Nice bump, Sharon
I do not claim to completely understand all the platelet specifics, but it appears that Zivadinov and the other docs are explaining platelets to a neurological world which has not considered them very important. This paper illuminates more connections of MS to venous disorders. Platelets are tiny, irregularly shaped cells that do not have a nucleus w/ DNA. They circulate in the blood and control clotting.
Here is CVI research-
Note: Chronic venous insufficiency of the legs shows extreme platelet activation-
Conclusion: All classes of CVI are associated with significantly increased percentages of platelet-monocyte aggregates and increased percentages of platelet-neutrophil aggregates throughout the circulation. The presence of more of these aggregates and the increased propensity to form aggregates in the presence of platelet agonists in all classes of CVI suggests an underlying state of platelet activation and increased reactivity that is independent of the presence of ulceration. http://cat.inist.fr/?aModele=afficheN&cpsidt=1180395
And now, from the Zivadinov paper, here are platelets in MS- also in a state of chronic activation...
The possible involvement of platelets in MS was first studied by Putnam in 1935, who considered a role for venule thrombosis in CNS demyelination . In the 1950’s- 60’s, at least ten studies appeared on the relation of platelets to CNS demyelination, several of which reported augmented platelet adhesiveness in MS, which correlated with disease activity [298-301]. More recently, a number of observations of platelet abnormalities in MS patients have appeared [302-304], and others cited below. We became interested when colleague W. Sheremata encountered MS patients with severe immune thrombocytopenic purpura (ITP) , leading to our report of increased platelet microparticles and platelet activation marker CD62P (P-Selectin) in MS . Thus, chronic platelet activation in MS may now be regarded as well established,
http://www.jneuroinflammation.com/conte ... 4-7-10.pdf
including by the report of Cananzi et al cited earlier .
One point Dr. Zivadinov made, emphatically, in Bologna- was that he believed the next ten years would generate thousands of new research papers explaining MS as a vascular disorder and CCSVI. This paper appears to be one of those promised papers.
If CVI of the legs is caused by venous blockage, which then signals platelet activation, the coagulation cascade, and resultant tissue damage (venous ulcers)- then CCSVI, created by venous blockage- could do the same thing to the brain. Both diseases share venous insufficiency, platelet activation, inflammation and tissue damage.
thanks for sharing it!
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS