CCSVI one year later
Posted: Sun Feb 21, 2010 9:33 am
From Dr. Cooke, endothelial researcher at Stanford University- the doctor I sent my endothelial health for MS program- who put me in touch with Dr. Dake. We've been discussing the progressive nature of MS, how Jacobs found that in more progressed MS, CCSVI is more severe. This is still theory, because the Stanford group is just beginning animal models of CCSVI, but I thought this was a good observation from Dr. Cooke-
From Dr. Simka-
His is a post from Shayk with three new papers relating to CCSVI-
http://www.thisisms.com/ftopic-7708-30.html (the hypoperfusion thread is a classic)
The mechanism of CCSVI is still only theory (although fact in other parts of the body)...and there will be thousands of new papers coming out in the months and years ahead. Jeff had his jugular veins repaired because our doctor told us his impaired venous drainage was bad for his brain. We'll report back at his one year check up to see how this repair has affected his MS. So far, all looks good- no relapses, no progression, much less MS fatigue.
take care,
cheer
Indeed, Dr. Zamboni's research shows how this process occurs in chronic venous disease in other parts of the body, but understanding the affects in the CNS will be the new goal.This observation of Rindfleisch anticipated the recent discovery by Zamboni at the University of Ferrara, and Dake at Stanford University- that there are anomalies of the veins draining the head and neck. It seems possible that the alteration in venous hemodynamics may induce alterations in the smaller tributaries (which will be "engorged with blood" as described by Rindfleisch). The change in flow and pressure experienced by these small veins may induce changes in the endothelial expression of adhesion molecules and chemokines that would promote inflammation, and perhaps favor the development of MS, if not cause it directly.
From Dr. Simka-
I hope that this board remains- as it began- a place to post research and discuss new papers and share pertinent information.Moreover, under normal conditions, cerebral endothelium expresses only low levels of adhesion molecules. Consequently, immune cells very infrequently adhere to endotheliocytes and transmigrate across the blood-brain barrier. It has not yet been studied before if the pathological venous flow could increase the expression of adhesion molecules by cerebral and spinal endotheliocytes. Yet, it is possible that such an abnormal flow, in analogy with the case of varicose veins and venous ulcers, could trigger overexpression of these adhesion molecules. In turn, an increased expression of adhesion molecules, ICAM-1 in particular, could lead to the further increased permeability of the blood-brain barrier. In these settings, monocytes could transmigrate across the blood-brain barrier, transform into dendritic cells, and initiate an autoimmune attack against nervous tissue.
His is a post from Shayk with three new papers relating to CCSVI-
http://www.thisisms.com/ftopic-7708-30.html (the hypoperfusion thread is a classic)
The mechanism of CCSVI is still only theory (although fact in other parts of the body)...and there will be thousands of new papers coming out in the months and years ahead. Jeff had his jugular veins repaired because our doctor told us his impaired venous drainage was bad for his brain. We'll report back at his one year check up to see how this repair has affected his MS. So far, all looks good- no relapses, no progression, much less MS fatigue.
take care,
cheer