This Is MS Multiple Sclerosis Community: Knowledge & Support

But why have so many of those treated later regressed? Dr Tomasz Ludyga, of the Euromedic Clinic in Katowice, who carried out the Scots’ procedures, offers an explanation.

“We can’t explain this entirely but we think when there is a blocked circulation some substances are secreted in the brain to protect it, which results in damage.”

He added: What we are looking at is a substance called Endoterin 1 and its levels before the procedure and after. After the procedure, the veinous obstructions are cleared and we think these substances disappear. And we can get some initial improvement in the body functions such as headaches going, feet warming, improved retina, balance improving.

“But if a patient, for example, had a disease for 20 years or more then you can’t expect them to be cured immediately. The damage to the neurons in the brain and the spinal cord means that the restoration could take several years. The feeling of the neurons has just started.”

CCSVI itself increases Endothelin- as hypoxia and shear stress are both triggers for its increased production.

And Endothelin also increases fibrosis, hypertrophy, inflammation and vasoconstriction. which can make the stenosis get worse over time.......so its a circle that has to be broken with PTA and vascular hemodynamic correction.

Eliminate hypoxia and shear stress with successful PTA,

and I'll bet with a good endothelial health Endothelin levels will go back to a normal range.

Dr. Guilio Gabbiani from the Centre Medical Universitaire in Geneve, Switzerland speaking on jugular wall changes in MS. His laboratory was interested in the fibrotic changes. He was interested in learning the importance of venous morphology, and is surprised so little is known.

Comparing arteries to veins: Arteries are thicker and there is more resistance.

Dr. Gabbiani took 5 specimens from IJV tissue removed by Dr. Zamboni from some of the patients he treated endovascularly. The tissue was from the area NOT damaged by angioplasty.
He compared it to healthy tissue from autopsy controls.
He looked at eosin, hematoxylin, Miller’s elastic stain and massons trichrome.
He found smooth muscle cells were numerous and increased in MS compared to controls. He then used isoelectric focusing to measure contractions in the smooth muscle cells via actin heterogeneity to ID the smooth muscle cells in the veins.
There is an increased expression of smooth muscle actin in MS, much more than controls.

By red staining for collagen and using unpolarized and polarized light, he saw that there is less collagen 1 type fibers in the MS jugular vein tissue, and more collagen III fibers in MS. This is the exact opposite of the controls.

Connective tissue in MS switches from collagen I to collagen III and this takes place in the IJVs. THis switch also happens in fibromatosis, colloids and hypertrophied scars, and this remodeling may play a role in CCSVI disturbances.

Dr. Lee makes a comment...
This collagen conversion from I to III happens in the arteries had no idea it could happen in the veins as well!

answer: Collagen III is stiffer, and fibrosis takes place for some reason. There was no inflammation on the tissue samples, but inflammation might have occurred before the the intervention and the fibrotic changes happened. All is still speculation, we do not know.

Dr. Zivadinov asks, so the testing was in the normal, non-stenosed part of the IJV?

Answer: Yes, we are trying to examine the normal part of the vein not affected by stenosis.

If I'm understanding this right, it puts paid to the argument that MS causes CCSVI. Instead, CCSVI causes worsening CCSVI, through the endothelin effects.

Just looked at the endothelial health page on CCSVI Alliance - there looks to be a real link between this theory and the ideas such as vit D, good fats etc that have been around for years. Seems this should definetly be a priority for further study.

Does anyone know if its possible to get tested for levels of Endothelin-1?

Just looked at the endothelial health page on CCSVI Alliance - there looks to be a real link between this theory and the ideas such as vit D, good fats etc that have been around for years. Seems this should definetly be a priority for further study.

Does anyone know if its possible to get tested for levels of Endothelin-1?

Does this suggest that stenoses are not congenital, but develop over time?

Does this suggest that stenoses are not congenital, but develop over time?