses in the veins, but he is not writing or speaking about what he thinks causes them...yet. Once they are surgically removed, they can be examined and cultured. Here's what I think...the blockage will be caused by different factors for folks. The consistent for MS will be venous insufficiency.

The azygous and internal jugular veins have been very difficult to scan until recent improvements in CAT and doppler. This is why most docs haven't really considered the venous drainage system important in relation to the brain- and why it will take a groundswell of research to change their collective minds. We can see leg swelling, venous ulcers on the legs and varicose veins. When I saw what was going on in my husband's legs that the docs said was "benign" and "not connected to his MS" I knew we were on our own. Venous insufficiency is not benign in the brain.

http://emedicine.medscape.com/article/461449-overview
AC
Last edited by cheerleader on Fri Jan 09, 2009 9:03 am, edited 1 time in total.
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby gibbledygook » Fri Jan 09, 2009 8:59 am

:lol: :lol: :lol:
It would be handy if this were so as it was a plausible cause for a stenosis to develop but the research on pubmed hasn't revealed that, yet. I have read 20 pages of abstracts on chronic venous insufficiency out of 140. They are mainly focussed on the surgical aspect.

There was only one interesting abstract out of the 400 I have glanced through which suggested that a loss of tropoelastin in the vein wall results in valve incompetence.

Seems like we shall all have to go under the knife! 8O
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 » Fri Jan 09, 2009 9:06 am

eems like we shall all have to go under the knife!


I'm glad you said it, I have come to the same conclusion there is no other solution really at all. :?

Good to know..................
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Postby cheerleader » Fri Jan 09, 2009 9:24 am

mrhodes40 wrote: And let's get eough magnesium to keep from straining in the bathroom....

Lew...and all "strainers" :oops:
Listen to Marie! Magnesium Citrate is the stuff they give you before a colonoscopy. This stuff works. My hubby is now a "regular" guy (well, almost!)
And Zamboni's Liberation procedure uses endovascular surgery, which is supposed to be less invasive. Fingers crossed.
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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