Sotris,
What does Dr Simka mean in slide 28:
"Does CCSVI account for the initiation of MS
-MS Patients who had their first attack of the disease at a younger age presented with less severe ccsvi
-Therefore, since a more severe blockage did not result in an earlier beginning of neurological symptoms , it may mean that the OTHER FACTOR, and not CCSVI, is responsible for the initiation of MS."
Is Dr Simka suggesting CCSVI and other factors are responsible for MS rather than CCSVI alone?
To me given the preliminary studies we have seen so far this does make more sense than the idea that CCSVI alone causes MS.
[/b]
Does MS cause CCSVI?
Re: Does MS cause CCSVI?
Please define MS. As far as I know, MS is the presence of disseminated scars in the brain. It is impossible that this could produce anything.gainsbourg wrote:I know this question was discussed on the recent "CCSVI and iron" thread but I'd be interested to hear the views of anyone who might have missed it.
gainsbourg
Maybe you mean by MS the underlying condition that produces the scars, but then you are speaking about something unknown and that could be not unique. It is difficult to assert anything in those conditions.
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gainsbourg
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The name "multiple sclerosis" can be misleading. The number of scars present often shows no correlation with the severity of symptoms experienced. MS is basically a disease of chronic inflammation of the white matter in the brain and/or spine. This is why anti-inflammatory drugs such as steroids, or immunosuppresents temporarily help with symptoms. It is also why the illness often has periods of remission.frodo wrote:as I know, MS is the presence of disseminated scars in the brain
My whole point concerns the inflammatory nature of MS. The CNS is constantly fed with huge amounts of blood - every second - because brain matter consumes blood like nowhere else in the body. The same amount is constantly drained. Once chronic, inflammatory problems arise within this tissue there is inevitably going to be a disruption in this blood flow - which the vascular system simply isn't designed to cope with.
There's no getting away from the fact that this unnatural flow could gradually, perhaps over a decade or so, put a strain on the venous drainage system and bring out congenital weaknesses.
Look at other parts of the body for comparison, like varicose veins in the legs. Don't be surprised if wearing high heels too often disrupts the blood flow to your leg muscles to the extent that you end up getting varicose veins. The same thing can happen if you disrupt the leg circulation by standing up to much in your job, or subjecting your legs to other unnatural strain over a long period of time. You bring out a congenital weakness.
Or what about that other notorious venous insufficiency - hemorrhoids - a congenital weakness that is brought on by restricting blood flow to the rectum, e.g. through constipation or pregnancy.
Cece - you made some valid points. I should have said it explains why MS progression isn't halted by fixing the veins (rather than saying "it explains why MS isn't cured").
Also, if as you claim, everyone with MS does turn out to have venous problems it could be that a tendency to venous problems in the CNS is shared by people in general - only it takes a long term disruption in cerebral blood flow to bring any weakness out - such as the chronic inflammation in MS.
After all, non MS people do get CCSVI - maybe that's why other illness like Parkinson's are also now being associated with CCSVI. Again, possibly due to a chronic disruption of cerebral blood flow which eventually puts a strain on the veins.
gainsbourg
or maybe it was this mechanism. Let's see if this get's heard: MS causes scar tissue cells. they wash down the pipes. These cells have a 'clenching' effect they use to close wound. Drawing tissue together. This causes the stenosis.
Issue: If there are no preexisting blockages why would the blood stop in the juglars? this model would describe an issue that would happen in the heart.
possible answer: While you are sleeping and lying horizontal the blood in your neck lies stagnant (?) and that's when the immune cells do their dirty work.
Let's see if this theory gets heard.
Issue: If there are no preexisting blockages why would the blood stop in the juglars? this model would describe an issue that would happen in the heart.
possible answer: While you are sleeping and lying horizontal the blood in your neck lies stagnant (?) and that's when the immune cells do their dirty work.
