This Is MS Multiple Sclerosis Community: Knowledge & Support

I am ready now. All i need is about $5M.

Dear Dr. Sclafani!
Happy Birthday from Slovakia! Všetko najlepšie k narodeninám!
Erika

Funding... That's nothing. For pwCCSVI proceeding is sometimes not even possible...

Actually I was going to ask you something: what regime do you use for anti-coagulation lately? Do you expect that to change soon?

My experiences with that:

1. was on Plavix for one year after my heart-attack related angio, where 3 stents were used. I bruised a lot then because I had not had the procedure, and I probably tried to do more than I should have, a few years ago. I'm learning. Anyway for whatever reason, every bump or fall made a bad bruise.

2. was on Plavix for 1 month following procedure for CCSVI in 2010.

3. since heart incident of early 2009 have taken 1 aspirin/day, initially regular adult size, but cut back to baby size because I thought I must be getting nosebleeds from the dry air in winter, combined with a blood thinner. If I was right, I will not have them this winter. I will go back to the adult size in May if that works.

What I want to know is, since length of treatment seems to matter, are we paying that any attention? I hope my heart stents keep working. I don't know if you get clots with arterial stenting and it must be different for veins.

I have heard of everything from none to coumadin for life.

Hi Doc,

How was ISNVD 2013 in Poland?

Rgds,

Robert

Hi Dr S.

Have there been any studies on valves over time? Valves that have not been touched/PTA'ed to see if there are any changes in their performance or function?

Separate question;
If after PTA the valve re-stenosis' then is it valve related or incomplete destruction of valve and annulus or is it another area that was previously unseen or missed?

I am wondering if there may be an issue with the valves and that thickening or generally non functioning valves may be changing over even short periods of time eg the 're-stenosis' average after PTA.

If for instance in normal life the function of the valve waxes and wanes like MS does!

It is mysterious how this disease is fluctuating in two scenarios, one to a healthy lifestyle (change) and two with PTA and both are very similar outcomes symptomatically

i am not sure that they are that similar.

Now that White Matter lesions are found to be less connected to MS disease symptoms there may at last be a shift to measuring actual symptoms! This 'should' help find the tools to measure PTA benefits with a 'real' assessment.


Nigel

Diet changes and medications seem to alter the relapse rate and in some even halt progression, so could that mean the flow has improved without PTA?

I hope you had a pleasant birthday!

You've got a question that landed in this thread: chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic21128-30.html#p205902

The worst news this week, or any week, was that we've lost the Greek from the D. Wheelchair Kamikaze has a memoriam up: http://www.wheelchairkamikaze.com/2013/ ... oriam.html

Thanks Cece for posting both of these.

Dr S I have been reading up on the research that shows infection is an early co-incident factor in heart attacks and strokes and I find that there is lots of talk about spasms in arteries.

*Does this also effect veins?

The work being done regarding vein health is indicating that the valve issues are more related to general vascular health. The research on diet, vit D, stress etc is really an extension of after the fact issues through life that have negative cumulative effects that create the problems you are treating. For instance endothelial health improvement is a must for CCSVI success!

My talking around the traps tells me that the doppler findings of CCSVI are actually changing over time (month by month), not fixed or only worsening. They are transient which makes sense for some of the findings.

The 'possibility' that plaque build up due to infection causing the fluctuating stenosis findings is very realistic. The process of build up and leakage of fluid plaque and then clots is a strong possibility for the waxing and waning post PTA. The collagen changes are an indication of healing from inflammation, which is likely to be caused by infections by pathogens such as Lyme and CPn bacteria.

*Do you see similarities in vein walls that correspond with artery spasms?

*And is there research and studies indicating vein wall spasm?


Nigel

I interpret that as the doppler being unreliable, not as the CCSVI abnormalities changing. It might also be due to the doppler technicians looking at vein wall narrowing, which could be physiological or transient depending for example on hydration, instead of looking at intraluminal abnormalities, which are fixed? I agree that infection if it is present would be bad for endothelial health.

I am waiting for Dr. Sclafani to return to see if he has any thoughts about the ASTRAL trial, which is not directly related to CCSVI! The ASTRAL trial was a trial on endovascular treatment of renal artery stenosis. It was a big randomized trial and it got negative results. In the ASTRAL study, during patient selection, they skimmed off the worst cases and did not include them because it was known that they needed to get endovascular treatment and so it would not be ethical to include them in a randomized trial. So the entire trial was only on the borderline cases and it got negative results, so maybe borderline cases of renal artery stenosis don't need to be treated or maybe more research is needed.

What if including borderline cases in the CCSVI trials is going to result in negative results? Would it be possible or practical for the selection criteria for CCSVI trials to use only people like me and Tiltawhirl who had nearly complete bilateral jugular stenosis? The up side would be that improvements might be more easily captured; it might be a proof-of-concept which is taking so so long to happen. The down side would be that the results might only apply to those of us with severe bilateral jugular stenoses.

Also if the need for funding is what is holding everything up, then how do we make that happen? Do you know what the NIH needs to see before it will fund CCSVI research?

Thanks Cece,
I think that same operator, same machine will decide the question. From what I understand the example I showed you in the PM is how there will be more definitive answers.

Question for Dr S,
** if people have atherosclerosis of arteries does that also effect capillary beds and then veins down stream?

The variety of findings from IVUS is very broad and I wonder what is the reason for the findings such as valve leaflet hardening and thickening as a group finding. Collagen involvement and fibrin increase points more to infection from my reading.

So there may be a subset of findings that relate to for instance infection and other subsets as well that are categories such as genuine malformation from birth like webs and septums.

The outcome (aka lesions of brain tissue) from impeded flow could generally speaking be from reflux within the outflow system which breaches the vein wall integrity.

The examples of less rapid reflux and impeded flow would also cause ischemia and low oxygen levels.

The repetitive damage at a cellular level will cause inflammation which will increase a cyclical pattern and that in turn will create a cascade effect as the repeating inflammation effects more tissue. Then that inflammation area is ripe for infection by opportunistic infection (bacteria) and also spread of any pre-existing infection such as atherosclerosis (CPn co-incidence finding in atherosclerosis) up stream of the new inflammation site.

Various diseases are the outcome of the variety of pieces in the matrix of 'causing factors' which require time, then once Medical Science decides on the label for the symptom expressions you have a name for the de-generation disease.

Does this sound like your findings?

Nigel

The flaw with using someone that knows what they are doing that has been involved in the theory and treatment from an early stage is the need for transparency and for results that can be replicated by others. These are the two biggest requirements of any study of this nature. They are also the most difficult to overcome.

The argument from the other side is that the experienced CCSVI IRs are inherently biased. Only inexperienced ones can be trusted as being independent.

Anyone heard from Dr. Sclafani lately? It's been awhile.

Feels like using à guy without drivers license to test à Ferrari