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Major topics covered:
Ultrasound and MR imaging in treatment planning
The role of iron in MS and neurodegenerative disease
Perfusion deficits and hypoxia and possible relationships to CCSVI
New evidence of CCSVI in animal models
Related vascular problems: venous embriology, idiopathic intracranial hypertension, normotensive hydrocephalus, carotid surgery in stroke
CCSVI treatment: procedure and neurological outcomes
Flow dynamics: modeling the cerebral venous system
Billmeik wrote:a bit off topic but where are the animal studies?I hoped the stanford ones would be either positive or negative by now. I dont see any mention of it in the march conference. How hard would it be to replicate putnam?(maybe very hard?)
cheerleader wrote:Shannon---the specific truncular venous malformation (like a web) won't be created in mice. The affect this web has on the jugular vein can be created by crimping, pinching and closing off jugular veins in mice. That is how animal models are created.
David1949 wrote:At least one study shows CCSVI to be more common among more advanced cases of MS and less common among early cases. That doesn't fit with the theory that CCSVI is congenital. Also if we are born with these defects then why does MS not manifest itself until we are in our thirties? (or 44 in my case?) I remain open to the idea that CCSVI is not congenital or at least not entirely congenital.
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