The different types of malformations Dr. Sclafani has described (backwards valves, atresia, membranes, ets) all seemed to be malformations, not build-ups of fat plaque. Which would fit with the congenital ccsvi theory?
If i understand the fat-induced theory, fat emboli act as an irritant to the endothelium, and this trauma to the endothelium is a large factor in the BBB breakdown. The emboli cause aggregation of blood cells, which further occlude the smaller vessels and capillaries, and you get slowing down of flow of blood. With the accumulation of fat emboli, you get a hyperplasia (thickening) of vascular walls--which includes the small arterioles, capillaries and venules in the brain and spinal cord--as they thicken,they often became twisted, nodular, and alternately constricted and dilated.
As far as the autoimmune part, the fat-induced theory would explain this I think by the fact the emboli and aggregated blood cells also cause hypoxia (low oxyygen) and ischemia (low blood supply), which would shift the blood and tissues to acid, which would activate the digestive enzymes in the lysosomes--which in turn could result in the erosion of the surrounding tissues, incl myelin. So it is not an autoimmune reaction that destroys the myelin.
As an overall scheme for CCSVI, I think this theory is much more reasonable than congenital CCSVI.
But I'm not sure where some of the malformations found when doing Liberation procedure would fit into the fat-induced theory--I see them as not congenital, but environmental--that is, dietary deficiencies as underlying cause. (might look like congenital, because often mother and child have same nutrient deficiencies).