CCSVI and BBB

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

Postby patientx » Fri Mar 19, 2010 6:39 pm

Mark,

I understand the point you are trying to make, but I would like to expound on one other thing:
MarkW wrote:For the record - If you have MS, get tested for CCSVI and treated if it is present. Then wait for the scientific community to explain if it stops progression of MS.

I see a few problems with this. One, it is not completely clear what constitutes CCSVI, and how best to identify it. Second, treating it is not without serious risks. One person has sustained damage to his heart due to stent migration, and it was later revealed the stents were installed for something that was not a problem. Now it appears someone else is having worsening problems as a result of his jugular valve being treated angioplasty.

Yes, almost all of the MS treatments involve some risks. But these risks need to be traded-off with the benefits. Further, the patient needs to know the risks.
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Postby sbr487 » Fri Mar 19, 2010 7:29 pm

ozarkcanoer wrote:Speculation can be rewarding if it doesn't get contentious. I think speculation is the start of true ideas. Like Dr Zamboni the first time he tried a Doppler wand on an MS patient : "Hmmmm, I wonder what would happen if I look here ????!!!!!".

One story that I love (I don't know if it is true or not) is that Galileo was at church and was bored and he watched the lanterns swaying from the ceiling. Voila, the first real observation of how a pendulum works. But poor Galileo, like many innovators, was stifled by the church for his sun-centered heresy. So let us always speculate !!!!!

ozarkcanoer


I am also not very comfortable in saying that non specialists cannot make observations on specialized topics (such as CCSVI).
Just imagine ... the world would have lost the most gifted mathematician, Ramanujam, if Prof. Hardy had dismissed his theorems as fruad since Ramanujam was not a formal mathematician. What Ramanujam wrote theorems just as matter of fact Prof. Hardy found it difficult to believe at first. What makes Ramanujam's story important is that he was self taught and had no formal training in mathematics.

http://en.wikipedia.org/wiki/Srinivasa_Ramanujan
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Postby Cece » Fri Mar 19, 2010 7:31 pm

Rokkit wrote:I've been wondering lately if it's going to be a moot point anyway. People appear to be lining up in droves for every doctor willing to do the procedure, so at some point you have to wonder if the large majority of patients are going to already be treated long before any study can prove anything about CCSVI.


In another thread, it was estimated that there have been about 200 liberations performed so far worldwide. While I don't know the number for the total afflicted with m.s. in the U.S. alone, it is certain that 200 is but a drop in the bucket. Plenty of time for those studies to get done!

In Dr. Sclafani's thread, he talked about the possibility of using an intravascular ultrasound catheter and the steps he'd take to get it out as an idea to other doctors and the scientific community (I'd have to double-check what he said but it involved writing a paper on it after keeping data on his usage of it)...so there are papers that can come out of this from the current wave of procedures. And of course there was Dr. Dake's paper, which was accepted for publication on its merits, as I understand it, and then dropped because of the controversy.

None of what I've said has much to do with the original topic, I'm afraid. I continue to vote for adhesion molecules as the explanation for how the BBB is breached, even though I find it hard to understand adhesion molecules. :)
"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 cheerleader » Fri Mar 19, 2010 9:08 pm

sooooo, back to the blood brain barrier, and the model proposed by Dr. Simka, Dake, Zamboni and others-

When Dr. Dake and I were first discussing Dr. Zamboni's research back a year ago, he mentioned that this model of CCSVI in MS looked a lot like congestive venous myelopathy. We already have a medical model for how venous congestion can create demyelinating lesions.

This is venous congestion created by DAVFs or AVMs. The demyelination in venous congestion is well documented. BTW, vascular steal is when there is a reduction of blood flow thru the arteries, due to venous blockage. This creates ischemic injury.

OBJECTIVE: Although venous congestion is considered to be a major cause of progressive myelopathy in patients with spinal dural arteriovenous fistulae (DAVFs), the neurological deterioration in patients with spinal intradural arteriovenous malformations (AVMs) has been attributed to hemorrhage or to vascular steal. To reexamine this theory, we analyzed our own cases of spinal vascular diseases. METHODS: In 24 patients with spinal vascular diseases, those who demonstrated progressive myelopathy with T2 hyperintensity in the spinal cord on magnetic resonance imaging (MRI) were diagnosed as patients with congestive myelopathy. We further examined the clinical courses, MRI findings, and reversibility of these cases. RESULTS: Venous congestion was judged to be a cause of neurological deterioration in 13 patients (7 DAVFs, 6 intradural AVMs). The T2 signals on these patients' MRI scans were located in the center and extended over several levels not corresponding to distribution of ischemia due to arterial steal. Of the patients who were diagnosed with congestive myelopathy, no differences between those with DAVFs and those with intradural AVMs were apparent in terms of clinical manifestations and reversibility. Eight (four DAVFs, four intradural AVMs) of 13 patients experienced neurological improvement after treatment. All patients with poor outcomes had intervals from onset of more than 3 years and showed contrast enhancement of the spinal cord on MRI studies. CONCLUSION: Spinal intradural AVMs as well as spinal DAVFs can be a cause of venous congestive myelopathy. Regardless of its etiology, congestive myelopathy is potentially reversible if properly diagnosed and treated.


an aside....this study states congestive venous myelopathy is potentially reversible if caught early...it seems 3 years after injury had poorer outcomes. This is why Dr. Zamboni urges studies now.
http://www.ncbi.nlm.nih.gov/pubmed/11383723

