Notes from CCSVI conference,
Bologna, Italy --September 8, 2009
September 9, 2009 at 7:37pm
Notes from the CCSVI presentation
September 8, 2009
Dr. Ellliot Frohman, University of Texas Southwestern Medical Center Neurology, Dallas, Texas and Robert Zivadinov, Jacobs Neurological Institute, Buffalo, NY are chairs for the morning session:
Dr. Frohman makes the introduction. CCSVI is removed from how we think about MS or any other immune mediated diseases. Could other diseases we currently classify as autoimmune be related to venous disease? Autoimmune diseases share in common molecular adhesion molecules. Perhaps Crohn’s could be venous? Validating CCSVI in MS may affect the classification of other autoimmune disorders. This venous model has been overlooked.
Micrographs, histopath proficles, periventricular cuffs, red cells we see in post capillary venules. This is not new. In 1863 -before Charcot.- G.E. Rindfleisch writes of venous congestion in MS.
Could the immune system go anywhere blood goes? Is this why there is an inappropriate immune response? He notes the large crowd in the room (it’s packed) and says he hopes people will speak out. (they will!)
+++++++++++++++++++++++++++++++++
Dr. Paolo Zamboni- Universita degli Studi di Ferrara, Italy director of vascular studies
The drama of CCSVI and MS is that of severe stenosis of the extracranial pathways. Everyone in this room can return home and establish a cooperation between vascular and neurology departments. A simple demonstration - he shows a video demonstration of doppler protocol to aid diagnosis. There is a blocked outflow of blood.
In the normal control groups, there is a monodirectional flow of blood. In MS the periventricular vein has a bidirectional flow. Substitute circles avoid intracranial hypertension. Mean transit time is increased.
Dr. Zamboni proposes a “Menu” for the day-
1. Entree- what is the origin of venous stenosis?
2. Pasta- May we assess consequences of CCSVI in the brain. Perhaps microbleeding is the source of lesions. Just like CVI in other parts of the body- there is microcirculation
Cerebral spinal fluid ultrafiltration and reabsorption depends on transmural pressure.
TMP = IVP-EVP
In venography, there is much higher pressure in MS patients then controls.
Histology- research cited:
-red blood cell extravastion during relapse
-fibrin cuffs in venous hypertension
-iron laden macrophages
are ALL found in MS patients.
3. Main Course- Is CCSVI treatable?
measuring pressure before and after Liberation procedure is significantly changed.
4. Dessert- What are the effects of CCSVI treatment?
and for Today’s Special---Chronic fatigue as a symptom of CCSVI
(you have to love the Italians and their food analogies.)
September 8, 2009
Dr. Ellliot Frohman, University of Texas Southwestern Medical Center Neurology, Dallas, Texas and Robert Zivadinov, Jacobs Neurological Institute, Buffalo, NY are chairs for the morning session:
Dr. Frohman makes the introduction. CCSVI is removed from how we think about MS or any other immune mediated diseases. Could other diseases we currently classify as autoimmune be related to venous disease? Autoimmune diseases share in common molecular adhesion molecules. Perhaps Crohn’s could be venous? Validating CCSVI in MS may affect the classification of other autoimmune disorders. This venous model has been overlooked.
Micrographs, histopath proficles, periventricular cuffs, red cells we see in post capillary venules. This is not new. In 1863 -before Charcot.- G.E. Rindfleisch writes of venous congestion in MS.
Could the immune system go anywhere blood goes? Is this why there is an inappropriate immune response? He notes the large crowd in the room (it’s packed) and says he hopes people will speak out. (they will!)
+++++++++++++++++++++++++++++++++
Dr. Paolo Zamboni- Universita degli Studi di Ferrara, Italy director of vascular studies
The drama of CCSVI and MS is that of severe stenosis of the extracranial pathways. Everyone in this room can return home and establish a cooperation between vascular and neurology departments. A simple demonstration - he shows a video demonstration of doppler protocol to aid diagnosis. There is a blocked outflow of blood.
In the normal control groups, there is a monodirectional flow of blood. In MS the periventricular vein has a bidirectional flow. Substitute circles avoid intracranial hypertension. Mean transit time is increased.
Dr. Zamboni proposes a “Menu” for the day-
1. Entree- what is the origin of venous stenosis?
2. Pasta- May we assess consequences of CCSVI in the brain. Perhaps microbleeding is the source of lesions. Just like CVI in other parts of the body- there is microcirculation
Cerebral spinal fluid ultrafiltration and reabsorption depends on transmural pressure.
TMP = IVP-EVP
In venography, there is much higher pressure in MS patients then controls.
Histology- research cited:
-red blood cell extravastion during relapse
-fibrin cuffs in venous hypertension
-iron laden macrophages
are ALL found in MS patients.
3. Main Course- Is CCSVI treatable?
measuring pressure before and after Liberation procedure is significantly changed.
4. Dessert- What are the effects of CCSVI treatment?
and for Today’s Special---Chronic fatigue as a symptom of CCSVI
(you have to love the Italians and their food analogies.)
