BTW, unlike "liberation", there are good randomized controlled trial showing that the current DMD drugs do slow the progression of plaques. Otherwise they could not be sold.
But progression of plaques (lesions) does not equal progression of MS disability...or someone like my husband, with 20 lesions, would not be able to mountain bike, while our friend, with one lesion, cannot walk.
DMDs do not address the true disability, which is brain atrophy and loss of gray matter. That continues, even on DMDs.--http://archneur.ama-assn.org/cgi/reprint/63/8/1175.pdf
Clinically relevant GM atrophy occurs in the cerebellum of MS patients and is more prominent than WM atrophy. As such, it may provide complementary data to other regional atrophy and intrinsic tissue measures. http://msj.sagepub.com/content/15/7/811.abstracthttp://onlinelibrary.wiley.com/doi/10.1 ... 7/abstract
The Review of DMDs by the British Medical Journal showed that even when DMDs stop relapses, MS disability continues. It's not about white matter lesions.....this is why the DMD program was called a failure in the UK. Because the drugs don't work.
To make things even more difficult, the calculations assessing whether disease modifying treatments might be affordable in the NHS were predicated on the putative effects of preventing the accumulation of disability in multiple sclerosis, not on relapse rates. To many this seemed hazardous—firstly, because only a proportion of patients (who are unidentifiable) become progressively disabled; and secondly, because the relation between relapses and disability is more complex and more indirect than many imagined.5 Reducing the frequency of relapses does not necessarily reduce the progression of disability. Indeed, studies with powerful monoclonal antibodies show that progression can continue unabated even when relapses are abolished completely.6
So...even with all of those wonderful trials of the drugs...we are not any further along in understanding the true cause of disability in MS....but it looks to be gray matter atophy, not white matter lesions. Interestingly enough, my husband's brain atrophy was reversed by increased blood flow after his angioplasty.
Which is why I find the autoimmune theory of MS to be surreal.
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS