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1eye wrote:Is 200 the number? The large Italian study said they had to reach 400 before the complications went to a low enough rate.

Yeah, I think 400 is the number but that's a high standard to reach. 200 might be a reasonable compromise. 0 is the number of procedures previously done by the doctors involved in Dr. Trabalousee's study. Now they're up to 7 but those are all being included as data, instead of discarded as being below the learning curve.

All other things being equal, we are interested in the effect of stenosis, or blockage, or malformation, on the individual vein flow rates in the neck. Assuming there are no more changes in flow resistance or local pressure before and after the stenosis, you can gauge neck flow rate reduction by measuring it in two places, for instance at neck arteries and neck veins, much as Dr. Zamboni has done.

This is helpful, thanks.

brocktoon wrote:Good question, it depends on where that stenosis takes place. But let's consider that a vein's largest area below the mandible is 18mm^2, and the smallest would be 6mm^2. So therefore, by Traboulsee's reading, the calculation would be 6mm^2/18mm^2 which is 33%, or ~66% stenosed, and therefore categorized as stenosis. Let's consider someone, who may have a closed vessel, or maybe a hypoplastic jugular vein and his maximum diameter is 8mm^2, and now let's say his smallest caliber size is 7 mm^2. The calculation comes out to 88%, or 12% stenotic, which would not be categorized as stenosis, even though this area size is very small and most likely has very reduced flow out of that vessel. What if the values were 2mm^2 and 3mm^2 (non-stenotic)? or 40mm^2 and 100 mm^2 (stenotic).

Using a fixed value may be a safer bet because it may only take a certain area size to guarantee XYZ ml/s amount of flow. And we have 4 papers using an approach where stenosis is defined as IJV calibier <= 12.5 mm^2 above the C3 neck level, and <= 25mm^2 below the C3 neck level, with consistent results.

This seems logical and I much prefer your approach to the percentage approach.
It seems there should be precedence for this in other diseases of veins or outflow obstructions. All these different ways of measuring are being worked out just for CCSVI.

So you compare the area of a vein to the average normal vein at that level in the jugular. I was trying to say that length of a narrow part of a vein can affect the flow rate, although not to the same degree as narrowing. A short narrowed part of a stuck valve may present a higher resistance than a longer but still tubular length of vein, just because of the slit shape of the opening as compared with the circular or ellipsoid shape of a vein.

Could you just measure flow rate at the vertically lowest part of the jugular (say where it empties out) and compare that to an average normal? Or would the normal be too big of a range? Might be better just to look at flow rates in two normal sized and similarly shaped points on either side of the suspect problem area, or top and bottom of the neck. But there could be veins which add to or divert the flow, in between. So the total is important to compare with normal too. Pressure could be different, as well as flow rate.

Total flow rate in all the largest veins into and out of the brain would be nice to compare to a normal.

Maybe you should look at plethysmographic results and compare those with a normal range too.

Does it matter which side of your body is on top when you are supine on your side?

1eye wrote:Might be better just to look at flow rates in two normal sized and similarly shaped points on either side of the suspect problem area, or top and bottom of the neck.

I think top and bottom of the neck is what they're doing. C2 is top and C6 is bottom.

from the presentation at sherbrooke wrote:Our Evidence of Flow Abnormalities
There are five levels of analysis:
1. Evaluate ST vs. NST patients
2. Compare individual IJV flows at C2 & C6
3. Evaluate total IJV flow at both C2 & C6
4. Evaluate normalized IJV flow at both C2 & C6
5. Establish a quantitative threshold that separates HCs from stenotic MS patients

In the material presented so far, we have presented the flow information for every patient in a 2D quantitative plot.
If one were to evaluate only point number two by merging all the patient information into a simple histogram it is unlikely that we would find any difference between MS and HC.

Chronic cerebrospinal venous insufficiency in multiple sclerosis:the first encore.

Introduction
I guess you have all seen the summary so I will not bother to include it here. I will try to give just the salient points in the rest of the paper. In his introduction Traboulsee makes great play of his study being the first to have catheter venography to 'validate' it's 'magnetic resonance venography.' He also emphasises this is the first blinded study of venography. He also puts emphasis on 'standardisation of imaging protocols.'

Stated Aims
1. “Clarify whether venous blockages are unique to multiple sclerosis”
2. “Assess the sensitivity and specificity of the 2 doppler ultrasound criteria for the disorder referred to as 'chronic cererbrospinal venous insufficiency' compared with catheter venography.”

