folks start to worry about Fingolimod

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby MegansMom » Wed Nov 03, 2010 4:54 am

I just want to point out that IF the MS lesions are formed as part of the CCSVI theory.......

say the veins are blocked
the reflux occurs, shear stress occurs, blood turbulance damages RBCs ( showly and insidiously) Iron iand other deposited on the vessel walls and
cerebral hypoxia ( low level) and cerebral hypogycemia starve brain cells
As a result of this
Oligodendrocytes die, Endothelin levels climb to reinforce the vessel walls
In an attempt to preserve the axon the Immune system rallies- Inflammation occurs, the WBCs remove debris, and form scar tissue to reinforce the stressed area ( sort of fiberglassing the walls)
At the beginning of MS there are only basic WBCs seen, the BIG gun B and T cells are evident well into the disease.

So IF you suppress the IMMUNE sysytem you will NOT see scars because the scar makers are unable to make the scar lesion. This does not mean that cerebral hypoxia and hypoclycemia and its sequalae ( side effects) will not be continuing. MS lesions were believed to be the ground zero of an Immune attack and thats very questionable in CCSVI theory.

Also worth mentioning is that the prescribing neurologists do not have a in depth knowledge of the vascular system ( most have just what they learned in medical school). I would discuss the use of the MS drugs with a physician well versed in vascular medicine and CCSVI theory.
Cat (Catherine Somerville on FB)
My 35 yo daughter is newly dx 8/19/10 (had 12 symptoms)
Dx with Type A CCSVI- 1 IJV & double "candy wrapper" appearance of her Azygos
Venoplasty done Sept 21, 2010
Doing extremely well-
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