This Is MS Multiple Sclerosis Community: Knowledge & Support

I, too, have PPMS. I'm not yet ready to give up hope that CCSVI angio is going to be beneficial. I did see improvements after angio #1 - noticeable to others, too - and was able to walk easier/longer/stronger. Sadly, the LIJV became occluded and untreatable (at this point in time) and angio #2 (valves) gave me the benefit of sweat (those w/o MS laugh but we all know this is a biggy when it comes to heat tolerance; I am miserable in this current heat but not anything like I was last summer in 80degrees compared to our triple digit heat index right now). I believe time & experience will offer more hope for PPMS.

And, Marc, I look forward to learning more.

newlywed4ever, that is encouraging.

We've always talked about MS being a disease of exclusion and about MS being a few different diseases with different etiologies lumped together. But then CCSVI comes along and, if we go by Dr. Sclafani's clinical findings, 99.5% of pwMS are also pwCCSVI. So I think we are more united as pwMS than we were before; we do all have something in common.

So then maybe the differences in MS are because of the different ways the body can respond to CCSVI and the severity of the CCSVI. Developing a tertiary lympatic system in the brain, well, that is definitely one undesirable way the body could respond to CCSVI! Before that I was mainly thinking of it in terms of a greater inflammatory response or not, depending on innate reactivity of the immune system, and that sort of thing.

One thing about the brain is that so much is recoverable and plastic. One thing I heard about was that animals have had their eyes hooked up surgically to "hearing areas" and auditory nerves hooked up to "visual centers" and they could still learn to see and hear.

_________________
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'_MS' is over - if you want it
Patients sans/without patience

I have had MS since I was 25, I'm 61 now, PPMS etc etc, and blah blah blaH. the EDSS scale never moved an iota, but my world changed exponentially after CCSVI treatment.
I say, get a new scale that includes the many minute details of everyday life that can prove change. I am happy again, there's hope, I can do lots of things I couldn't do before, a simple thing - turning on my own electric toothbrush,, for example. bladder control, oh mY, the list goes on, yet, not an iota on that stupid scale, its too vague, the Polish forM is way bettter, and shows these improvements...
never give up
- i'm going to Dr Areta in Calif.,and will always, no matter how many times I restenose, have great thrills finding new things i couldn't do before.

they'll figure it out, but to not give a glimmer of hope to PPMS? NOT!! IT'S ALWAYS WORTH IT. just being able to unwrao a candy...

_________________
PPMS. Liberated Katowice, Poland
06/05/10 angioplasty RJV-re-stenodsed
26/08/10 stent RJV
28/12/10 follow-up ultrasound intimal hyperplasia

PPMS here as well, and not willing to give up hope either.

I have seen changes that are hard to put in the placebo column, they are also hard to measure. I awake much easier in the morning. I sweat (which I agree is huge), not like I used to but I had quit sweating all together. I am more alert than pre-angio. I can lift my right arm off the bed when laying flat. I feel like I have energy, just can't get the body to follow along.

Not giving up on the theory for PPMS until my left jugular is open, and stays open.

This part was likely accidentally left out of the article you posted Cheer:


Usually this type of information is used to discredit trials that do not support the CCSVI hypothesis so I am sure it is information many of you will find a critical part of the trial!!!!

wrong . It is part of the post .
Mr.Success

I also add the length of time with the disease. In my case it was very very slow in progessing, but I have had it for over 35 years. I think that the likelihood that damage to the neurons and other central nervous system tissue is permanent is greater if you have had the disease longer.

I don't mean to sound quite so negative. I still think it is possible that certain symptoms may be improved or even corrected with improved blood flow. I think Dr. Sclafani mentioned autonomic functions, and certainly congnative and energy functions would improve with overall better blood flow through the brain. The speed at which we are progressing with this new techniques for treating CCSVI and my own slow progression made it advisable to hold back on getting a second treatment for the time being, that's all.

