oops, I think I spilled my alphabet soup...
...SPMS cases. I think that's also adding new questions, such as
What makes F- SPMS patients get worse?
What's the mechanism of ITMTX in PwPPMS?
I will not ask about acronyms for stuff I don't believe exists. However, in order to answer the last question, for me, "ITMTX" would have to have more discrete words. I guess maybe my answer could never make sense anyway to someone who believes "RR" patients are not == "PP" or == "SP". I think I read somewhere that there is atrophy and axon loss even as soon as the first clinical indication. The divide and conquer strategy only works if you are fighting patients, not disease. Is there a physical, non-venous indication that a person with "MS" is one "phenotype", and not also the others? Is the presence of these follicles to be the new tatoo, since we have recently become aware of it?
This "SPMS" course of mine seems to have been getting milder lately. Where does that fit in?
The remission is a myth that needs busting. Nobody on earth could convince me I was free from progression, back when I was having "remissions". I claim this is not my imagination or some cognitive problem fooling me. If I have not lost touch with reality completely, "MS" is a continuum, a sentence at first punctuated with attacks. You keep adapting to it, until the body runs out of resources (like room for new collateral drainage).
I put all my remissions down to the growth of new collateral veins. Isn't that really why steroids help, and why they only help once or twice? Do they not induce rapid "remissions", or more accurately, adaptations?
Some people, called "PPMS", are just unable to adapt for physical, spatial, likely congenital, plumbing reasons.
I have "PPMS", and "SPMS", and "RRMS", because it is all just "MS". If you want to call it that.