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A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby fernando » Mon Mar 22, 2010 11:46 am

Patientx

Except neither of those citations mention demyelination.


Maybe this paper is a little more suited to you:

http://www.nature.com/modpathol/journal ... 0350a.html

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 .
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Postby patientx » Tue Mar 23, 2010 6:59 am

There's the demyelination - good find.

But I'm still not sure how good a comparison this is to what would happen in CCSVI. The papers still seem to suggest that the myelopathy is from the pressure on the spinal cord caused by the venous congestion:

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.

It would seem this is why relieving the venous congestion, i.e pressure on the cord, brings almost immediate relief from the myelopathy.
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Postby fernando » Tue Mar 23, 2010 8:15 am

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.
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Postby patientx » Tue Mar 23, 2010 11:21 am

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.


You could be right. Sometimes these medical articles sound like a different language to me.
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