Dr. Zamboni Responds"I Invite Scientists to Develop MS
Posted: Mon Dec 07, 2009 8:52 am
From the CCSVI in Multiple Sclerosis's Notes Facebook Fanpage
Printed in the Ottawa Citizen
http://www.ottawacitizen.com/health/inv ... story.html
I want to respond to the Citizen article on chronic cerebrospinal venous insufficiency (CCSVI) syndrome, a vascular disease we found 40 times more frequent in multiple sclerosis (MS) sufferers.
I never discouraged MS patients from following treatments prescribed by their specialists. I never had "a hard time in answering any of the questions from the MS experts." Rather, I think that scientific exchanges between experts in venous circulation and experts in MS are still insufficient.
Beno Schlessinger, in 1939, while injecting the cerebral venous system with increased pressure, noted the extravasations produced around the lateral ventricles "closely stimulate the distribution and even shapes of plaques in multiple sclerosis." So we have a model of venous MS from 60 years ago.
Dr. Mark Freedman is right when he suggests we develop an animal model of CCSVI. Despite all the models of tissue injury from venous insufficiency described in the medical literature, such a scientific step will be certainly necessary.
On the other hand, the autoimmune concept in MS is built on feet of clay -- the animal model EAE (experimental autoimmune encephalomyelitis) where the antigen is brain tissue from another animal. In contrast, the recent description of CCSVI in MS demonstrates how inadequate EAE is. EAE assumes that brain circulatory function is normal and thus does not reflect what really happens in humans.
In turn, I invite scientists to develop a new model of MS, which takes into account the presence of extracranial venous blockages. I disagree that the development of a new animal model has to precede further studies on patients. This would be a parallel track.
It is irresponsible to delay further studies on the value of the endovascular treatment of CCSVI in MS, the so-called liberation procedure. Patients need to have clear answers and it is mandatory to face the problem. Either to organize educational programs for Doppler screening of CCSVI in MS, or to find support for a randomized controlled trial on liberation procedure are more than urgent and reasonable projects.
Paolo Zamboni, MD,
Director Vascular Diseases Center,
University of Ferrara,
Ferrara, Italy
Printed in the Ottawa Citizen
http://www.ottawacitizen.com/health/inv ... story.html
I want to respond to the Citizen article on chronic cerebrospinal venous insufficiency (CCSVI) syndrome, a vascular disease we found 40 times more frequent in multiple sclerosis (MS) sufferers.
I never discouraged MS patients from following treatments prescribed by their specialists. I never had "a hard time in answering any of the questions from the MS experts." Rather, I think that scientific exchanges between experts in venous circulation and experts in MS are still insufficient.
Beno Schlessinger, in 1939, while injecting the cerebral venous system with increased pressure, noted the extravasations produced around the lateral ventricles "closely stimulate the distribution and even shapes of plaques in multiple sclerosis." So we have a model of venous MS from 60 years ago.
Dr. Mark Freedman is right when he suggests we develop an animal model of CCSVI. Despite all the models of tissue injury from venous insufficiency described in the medical literature, such a scientific step will be certainly necessary.
On the other hand, the autoimmune concept in MS is built on feet of clay -- the animal model EAE (experimental autoimmune encephalomyelitis) where the antigen is brain tissue from another animal. In contrast, the recent description of CCSVI in MS demonstrates how inadequate EAE is. EAE assumes that brain circulatory function is normal and thus does not reflect what really happens in humans.
In turn, I invite scientists to develop a new model of MS, which takes into account the presence of extracranial venous blockages. I disagree that the development of a new animal model has to precede further studies on patients. This would be a parallel track.
It is irresponsible to delay further studies on the value of the endovascular treatment of CCSVI in MS, the so-called liberation procedure. Patients need to have clear answers and it is mandatory to face the problem. Either to organize educational programs for Doppler screening of CCSVI in MS, or to find support for a randomized controlled trial on liberation procedure are more than urgent and reasonable projects.
Paolo Zamboni, MD,
Director Vascular Diseases Center,
University of Ferrara,
Ferrara, Italy