The oligodendrocytes are fragile they are separate cells that wrap the myelin around the axons. See it here:
CLICK FOR OLIGO
because of the thin connections between the axon and the oligo the oligodendrocyte is more vulnerable to damage. When the endothelium becomes leaky and the fluids and cells from the congested veins slips into the brain tissue, it is the oligodendrocytes that get hurt first, it is even possible that congestion, or edema and inflammation in the area can break the bonds between the oligo and the axon of the nerve.
From Schelling page 30. see research thread....
neuropathologists have sometimes proposed that any edema in fact any intense vascular seepage or leakage into some part of the brain or spinal coord preferentialy damages the myelin sheaths. One researcher even posited that there is no demyelination other than that attributed to perivascular edema.
It is also known that in spinal cord injury there is demyelination.
Spinal cord injury has an immense amount of inflammation/swelling/fluid in the area.
So even though we have not been taught to think in terms of edema or fluid or congestion as being the START of the MS process by causing demyelination, it is absolutely true that it can do that.
Go back to the picture of the oligodendrocyte and then imagine a lot of fluid gets in the area, pushing the structures apart. It is easy to see that the thin fragile threads connecting the oligo to the nerve could be the thing that breaks first, then the myelin dies because it is not attached to the oligo any more then the macrophages come and clean it up...... and all the stuff that was thought to be proof of an attack by the immune system is suddenly explained: the myelin filled macrophages, the dead myelin and the demyelinated nerve which functions poorly, the activated miroglia and the inflammation cascade.
This even explains why Prineas and Barnett, who looked at a young girl who died 17 hours into her MS attack found that the oligodendrocytes were dead but the immune system was NOT there yet. In fact the microglia were only starting to respond to the dead oligo. They concluded that MS is not autoimmune but something else is killing the oligos first.
this new model of CCSVI explains all that very nicely it seems.
I hope I made that easy enough and plain enough.