Thoughts on the spreading of lesions and symptoms in CCSVI
Posted: Wed Sep 09, 2009 9:39 am
CCSVI is not the only problem in MS, but the immune systems response to exposed CNS matter plays a crucial role in beginning a cascade of inflammation that leads to loss of neurological function.
I have a thought about this. Once the blood brain barrier has been perforated (via reflux, edema, leakage caused by hypoxia) and there's an immune system response against the exposed CNS-matter, this might also affect other areas, and cause new lesions by itself, i.e. without stenosis involvement in those areas. A load of T/B-cells and antibodies that have been primed to attack e.g. a lesion around the ventricles could circulate to other areas.
I've never had any neurological symptom until earlier this year, when I came down with symptoms likely emanating from different regions in my CNS. Now it seems an unlikely coincidence for the endothelium of vessels in these different regions to break down around the same time. My only explanation is that one lesion caused an increased number of circulating myelin-reactive T/B-cells and antibodies that facilitated demyelination in a different region. This is comparable to the infection of rodents with EAE in the lab by immunizing them in a location far away from the brain, in the absence of stenoses, where upon administration of MOG or MBP antigenes the immune system causes demyelination in multiple places (I believe there might be a difference in the lesion pattern seen in EAE versus that in MS - it would make sense that the primary lesions in MS are closer to venous outflows, and those in EAE closer to arterial inlets, but I don't know whether this is the case. Anybody?).
This would also help to explain why patients who had the "liberation procedure" didn't experience complete stopping of their MS activity, but that the percentage of them that had new lesions went "only" from 50% to 12%, and relapse rate from 50% to 23% over two years respectively: there were still plenty of circulating myelin-reactive immune cells and antibodies that can cause further damage. However once blood flow has been improved, one may hope that eventually those T-cells die off (if you have been immunized to a certain pathogen you need re-immunization a few years later as well, I don't know about myelin reactive cells. Anybody?), but it could be that some amount of immune suppression may be useful (not just steroids, but longer term suppression, focusing on the Th1 and Th17 channels) to prevent the immune system from creating further lesions and lead to a renewed cascade of increased immune reaction.
I have a thought about this. Once the blood brain barrier has been perforated (via reflux, edema, leakage caused by hypoxia) and there's an immune system response against the exposed CNS-matter, this might also affect other areas, and cause new lesions by itself, i.e. without stenosis involvement in those areas. A load of T/B-cells and antibodies that have been primed to attack e.g. a lesion around the ventricles could circulate to other areas.
I've never had any neurological symptom until earlier this year, when I came down with symptoms likely emanating from different regions in my CNS. Now it seems an unlikely coincidence for the endothelium of vessels in these different regions to break down around the same time. My only explanation is that one lesion caused an increased number of circulating myelin-reactive T/B-cells and antibodies that facilitated demyelination in a different region. This is comparable to the infection of rodents with EAE in the lab by immunizing them in a location far away from the brain, in the absence of stenoses, where upon administration of MOG or MBP antigenes the immune system causes demyelination in multiple places (I believe there might be a difference in the lesion pattern seen in EAE versus that in MS - it would make sense that the primary lesions in MS are closer to venous outflows, and those in EAE closer to arterial inlets, but I don't know whether this is the case. Anybody?).
This would also help to explain why patients who had the "liberation procedure" didn't experience complete stopping of their MS activity, but that the percentage of them that had new lesions went "only" from 50% to 12%, and relapse rate from 50% to 23% over two years respectively: there were still plenty of circulating myelin-reactive immune cells and antibodies that can cause further damage. However once blood flow has been improved, one may hope that eventually those T-cells die off (if you have been immunized to a certain pathogen you need re-immunization a few years later as well, I don't know about myelin reactive cells. Anybody?), but it could be that some amount of immune suppression may be useful (not just steroids, but longer term suppression, focusing on the Th1 and Th17 channels) to prevent the immune system from creating further lesions and lead to a renewed cascade of increased immune reaction.