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I think it's also important to remember that, until recently, the technology did not exist to identify or treat the vascular malformations.Cece wrote:Fat-induced vascular problems is a previous theory.
Congenital truncular vascular malfomations is the current theory of ccsvi.
It seemed important to keep that clear.
http://www.medlink.com/medlinkcontent.aspTransverse lesions of the spinal cord were attributed to thrombosis caused by arteriosclerosis, syphilis, and other infections by Bastian in the 1880s (Follis and Netsky 1970). Foix and Alajouanine also believed that transverse myelitis had a vascular etiology (Foix and Alajouanine 1926). They described 2 patients with subacute necrosis in the sacral or thoracolumbosacral cord associated with massive dilatation and endomysial hypertrophy of the extramedullary veins and similar but less marked changes in the intramedullary vessels. The lumens were not obliterated, and the arteries were not involved. The term "angiodysgenetic necrotizing myelopathy" is sometimes applied to this condition (Follis and Netsky 1970). A similar syndrome is believed to be caused by spinal dural arteriovenous fistulae, although Mirich and colleagues found no arteriovenous malformations in 4 typical cases of subacute necrotizing myelopathy (Mirich et al 1991).
Paine and Byers were the first to report a large clinical series with follow-up exams and used the term “transverse myelopathy” (Paine and Byers 1953). They also postulated a vascular cause but did not present any pathological evidence. In most of these early reports, 1 or 2 patients were studied, and the autopsies were performed months to years after the original illness (Jaffe and Freeman 1943).
In more recent series, autopsies from patients with acute transverse myelitis seldom show significant vascular alterations. Lipton's series of 34 contained only 2 cases with infarcts of unknown etiology and one with hemorrhage plus telangiectasias (Lipton and Teasdall 1973).
That is really interesting, that's very similar to MS having its original vascular theory.TMrox wrote:Transverse Myelitis (a demyelination of the spinal cord only, monophasic)was also thought to be vascular.
But most important is to keep in mind that both are only theoriesFat-induced vascular problems is a previous theory.
Congenital truncular vascular malfomations is the current theory of ccsvi.
It seemed important to keep that clear.
No, it isn't a stretch to say that the theory dates back to the 19th century. The vascular connection has existed since the time of Charcot who is considered the father of modern neurology. I don't know if I'd say that neurologists have been "poo poo-ing" it for that long. But they've certainly been stuck on the auto-immune theory since Thomas Rivers came up with the EAE model of MS in the 1930's.concerned wrote:So, would you say it's a big stretch of the imagination then to say that this theory dates back to the 19th century? That neuros have been poo poo-ing it for that long? (Even the 60's-70's)
I especially like applying the same logic to autoimmune THEORY.shye wrote:But most important is to keep in mind that both are only theories
Maybe I'm over-simplying things but I believe there's credence in both theories and it's a cause and effect thing. It's really no wonder, to me, that there has never been anything conclusive to determine the cause of MS. It has to be one of the most complicated diseases known to man. It can be congenitally caused or trauma caused. It's vascular and it's auto-immune. We need doctors and researchers in a variety of different fields working together to learn more. I believe that's finally going to happen now because of Dr. Zamboni's discovery and because patients are more knowledgable now than ever before.Cece wrote:I especially like applying the same logic to autoimmune THEORY.shye wrote:But most important is to keep in mind that both are only theories
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.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?