Sorry, Jugular, but I'm not sure I follow your logic. The theory that CCSVI is the primary causal factor of MS does not say that it is the thing that directly causes MS symptoms (except perhaps hypoxia): iron deposits in the brain and auto-immune reactions possibly being the secondary direct causal mechanisms of symptoms. If CHRONIC CSVI is a major primary cause, I would think that the CCSVI condition would be almost always present and detectable, regardless of MS symptoms. The only caveat to that would be cases where the stenosis is an "on-again/off-again" thing, where a collapsed vein periodically reopens and closes spontaneously or a valve mis-functions only part of the time.
Hey Ted. My "variable" logic is that the secondary effects of CCSVI such as auto-immune reactions to iron deposits and the like will vary with the primary causal factor, i.e. venous insufficiency. Lets presume that the toxic agent of interest here is iron deposits caused by blood reflux. If the reflux is greater (one would expect) so should be the secondary damage. Variations in the degree of venous insufficiency would account for the variation in MS symptoms and nerve damage that is typical of the disease.
The variations of which I speak are not just about the RR course of the disease, but also on fluctuations in the "progressive" part of SP and PP courses.