The fact that the IRs are finding such high numbers of patients with CCSVI is actually problematic. Studies indicate that the the misdiagnosis rate of MS is generally acknowledged to be between 5%-15% (the NIH puts the number at 10%, so high, in fact, that they believe misdiagnosed patients have polluted much of their research data). There are literally dozens of diseases that can be mistaken for MS, yet interventional radiologists doing CCSVI venoplasty are only finding minute numbers of patients with "healthy" veins.

Here's a quote from the book "Multiple Sclerosis: Diagnosis, Medical Management, and Rehabilitation":

"… early accurate diagnosis is critical. It guides optimal therapy, removes uncertainty, allows informed planning, and improves the patient's sense of well-being by providing an explanation for their problems. Unfortunately, the misdiagnosis rate for MS approximates 5% to 10%, even by experienced healthcare providers"

Here are two terrific papers on the possible differential diagnoses of MS:

http://www.neurologia.org.mx/portalweb/ ... ulos/6.pdf

http://msj.sagepub.com/content/14/9/1157.full.pdf+html


The high rate of venous lesions being found by the physicians doing CCSVI venoplasty lead me to believe that venous abnormalities may be more common than previously believed, and possibly could be linked to a variety of neurologic conditions.

Furthermore, there's more and more evidence mounting that there is a viral components to MS, most likely in the form of EBV. Here's a fascinating new study that indicates MS patients are infected with both types of EBV in far greater numbers than healthy controls:

http://www.ncbi.nlm.nih.gov/pubmed/21757537

Interestingly, EBV "hides" in the human body in B cells, the likely culprits in the tertiary lymphatic organ scenario…

And, there was the recent study out of Taiwan, which looked at hundreds of thousands of patients, and showed that patients who suffered an outbreak of shingles (caused by the varicella zoster virus, a cousin of EBV) were almost 4 times as likely to develop MS within the year as those not afflicted with shingles.

http://ca.news.yahoo.com/multiple-scler ... 34680.html

We also know that there is certainly a genetic component to predisposition to the disease, and all of the genes thus far associated with MS are also associated with immune response.

All this is to say that looking at CCSVI as THE primary driver of MS is probably oversimplistic. I believe the evidence points to CCSVI playing some sort of role in MS disease pathogenesis, but multiple sclerosis is definitely a multifactorial disease, and there are likely many people walking around with CCSVI to no ill effect, and some segment of the MS population that does not have CCSVI.

IMO, CCSVI is likely responsible for a subset of MS symptoms, but blood flow problems alone don't account for the infectious and genetic evidence that is quickly accumulating, which also reveals itself in geographical and migratory incidence of the disease, and the existence of MS clusters.

_________________
Marc
www.wheelchairkamikaze.com

.

So much to be determined still. I look forward to knowing reliable figures for CCSVI in MS patients, CCSVI in healthy controls, and CCSVI in other neurological conditions. I like the possibility of that last one, maybe patients with Lyme disease or other conditions might yet benefit. (Lyme being a possibility if CCSVI creates BBB conditions that facilitate the Lyme going neurological, which in most cases Lyme does not.)

I wonder what is the smallest percentage of stenosis that our CCSVI docs would include in the definition of CCSVI and treat. One way to get to 99% is to include stenoses that are smaller, such as 20 - 30%.

That is only one of the reasons why a judgement against the results of one or two smallish trials is not a very scientific way of looking at things, and why even Dr. Zivadinov's results are not so damning. Consider that some proportion of his normals may actually have MS, and some sizable proportion of his MS patients have most likely been misdiagnosed.

_________________
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'_MS' is over - if you want it
Patients sans/without patience

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2276727/


well, that explains it all..... ow
since when did understanding my disease require physics, immunology, IR image reading and techniques (ok, that part is fun), neurology, etc, etc, etc?
multidisciplinary, multifactorial!

*bump*
MrSuccess, is this what you were looking for in terms of studies similar to Dr. Zamboni's that included endovascular treatment?

Yes ... this clinical trial prelim. results appear more in line with Dr.Zamboni's original work.

Has more of Dr. Mehta's data been published ?



MrSuccess