Chronic Cerebrospinal Venous Insufficiency (CCSVI)-

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

Postby CureOrBust » Wed Jan 28, 2009 4:28 pm

cheerleader wrote:From what Zamboni has told me, this is an endovascular procedure, meaning it is with local anesthetic only and uses a catheter to open the vein. Not a major cutting open surgery, it's an outpatient procedure. It sounds like stents are in the works, according to Wobbly. This would provide a permanent solution to keeping the vein open and might involve a more complex operation.
I can understand restrictions (stenosis) being easily resolved with fairly minor surgery, it is the valve failures that I do not understand a procedure for repair. Did Zamboni mention anything in regards to these? anyone got any ideas? I originally did a google search, and do not remember any clear answers.

Jimmylegs, when you say "nice work cureo", all I hear is a sarcastic tone, as I made a pretty weak boo-boo on the email. I took down the email address as being ".Msw.gov.au" when the state that I am in is "NSW" :oops:

Artifishual, "street-cred" is earned 8) , not handed out. word. :wink:
User avatar
CureOrBust
Family Elder
 
Posts: 2914
Joined: Wed Jul 27, 2005 3:00 pm
Location: Sydney, Australia

Advertisement

Postby mrhodes40 » Wed Jan 28, 2009 4:46 pm

The amount of research and published papers he has generated show the determination of a "man possessed."

No kidding Cheer! three large studies in just over a year! Just so it's in one place and updated with the new study you sent that I added to the thread, I'll tally them up here

All three studies looking at the results of 5 color doppler venous studies in the head.
2007 89 MS patients 60 matched controls
2008 65 MS patients 235 controls, including some with other types neurological disease and some with other vascular disease
2009 109 MS patients 177 matched controls including OND again.

In every study, every person with two abnormal findings out of the 5 had MS and none of the normal subjects had more than one abnormal finding. that's total 263 MSers and 472 controls with 100% concordance over three studies by this team.

It still just blows me away 8O :D :D :D . I'm kind of like "pinch me, is this real?"

Someone argued with me that he is just one man, maybe it is not there as he says, but notice that the team of researchers is 8 people and the dopplers were blinded. It seems incredibly far fetched to imagine that a team of people that large and at that research level is faking it or somehow being wishful about the findings when they are running those numbers of people through the doppler clinic BLINDED (not knowing who has MS and who not). :? How could they possibly tweak the results and "make sure" all the MS patients had 2 abnormal findings? You can't.

It just seems this poses at the minimum a new avenue for research ie what does this venous abnormality mean, is it helpful to improve it, what measures do improve it best, is it the sole instigator to MS and do all other things flow from there or is it a side effect of the real disease process. I can't wait to see where it goes! :wink:

I find it really hard to wait for what is next........I am so impatient for this to play out :roll:

my vascular guy is a part time adjunct professor so the email I used at the U is not his main one. Doh! I'll start again at it..........
User avatar
mrhodes40
Family Elder
 
Posts: 2066
Joined: Thu Sep 23, 2004 3:00 pm
Location: USA

Postby DIM » Thu Jan 29, 2009 12:21 am

Now knowing that Zamboni's wife has MS explains so much to me. The amount of research and published papers he has generated show the determination of a "man possessed."

...the above explains to me why his research may not be fake!
User avatar
DIM
Family Elder
 
Posts: 384
Joined: Thu Feb 28, 2008 4:00 pm
Location: GREECE

Postby CureOrBust » Thu Jan 29, 2009 5:02 am

I just posted on another thread, thinking it was this one. :oops: so I just simply copied what I posted, for the most part.

I have an actual appointment for the 17th of Feb, with the neurologist that said he could do the scans. I asked the assistant making the appointment with me, and she could not confirm if it was simply an initial consult, or if he would actually do some sonography. From previous discussions, Tuesday afternoons are when they are most likely to perform any sonography. Also, in all my emails, I kept using the word "tests".