Groups and blinding
He has three groups: 1) pwMS 2) their healthy siblings and 3) age and sex matched controls all of whom were naïve subjects in terms of vasoactive drugs and venous procedures. He says all study team members were masked to the participants status also canes aids etc belonging to participants were hidden. In fact the bodies of the participants were also draped leaving only the head and neck visible. He also asked the study team members to guess which subjects belonged to which group to confirm his masking. No evidence of unmasking was reported. So far so good.

Methodology
Regarding the procedure: a fair amount of detail is given about the catheter venography I will not recount it all here. It seems reasonable in general . I would say the same about the ultrasound protocol. He also says that the sonography equipment was identical to Zamboni's and the operators were trained by Zamboni. He says the catheter venography protocol was standardised across the three centres and that there were three training sessions for the performance and interpretation. He doesn't explain whether he is using 'and' exclusively or inclusively so it is not clear whether there were nine (three at each centre) training sessions or three in total. In fact 18 and 6 in total are also a possible interpretation – three sessions for operators + three sessions for assessors x three centres =18 or 3 at BC and 3 at Sask = 6. The content, length and depth of the training is not indicated. Subsequent (or previous) practice and experience is not mentioned. Training and experience of the sonographers is not described. Training and experience are critical in relation to both sonography and venography. Traboulsee does not describe it in detail. Whether or not it all really amounts to a true use of Zamboni's protocols (or better) is not clear to me. Whether it was good enough for the purpose of this study needs careful scrutiny. He spells out the 4 criteria he used to define pathology for his sonography and catheter venography and they seem to me to agree with Zamboni's.

Results

There are three main tables summarising the results which I have tried several ways to insert but I can't get it to work.

The aggregated data shows basically no difference between pwMS and controls, But these are the figures for Saskatchewan compared to British Columbia. There are clear differences throughout.

For the ultrasound:
pwMS Controls
British Columbia 16 (38%) 21 (36%)
Saskatchewan 19 (51%) 13 (38%)

For the Catheter Venography:

pwMS Controls
British Columbia 27 (77%) 41 (80%)
Saskatchewan 21(70%) 16 (48%)

I am not sure it is worth saying much about the sonography as it is well known to be unreliable but even here Sask seems to find greater evidence of pathology in the MS group than BC 51% to 38%. But look at the catheter venography BC finds slightly more in the control group (77% to 80%) where Sask finds a lot more in the MS group (70% to 48%.) BC has the two groups scoring about the same. Saskatchewan has a 45% higher score in the MS group than in the control group. That is a big difference. The obvious questions to pose are 'Is the Sask group doing something different to the BC group?' and if so 'Is the Sask group doing it right and the BC group doing it wrong? (or vice versa?)' Traboulsee should acknowledge and address this in his discussion as a possible source of error. He mentions it and even records that the difference is significant but there is no attempt to explain or mitigate the potential error or justify the aggregation of the two sets of data. He just goes ahead and does it. He may be relying on his claim to have 'standardised' the testing across the centres. If he was applying a well known and well validated and standardised published test that had already been used extensively then there would be some justification for ignoring the discrepancy. But he isn't. He is applying a protocol which has developed himself and which he says is the first attempt ever made to create one.

Now basic steps to ensure that the different centres are doing the same thing is absolutely necessary and can be called standardisation but it is not the same thing as using a 'standardised test.' I also accept it is very early to address issues of the validity and reliability of his protocol in this study but it may have helped his case a lot if he had gone some way towards that. Without it we are left wondering: Was any attempt made to validate their protocol by retests or by testing assessors against each other? Is there other evidence to support the assumption that what BC was doing was the same as what Sask was doing? Did the operators and assessors share their work equally between all sites or did they only work at one? How many operators/assessors were there?

Discussion
Traboulsee has chosen to go along the route of refusing to do treatment trials and instead to attempt to measure and compare the degree of 'pathology' as defined by Zamboni's criteria in people with MS and normals. I have never been convinced that would be a fruitful path to follow and so it seems here. If we accept his aggregated results they do show no difference between the two groups so that if his testing is reliable and his aggregations are justifiable then the conclusions he has drawn are reasonable. Even then a first small study of 143 subjects would not justify the fanfare which has accompanied this paper.

