marcstck wrote:My understanding is that reflux is a key component to the CCSVI hypothesis, in that it explains the breakdown in the blood brain barrier that allows for the immunological response that is a hallmark of MS. A simple reduction in blood flow, while certainly capable of doing harm to the CNS over the course of decades, would not explain the infiltration of T cells into the CNS, as is proven by the presence of O-bands in the CSF of MS patients. Reflux, resulting in a breakdown of the BBB, would account for the inflammation seen in RRMS; a long-term reduction in overall blood flow likely would not. If CCSVI is to eventually be determined to be a causal factor in MS, it must play a role in the breakdown of the BBB.
Actually, not true, Marc. A reduction in bloodflow, hypoperfusion and low O2 could create demylinating lesions. No need for reflux. People who suffer from diffuse cerebral hypoxia due to low O2 can have demyelination in the brain. It's called delayed cerebral hypoxic demyelination--happens to mountain climbers, divers, folks poisoned by CO2. This is why I continue to urge the doctors to test O2 levels pre and post angioplasty, and why Dr. Haacke is doing just that. I believe Jeff falls into the category of pwMS who had low cerebral O2 levels due to hypoperfusion and CCSVI. He came home from a week at high altitude and soon had an MS diagnosis and seven enhancing lesions. Granted, this is not everyone.
http://neuro.psychiatryonline.org/cgi/c ... l/20/4/473
Hypoperfusion and white matter lesions in rats-
Multiple sclerosis (MS) is a disease of the central nervous system characterized by patchy areas of demyelination, inflammation, axonal loss and gliosis, and a diffuse axonal degeneration throughout the so-called normal-appearing white matter (NAWM). A number of recent studies using perfusion magnetic resonance imaging in both relapsing and progressive forms of MS have shown a decreased perfusion of the NAWM, which does not appear to be secondary to axonal loss. The reduced perfusion of the NAWM in MS might be caused by a widespread astrocyte dysfunction, possibly related to a deficiency in astrocytic beta(2)-adrenergic receptors and a reduced formation of cAMP, resulting in a reduced uptake of K+ at the nodes of Ranvier and a reduced release of K+ in the perivascular spaces. Pathologic and imaging studies suggest that ischemic changes might be involved in the development of a subtype of focal demyelinating lesions (type III lesions), and there appears to exist a relationship between decreased white matter perfusion and cognitive dysfunction in patients with MS
There are many, many discussions on this slowed blood flow detected in MS brains, called hypoperfusion, fogdweller--this has been a very important part of the puzzle--
Here's a good one: