Friday, November 19, 2010

Dr. Michael Dake on CCSVI


November 19, 2010 at 11:26am

from the V-Aware November issue.

Dr. Dake is the cardio-thoracic specialist I contacted with Dr. Zamboni's research in January 2009.  He was our local doctor at Stanford University.  The damage that Dr. Dake saw in Jeff's brain on MRI, and the damage he found in Jeff's jugular veins on MRV made sense to him.  As a vascular doctor, he understands the correlation of venous drainage and disease.

Important Points to note in this article:
1. CCSVI resembles a known venous disease, superior vena cava syndrome.  Symptoms related to this condition are similar to those in CCSVI.  Relieving CCSVI via angioplasty produces similar results in angioplasty for superior vena cava occlusion.

2. CCSVI might account for the low flow states (hypoperfusion) found in pwMS.

3. Slowed blood flow changes the endothelial layer of blood vessels, allowing for a break in the blood brain barrier and immune cell penetration 

4. Inflammation created by disturbed blood flow in CCSVI continues to damage the vein lining.  Thus, CCSVI will progress with age of patient and length of disease.
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Here is Dr. Dake on CCSVI---


Evidence presented recently in the medical literature proposes that patients with multiple sclerosis (MS) have a coexisting high frequency of obstruction to veins that drain the brain and spinal cord.

These data suggest that MS is associated with blockages in veins located in the neck or chest that alter cerebral venous hemodynamics, causing alterations in venous pressure and flow patterns. This venous obstruction is called chronic cerebrospinal venous insufficiency (CCSVI).

Wednesday, November 10, 2010


Dr. Zamboni's published letter in response to the Doepp study

November 10, 2010 at 2:00pm

Published in the Annals of Neurology-

Regarding ‘‘No Cerebrocervical Venous Congestion in Patients with Multiple Sclerosis. Intraluminal Jugular Septation’’ Paolo Zamboni, MD

I read with interest the article titled ‘‘No Cerebrocervical Venous Congestion in Patients with Multiple Sclerosis’’ by Doepp and coworkers.1   Contrary to their conclusions, I believe that the authors’ results are a further validation of venous flow irregularities in multiple sclerosis (MS) patients.

One of the major regulators of cerebral venous outflow is posture, due to the gravitational gradient between the cerebral parenchymal veins and the base of the neck (␣30mmHg).2   The authors demonstrate a much larger change in blood flow volume in normal subjects compared to MS patients when the subjects go from a supine to an upright position. They find a change of 128ml/min and 56ml/min for the right and left sides, respectively, for MS patients. But they find a much larger change of 266ml/min and 105ml/min for their normal subjects. This result actually suggests the presence of chronic cerebrospinal venous insufficiency (CCSVI). Possible causes include intra-luminal septum, membrane, and immobile valve affecting the hydrostatic pressure gradient in the upright position. The presence of such blockages in the extracranial and extravertebral cerebral veins has been proven also by using catheter venography, the unquestionable gold standard in medicine.3,4

There was a trend toward significance (0.06) when comparing the mean global cerebral blood flow (CBF) in MS patients with that in controls. However, the level of significance is under- estimated by the low control sample, 20 versus 56 patients. The reduction in CBF in MS, meaning in practical terms stasis, might become significant by simply increasing the control sample.