This Is MS Multiple Sclerosis Community: Knowledge & Support

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One thing that struck me is that Zamboni's original tests weren't truly blinded. If an MS patient had an obvious physical problem, the doctors and techs would realize the person probably had MS. The article seems to confim this:



Also, some people have been arguing that the big difference in percentages between Zamboni and the Buffalo group was due to differences in ultrasound machines. But

I don't understand.. why can't it just be accepted that these abnormalities are very common and effect people in different ways.. I refer to MS and the wide scope of symptoms and varying degrees of disability. For me, the need to diagnos CCSVI in healthy controls is critical and only serves to reinforce the validity of this theory..

How so, PCakes?

Are you saying that you think CCSVI being found in healthy controls is beneficial to this theory of MS?

Finding CCSVI in healthy controls is a benefit to the science of CCSVI. If Stenosis is found then they can be watched for development of MS or other diseases.
MS isn' an all or nothing disease. Some people can have the disease and not even know it, while some can have it affect them profoundly.

I think CCSVI needs to be studied and researched, on the other hand it has some positive results from the "casual observations". These aren't to be ignored and in some cases you or your dr are remiss on not moving on it.

IMHO

Just a thought........as a layperson....

Not every person with elevated lipids/ cholesterol has Atherosclerotic/ vascular disease. Other factors like genetics, hypertension, Diabetes etc make it more likely that this person will develop the vascular complications of the elevated Cholesterol. Cholesterol lowering is nevertheless an integral part of preventing the onset of vascular disease if it is not yet present and of treatment when it is already present. If a person with Coronary artery disease has elevated Cholesterol you definitely want to lower the Cholesterol aggressively.

Similarly, not every person with CCSVI may have MS ( perhaps 20% ). Other factors like Vit D Deficiency, genetics, Chronic EBV infection make it more likely that the person may develop MS. Treating the CCSVI should similarly be considered as part of preventing the onset of MS and definitely as part of the treatment if MS is already present. The other factors should be treated as well whenever possible along with immunomodulators/ CRAB's.

Just my 2 cents....

WHO CARES IF THE TESTS ARE BLINDED OR NOT. Treat the patients. Time and Tim again we get lost in the trees. I have seen so many people get better so fast. Let them get the surgery.

i might be mistaken here, but my understanding of it all, after watching the web meeting is
the buffalo study did not use venogram, only non invasive scans. and that the non invasive scans only will give an indication of ccsiv or not ccsiv

and that if they added venogram examination it is not only highly likely that they would confirm ccsiv in the ms patients that didnt have any indication of ccsiv with non invasive scans, as well as it is highly likely that ccsiv would come back negative of ccsiv if they used venogram on them as well.

didnt the doctor conducting the buffalo study say that, or did i just misunderstand it all. didnt he say that if venogram had been used ccsiv would only be reported in about 6% of healthy population, and in 90 odd percent of ms patients.
wsnt there something about that the controll groups with ccsiv but no ms, were patients with other disorders, and patients with close genetic link to ms patients.

i mean ccsiv might be a very effective treatment of ms, but it still leaves a lot of question unanswered to cuase and effect.
as a patient my main consern is, will it make me feel better, will i benefit. i belive so, that is why i am having it done.

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<div>I have lived with ms for 8 years. The last year has been hell, I've gone from shite to even worse every single month, until my liberation in May. </div>

also like to add.....i second gordon above. treat the ptients, time will tell, sureley the cost and risk of doing so is a lot smaller then waiting.
and then we would have some very convinsing results, one way or the other.
it is a low risk, low cost procedure, comepared to tysabri, chemo and a lot of the other shit that we get infused with.
not everybody dies from tysabri, but there is a lot of other nasty sideeffects as well. even if it has been proved to slow down the disease in a lot of patients, they do not know if it will work for you.

