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Except neither of those citations mention demyelination.

Venous congestive myelopathy: a mimic of neoplasia
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Pathology Findings
Given their small size, the spinal cord biopsies frequently showed distortion of architecture. Gliosis and mild glial atypia were often seen (57%) (Figures 2, 3, 4 and 5). In all cases, there was an increased number of small vessels with markedly hyalinized vascular walls (Figures 2 and 5). There was frequently (71%) a relative myelin loss as best demonstrated on LFB/PAS (Figure 5b). Neurofilament stains showed axonal loss only in the two cases featuring necrosis. The findings were not those seen in primary demyelination given the following observations: hemosiderin deposition, predominantly perivascular and indicative of previous bleeding, was commonly seen (71%) (Figures 2b, inset and 5c). Scattered Rosenthal fibers were present in some cases (43%) (Figures 3b and 5e). Vascular thrombosis and necrosis were seen each in two cases (29%) (Figure 4). Vascular thrombosis was the only feature seen exclusively in patients found subsequently to have a spinal dural arteriovenous fistula (two of three patients). Vessel wall calcification was not observed in any of the cases. The distribution of these various findings is summarized in Table 2 .

The underlying pathophysiologic mechanism of the myelopathy induced by arteriovenous fistulas is now believed to involve passive venous congestion of the cord,1, 2, 3, 4, 31 because arterial blood originating from the fistula enters the perimedullary venous plexus, a valveless system, increasing pressure and impairing normal drainage from the cord parenchyma.

fernando wrote:For me "impairing normal drainage from the cord parenchyma." sounds a lot like CCSVI. I suppose that the thing that is not draining well is venous blood.

But, maybe I'm plainly wrong.