500 patients traités à Seatle! Et il a pas mal d'éléments intéressants à communiquer! Je suppose que ce médecin n'a plus besoin qu'on lui prouve qu'il y a un lien!Par contre, l'histoire des valves est fort intéressante! Pas de sténose, pas de balloning! On est à l'étape suivante: l'étude de la CCSVI, plus du lien avec la SEP! 2 types de CCSVI? Quand cela arrivera enfin en France, l'avantage, c'est que le problème sera mieux connu et mieux traîté! Pas grâce aux français mais bon...
Van FB: Dr. Michael Arata presentation January 29, 2011 (Seattle) - MS in a new light -- CCSVI
Citaat:
Dr. Arata wanted to share some of his observations based on one year of treating CCSVI. With over 500 patients now treated at his clinic, Dr. Arata feels there are a few exceptions to the MS - CCSVI connection. Dr. Arata sees flaws in the jugular valves in almost all patients on both sides and believes this causes a form of cerebrospinal venous hypertension. In fact, Dr. Arata thinks CCSVI should more accurately be called CCSVH because of this connection (however, he gives great credit to Dr. Zamboni for being a visionary to come up with this theory in the first place!).
Citaat:
The main symptoms addressed by correction of this situation are circulatory in nature, such as sleep disturbance, fatigue, headache, brain fog, impaired brain plasticity, and autonomic nervous system dysfunction.
Citaat:
Other symptoms commonly associated with MS are more likely to be caused by damage to the nerves themselves and not a direct result of the hypertension. These are the symptoms that take longer to respond to angioplasty and may never improve if the damage is significant enough.
Citaat:
He felt impaired brain plasticity was a complication of end stage venous hypertension (i.e., where the brain can no longer recover from MS attacks and is left with lasting damage). Dr. Arata felt that combined therapy aimed at reducing venous hypertension (CCSVI treatment and valvuplasty) and reducing inflammation (drug therapies and nutritional approaches) is most effective.
Citaat:
Dr. Arata described primary CCSVI, the most common type, is generally a result of malformed valves in the jugular and azygos veins. Primary CCSVI causes venous hypertension of the jugular and azygos veins. The valvular deficits may or may not narrow the vein. What appears to be upstream venous lesions (narrowings) are actually collapsed veins, not stenoses, and should not be ballooned. These are in the mid-jugular region and ballooning in this region just introduces unnecessary venous damage and trauma. According to Dr. Arata, “it’s all about the valve.”
Citaat:
A secondary type of CCSVI is imaged through MRI involves hypoplasia or aplasia of the sinus of the brain.
Citaat:
In the azygos, secondary CCSVI can manifest as a compression of the vein between the heart and spine and, in the hemiazygos, against the aorta.
Citaat:
Secondary CCSVI caused by problems situated at at the craniocervical outlet (base of the skull) is a poorly suited environment for current endovascular techniques.
__________________
https://www.facebook.com/notes/ccsvi-at-ubc-ms-clinic-information-and-support/ms-in-a-new-light-ccsvi-dr-michael-arata-presentation-january-29-2011-seattle/495917362733
www.ccsvi-tracking.com
Van FB: Dr. Michael Arata presentation January 29, 2011 (Seattle) - MS in a new light -- CCSVI
Citaat:
Dr. Arata wanted to share some of his observations based on one year of treating CCSVI. With over 500 patients now treated at his clinic, Dr. Arata feels there are a few exceptions to the MS - CCSVI connection. Dr. Arata sees flaws in the jugular valves in almost all patients on both sides and believes this causes a form of cerebrospinal venous hypertension. In fact, Dr. Arata thinks CCSVI should more accurately be called CCSVH because of this connection (however, he gives great credit to Dr. Zamboni for being a visionary to come up with this theory in the first place!).
Citaat:
The main symptoms addressed by correction of this situation are circulatory in nature, such as sleep disturbance, fatigue, headache, brain fog, impaired brain plasticity, and autonomic nervous system dysfunction.
Citaat:
Other symptoms commonly associated with MS are more likely to be caused by damage to the nerves themselves and not a direct result of the hypertension. These are the symptoms that take longer to respond to angioplasty and may never improve if the damage is significant enough.
Citaat:
He felt impaired brain plasticity was a complication of end stage venous hypertension (i.e., where the brain can no longer recover from MS attacks and is left with lasting damage). Dr. Arata felt that combined therapy aimed at reducing venous hypertension (CCSVI treatment and valvuplasty) and reducing inflammation (drug therapies and nutritional approaches) is most effective.
Citaat:
Dr. Arata described primary CCSVI, the most common type, is generally a result of malformed valves in the jugular and azygos veins. Primary CCSVI causes venous hypertension of the jugular and azygos veins. The valvular deficits may or may not narrow the vein. What appears to be upstream venous lesions (narrowings) are actually collapsed veins, not stenoses, and should not be ballooned. These are in the mid-jugular region and ballooning in this region just introduces unnecessary venous damage and trauma. According to Dr. Arata, “it’s all about the valve.”
Citaat:
A secondary type of CCSVI is imaged through MRI involves hypoplasia or aplasia of the sinus of the brain.
Citaat:
In the azygos, secondary CCSVI can manifest as a compression of the vein between the heart and spine and, in the hemiazygos, against the aorta.
Citaat:
Secondary CCSVI caused by problems situated at at the craniocervical outlet (base of the skull) is a poorly suited environment for current endovascular techniques.
__________________
https://www.facebook.com/notes/ccsvi-at-ubc-ms-clinic-information-and-support/ms-in-a-new-light-ccsvi-dr-michael-arata-presentation-january-29-2011-seattle/495917362733
www.ccsvi-tracking.com