Is anyone possibly going to beat me to the test before 17th Feb? Image Image
User avatar
CureOrBust
Family Elder
 
Posts: 2914
Joined: Wed Jul 27, 2005 3:00 pm
Location: Sydney, Australia

Postby jimmylegs » Thu Jan 29, 2009 5:18 am

oh shush cure. nice work that you got it all sorted. i mean sheesh it's not like you mixed up N with Q, or Z, or something, M's pretty close ;) mew south wales that's kind of cute :)
jimmylegs
Volunteer Moderator
 
Posts: 9025
Joined: Sat Mar 11, 2006 4:00 pm

Postby gibbledygook » Thu Jan 29, 2009 5:18 am

I'm trying! But I think you'll beat me to it!
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,
User avatar
gibbledygook
Family Elder
 
Posts: 1414
Joined: Mon Feb 14, 2005 4:00 pm
Location: London

Postby gainsbourg » Thu Jan 29, 2009 5:26 am

I have finally got around to reading the latest Zamboni study (published online Jan 2009). The consistency of his findings on venous drainage in MS is remarkable but what strikes me is his increasing interested in the role of iron in these abnormalities. This is how he begins and ends the abstract:

Iron stores in the white and deep grey matter in course of multiple sclerosis (MS) have never been explained and could be related to abnormalities in venous drainage, but this possibility has never before been investigated…..

…..this study demonstrates a significant impairment of cerebral venous drainage in patients affected by MS, a mechanism potentially related to increased iron stores.



gainsbourg
User avatar
gainsbourg
Family Elder
 
Posts: 218
Joined: Sat Sep 06, 2008 3:00 pm
Location: London

Postby CureOrBust » Thu Jan 29, 2009 6:02 am

jimmylegs wrote:i mean sheesh it's not like you mixed up N with Q, or Z, or something, M's pretty close ;) mew south wales that's kind of cute :)
The "cute" part is that I was carefully typing his email address as he spelt it out to me, and I went out of my way to ensure it was an "M". and he repeated, that yes it was an "M". When in reality, he thought he heard me say "N" (what idiot would not of got "NSW"), I was sure he confirmed back to me an "M"; it did not click to me what the following two letters were.
Image

I want someone to "beat me", so we can confirm or possibly deny his absolute results.

gainsbourg, when you say you "finally got around to reading the latest Zamboni study", do you mean the full article? or just the abstract and table of contents?

As for the iron link, without actually seeing the full article, I personally can not see how he can tie this in with any scientific certainty, if he only ran similar test to his previous papers; the abstract implies he only performed TCCS-ECD, as in the last paper.
User avatar
CureOrBust
Family Elder
 
Posts: 2914
Joined: Wed Jul 27, 2005 3:00 pm
Location: Sydney, Australia

Postby jimmylegs » Thu Jan 29, 2009 6:22 am

oh dear, i hope it didn't go to 'm as in mancy?' ;)
jimmylegs
Volunteer Moderator
 
Posts: 9025
Joined: Sat Mar 11, 2006 4:00 pm

Postby Terry » Thu Jan 29, 2009 7:19 am

Gainsbourg,
I have a very small understanding of all this, but I wonder about the oligodendrocytes. They are the chief iron carriers in the brain (I think) , and since they are meeting untimely death, I wonder where the iron goes that they carried. Well, maybe I know where it goes, NOWHERE, but I do wonder if the iron doesn't come from those and not the veins.
Terry
User avatar
Terry
Family Elder
 
Posts: 500
Joined: Fri Oct 26, 2007 3:00 pm

Postby notasperfectasyou » Thu Jan 29, 2009 8:42 am

Circling back. Iron is a nutrient for bacteria.

How Some Bacteria May Steal Iron From Their Human Hosts
User avatar
notasperfectasyou
Family Elder
 
Posts: 774
Joined: Thu Feb 09, 2006 4:00 pm
Location: Northern Virginia

Postby gainsbourg » Thu Jan 29, 2009 5:27 pm

Terry, your suspicion about oligodendrocytes is shared by George Bartzokis of The University of California who did research (2007) about iron deposition in neurological illness in general.

Oligodendrocytes and myelin have the highest levels of iron of any brain cells. He suggests that myelin breakdown releases iron, which promotes the development of the toxic amyloid oligomers and plaques, which in turn destroy more myelin.

http://www.universityofcalifornia.edu/news/article/9191

There are theories abounding about why iron accumulates in the MS brain:

Zamboni (2006) suggested that iron may accumulate in MS in much the same way as it does in chronic venous disease (CVD) “The origin of increased leg iron stores is extravasation of red blood cells (erythrocytes) in conditions of significant venous stasis” (This basically means the blood is soaking through capilliary walls into surrounding tissue, taking the iron with it).

http://www.societaitalianaflebologia.it ... amboni.pdf

Since this study, elevated excretion of iron has been found in the urine of both MS and CVS patients, which is suggestive that faulty metabolism may be behind the excess iron.

