Lyon wrote:Considering all the new testing that is available...and expensive, I sometimes wonder whether someone with the motivation and funding to do exhausting testing on a group of MS'ers at this point could determine what MS "IS" and isn't?
MS is an inflammatory disorder believed to be autoimmune in etiology, and can present with features resembling APS [294-297]. Several reviews of the neurological symptoms of APS/SLE are available [298-300], and many case reports, e.g., cerebral ischemia . However, MS is not thought to involve ischemia, although elements of the coagulation cascade are present in MS lesions, including fibrinogen and recently, tissue factor and protein C inhibitor .
In 2000, our collaborative investigation demonstrated elevated endothelial microparticles (EMP) during exacerbations of MS [303,304]. Those findings motivated further investigations, this time of aPL in MS, with the hypothesis that aPL might be involved in endothelial activation in MS. Several prior reports had established that aPL commonly occur in MS, but in most of them the patient population was heterogeneous or inadequately defined, and there was no indication of a relation between aPL and the pathophysiology of MS.
The combination of hypoxia to ischemia may trigger pathological events that are not induced by ischemia alone. One potential pathological event is hypoxia-induced fibrin deposition that results from altered anti-coagulant properties of endothelial cells as demonstrated in pulmonary vessels.3,4 Thus, the reduction of CBF in conjunction with hypoxia may induce spontaneous thrombus formation to reduce blood perfusion further. This ischemia/hypoxia-induced microvascular thrombosis may also prevent cerebral reperfusion after the release of the large artery occlusion, similar to the previously described no-reflow phenomenon after brain and cardiac ischemia.5,6
What I'm thinking is that as the hypoxia is healed- after returning oxygen to the brain and spine- then the coagulation cascade should STOP. Right? Maybe ending CCSVI with your stents will end the blood issues for you and others? Maybe your coag numbers will normalize now?
I agree there is something going on here and it ties in. I too am very hopeful for a new line of research.And the expert said that even though I tested positive on cadiolipin test and anti-beta 2-glycoprotein that it didn't mean I had APS/sticky blood because lots of MSers sometimes have weird somewhat abnormal t
I also don't think all of us have congenital issues that block the veins, I think it will be many different issues but the common thread is blocked veins from the headI have been unconvinced that we all have a congenital issue. But, for those who do, this could be the answer
A family friend is an MSer. She had a car accident with injury a few years back and had neck surgeries to repair]
I meant my Gd enhancement is gone and no inflammation in my MRI. I have RA so my sed rate is always up. AND my reg doc is a chronic disease specialist and she sees coagulation problems in the blood of people with chronic disease all the time and that is why I was tested and knew that my blood was sticky. I regularly test for fibrin manometer and thrombin with numbers so high occasionally they can't even quantify it. My d-dimer which is a little non specific but which can mean that a clot is breaking down, is usually high. 4 days before I left for stanford it was 4 when1 or less is normal. It was this that brought it to Dr D's radar he does expect it may drop into normal ranges he said.n the CCSVI model, where stenosis causes reflux and hypoxia.... this is activating the coagulation cascade. In other words, CCSVI could have been responsible for the elevated levels of fibrinogen in your blood. (Also, you've mentioned that you no longer have inflammation...was this in reference to gad-enhancing lesions, or inflammation in your blood? Do you have a high SED rate?)
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