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<div>I have lived with ms for 8 years. The last year has been hell, I've gone from shite to even worse every single month, until my liberation in May. </div>

This is a very good point. CCSVI likely does not by itself contribute to the development of MS, as shown by Zamboni's study where 20% of healthy controls had CCSVI but not signs of MS. (In addition, there are many examples of jugular vein issues, including dialysis patients.) Thus, we can infer that there may likely be another contributing factor in the CCSVI and MS association. My logic is a little rusty, but I think this is correct:

If CCSVI and factor X, then MS
If not MS, then not CCSVI or not factor X

So, to develop MS one must have CCSVI AND factor X. If one does not have MS, then either one does not have CCSVI or does not have factor X. Those without MS can have CCSVI or factor X, but not both.

Hi Hope , Greenfields' answered this perfectly and much more eloquently than I could. Thank you. I only might add.. eventually they will know what type of stenosis/ insufficiency should be treated proactively.
Till then.. default to 'all'.
p

it would be excellent news if studies came back with the results you are portraying there.
but it should not be the end of the research or the hope for treating ccsiv as an effective treatment for ms, even if the numbers do not come back quite as conclusive.

To diagnose ms today, you need leasions on mri, you need protines in spinal fluid, and you need two seperate neurological attacks.

we know attacs and lesions are due to auto imune responses to leaks in blood-brain-barrier. question is, what is causing the b-b-b to be faulty?
does it have to be the same cause in all ms patients? can it be ccsiv in some of us, and something else in others? maybe at some point they will be able to say, you got ms brought on by ccsiv, and you got ms due to lack of vitamin d? just thinking out loud here.

they say that attacks and lesions is just the tip of the iceberg, and that the real disabeling part of the disease is the reduction in brain volume that happens over time, and can not be measured by counting placks shown on mri. but this stage is not part is not even part of the current definition of ms. question is what is causing our brains to shrink
could it be ccsiv?

could attacks be caused ny one thing, and brain shrinking by somehting else? does it have to answer everything to be valid?

as the doctors have commented on in their articles, ccsiv is a venous problem, when set straight patients have a lot of symptoms relived. symptoms that are common in ms, but is not even part of the definition. symptoms like cogfog, fatigue, balance head aches etc.

i do not think that your ccsiv + factor unknown = ms model is apropriate here. i think we are looking at a much more complex model. not saying that ccsiv is unimportant. if i thought that i would not have it done.

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<div>I have lived with ms for 8 years. The last year has been hell, I've gone from shite to even worse every single month, until my liberation in May. </div>

I think you mean Zivadinov and the BNAC study. Zamboni did not find CCSVI in healthy controls. Or did he? (my mind is muddy these days)

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My name is not really Johnson. MSed up since 1993

I think that the most important thing will be to follow the progress of treated people over time and see what symptoms and measurable "ongoing damage" is left once the CCSVI problems are overcome.
It seems that if we look at the CCSVI drainage issues and remove them from the puzzle we will be able to look at the resulting situation and work with that. There is no doubt that there is a link between the two so lets look at what can be learned by removing one part of the equation. CCSVI is one thing at last that can be adjusted in the equation.
We need to let go of what has been said about the MS disease so far, such as the immune theory as it is restricting the flow of other proven influences in the disease process from standing out and adding to the learning process. For example diet and hyperbaric oxygen also LDN and 4aminoperidine had some effect for some people does this have links to CCSVI. I think sometimes we go too far into the science and get lost in the grey area of possibilities science brings.
Thinking outside the box has more merit.

please note that Jane Qiu is a writer, not a M.D. Of any kind, and I would suspect, not as knowledgeable about MS and CCSVI as some of the contributors here. She does say that she has post-doc work in neuroscience. Sounds to me like she is an apologist for those opposed to CCSVI in the MS societies.

According to Zivadinov's numbers, less than 0.37% of people with CCSVI have MS.

U.S. MS prevalence 133 per 100.000, (133*0.62)/(100000*0.22+133*0.62) = 0.0037; possibly less, once one includes stenosis prevalence in other neurological diseases etc