Dr Trevor Tucker with his understanding of CCSVI and flows

[1eye]

(Some day, 1eye, we should discuss over lunch at the Swan in Carp, or perhaps the Cheshire Cat)
Trev. Tucker

The Cheshire Cat is more my speed, but both great. Good beers to be had. Somebody should open a Dirty Duck (on the Beaverbook?)...

[Squeakycat]

Dr. E. Mark Haacke's presentation on Flow Quantification in CCSVI by MRI at the CCSVI Symposium 2011 has now been uploaded to YouTube.

[1eye]

for comment

[Cece]

Dr. Tucker's paper has been published:

A physics link between venous stenosis and multiple sclerosis

Trevor W. Tucker

Abstract

This paper hypothesizes that a stenosis or obstruction at a lower extremity of an internal jugular vein (IJV) would, in accordance with the physics of fluid dynamics, cause 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 hypothesized 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 would be substantially greater than those that would exist in a healthy unobstructed vein. This increase in blood pressure fluctuation located 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. Also the deprivation of oxygen in the brain tissue may result in the death of oligodendrocyte cells, which, in turn would result in the deterioration of the myelin surrounding the brain’s neural axons.

In addition, the paper also predicts that, in cases of extreme obstruction, the predicted localized hypertension at the venule end of the capillary bed may be sufficiently high to cause a localized disruption in the blood–brain barrier. Such a disruption of the blood–brain barrier could then allow the migration of leukocytes (auto-immune attack cells), from the blood into the brain tissue, enabling them to attack myelin, which has degenerated or deteriorated from the reduction in repair function normally provided by oligodendrocyte cells. Such leukocyte attack on myelin has long been associated with multiple sclerosis.

http://tinyurl.com/5w7vkgo

[1eye]

Can't get the paper without paying $ for it, which I may do anyway. I tried to figure out the expected wavelength, of these pressure waves in blood, just to ballpark it, or get an order of magnitude, anyway. It is non-trivial! It's not clear what kind of waves are expected, and it makes a difference. This branch of physics is full of things with names like capillary waves, gravity waves, and Bernouilli, which is something that makes airplanes fly. Physicist Richard Feynman even complained about the non-triviality of using fluids to teach wave physics in high school.

Thank heaven it has not much to do with the "Bernoulli-Leibniz-Feynman quantum parallax topology effect", in which "the engines cannae tek any mooore than warp 9. This is because the warp drive slows the rate of spin of the dilithium crystals to such an extent that the effect becomes an issue at about warp 7." Apparently "liberal applications of WD-40 to the dilithium crystals will excite the quark-boson-neutrinos in such a way as to counteract the detrimental warp drive de-spinnification."

Seriously, though, the science may be non-trivial. Anybody got a guess on wavelength? Period of a heartbeat I used was 1/(70 BPM/60 s). These are not sound waves, nor is the medium air (though they might be longitudinal), or the length would be on the order of 1000 feet.

Constructive interference would not be much of an issue, though heartbeat-driven earthquakes might be, and you might have to watch out for whales and elephants.

[ttucker3]

1eye

Pleased to have had the opportunity to meet you at the VAS Conference in Ottawa recently. Sorry I had not picked up on your last query before now. My TIMS prowls are somewhat intermittent. From my understanding, on average the length of the internal jugular vein is something like 13 to 15 cm long. The normal flow rate is also something like13 to 15 cm/sec. So it takes about a second for a pulse to transit down the vein, hit an obstructed valve and another second to bounce back to the venules. If the pulse rate is about 60 pulses/min or 1 pulse/sec at the time a pulse is emerging from the venules another reflux pulse is crashing into it, substantailly increasing the pressure at the venules - localized hypertension. I will be providing another presentation of this on the 36 hour Global CCSVI Expo - my time slot is 6:00 pm EST on Sunday Nove 20. I will be describing this with some graphics. Hope you and Triana can watch (enjoyed her presentation in Ottawa immensely.)

Trev. Tucker

[cheerleader]

Hi Dr. Tucker--
Jeff and I will be after you and CCSVI Alliance (6:30) at 7pm Sunday on the global expo.
Wanted to let you know that I bumped up a terrific older thread on hypoperfusion and MS for you to read (in your spare time
http://www.thisisms.com/forum/chronic-c ... c7708.html
thanks for all your hard work,
Joan/cheer

[MarkW]

Great explanation of stenosis of vein valves. Then a link to MS which is weak in the science as it refers to the work CCSVI advocates. Please provide us with good background to why pwMS should have get treatment for stenoses in their vein valves. This is good info, the rest I can pick holes in but don't because treating CCSVI syndrome is a good idea.

