I won't reiterate what has been so well elaborated by Dr. Simka and Dr. Zamboni, but I'll try to bring you a perspective on where we are in Canada.
The essence of the problem is an assumption that venous abnormalities to drainage from the brain circulation cause venous hypertension, causing, if you will, dilatation and leakage of fluid and red cells into the brain matter, causing inflammatory reaction—possibly an immune reaction—and that this may be associated with MS. This has been very well described, as you've heard, by two excellent reporters.
I guess the issue for Canada is, where do we go in Canada to test the hypothesis? As you're probably aware, the MS Society has spent $700,000 in funding for studies that are essentially evaluating not the hypothesis of whether or not these lesions and the treatment thereof can improve the MS symptoms; rather, we're spending $700,000 in evaluating the techniques that have been described on how to evaluate stenoses and how the frequency of stenoses in MS patients compare with the frequency of stenoses and venous abnormalities in the normal population.
I put to you that this is very interesting and will give us some interesting academic information, but I'm not really sure that it is relevant to the issue at hand. If one wants to test my hypothesis of a new drug being efficacious in the treatment of a disease disorder, one has to put that medication into the patient and test it compared to a normal cohort that may receive placebo.
In this particular case, I personally know that not everybody with venous outflow obstructions has MS. Probably, if one looks at a general population of normal individuals, there will be significant venous abnormalities found.
We know from the surgery that we do for cancer that we resect the jugular vein not infrequently when we're doing neck dissections. We also know that when we do carotid surgery, we not infrequently ligate venous outflow from the brain and from the face. None of these people develop complications of MS. So probably there is significant venous abnormality noted in the normal population.
That doesn't preclude the notion that in these particular patients who may have some underlying tendency to neurological disorders, their pathology and the venous disease may be correlated with neurological damage.
A case in point here would be in venous disorders of the lower extremity. I've been practising vascular surgery for the last 30 years and routinely, through Doppler ultrasound, I evaluate people with venous insufficiency, both of the deep and the superficial venous system. Infrequently, some of those patients will develop what we call the “postphlebitic leg”, with ulcerations and hemosiderin deposits, which reflects what Dr. Zamboni was talking about: the iron deposits noted in the brain of MS patients.
But the point is that not all patients with venous insufficiency develop these complications, so there's obviously a predisposition in some patients to develop iron deposits that could lead to inflammation and the immune response known to be involved in MS patients.
From the point of view of Canada, we obviously don't have a lot of experience in the treatment of the venous blockages that have been identified in patients with MS. We've done a few anecdotal cases—I haven't, but friends of mine have—that are reporting, again, anecdotal improvement in the symptomotology.
But the question begs to be asked that if we are going to evaluate the notion, the hypothesis, that CCSVI and its treatment is related to and can benefit patients with MS, I think we have to do a proper, randomized, blinded, and controlled study to test the hypothesis, and not do what the MS Society in Canada is proposing or has funded, which is really to fund the best means of investigating venous abnormalities and how the MS population and the normal population relate to one another in the frequency of this disease process.