Dr. Tucker at ISNVD

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Dr. Tucker at ISNVD

Postby Cece » Sat Feb 25, 2012 5:38 pm

page 40 http://www.isnvd.org/files/ISNVD%20Abstract%20Book.pdf
A Physics Link Between Cerebral Venous Reflux and Venous Hypertension, Hypoxia and Scleroses
(Trevor Tucker, CANADA)

This presentation postulates that an obstruction at a lower extremity of an internal jugular vein (IJV), in
accordance with the physics of fluid dynamics, causes a standing pressure wave within the vein. This pressure
wave would possess regions of large pressure fluctuations and other regions of relatively little fluctuation which
also have substantially lower peak pressure values. If the wavelength of the pressure wave is comparable to the
distance from the obstruction to the venule end of the capillary bed, then a region of high pressure fluctuation
would exist at the venules. Depending on the degree of obstruction, the pressure fluctuations at the venules of
the capillary bed could be substantially greater than those that would exist in a healthy, unobstructed vein.
This increase in blood pressure fluctuation at the venule end of the capillary bed, which would be equivalent to
local hypertension, is predicted to reduce the pressure drop across the bed which, in turn, would reduce blood
flow through the bed in accordance with Darcy’s Law. Such a reduction in blood flow through the bed would
be accompanied by a reduction in the transfer of oxygen, glucose and other nutrients into the brain tissue in
accordance with Fick’s Principle. The reduction in oxygen levels in the brain tissue (i.e. hypoxia), would, in turn,
be associated with increased fatigue and decreased mental acuity in the subject patient. In addition, cerebral
hypoxia may be associated with vasoconstriction of the endothelium and promotion of both leukocyteendothelial
adherence and angiogenesis (ie. growth of collateral veins). The deprivation of oxygen adjacent to
the venules may also result in cell death, including endothelial, and oligodendrocyte cells. The death of
oligodendrocyte cells would result in the deterioration of the myelin surrounding the brain’s neural axons. The
presentation also postulates that, in cases of sufficient obstruction, particularly with a hypoxia-weakened
endothelium, localized hypertension at the venule end of the capillary bed may be sufficiently high to cause a
disruption in the blood-brain barrier. Such a disruption of the blood-brain barrier could then allow the
migration of leukocytes from the blood into the brain tissue, enabling autoimmune cell attack on myelin, which
has deteriorated from the reduction in repair function normally provided by oligodendrocyte cells. In addition,
the presentation also briefly addresses other factors, such as gender, aging, vitamin D deficiency, cigarette
smoking and viral infection on the potential amount of local hypertension, on endothelium compliance and on
a potentially enhanced predisposition toward blood-brain barrier disruption and leukocyte cell attack on
weakened myelin. Such leukocyte attack on myelin has long been associated with multiple sclerosis.
How was Dr. Tucker's presentation received? Was there any sense as to what is doing the most damage in CCSVI: iron diapedesis or hypertension or reduced perfusion and hypoxia?
Cece
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