But he has not really achieved either of those things. He posed the question 'whether venous blockages are unique to multiple sclerosis? Now it would be easy simply to say 'obviously not every venous blockage causes MS.' Varicose veins are an obvious example of venous blockages which do not cause MS. There are other syndromes I could name where blockages in jugular veins have other outcomes than MS. He really needs to state this aim more precisely. Sadly imprecise statements of aims are often accompanied by lack of precision elsewhere as happens here.

So I am assuming the real question which Traboulsee wants to address is 'whether the claimed pathological conditions which are called CCSVI are present in pwMS and not in normals.' To do that he has to address the real difficulties in assessing those conditions using sonography and catheter venography. Using Zamboni's criteria (and training and equipment) and ensuring blinding and rigid conformity in the testing is simply not good enough. I would say that is very obvious now in late 2013 but was fairly obvious even in 2010.

Sonography
The problem with ultrasonography is that it is very operator dependent. In which case the training and experience of his operators and their precise instructions are critical. But none of that is detailed in this report. I have seen 50 procedures stated as a bare minimum to start to become proficient. Sonographers experienced in assessing CCSVI now have hundreds maybe thousands of procedures under their belts. So if Traboulsee's operators were naïve to the procedure at the start they may have achieved basic proficiency by the time they finished. But we don't know they were as Traboulsee does not say. Similarly we know at least three days of training were performed but not what it was? How much of it was given to sonography? How many sonographers in total were used?

The claim from proponents of CCSVI is not just that a trained and experienced operator/assessor (which may be one person or a team) is able to identify CCSVI using sonography but they claim that they use that high level of expertise and experience to guide their investigation. So in addition we need to ask 'Were Traboulsee's team given leave to operate in the same way to search intelligently for pathology?' Or were they instructed to mechanically perform exactly the same tests in exactly the same places? If that was the case how sure can we be that they correctly identified the pathologies which may have been present? Was the operator the same person as the assessor? If not was the assessor allowed to guide the actions of the operator or was he later presented with the data which the operator had gathered independently? Separating the operator from the assessor helps in respect of blinding but it could pose a problem in terms of the quality of the data gathering. You really need expert operators and assessors with the freedom to use their expertise to find the pathology. It is hard to see how that could be done if the operator and assessor were not the same person or did not collaborate. I get the impression here that they were separate people who did not collaborate but it is not explicitly stated. I quite understand that Traboulsee may be striving for an objective standardised protocol and therefore does not want a free-ranging investigation but I would question whether that is an appropriate experimental design in this field.

But actually we don't know exactly what the protocol was so without knowing answers to those questions why should we not simply conclude the sonography was flawed and ignore it? Traboulsee needs to do a lot more to make this convincing.

Venography
Catheter venography has the same problems as the sonography does. The images may be clearer but the experience, training, expertise of the operators and assessors are still critical. And Traboulsee's precise protocol is again not spelled out. Where there separate operators and assessors? Did they collaborate? Did the protocol allow the operator/assessor to search for problems like an experienced IR would or did they just mechanically repeat the same measurements in the same place for each subject? The same caveats I have made above apply. If you wish to identify as accurately as possible the same set of problems which it's proponents call CCSVI you really need to follow the same procedure they use. Imposing restrictions for the sake of standardisation and objectivity could reasonably be viewed as deliberately prejudicing the data collection. (I would very much welcome the opinions of practising IRS about that view.)

Traboulsee's protocol mentions measurements being taken at two places in each jugular vein as well as pressure readings. But he does not say how the jugular vein was identified? Did the IR first advance the wire to the sigmoid sinus? If not how are we sure the jugulars were correctly identified? Traboulsee records injecting dye twice in the upper and lower jugular vein and I am guessing this was above the valve (T doesn't say.) He repeats the procedure in the azygous vein. It is not clear to me how many different sites in the azygous vein were used. This sounds like a mechanical procedure that was repeated as near identically for each subject. If that is correct Traboulsee is obviously striving to control operator bias and maintain an objective standard. He does not mention variations and does not describe the IR actively searching for pathology. For example incompetent valves can be identified by placing the catheter below the valve and injecting dye against the valve. This does not seem to have been done. Intraluminal defects are best detected by IVUS as is cross sectional area. This was not done. So the answer to the question “Would this procedure detect all existing potential CCSVI pathology?” has to be probably not.

