This Is MS Multiple Sclerosis Knowledge & Support Community

sorry to hear that, concerned, hopefully if she is interested in CCSVI she'll have the opportunity for local treatment someday, if it is what she wants.

CCSVIhusband wrote:But not according to this study. As I said, any researcher worth his or her salt, can conduct a study to tell you anything you want to hear about a topic. It just so happens that this is what they wanted to hear for this study. At least it admits that CCSVI is real ... now, define CCSVI ... (I think we can agree it's insufficient drainage) OK ... so did they include all possible insufficient drainage? Nope ... OK so invalid study in that respect.

Yes, they did not include all possible insufficient drainage, which I was really upset by. Invalid in that respect but not in all respects. It means that even though the criteria to have something count as CCSVI was extra stringent, they still found CCSVI. Would love to have seen if they'd found anything in a control group using catheter venogram but that was not a part of the design of this study and poses certain difficulties too (running cath venograms on healthy people).

I've said, I'll volunteer, find a doctor to do it on me. People volunteer for science all the time. I'm sure I'd volunteer (... should volunteer just to prove the point - and so would a lot of other husbands and wives who aren't blood related though they could separate out that criteria and see if relatives are or are not a factor ... so maybe that wouldn't even matter).

concerned wrote:My mother can hardly make it to local doctors appointments, travel is basically out of the question.

Sorry to hear that concerned.

.

CCSVIHusband I still wonder if you are slightly missing the point - even if you broaden the definition of CCSVI as you suggest there will still be a substantial relative difference between CIS and LMS with CCSVI. This strongly suggests that it is unlikely CCSVI causes MS.

Cece I agree it would have been fascinating to see a comparison with helthy controls. I do suspect under this strict criteria that the CIS and controls groups would have been very similar as congential defects were removed from the criteria.

My daughter was diagnosed officially with CIS in August, her first symptoms appeared months earlier.


She had angioplasty for 2 vessels - a double "candy wrapper" twist in the azygos with little flow and a partially blocked L IJV. 1 month after diagnosis.

IF a person early on has chronic ( but mild) cerebral hypoxia and chronic cerebral hypoglycemia and reflux with shear stress the endothelin 1 level would raise (it does) in the body's attempt to strengthen the vessels assault.

Endothelin 1 causes vein stiffness( lack of compliance and elasticity), vessel wall fibrosis, valvular hypertropy (thickening) this would over time make the CCSVI worse-------


If the CCSVI is worse , the cerebral hypoxemia and hypoglycemia get worse. The worse these get the more damage to brain tissues such as myelin, oligodendrocytes, etc. MS gets worse.

It is a viscious circle and CCSVI- the actual lesions would get worse over time even if they are congenital.

dreddk wrote:CCSVIHusband I still wonder if you are slightly missing the point - even if you broaden the definition of CCSVI as you suggest there will still be a substantial relative difference between CIS and LMS with CCSVI. This strongly suggests that it is unlikely CCSVI causes MS.

Cece I agree it would have been fascinating to see a comparison with helthy controls. I do suspect under this strict criteria that the CIS and controls groups would have been very similar as congential defects were removed from the criteria.

BUT that's not what they tested, ... so you can't extrapolate that from the air

All I'm saying is, my wife was diagnosed with, and treated for CCSVI before she had an MS diagnosis. She had a web in her veins, a stuck valve, and narrowing.

After those things were treated, a lot of her symptoms went away. Did her MS go away? No not as far as I know (but she didn't have any MRIs) ... so let's see. CCSVI treated, symptoms go away ... what caused the symptoms, it would seem CCSVI. Sounds "causal" in my books.

I just want people to see what we're dealing with here ... I don't think it's too much to ask that they understand the relationships people have to MS or CCSVI ... and whether they have any personal experience with it or not.

All I want is for people to go back and read the research from Cheer and her gang originally and take it to doctors and see if this is for them ... (and there is a lot of research) - Heck, SBR8R (or whatever the name is) posted two great articles about CCSVI like linkings to MS from decades ago today - new ones that weren't even mentioned before.

(EDIT - my edits were all on spelling errors I found while re-reading)

MegansMom wrote:My daughter was diagnosed officially with CIS in August, her first symptoms appeared months earlier.


She had angioplasty for 2 vessels - a double "candy wrapper" twist in the azygos with little flow and a partially blocked L IJV. 1 month after diagnosis.

IF a person early on has chronic ( but mild) cerebral hypoxia and chronic cerebral hypoglycemia and reflux with shear stress the endothelin 1 level would raise (it does) in the body's attempt to strengthen the vessels assault.

Endothelin 1 causes vein stiffness( lack of compliance and elasticity), vessel wall fibrosis, valvular hypertropy (thickening) this would over time make the CCSVI worse-------


If the CCSVI is worse , the cerebral hypoxemia and hypoglycemia get worse. The worse these get the more damage to brain tissues such as myelin, oligodendrocytes, etc. MS gets worse.

It is a viscious circle and CCSVI- the actual lesions would get worse over time even if they are congenital.

Exactly MM ... we'll argue about the chicken or the egg all day long - it's been thousands of years and that hasn't been solved (see my references to circular logic and we'll all be dead and gone before ALL of the answers are found).

Did your daughter get any results from the procedure (I'm sorry, I truly forget).

Sounds like your daughter and my wife had a similar experience though with this EARLY MS/CIS and CCSVI. Odd that two people on this small collection of a board would have that, when they found it so seldom in this study we're bantering about.