Rohit Bakshi (and others) suspect the BBB: Dr. Yulin Ge believes that the iron deposits may form because “the axons are transected by the MS lesions, interrupting iron outflow pathway from iron-rich deep gray matter nuclei to projected cortical sites”

Simka and Rybak (2008) also have some very interesting things to say about the similar role of iron and T-cell proliferation in Venous Leg Ulcers and MS

http://www.labmeeting.com/paper/2818751 ... is-lesions



But, as you know, I’m most concerned with how to get rid of the stuff!


gainsbourg
Last edited by gainsbourg on Thu Jan 29, 2009 5:40 pm, edited 2 times in total.
User avatar
gainsbourg
Family Elder
 
Posts: 218
Joined: Sat Sep 06, 2008 3:00 pm
Location: London

Postby mrhodes40 » Thu Jan 29, 2009 5:38 pm

I got a "GO" for sending my materials to my hoped for vascular dude he is interested enough to read the papers. :D No appointment yet, he said we'd set that up after he gets a gander. :roll:

Hubby read all the papers and he is a go too-even though this will not be covered by insurance and it will require some funds. He's all for it...Wow! :D

There'll be a bake sale in the foyer........ :lol:

So cur-o maybe we'll have something to compare. my lesions are large few and periventricular.
marie

Gain, I'm with you on getting rid of it! Anemic rats don't even get EAE!
This could be why MS is so hard on post menopausal women and men. Premenopause women tend to be a little on the anemic side of things.
Last edited by mrhodes40 on Thu Jan 29, 2009 6:07 pm, edited 1 time in total.
User avatar
mrhodes40
Family Elder
 
Posts: 2066
Joined: Thu Sep 23, 2004 3:00 pm
Location: USA

Postby mrhodes40 » Thu Jan 29, 2009 6:00 pm

Napay,
Stratton did a paper on venous ulcers and CPn......

People do not really know what the mechanism is for venous ulcers other than if they reduce the stricture in the femoral vein, the lesion usually heals a lot.

People should not get the idea that saying the MS lesion may be the same as a venous lesion means that we all of a sudden know everything about these lesions, we do not. It also does not mean that past MS research is somehow no longer important or that this necessarily counters it.

Researchers write paper all the time on some new MMP9 thing or iron thing or other thing related to the venous ulcer and how it got there. It is just as widely varied as reading MS lesion research, the difference is that they know how to impact the lesion in venous ulcers: relieve the stricture.
Most of the time, that makes a huge difference, but not all the time, so there is still interest in how these dang things got started in the first place.

The Schelling & Zamboni idea is that this causes it straight up, no other factors, but there may be more to the story than that if venous ulcers are like MS lesions

If MS lesions and venous ulcers are both similar and the pathology is related to the upstream vein and stricture, then we can assume likewise there remains unknowns about the MS lesion as well; how did it get there and why did it start and what caused the strictures anyway.

And as I said Stratton did a paper on CPn in venous ulcers proposing they play a role in the causation of them. So Cpn MS research, Cpn venous ulcer research, threads everywhere, it is not a done deal. More research will clarify it hopefully! I am thankful for this line of thinking personally and feel it offers a great new line of exploration even if all is not known.

I also take abx and think they help a lot, though I progressed too, so more co factors interest me, personally. I am planning both abx and venous stuff, if I can get it!
User avatar
mrhodes40
Family Elder
 
Posts: 2066
Joined: Thu Sep 23, 2004 3:00 pm
Location: USA

Postby notasperfectasyou » Thu Jan 29, 2009 8:53 pm

mrhodes40 wrote:Stratton did a paper on venous ulcers and CPn......


Do you have link for it? I'm still working on Schelling. It's hard to read schelling, it reminds me of the OJ case. Ken
User avatar
notasperfectasyou
Family Elder
 
Posts: 774
Joined: Thu Feb 09, 2006 4:00 pm
Location: Northern Virginia

PreviousNext

Return to Chronic Cerebrospinal Venous Insufficiency (CCSVI)

 


  • Related topics
    Replies
    Views
    Last post

Who is online

Users browsing this forum: No registered users


Contact us | Terms of Service