第26屆歐洲MS治療研究委員會議 CCSVI新消息

CCSVI--the new strategy to come out of ECTRIMS---
會中的討論很棒, 值得大家參考!!

There are two new studies that are approaching CCSVI from a new angle...that of proving that CCSVI is not the cause MS. They both look at clinically isolated syndrome (CIS) and early MS are conclude there is no CCSVI. Both studies appear to be doing the doppler and venography testing incorrectly, and we'll get into more specifics tomorrow...but what I found interesting is that these studies actually found CCSVI in more progressed or later-stage MS. They do not deny CCSVI exists...but they are trying a new tactic. They are saying CCSVI is created DUE TO brain damage from MS. It's the old chicken and egg switcheroo.

Here's why this is interesting. It is obvious that the correlation to CCSVI and MS is undeniable. More and more patients are coming forward with positive venograms showing stenosis and reflux in the central veins. It is becoming impossible to ignore or deny. So, the neurologists and MS specialists are going to re-write the script and say, Yes...you do have CCSVI. But it's because you have MS. MS causes CCSVI. Let us treat your MS with our drugs, and your CCSVI won't progress.


Now, this was the question raised by the Alberta document (maybe MS causes CCSVI?) and I think those who hope to disprove CCSVI were very smart to pick up on this line of logic. Problem is...CCSVI exists. And it exists early in the MS disease process. Other doctors are finding it in early MS and clinically isolated syndrome. I've told the story of Dr. Dake testing the daughter of one of his first patients, and finding she had occluded veins, even though she did not have an MS diagnosis. She later had an MRI, and there were the white matter lesions. Dr. Dake treated her with angioplasty, even before she ever had an official MS diagnosis. The other daughter had great veins, no CCSVI and no MS. And Dr. Zivadinov told a similar story in Bologna, about the daughter of an MS patient in his study who was part of the healthy control group. Sure enough, she had CCSVI and it was a few months later she showed white matter lesions on MRI and received an MS diagnosis. And this is happening world wide.

Those who've been following this page already know that Dr. Byung B. Lee and a panel of international vascular experts have classified CCSVI stenosis as truncular venous malformations, formed in utero. Here's Dr. Lee's paper.

http://www.fondazionehilarescere.org/pdf/03-2518-ANGY.pdf

And we also know that these truncular venous malformations grow with the body, and get progressively worse with age. And yes, as inflammation in the body increases, the stenotic lesion will worsen as well. MS is a chronic disease which progresses over the duration of the disease...and venous malformations get worse as the body ages and disturbed blood flow continues to damage the veins. Chronic venous disease gets worse. CCSVI gets worse.

So, be prepared for the neurologists' new tactic...telling you that your MS has created your CCSVI. It's getting more interesting all the time....til tomorrow---

Joan (參與研討會者)
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會中有一派說法 說MS形成CCSVI 請看原文第1段 (these studies actually found CCSVI in more progressed or later-stage MS)

另一派的說法是 : CCSVI形成MS. 特別是在MS發展初期階段, 就可以看到CCSVI的 請看原文第3段 由美國史丹佛Dr. Dake的病人以及 Dr. Zivadinov的病人也都有看到同樣的狀況.. 在CCSVI症狀已經被診斷出來的時候, MS的症狀尚未出現(腦部未出現斑塊), 但是經過血管擴張之後, MS也不會再繼續發展..

共識: It is obvious that the correlation to CCSVI and MS is undeniable. 毫無疑問的，兩者彼此相互關聯,Problem is...CCSVI exists. 問題是CCSVI的本身的存在 會影響中樞神經導致肢體的障礙!

若是前者的說法為真, 那麼MS衍伸出CCSVI的結果只會造成病人肢體殘障且無法回復之不可逆的結果,-->輪椅要坐一輩子, 永遠無法再用自己的雙腳行走.... (文獻指出有50%的反覆發作型的MS有可能進一步的轉變為Secondary progressive MS 也許就是因為這個原因吧。)

若是後者的說法為真, 那麼能夠在MS的初期(臨床症狀 如腦部的斑塊 尚未表現出來的時候) 就可以先診斷出CCSVI的症狀再加以處理，就不用進展到MS了.(Dr. Dake treated her with angioplasty, even before she ever had an official MS diagnosis.)

所以不管是哪一種原因, 不管是先有雞還是先有蛋, 狹窄的靜脈是一定要被擴張的，不然 病情只會隨著時間而繼續惡化!!

既然如此, 還有什麼可以爭論的呢? 就解決這個狹窄靜脈的問題吧!

第26屆歐洲MS治療研究委員會議 CCSVI新消息