Trasboulsee claims catheter venography is the gold standard. It is certainly not true today to say that catheter venography alone is the gold standard. Catheter venography plus IVUS in the hands of an experienced IR allowed to freely search for symptoms may now (for the time being) be considered a gold standard. That being the case some may then say that this research has only historical value. It was said clearly in 2010 and has been repeated since that CCSVI first needs to be investigated qualitatively because we do not yet know enough to design trustworthy protocols to support more quantitative research. Similarly the criteria that Zamboni originally proposed have also evolved. I don't think any IR now relies on them.

It can reasonably be concluded that Traboulsee's catheter venography protocol will have identified some of the conditions present in his subjects which may be thought to contribute to CCSVI but certainly not all. The next question is clearly can we reliably assume that the amount of missed data will be more or less the same for each group so that there is no significant bias either way? Well not really if the contention is that pathology exists in the MS group and not the control group then it is possible to miss something that exists in the MS group but that pathology is assumed not to exist in the control group so cannot be missed there. If the effect is there then it can only be considered a source of uncontrolled error. Traboulsee's data throws up another oddity here: the high rate of narrowing found in the healthy control group. No other study has found this. I think we can safely assume this is non-pathological narrowing and there is a lot of it. The existence of phasic narrowing which disappears after CCSVI treatment has been known about for the past three or more years so there seems a basis to consider it possible to have both pathological and non-pathological narrowing. So we have to consider the possibility that there are a lot of false positive results in this data. For the data to be valid for the purpose I set out then we have to assume that there is missed data which may be positive and a fairly large amount of false positive data. I should say at this point that Traboulsee would consider the high rate of narrowing in normals as not false positive at all but as proof that everyone has narrowing so it is entirely normal. He would say the narrowing found by CCSVI proponents is just more of the same. But to do so is to rule out the possibility of pathological narrowing from the outset. If Traboulsee rejects the possibility of pathological narrowing from the outset then this research is pointless. If he accepts for the sake of the study that pathological narrowing may be possible then he needs to be able to distinguish one from the other. If he had found a wide difference of the prevalence between the two groups it would have supported the idea that CCSVI exists. Unfortunately even if we take his results as accurate, finding the same amount of narrowing in both groups does not prove the opposite view unless we can say which portion of the narrowing is claimed to be pathological by proponents of CCSVI and which isn't. As Traboulsee himself (and proponents of CCSVI would agree) has shown that non-pathological narrowing may exist in large amounts. For this data to be valid we have to have a way of quantifying the amount of CCSVI pathology missed by Traboulsee's protocol and a way of isolating narrowing which would not be considered pathological by CCSVI proponents. If you could do that then credible adjustments to the data might be made to increase it's accuracy. Phasic narrowing seems to have been found most often (but not exclusively) in the upper jugular veins. Traboulsee could have tried removing the data for narrowing found in the upper jugular veins and run his statistics again. If the new figures then tilted in favour of CCSVI could be construed as support for the idea that those data were non-pathological narrowing. If it doesn't then it would strengthen his view.

Of course there may be another reason for the high rate of narrowing in normals that we don't know yet but until we know what it is or corroborating data is found in other research this very unusual finding must leave a question mark over the whole data set. That coupled with the possible effect of the rigid protocol in missing existing pathology in the MS group leaves another question mark. I am of course not ruling out the possibility that Traboulsee has in fact considered all these points himself already and has convincing replies to them. If so I would like to hear them.

Inconsistency in the Data and Conclusions
Two areas of potential error have been pointed out above. The third is the variability between the data collected in BC and the data collected in Sask which I mentioned earlier. In my view Traboulsee does not adequately deal with any of them.

Traboulsee set out to design a study which would make up for the deficiencies he perceived in previous research which lacked blinding and controls. He claims his is the first study 'with careful attention to standardisation of imaging protocols and blinding.' As far as I can make out he has made a pretty good job of that although I am still unclear exactly what his protocols are. But the question is does his experimental design actually enable him to get at the things he wants to isolate and study? He has ensured blinding and conformity of testing as far as was possible with the equipment he has used. But in doing so he seems to have thrown the baby out with the bath water. Rigid conformity in his protocols has 'shaped' his data at the outset because he has not allowed his operators and assessors to freely search for pathology placing the catheter wherever they want. Lack of IVUS means he may have missed a whole class of pathology which may have been present. The inability to distinguish the apparently high level of non-pathological narrowing from claimed pathological narrowing makes it very difficult to know exactly what his data does represent. An obvious question is “Is it largely made up of noise?”