Let's see if this theory gets heard.
http://www.albertahealthservices.ca/fea ... -sheet.pdf
a paper by alberta health where they present the same idea.
discussed in this thread
http://www.thisisms.com/ftopict-10341-alberta.html
a paper by alberta health where they present the same idea.
discussed in this thread
http://www.thisisms.com/ftopict-10341-alberta.html
Would this be a suggestion to support the idea that MS had become a 'catch all' classification? I ask as the theory you propose would predispose CCSVI while those structural anomalies listed, the opposite.Billmeik wrote:Im not saying this is true. Im just saying there is another model that can work to explain ccsvi. If it was that way I don't see why clearing the ccsvi wouldn't help anyways...
no argument here.. imho, in order of importance.. effective immediate - treat all 'late stage' with the skills at hand!!.. at the same time - expidite 'best practice' to treat all others then, get it done!!.. in parallel, research 'cause & effect'.Billmeik wrote: If it was that way I don't see why clearing the ccsvi wouldn't help anyways...
a lot of the structural anomalies can be explained. If you do some reading on varicose veins you see the weirdest stuff, veins that do backflips, turn in on themselves. Iron deposition.
The bone stuff can't be explained though and is the strongest point for ccsvi->ms
The strongest point for ms->ccsvi is that it is the most obvious idea to many doctors. It needs to be ruled out. It shouldn't be hard but yes that's how science works.
It's interesting to note that patients can do this research. Patients, like Ashton Embry the geologist, can write papers and add valuable input to the discussion. Can we prove ccsvi->ms?
I think the first big patient contribution to the actual research would be someone trapping restenosis. Time stamped pictures proving that chicken egg problem goes restenosis->ms attack.
Thar would kind of solve this problem too.
The bone stuff can't be explained though and is the strongest point for ccsvi->ms
The strongest point for ms->ccsvi is that it is the most obvious idea to many doctors. It needs to be ruled out. It shouldn't be hard but yes that's how science works.
It's interesting to note that patients can do this research. Patients, like Ashton Embry the geologist, can write papers and add valuable input to the discussion. Can we prove ccsvi->ms?
I think the first big patient contribution to the actual research would be someone trapping restenosis. Time stamped pictures proving that chicken egg problem goes restenosis->ms attack.
Thar would kind of solve this problem too.
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MS_HOPE
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Does MS cause CCSVI?
Gains, it appears that Dr. Sclafani may have answered your original question about MS causing CCSVI "Yes", though frankly I don’t know why. I was rather stunned to read his post describing his recent presentation on CCSVI and MS in Belfast, where one of the four major points he made was: " 1. that ccsvi has many causes although ms was the most common cause".
I'm sorry I don't have the "Quote" thing down, but you can read Dr. Sclafani's original post about this on p. 228 of the topic "DrSclafani answers some questions”. My question/post is on p. 229, and his response on p. 231.
I said, in part (p. 229):
Oh dear, Dr. S, now I'm really confused. Thanks so much for your summary of the Belfast debate. One statement you made really got my head spinning: "I made four major points
1. that ccsvi has many causes although ms was the most common cause...."
YIKES. From all I've read, I'm convinced it's the other way around - that MS is probably caused, at least in large part, by CCSVI (and other concurrent, and probably variable factors, depending on the individual pwMS.) I am persuaded by the thinking of Ashton Embry (cited on p. 226 of this thread by NZer1) as to the probable causes of MS.
Dr. Sclafani replied (p. 231):
CCSVI is a clinical entity caused by outflow obstruction of veins. The most common association is with MS but it is not proven that ccsvi causes ms. CCSVI may result in symptoms seen in patients with MS. Those symptoms may not be resulting from ms, but rather from ccsvi
So (Liz speaking again), while I agree that causation of MS by CCSVI has not (yet?) been proven, to me neither has the converse! I still don’t understand why Dr. Sclafani made that statement.
