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.
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
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:
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.