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


Postby sou » Mon May 04, 2009 6:46 am


I have found this in the news:


It is about the long term effects of plasmapheresis. I wonder what in the plasma could erode the BBB, so that despite the stenoses, the nervous system keeps working...

The 100% freaked out,
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Postby cheerleader » Mon May 04, 2009 6:58 am

Stay calm, sou.
We've been discussing plasmapheris on this thread.

Once veins are open, blood can flow, inflammation will be lowered, cell apoptosis due to hypoxia will stop, oxygen can reach cells, perfusion times will become normal. Blood will normalize with correct flow. The BBB will heal.
CCSVI is a chronic condition and moves slowly in takes many years of reflux and slowed transit time for the damage to the brain and spine to be significant enough to show.
Let us know how the MRV goes-
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
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Postby mrhodes40 » Tue May 05, 2009 6:09 am

here's the thing to me:
Because this has not been the accepted model of MS causation, there is no research into how something like PLEX might impact MS given a stenotic causation.

People with MS and people with venous ulcer have different things about them in the blood: hemosiderin is present, iron is crossing the BBB/endothelium inflammation is happening as a result of inflammatory cells crossing in, etc
from Zamboni "The big idea"

Inflammation in MS is characterized by expression of
adhesion molecules,26 followed by a migration of
macrophages and T-cells across the BBB. Infiltration of
the matrix by macrophages, as in CVD, is considered a
crucial step27 (Figure 3A and B). In both situations,
macrophages appear with considerable intracellular iron
stores due to phagocytosis of senescent erythrocyte. Iron
overload in MS plaques has been demonstrated in vivo by
MRI.28 In addition, we observed haemosiderin in the urine
of patients with active inflammation of MS (personal
unpublished data).
Iron-laden macrophages carrying the HFE mutation
display increased iron export, increasing the risk of
generation of free iron and free radicals, possibly extending
tissue lesions.5,6 A study from Australia29 suggests that
C282Y-HFE mutation is increased in MS cases of North
Western European origin and supports further investigations
into the role of iron metabolism in the severity of MS.
As in a venous ulcer, a key determinant of tissue injury
is played by MMP9. Exactly as in CVD, the over-expression
of MMP9 is insufficiently counterbalanced by its tissue
inhibitor TIMP-1. MMP9 can trigger leukocyte transendothelial
traffic through an altered BBB, and serum active
MMP9/TIMP-1 is now considered an appropriate indicator
of ongoing MS inflammation.30 Despite histological findings
showing haemosiderin deposits encircling the central vein of
MS lesions (Figure 2A), the iron-MMP pathway of
activation is not considered in MS literature.

Another group32 investigated the serum concentration
of soluble transferrin receptor (sTFR) in a group of MS
patients. The levels were found to be significantly higher in
patients with active MS, either in progressive or relapsingremitting
clinical form, than in controls

These things will be impacted by PLEX.

And I agree with Cheer in that one thing that is not appreciated is how slow the natural course of MS is: it takes years most of the time for a person to accumulate significant disability.

These venous differences are key to development of lesions if the model is correct, but it is not like a stroke where the artery is totally blocked off resulting in dramatic injury immediately: it is an issue of partial blockage, so that the drainage still happens it is just hampered compared to normal. If the immune stuff from the blood can't cross into the brain it can't hurt it there either, considering a significant amount of the damage is from the immune activation itself.

I think as people look at MS from this new persepctive we will find out much more about how these things relate.
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