For me the major conclusion to draw is that this type of study is simply not the right way to go and only serves to confuse matters further. Striving for objectivity and conformity in testing when the instruments used demand to be guided by an experienced and expert hand using that experience and his own intelligence to decide which way the investigation should go. I have tried to think of obvious analogies to express this one might be

“If the person aiming the gun is not the same person pulling the trigger does that make it more likely you will hit the target or less?”

That is the situation you are creating when you separate the operator from the assessor.

Another is: If you had been injured in a car crash and the doctor treating you was told he could not talk to the nurse who was injecting you (and vice versa) would that make it more or less likely they would identify all your injuries?

That is the situation we have when the operator and assessor cannot collaborate.

The experimental design Traboulsee has constructed does not seem to me suitable to support the aims he has set himself and the result is that his data is seriously flawed in several ways. Another word which comes to mind repeatedly is inconsistency. Inconsistency between sites – between sonography and venography – in respect of narrowings in normals between these and other published results.

His gold standard is now at best silver.

Friedmann and Wattjes' headline “Chronic cerebrospinal venous insufficiency in multiple sclerosis: the final curtain” is simply laughable. Small flawed study with as yet no confirmatory studies (which is more or less what they said about Zamboni) would be nearer the mark.

In conclusion it seems even more obvious to me that trying to prove a link between CCSVI and MS or that CCSVI causes MS or vice versa by this type of study is largely a fool's errand. The emphasis should always have been on treatment trials.

I don't like the inclusion of siblings. Venous obstructions may not have led to MS in the unaffected sibling but may still be present if such malformations are hereditary.
It is disturbing that the two centers found such disparate results, and that the data was then combined.

AMcG wrote:...He doesn't explain...it is not clear...is not indicated... is not mentioned...is not described...does not describe it in detail...is not clear to me...needs careful scrutiny...spells out...BC finds slightly more...where Sask finds a lot more...about the same. Saskatchewan has a 45% higher...

Sounds like either the reader or the author are uncertain. Where there is the least possibility of confusion or ambiguity the paper must clarify. I would have thought these questions would all have been answered by peer review.

AMcG wrote:That is a big difference. The obvious questions to pose are 'Is the Sask group doing something different to the BC group?' and if so 'Is the Sask group doing it right and the BC group doing it wrong? (or vice versa?)' Traboulsee should acknowledge and address this in his discussion as a possible source of error. He mentions it and even records that the difference is significant but there is no attempt to explain or mitigate the potential error or justify the aggregation of the two sets of data. He just goes ahead and does it. He may be relying on his claim to have 'standardised' the testing across the centres. If he was applying a well known and well validated and standardised published test that had already been used extensively then there would be some justification for ignoring the discrepancy. But he isn't. He is applying a protocol which has developed himself and which he says is the first attempt ever made to create one.

AMcG wrote:...it may have helped his case a lot if he had gone some way towards that. Without it we are left wondering: Was any attempt made to validate their protocol by retests or by testing assessors against each other? Is there other evidence to support the assumption that what BC was doing was the same as what Sask was doing? Did the operators and assessors share their work equally between all sites or did they only work at one? How many operators/assessors were there?...

I think I see definite signs of curiosity insufficiency here. Besides, this multi-center study has the collective good will of the Conservative Party of Canada and the Canadian MS Society's need for cash at the helm. The results from different provinces are expected to be as different as their economies and their cultures.

AMcG wrote:...He really needs to state this aim more precisely. Sadly imprecise statements of aims are often accompanied by lack of precision elsewhere as happens here...

...If that was the case how sure can we be that they correctly identified the pathologies which may have been present? Was the operator the same person as the assessor? If not was the assessor allowed to guide the actions of the operator or was he later presented with the data which the operator had gathered independently? Separating the operator from the assessor helps in respect of blinding but it could pose a problem in terms of the quality of the data gathering...

He only needs to state his aims more clearly if he actually wants people to know what they are.

AMcG wrote:...I would question whether that is an appropriate experimental design in this field...

...we don't know exactly what the protocol was so without knowing answers to those questions... why should we not simply conclude the sonography was flawed and ignore it? Traboulsee needs to do a lot more to make this convincing.

AMcG wrote:Venography...
...has the same problems as the sonography does....Traboulsee's precise protocol is again not spelled out...[they]need to follow the same procedure[used]...restrictions for the sake of standardisation and objectivity could reasonably be viewed as deliberately prejudicing the data collection...Traboulsee's protocol mentions measurements being taken at two places in each jugular vein as well as pressure readings. But he does not say...sounds like a mechanical procedure...identically for each subject...the answer to the question “Would this procedure detect all existing potential CCSVI pathology?” has to be probably not...

...Catheter venography plus IVUS in the hands of an experienced IR allowed to freely search for symptoms may now (for the time being) be considered a gold standard. That being the case some may then say that this research has only historical value...can we reliably assume that the amount of missed data will be more or less the same for each group...it can only be considered a source of uncontrolled error...

Also refusing to answer an offer of help from an experienced IR who advocates IVUS betrays an intention to avoid a specific, unwanted result, which IVUS might have provided.

AMcG wrote:...Traboulsee himself (and proponents of CCSVI would agree) has shown that non-pathological narrowing may exist in large amounts. For this data to be valid we have to have a way of quantifying the amount of CCSVI pathology missed by Traboulsee's protocol...this very unusual finding must leave a question mark over the whole data set. That coupled with the possible effect of the rigid protocol in missing existing pathology in the MS group leaves another question mark....

..the variability between the data collected in BC and the data collected in Sask.

...I am still unclear exactly what his protocols are...Lack of IVUS means he may have missed a whole class of pathology which may have been present. The inability to distinguish the apparently high level of non-pathological narrowing from claimed pathological narrowing makes it very difficult to know exactly what his data does represent. An obvious question is “Is it largely made up of noise?”...

...this type of study is simply not the right way to go and only serves to confuse matters further...

...Another word which comes to mind repeatedly is inconsistency. Inconsistency between sites – between sonography and venography – in respect of narrowings in normals between these and other published results.

His gold standard is now at best silver...

...Friedmann and Wattjes' headline “...the final curtain” is simply laughable...trying to prove a link between CCSVI and MS or that CCSVI causes MS or vice versa by this type of study is largely a fool's errand. The emphasis should always have been on treatment trials.

So our plucky hero drops an imaginary curtain in front of himself, and goes out to the front of the stage for some well-deserved applause. Well, one or two applause anyway...

This paper is being published in the Lancet. It should have a strong reply from pwMS (20,000+ ?) who have undergone Balloon Venoplasty. Anyone up for working on a letter???
MarkW

Lancet. 2013 Oct 8. pii: S0140-6736(13)61747-X. doi: 10.1016/S0140-6736(13)61747-X. [Epub ahead of print]
Prevalence of extracranial venous narrowing on catheter venography in people with multiple sclerosis, their siblings, and unrelated healthy controls: a blinded, case-control study.
Traboulsee AL, Knox KB, Machan L, Zhao Y, Yee I, Rauscher A, Klass D, Szkup P, Otani R, Kopriva D, Lala S, Li DK, Sadovnick D.
Source
Department of Medicine, University of British Columbia, Vancouver, BC, Canada. Electronic address: t.traboulsee@ubc.ca.
Abstract
BACKGROUND:
Chronic cerebrospinal venous insufficiency has been proposed as a unique combination of extracranial venous blockages and haemodynamic flow abnormalities that occurs only in patients with multiple sclerosis and not in healthy people. Initial reports indicated that all patients with multiple sclerosis had chronic cerebrospinal venous insufficiency. We aimed to establish the prevalence of venous narrowing in people with multiple sclerosis, unaffected full siblings, and unrelated healthy volunteers.
METHODS:
We did an assessor-blinded, case-control, multicentre study of people with multiple sclerosis, unaffected siblings, and unrelated healthy volunteers. We enrolled the study participants between January, 2011 and March, 2012, and they comprised 177 adults: 79 with multiple sclerosis, 55 siblings, and 43 unrelated controls, from three centres in Canada. We assessed narrowing of the internal jugular and azygous veins with catheter venography and ultrasound criteria for chronic cerebrospinal venous insufficiency proposed by Zamboni and colleagues. Catheter venography data were available for 149 participants and ultrasound data for 171 participants.
FINDINGS:
Catheter venography criteria for chronic cerebrospinal venous insufficiency were positive for one of 65 (2%) people with multiple sclerosis, one of 46 (2%) siblings, and one of 32 (3%) unrelated controls (p=1·0 for all comparisons). Greater than 50% narrowing of any major vein was present in 48 of 65 (74%) people with multiple sclerosis, 31 of 47 (66%) siblings (p=0·41 for comparison with patients with multiple sclerosis), and 26 of 37 (70%) unrelated controls (p=0·82). The ultrasound criteria for chronic cerebrospinal venous insufficiency were fulfilled in 35 of 79 (44%) participants with multiple sclerosis, 17 of 54 (31%) siblings (p=0·15 for comparison with patients with multiple sclerosis) and 17 of 38 (45%) unrelated controls (p=0·98). The sensitivity of the ultrasound criteria for detection of greater than 50% narrowing on catheter venography was 0·406 (95% CI 0·311-0·508), and specificity was 0·643 (0·480-0·780).
INTERPRETATION:
This study shows that chronic cerebrospinal venous insufficiency occurs rarely in both patients with multiple sclerosis and in healthy people. Extracranial venous narrowing of greater than 50% is a frequent finding in patients with multiple sclerosis, unaffected siblings, and unrelated controls. The ultrasound criteria are neither sensitive nor specific for narrowing on catheter venography. The significance of venous narrowing to multiple sclerosis symptomatology remains unknown.
FUNDING:
MS Society of Canada, Saskatoon City Hospital Foundation, Lotte and John Hecht Memorial Foundation, Vancouver Coastal Health Foundation, and the Wolridge Foundation.
Copyright © 2013 Elsevier Ltd. All rights reserved.
PMID: 24119384

