Yes I believe the graphic is perfect!!! LOL!
I think the operative word in that abstract is ARTERY.... in that case the patients had an artery that was problematic and which was directly ischemic to an area of the brain, meaning the oxygen was not delivered and the tissue died because of that.
Ischemia is not the main issue with venous insufficiency because veins take the blood back to the heart after it is already de-oxygenated to be re delivered to the lungs for a new load of O2. If the veins are not getting stuff back, there is pooling of the blood, inflammation, swelling is often obvious (think ankles of pregnant or old people).
The arterial problems they were addressing in the abstract would have resulted in a different inury, the blood was not getting there in the first place so the area of the brain was deprived of oxygen, what the Schelling/Zamboni theory is is that venous pooling is causing damage with different mechanisms for injury like iron deposits and direct mechanical injury.
Here's the BIG BONUS of that arterial study;
experienced partial restoration of lost neurologic function
That may well apply to us also!
As for the Faroe Islands, I remain convinced that there is a germ angle to this. I can't help but remember that many people all over the world have found chlamydia pneumoniae in MS brains, CPn is a vascular germ, and it colonizes any area that infected blood cells can get to. CPn has been repeatedly found in atherosclerotic plaques of the arteries and is involved in narrowing of those arteries. While in general people worry more about arterial flow and the studies are mostly in that field, it is possible that the strictures they have found in the jugular vein will turn out to have the same kind of plaques with CPn in them as well. Such an idea is entirely speculative of course, but not unreasonable.
I am really glad for Dignan and Cheer for bringing this to the forefront. I am really glad to have this to work with NOW. I hope I can find a good vascular person to help!