MarkW

[Cece]

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.

Such a cascade of bad effects.

[violin]

You can find this paper (the same Abstract) on PubMed.
PMID: 21958625

"A physics link between venous stenosis and multiple sclerosis." Tucker TW.
Med Hypotheses. 2011 Dec;77(6):1074-8. doi: 10.1016/j.mehy.2011.09.006. Epub 2011 Sep 29.
PMID: 21958625

[violin]

In this 2015 paper, Dr. Zamboni cited Dr. Tucker's paper.

"The Oscillating Component of the Internal Jugular Vein Flow: The Overlooked Element of Cerebral Circulation."
Sisini F, Toro E, Gambaccini M, Zamboni P.
Behav Neurol. 2015; 2015:170756. Epub 2015 Dec 9.
PMID: 21958625 DOI: 10.1016/j.mehy.2011.09.006

[violin]

Here is another, more recent paper by Dr. Tucker on PubMed.
PMID: 31443762

Med Hypotheses. 2019 Oct;131:109255. doi: 10.1016/j.mehy.2019.109255. Epub 2019 Jul 2.
Fluid dynamics of cerebrospinal venous flow in multiple sclerosis.
Tucker T1.
Author information
1
T. Tucker Inc., Canada.
Abstract
Stenotic immobile valves and other malformations obstruct normal cerebrospinal venous outflow, resulting in reflux flow which combines with the normal outflow to produce standing pressure waves in the internal jugular and other cerebrospinal veins. It is hypothesized that, if the cerebrospinal venous structure between the obstruction and the deep cerebral veins is sufficiently non-compliant, the standing wave will result in bidirectional flow in the fine cerebral veins. Bidirectional flow in the fine veins, over extended periods of time, will cause disorder in the veins' endothelial morphology, and ultimately, result in the disruption of the blood-brain barrier as observed in multiple sclerosis. This physics-based analysis demonstrates a positive correlation between clinically observed MS attributes with the predicted flow patterns and venous malformations that are based on fluid dynamics principles that include venous compliance influences. The physics-based approach used in this analysis provides new insights into MS pathologies based on predicted pressure and flow patterns.

Copyright © 2019. Published by Elsevier Ltd.

PMID: 31443762 DOI: 10.1016/j.mehy.2019.109255

[violin]

Here is another paper, 2019, by Dr. Tucker.
Prerviously posted on ThisIsMS under THORACIC CAVITY VENOUS FLOW

2019 Oct
T. Tucker Inc., Ottawa, Ontario, Canada
Fluid dynamics of thoracic cavity venous flow in multiple sclerosis.
https://www.ncbi.nlm.nih.gov/pubmed/31443776

Abstract
This paper hypothesizes, based on fluid dynamics principles, that in multiple sclerosis (MS) non-laminar, vortex blood flow occurs in the superior vena cava (SVC) and brachiocephalic veins (BVs), particularly at junctions with their tributary veins. The physics-based analysis demonstrates that the morphology and physical attributes of the major thoracic veins, and their tributary confluent veins, together with the attributes of the flowing blood, predict transition from laminar to non-laminar flow, primarily vortex flow, at select vein curvatures and junctions. Non-laminar, vortex flow results in the development of immobile stenotic valves and intraluminal flow obstructions, particularly in the internal jugular veins (IJVs) and in the azygos vein (AV) at their confluences with the SVC or BVs. Clinical trials' observations of vascular flow show that regions of low and reversing flow are associated with endothelial malformation. The physics-based analysis predicts the growth of intraluminal flaps and septa at segments of vein curvature and flow confluences. The analysis demonstrates positive correlations between predicted and clinically observed elongation of valve leaflets and between the predicted and observed prevalence of immobile valves at various venous flow confluences. The analysis predicts the formation of sclerotic plaques at venous junctions and curvatures, in locations that are analogous to plaques in atherosclerosis. The analysis predicts that increasing venous compliance increases the laminarity of venous flow and reduces the prevalence and severity of vein malformations and plaques, a potentially significant clinical result. An over-arching observation is that the correlations between predicted phenomena and clinically observed phenomena are sufficiently positive that the physics-based approach represents a new means for understanding the relationships between venous flow in MS and clinically observed venous malformations.