Mark wrote:It should have a strong reply from pwMS (20,000+ ?) who have undergone Balloon Venoplasty. Anyone up for working on a letter?

I can't do it. I'm in mid-exacerbation. Just reading this thread gives me too much stress. Don't want to blow a fuse. (reaches for sub-lingual nitro spray -- outdated, must remember to renew)

Mark,

I have the doc of the full study, interested?

Rgds,

Robert

Hello Robert,
I need to read the whole Lancet paper but am away from Oxford. Please send it to mark@walkerm.com.
Thanks,
Mark

Okay. We now have more CCSVI > MS study results to discuss.

Apart from masking everything but faces and necks .... and hiding canes ..... this study appears to be conducted in a fairly straight forward manner.

As with all things CCSVI ...... results are all over the map.

From my perspective ..... MrSuccess could give a rats ass about the size and shape of veins. Round . Oval. Square. Figure of eight..... IT PLAYS NO ROLE.

It is the ABILITY to successfully move blood from the brain >>>> back to the heart that matters most. The FLOW rate and Volume are what need to be studied.

This is what Dr.Zamboni is trying to achieve. Again , Dr.Zamboni is so far in front of this race ..... it's laughable. Try to keep up boy's.

Interestingly of all ....... Dr. Traboulsee makes no mention of any symptom changes - for better or worse - in any of the treated pwMS.

That's all MrSuccess is interested in . That's where the rubber hits the road.

This study could be a huge waste of time and money.


MrSuccess

MarkW wrote:Hello Robert,
I need to read the whole Lancet paper but am away from Oxford. Please send it to mark@walkerm.com.
Thanks,
Mark

It's in your mailbox....

Regards,

Robert

"Sometimes these things can become separated, and what we've found is that although CCSVI as defined by Zamboni doesn't really exist ... we still have the situation where thousands of Canadians have gone abroad and have had a treatment ... (and many have) reported significant improvement."

Trying to stay true to your masters and still qualify for research dollars isn't so easy is it, Doctor Traboulsee? You have to pretend to accept some anecdotal numbers, empirical evidence, you might call it, yet still adopt the attitude of never being heard to call him 'Dr. Zamboni' in public. Just 'Zamboni' as if he might be a faceless corporation. It wears thin after a while. But remember, people will not need to know Dr. Einstein's "qualifications", because of what he did. They might even use his full name.

Again with that 'doesn't really exist' horse-manure? Please, give it a rest, Dr. Traboulsee! Call it what you must, better men than you believe it exists, and have documented the proof. I'm really tired of this dead-horse flogging, as I believe the thinking public is, also. Half of all studies are below average, by definition, and this one doesn't even come close.