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Three steps to demonstrating that CCSVI can be found with either MRI or for those sites able to do so with MRI and ultrasound (US).
1) Demonstrate with on the order of 10 or so cases per site that there are problems with either the jugular vein or reflux in the brain, or with the azygous vein and prepare a white paper for this topic for publication using the proposed first pass protocol.
2) Refine the protocol as needed to include US if MRI alone proves unable to see all the damage (and this may be indeed the case if there is valvular damage that MRI cannot see). Prepare a white paper on this protocol and get all the MR manufacturers to offer such a protocol on their systems. Such protocols should be available on both 1.5T and 3T scanners worldwide.
3) Propose a second phase study with again 10 or more cases per site with the refined protocol and where possible ultrasound validation. Increase the number of sites

If the thalamostriate system is affected with increased iron content along the venous system as I believe it is, then this all falls into place. CCSVI may just be the etiological source we have all been looking for. If so it provides great hope for MS patients worldwide and we cannot and should not wait years for funding to allow us to demonstrate this point. We need to establish an international protocol to attack this as the torch bearers for people suffering from MS.

Here is what I want to know: shall we TIMSers actively contact radiology departments with THIS information?

Here is what I want to know: shall we TIMSers actively contact radiology departments with THIS information?

In the last few years, I have been proposing that venous damage in multiple sclerosis is implicated by increased iron content in the basal ganglia and thalamus. But the interest and association of MS with veins dates back to Fog (1) in 1964 with a major decade's long effort to convince people of the role of the mechanical effects of changes in venous flow by Schelling (2). However, the excitement comes from a proof of concept that MS is a chronic cerebral spinal venous insufficiency (CCSVI) by Paolo Zamboni and his team (3). This exciting work done with ultrasound and followed by a corrective surgical procedures shows that we should have been looking outside the box (brain) to find the problem in the brain. There is a great deal of evidence in both atherosclerosis and chronic venous disease that changes in shear stress can cause a biological response that is very similar to what we see in MS (see for example the work by John Bergan (4)). In fact, it is a logical explanation as to why the entire brain is affected in MS, why the disease tracks backward along the venous drainage system, and why it emanates from the white matter near the ventricles in the drainage of territory of the medullary veins. If the thalamostriate system is affected with increased iron content along the venous system as I believe it is, then this all falls into place. CCSVI may just be the etiological source we have all been looking for. If so it provides great hope for MS patients worldwide and we cannot and should not wait years for funding to allow us to demonstrate this point. We need to establish an international protocol to attack this as the torch bearers for people suffering from MS.

Having Dr. Haacke come forward in this brave and provocative way is so heartening. He is saying, "This is real- look at it for yourselves! We cannot wait to help these people! Let's do it NOW!"