Here’s most of his original post (p. 228):
"ok let me share the discussions that occurred in Belfast it was quite a challenge and I am not sure there was a winner.
There were four speakers. Dr. Goianfranco Campalani, an MS patient who is a cardiothoracic surgeon at the Royal Victgoria was first.
Then TWO neurologists spoke back to back. Dr Stanley Hawkins is the senior neurologist in Belfast and is a consulting neurologist in the Royal Victoria Hospital, Belfast City Hospital and the Causeway hospitals. He is a well written MS neurologist. He was fol.owed by Martin Duddy who was also a consulting neuorogist with special interest in MS. He is a busy clinician. Finally yours truly got to speak
Dr Campalani gave a detailed account of his disease and the effects of balloon angioplasty on his life. It was the common description of progressive deterioration to the point of dysfunction and his dramatic improvements after balloon angioplasty. Followed again by recurrence, repeated angiopastly and a satisfied patient. Dr Campalani passionately spoke in favor of the procedure as a patient. He acknowledged that existing disease was not likely to be totally reversed and accepted his residual symptoms. He argued in support of universal availability of the liberation procedure.
Dr Hawkins then proceeded to state that neurologists understood this disease better than most. Perhaps in a wry joke, he showed a line illatration of the brain and spine and then insisted on repeating this in case it was too complicated for the audience. I could not tell whether he was insulting or just making a bad joke. He then reviewed the natural ihistory of MS, indicated that it took a long time to reach SPMS. He showed various tables indicating the waxing and waining course of MS, indicating that long periods of remision occured without treatment, that placebo was a real problem for assessing research, He pointed out that quality of life scores were not really very scientific and then stated that Zamboni's paper in JVS would not have been published in a neurology journal for its statistical deficiencies.
I had a lot of difficulty with Dr Duddy's presentation. He seemed to be mocking the entire subject as irrelevant. He kept pointing out things that proponents put forth and kept snickering and laughing about it. I could not tell whether he was mocking in a conptemptuous way.
he then reviewed samboni's papers, deconstrucing them as poor science with suboptimal outcomes abd crappy data. He discounted Zamboni's work because he had 100% correlation in ultrasound. he dsmissed zivadinov's confirmation because zivadinov know zamboni so "we couldnt really accept that, could we?" biased and all.
He showed some placebo studies and argued that the improvements seen by zamboni were less than those improvements reported for placebo trials. Interesting how he brought up the "unacceptable" zamboni data and then used that data to prove his point.
He then brought out the big hitters, the kahn editorial (lots of good data there) and the doepp paper as proof positive that zamboni was wrong.
Finally the commercial enterprises that are performing liberation were charlatons. That a 7,000 pound expense for this procedure was a real hardship. I wondered what he thought of the expense of some of the DMDs
Finally I had an opportunity to speako
I made four major points
1. that ccsvi has many causes although ms was the most common cause
2. that other causes of ccsvi are treated. I asked why MS patients could notgg be treated.
3. I argued that demands for a randomized trial were very premature if needed at all. i showed them the diagnostic challenges, the laack of clarity about the type, size, duration of balloon angioplasty, the unclear role of doppler, MRV, venography etc made it very unclear what represented best practice. without that knowledge we cannot compare liberation to durgs or to sham, etc. I gave countless examples of the confusing issues and numerous examples of bizarre veins
Finally I argued that the patients were not satisfied with the status quo. That they were intelligent and could make up their minds about whether it was worth their while to seek treatment. I warned the neurologists that a paternalistic attitude would one day bit them in the ass.
a vote was taken at the end and most did not commit one way or the other. the surgeons told me that their minds were opened by the debate.
I spoke to dr hawkins at the evening's dinner. I reiterated my need for collaboration between neurologists and interventionalists. I asked him how he would propose that i create that collaboration. He didnt give me a satisfying answer.
was the trip worth it? I thought it was . i think minds were opened a bit. Lets not give up hope about neurologist partnerrs. We really do need them
Hey......I am jet lagged beyond belief....have a good evening."