We describe three patients with progressive myelopathy, in whom autopsy revealed spinal cord pathology compatible with that of venous congestive myelopathy (VCM) associated with dural arteriovenous fistula (AVF), formerly known as angiodysgenetic necrotizing myelopathy (Foix–Alajournine syndrome). In these three patients, common symptoms were gait disturbance and sensory disturbance of the extremities, and these symptoms slowly worsened. The clinical diagnoses varied and included spinal cord intramedullary tumor, cervical spondylosis and multiple sclerosis. At autopsy, all the patients showed enlarged, tortuous venous vessels on the dorsal surfaces of the spinal cord at the affected levels. In the affected spinal cord parenchyma, necrotic lesions manifested by various degrees of neuronal loss and gliosis, with increased numbers of hyalinized vessels, were evident. The presence or absence of associated spinal dural AVF could not be identified histopathologically. Even with the help of modern neurological examination methods, early and accurate clinical diagnosis of VCM is sometimes difficult. When encountering patients with progressive myelopathy, VCM, although recognized as rare, should be considered as an important differential diagnosis.

http://www3.interscience.wiley.com/jour ... 1&SRETRY=0

So, here is someone diagnosed with MS who had tortous veins upon autopsy....creating progressive myelopathy.
I know, I know...this isn't exactly what Dr. Zamboni....this is DAVFs or AVMs in the spinal veins creating venous congestion, rather than stenotic lesions in the jugular and azygos veins creating venous congestion. But as Dr. Dake told me, we have a medical model for how venous congestion creates neurodegeneration and demyelination in the body. And it was a better explanation than the unknown mystery antigen the autoimmune proponents hypothesize. That was enough for me and Jeff.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby Vhoenecke » Fri Mar 19, 2010 9:33 pm

Thanks, that's enough for me too.


Val
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Postby Lyon » Sat Mar 20, 2010 7:42 am

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Postby Rokkit » Sat Mar 20, 2010 8:01 am

Lyon wrote:What needs to be done is to determine a conclusive test (venography?) to run on an even number of people with and without MS with absolutely equal effort to determine what the numbers are and whether stenosis does have some kind of unique relationship to MS. That would be a good first step towards believability.

I agree with this. I don't know if it's ethics or expense that is preventing it. I wish Buffalo would do venography on a subset of people from each of their groups to see if the results match the dopplers.
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Postby Lyon » Sat Mar 20, 2010 8:19 am

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Postby fogdweller » Sat Mar 20, 2010 9:27 am

What needs to be done is to determine a conclusive test (venography?) to run on an even number of people with and without MS with absolutely equal effort to determine what the numbers are and whether stenosis does have some kind of unique relationship to MS. That would be a good first step towards believability.


I am confused. Isn't this what Buffalo did?
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Postby Lyon » Sat Mar 20, 2010 10:37 am

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Postby fogdweller » Sat Mar 20, 2010 12:11 pm

thanks, Lyon.
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Evaluating Risks

Postby MarkW » Sun Mar 21, 2010 6:41 am

Evaluating Risks is important and to contine this conversation:
Patientx wrote:
I understand the point you are trying to make, but I would like to expound on one other thing:
MarkW wrote:
For the record - If you have MS, get tested for CCSVI and treated if it is present. Then wait for the scientific community to explain if it stops progression of MS.

Patientx: I see a few problems with this. One, it is not completely clear what constitutes CCSVI, and how best to identify it. Second, treating it is not without serious risks. One person has sustained damage to his heart due to stent migration, and it was later revealed the stents were installed for something that was not a problem. Now it appears someone else is having worsening problems as a result of his jugular valve being treated angioplasty.

Yes, almost all of the MS treatments involve some risks. But these risks need to be traded-off with the benefits. Further, the patient needs to know the risks.

MarkW: To be crystal clear on what I mean -
If you have MS, get tested for venous restrictions in the areas shown by Prof Zamboni. If any are present get balloon venoplasty performed to eleviate the restriction(s). If venoplasty is not successful then consider stents to reverse the restriction(s). Then wait for the scientific community to explain if it slows/stops progression of MS or not. Keep in mind that it could be many years before a fully researched explanation is available. Of course there are risks in doing this and understand them before doing anything. Personally I judge the risks as similar to taking part in an early drug trial. I have done drug trials so find the CCSVI risks as acceptable, but risk is a personal matter so YOU decide. Always remember that MS is a progressive disease so doing nothing does have risks. Of course if your current therapy has stopped your MS progession you are in a different position.

Hope this helps readers in thinking about what to do.

Kind regards,
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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BNAC Study

Postby MarkW » Sun Mar 21, 2010 6:50 am

I am expecting the Buffalo study to give the correlation coefficient between CCSVI and MS on a sample of 500 in April, not more. Later studies will give us more info. If as expected the answer is 0.55 or greater this is a definite reason for testing pwMS for CCSVI.

MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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BBB is too complex for me

Postby MarkW » Sun Mar 21, 2010 7:16 am

The BBB and MS is too complex for me but I will share a few probable points:
1 - In MS the BBB becomes permeable to cells which are usually blocked
2 - the permeabilty occurs at the time of a relapse in RRMS
3 - steroids 'repair' the BBB if a steroid pulse is given during a relapse
4 - pwMS have different genes/alelles from the average person
5 - MS incidence is governed by latitude except for places like Sardinia or where mothers/children have high vit D in diet
6 - MS incidence differs by birth month

With these clues and indicators (there are many more), I do not feel a complete answer to the cause of MS will emerge in the near future. However CCSVI appears to be a treatable symptom of MS, so why not treat the symptom ?

Kind regards,
Mark
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Postby patientx » Sun Mar 21, 2010 8:43 am

...This is venous congestion created by DAVFs or AVMs. The demyelination in venous congestion is well documented....
....But as Dr. Dake told me, we have a medical model for how venous congestion creates neurodegeneration and demyelination in the body. And it was a better explanation than the unknown mystery antigen the autoimmune proponents hypothesize.


Except neither of those citations mention demyelination.
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