(funny too all the youtube videos and postings on facebook tell similar stories) ... but I guess we're not a formal study, so it's all anecdotal and doesn't count.

y'know I linked to this thread in Dr. Sclafani's thread, to support fogdweller's question, and he's going to come here to all this?

CCSVIhusband, could we move any discussion of skeptics to the Skeptics Mentality thread? I like having that thread, thank you Lyon for starting it.

MegansMom, endothelin-1! Forgot about that.

.

MegansMom wrote:My daughter was diagnosed officially with CIS in August, her first symptoms appeared months earlier.


She had angioplasty for 2 vessels - a double "candy wrapper" twist in the azygos with little flow and a partially blocked L IJV. 1 month after diagnosis.

IF a person early on has chronic ( but mild) cerebral hypoxia and chronic cerebral hypoglycemia and reflux with shear stress the endothelin 1 level would raise (it does) in the body's attempt to strengthen the vessels assault.

Endothelin 1 causes vein stiffness( lack of compliance and elasticity), vessel wall fibrosis, valvular hypertropy (thickening) this would over time make the CCSVI worse-------


If the CCSVI is worse , the cerebral hypoxemia and hypoglycemia get worse. The worse these get the more damage to brain tissues such as myelin, oligodendrocytes, etc. MS gets worse.

It is a viscious circle and CCSVI- the actual lesions would get worse over time even if they are congenital.

I get it. CCSVI causes the MS which causes the CCSVI which causes the MS which causes our lives to go spiraling down the toilet.

But how would you relate into your theory the study’s finding (assuming that it is valid!) that the presence of stenoses seemed to relate solely to length of time from disease diagnosis, rather than lesion load or disability?

And how would your theory account for the fact that patients who have had bone marrow transplants from their own regenerated "cleaned" cells have demonstrated on several studies a stoppage of disease progression and even some disease reversal? This procedure is done without touching the veins draining the brain.

I’m not disagreeing with you, I would just like to know how you would account for it.

And how would your theory account for the fact that patients who have had bone marrow transplants from their own regenerated "cleaned" cells have demonstrated on several studies a stoppage of disease progression and even some disease reversal? This procedure is done without touching the veins draining the brain.

I will concentrate on this point only. My energy and time are limited.

There is no proven therapy that stops MS. Proven as in multi center double blinded yada yada.

AFAIK those studies are mainly for RRMS. There are studies for SPMS or PPMS but they are very very few and their results are not clear. Again, AFAIK.

If we believe that in RRMS there is a strong inflammation we can think that those therapies are mere sophisticated antiinflammatories as someone in this forum once said .

so you can't extrapolate that from the air (as the skeptics have questioned others who have done that from studies) ...

All I'm saying is, my wife was diagnosed with, and treated for CCSVI before she had an MS diagnosis. She had a web in her veins, a stuck valve, and narrowing.

CCSVI treated, symptoms go away ... what caused the symptoms, it would seem CCSVI. Sounds "causal" in my books.

I take your point CCSVIHusband and I was merely speculating.

Coming back, as you suggest, to the hard facts, CIS subjects did not exhibit stensosis relative to LMS patients. If you broaden the criteria then yes, more people may be defined as CCSVI (and probibly more false positives too which may explain the Buffalo study controls). However the fact will remain that most CIS people do not have CCSVI.

The inference from this must be that CCVSI cannot be causing MS. This would also explain why a large percentage of those who have the liberation procedure experience no relief from their MS symptoms.

As Spock said " Logic is wreath of pretty flowers that smell bad"

PS I would have thought CCSVI believers would be heartened by this. It appears to show CCSVI does exist. Surely thats better than the alternative even if it doesnt cause MS.

Couple of points.
This study once again highlights that there is blind spots in the research done so far to disprove Dr. Zamboni's theory. (Are they on purpose?)

The studies that use MRI are proven to be variable over a time sequence, especially for RRMS and early possible MS. The monthly scans sequences have shown that the lesions appear and disappear monthly and likely more frequently if the scan interval was shorter.

The RRMS form of the disease is less predictable than SPMS and PPMS. The studies on RRMS cannot predict disease progression or cannot show cause for relapses. NO TWO people with MS are the same, similar but not the same.

Studies of PPMS and the outcomes of CCSVI treatment are going to require longitudinal study but will be more consistent than guessing reason for changes in RRMS disease, changes due to CCSVI treatment.

Until the same group of 'patients' are used in studies by the researchers, there will be speculation and discrepancies in published results.

Until there is more money at stake to prove CCSVI there will be slow progress in understanding the vascular involvement. While the nay sayers (with the financial backing) have the upper hand to drag this out and cause doubt and confusion to discredit vascular involvement time is wasted for PwMSers.

It will take someone to challenge directly by accessing the same research participants to resolve this wasted energy and resources avoiding duplicating what Dr. Zamboni has found and then treating options can be sort. It is possible to contact some of the trial participants of the naysayers research through Facebook and TiMS as they have commented for time to time. It would be more proactive to find these people and organize through the networks of treating IR's to test these same people using Dr. Zamboni's protocols, and end the speculation.

I have said before that the PwMS have to take the stand to get the truth out and end the impasses caused by financial interests. Use the same people in studies, MS is not a disease were you can use differing cohorts in different studies and attempt to 'conclude' any position on MS especially Vascular Involvement!