I thought the jet lag might explain it, but am still confused even after his reply to my post.
Liz
I'm sorry I don't have the "Quote" thing down, but you can read Dr. Sclafani's original post about this on p. 228 of the topic "DrSclafani answers some questions”. My question/post is on p. 229, and his response on p. 231.
I said, in part (p. 229):
Oh dear, Dr. S, now I'm really confused. Thanks so much for your summary of the Belfast debate. One statement you made really got my head spinning: "I made four major points
1. that ccsvi has many causes although ms was the most common cause...."
YIKES. From all I've read, I'm convinced it's the other way around - that MS is probably caused, at least in large part, by CCSVI (and other concurrent, and probably variable factors, depending on the individual pwMS.) I am persuaded by the thinking of Ashton Embry (cited on p. 226 of this thread by NZer1) as to the probable causes of MS.
Dr. Sclafani replied (p. 231):
CCSVI is a clinical entity caused by outflow obstruction of veins. The most common association is with MS but it is not proven that ccsvi causes ms. CCSVI may result in symptoms seen in patients with MS. Those symptoms may not be resulting from ms, but rather from ccsvi
So (Liz speaking again), while I agree that causation of MS by CCSVI has not (yet?) been proven, to me neither has the converse! I still don’t understand why Dr. Sclafani made that statement.
Here’s most of his original post (p. 228):
"ok let me share the discussions that occurred in Belfast it was quite a challenge and I am not sure there was a winner.
There were four speakers. Dr. Goianfranco Campalani, an MS patient who is a cardiothoracic surgeon at the Royal Victgoria was first.
Then TWO neurologists spoke back to back. Dr Stanley Hawkins is the senior neurologist in Belfast and is a consulting neurologist in the Royal Victoria Hospital, Belfast City Hospital and the Causeway hospitals. He is a well written MS neurologist. He was fol.owed by Martin Duddy who was also a consulting neuorogist with special interest in MS. He is a busy clinician. Finally yours truly got to speak
Dr Campalani gave a detailed account of his disease and the effects of balloon angioplasty on his life. It was the common description of progressive deterioration to the point of dysfunction and his dramatic improvements after balloon angioplasty. Followed again by recurrence, repeated angiopastly and a satisfied patient. Dr Campalani passionately spoke in favor of the procedure as a patient. He acknowledged that existing disease was not likely to be totally reversed and accepted his residual symptoms. He argued in support of universal availability of the liberation procedure.
Dr Hawkins then proceeded to state that neurologists understood this disease better than most. Perhaps in a wry joke, he showed a line illatration of the brain and spine and then insisted on repeating this in case it was too complicated for the audience. I could not tell whether he was insulting or just making a bad joke. He then reviewed the natural ihistory of MS, indicated that it took a long time to reach SPMS. He showed various tables indicating the waxing and waining course of MS, indicating that long periods of remision occured without treatment, that placebo was a real problem for assessing research, He pointed out that quality of life scores were not really very scientific and then stated that Zamboni's paper in JVS would not have been published in a neurology journal for its statistical deficiencies.
I had a lot of difficulty with Dr Duddy's presentation. He seemed to be mocking the entire subject as irrelevant. He kept pointing out things that proponents put forth and kept snickering and laughing about it. I could not tell whether he was mocking in a conptemptuous way.
he then reviewed samboni's papers, deconstrucing them as poor science with suboptimal outcomes abd crappy data. He discounted Zamboni's work because he had 100% correlation in ultrasound. he dsmissed zivadinov's confirmation because zivadinov know zamboni so "we couldnt really accept that, could we?" biased and all.
He showed some placebo studies and argued that the improvements seen by zamboni were less than those improvements reported for placebo trials. Interesting how he brought up the "unacceptable" zamboni data and then used that data to prove his point.
