This Is MS Multiple Sclerosis Community: Knowledge & Support

1. The root cause: A Permeable blood-brain barrier (BBB) and transmission of provocative
substances, antibodies and leucocytes into the brain. This may be caused by chronic cerebrospinal vascular insufficiency (CCSVI, and associated microclotting due to stagnant cerebrovenous blood flow), latent infections that cause a Th1-dominated immune response and release
of matrix metalloproteases (MMPs) which can alter the BBB, or a general pro-inflammatory state created due to dietary factors.

I've wondered if Diamox might help me or others with CCSVI, there's a lot of reason to think it could. Please keep us posted & I hope it works.

(V-2-b) Specific Spinal Scars: Also Venous in Origin?


However, Oppenheimer, who first realized the denticulate ligament's pivotal role in specific spinal patch developments, stressed that only few of the lesions which he had studied had shown a relationship to veins, and that the only patches which had done so were found to irradiate the spinal cord's sides. Oppenheimer supposed that it was full flexions of the cervical spine, especially in the presence of rigid antero-lateral fixations of the spinal dural sac, which exerted the detrimental stresses upon the denticulate ligament's attachments to the spinal cord.


Regarding the mechanisms capable of producing bilateral cord lesions, even the most detailed accounts on classic instances of spinal multiple sclerosis consistently lack any indications of either some massive thrust upon the spinal cord’s front or of a heavy impact upon walls or surroundings of the vertebral canal. It is difficult to believe that in all these observations (series of) corresponding injurious processes or events were consistently overlooked. Therefore the search must begin for an endogenous source of comparably effective injurious impulses capable of continually injuring the spinal cord's specifically affected parts.


As to spinal cord flank lesions, the development of minimally traumatizing surgical procedures for interrupting the pathways of vehement venous regurgitations into the lowermost spinal canal appears – as challenging as this task may appear – equally promising.

cheer, terrific post.

Dr. Flanagan is in Albany, NY, too.

But why a permeable BBB? Taking a giant step back....it's possible to tie it all together when we look at slowed cerebral perfusion.

Hypoperfusion can be caused by injury, mechanical defect (in spine or vasculature). It can be exacerbated by endothelial dysfunction, which is caused by a number of things. It may be related to autonomic dysfunction.

Slowed bloodflow affects drainage of CSF, as shown by BNAC and Dr. Zamboni
http://registration.akm.ch/einsicht.php ... KEN_ID=900
http://www.ncbi.nlm.nih.gov/pubmed/20018140

Slowed bloodflow activates fibrinogen in the brain in all neurodegenerative disease and brain trauma.
http://www.ncbi.nlm.nih.gov/pubmed/19630789


Find out why your cerebral bloodflow is not normal....what is causing hypoperfusion, and you can help hopefully slow and stop neurodegenerative disease. This means each patient needs to go thru the list. CCSVI, neck injury, chiari, NPH, co-infections, diet and exercise. CCSVI Alliance is working on bringing these doctors together. Fortunately for all of us, Dr. Siskin, Mehta and Rosa are all in Albany And Dr. Flanagan and Dr. Schelling, Zamboni, Zivadinov, Haacke and others are connecting. There are answers for all diseases of neurodegeneration.

Yes, it's an exhausting process for those with neurodegenerative disease, and my heart goes out to Dania, 1 eye, blossom and others still looking for their personal answer. Jeff was lucky to find his with the endothelial health program and stenting. But it will not be the same game plan for everyone. And that makes this journey more complex....but hopefully, not impossible.
cheer