He then brought out the big hitters, the kahn editorial (lots of good data there) and the doepp paper as proof positive that zamboni was wrong.
Finally the commercial enterprises that are performing liberation were charlatons. That a 7,000 pound expense for this procedure was a real hardship. I wondered what he thought of the expense of some of the DMDs
Finally I had an opportunity to speako
I made four major points
1. that ccsvi has many causes although ms was the most common cause
2. that other causes of ccsvi are treated. I asked why MS patients could notgg be treated.
3. I argued that demands for a randomized trial were very premature if needed at all. i showed them the diagnostic challenges, the laack of clarity about the type, size, duration of balloon angioplasty, the unclear role of doppler, MRV, venography etc made it very unclear what represented best practice. without that knowledge we cannot compare liberation to durgs or to sham, etc. I gave countless examples of the confusing issues and numerous examples of bizarre veins
Finally I argued that the patients were not satisfied with the status quo. That they were intelligent and could make up their minds about whether it was worth their while to seek treatment. I warned the neurologists that a paternalistic attitude would one day bit them in the ass.
a vote was taken at the end and most did not commit one way or the other. the surgeons told me that their minds were opened by the debate.
I spoke to dr hawkins at the evening's dinner. I reiterated my need for collaboration between neurologists and interventionalists. I asked him how he would propose that i create that collaboration. He didnt give me a satisfying answer.
was the trip worth it? I thought it was . i think minds were opened a bit. Lets not give up hope about neurologist partnerrs. We really do need them
Hey......I am jet lagged beyond belief....have a good evening."
I thought the jet lag might explain it, but am still confused even after his reply to my post.
Liz
CCSVI: Making Sense of MS
Hey, I have the quote thing down! 
He's talked before at the Michigan fundraiser and the Sclafani symposium that CCSVI is found and treated when it's caused by other things, such as dialysis catheterization. So I understood this to be the same point: that it doesn't matter what caused the CCSVI, that it warrants treating.
He's talked before at the Michigan fundraiser and the Sclafani symposium that CCSVI is found and treated when it's caused by other things, such as dialysis catheterization. So I understood this to be the same point: that it doesn't matter what caused the CCSVI, that it warrants treating.
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1eye
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Re: Does MS cause CCSVI?
gainsbourg wrote: ...conclusion that CCSVI causes MS. Surely we should be considering the possibility that it might be the other way round.... that the blood flow problems come first and weak veins are exploited second (as a result of those blood flow problems).
I don't see how this even describes 'MS' causing CCSVI. All you have said is that blood flow problems come first. Are you saying 'MS' has caused them? How?
Remember, MS is basically chronic inflammation of these nerves, and once inflamed, the delivery of blood must surely alter or be disrupted in some way or other.
This sounds pretty vague. What way or other? Oh, you were getting to that...
Maybe the body tries to compensate for the inflammation by delivering even more blood to help the sick nerves, or, perhaps blood flow is reduced, simply because it moves more slowly through inflamed tissue.
Does it? I thought inflamed tissue required direct delivery of oxygenated blood. That's why inflamed areas turn red. This would make problems already present with drainage worse, and if the inflamation is directly caused by reflux, say, you have a vicious cycle, all caused by CCSVI (which seems to be either congenital or traumatic). CCSVI includes stenosis and reflux. It is hard to imagine how inflammation could cause them in the first place. It is a question of degree.
Your description seems to depend on a large increase in red blood to the brain.
The brain is designed to pump 1.5 pints of blood per minute back to the heart - even a slight change (more or less) over a long period of time, could start exploiting weaknesses.
The brain does not pump. It drains. If there is pumping it is done by the heart or by the thoracic muscles.
Let's avoid use of 'exploit'. That implies motivation on the part of 'MS'. And thinking. Whatever it might be, it doesn't think.
You mean it causes weaknesses to get worse. That means they have to precede 'MS'. So 'MS' is now making an existing problem worse. And since it is caused by CCSVI (the existing problem) 'MS' gets worse, causing (by more inflammation?) CCSVI to (maybe) get worse. Wasn't it bad enough for you? Aren't we chasing our tail here?
Inflammation cannot affect the amount of blood pumped into your brain enough to cause any amount of insufficiency or reflux. The problem of CCSVI is a higher degree of problem, which though it may be chronic is also acute enough to directly cause fatigue, nauseating dizziness; immediate problems. To do that you would probably have to have enough inflammation to kill you too. Once dead, you will not care if CCSVI causes 'MS' or not.
It explains why MS doesn't always seem to be cured by fixing the veins (because the venous problems weren't causing the MS, it was the other way round).
We are not gods and cannot 'fix the veins' so well that they are always 100 percent fixed. Plus we are not taking nearly enough time or concentrated effort to always be able to discover all the abnormalities first time. Plus we are deliberately staying out of the brain, because ballooning is not such a good idea up there.
It explains why the venous problems often come back so quickly after repair (because MS is the real cause of the venous problem - and MS hasn't gone away).
Our simple procedures cannot be a long-term fix like a stent is. If you leave 'MS' out of it, we could use something more permanent. Do you have something? I say elastic recoil is less the older you get. That might be a good thing to scientifically prove. We are depending on veins to be nice and stay open. Sometimes, they don't.
It explains why so many people have MS, yet show no signs of CCSVI (because MS isn't caused by CCSVI).
There aren't enough of them to worry the people doing the Liberating.
It explains why an increasing number of people are being found to have CCSVI but no MS (because MS isn't caused by CCSVI).
Increasing? More than, say, misdiagnosis of 'MS'?
...Blood flow to the inflamed nerves of the CNS is greatly improved, therefore easing MS symptoms.
But I thought you said CCSVI doesn't cause those symptoms. So how could fixing it reduce them? Are you trying to confuse me?
Besides, it is de-oxygenated blood we are Liberating. So how does that directly affect oxygenated blood to the inflamed area?
You have one hour until all pencils must be down.
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Not a doctor.
"I'm still here, how 'bout that? I may have lost my lunchbox, but I'm still here." John Cowan Hartford (December 30, 1937 – June 4, 2001)
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gainsbourg
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Thanks again for so many interesting comments - please note that I am not against treatment of CCSVI and hopefully it will eventually turn out well for all those brave pioneers. Only time will tell, in the meantime, the more we understand about it, the better.
Liz, I hadn't read your interview before with Dr Sclafani...glad someone had the courage to ask those difficult questions!
My reasoning is that people with MS, like everyone else have approximately a 22% chance of having or developing CCSVI in any case before you take into account the effect of the MS disease process. So these prior defects could include any of those in your list. The diseased MS brain then puts a chronic strain on the vasculature that exploits congenital venous defects much more seriously - resulting in a greatly increased incidence of CCSVI than in healthy people.
gainsbourg
Liz, I hadn't read your interview before with Dr Sclafani...glad someone had the courage to ask those difficult questions!
I think I see where you're coming from - but I'm not saying that all venous abnormalities found in those with MS are caused by MS. Obviously some congenital defects would certainly have been there at birth, such as your example of a "missing vein." You have to remember that almost a quarter of non MS-rs have also been found to have CCSVI, so presumably a whole range of venous defects are common at birth in the population as a whole.Pcakes wrote:your theories although intriguing, seem to neglect to address the variety of structural anomalies reported.. webs, septums, inverted valves, malformed valves, missing veins, etc..
My reasoning is that people with MS, like everyone else have approximately a 22% chance of having or developing CCSVI in any case before you take into account the effect of the MS disease process. So these prior defects could include any of those in your list. The diseased MS brain then puts a chronic strain on the vasculature that exploits congenital venous defects much more seriously - resulting in a greatly increased incidence of CCSVI than in healthy people.
gainsbourg