This Is MS Multiple Sclerosis Community: Knowledge & Support

Cosmos

In his thirteen part TV series, Cosmos: A Personal Voyage (1978-1979), Sagan briefly discusses Velikovsky in Episode 4: "Heaven and Hell" in a section on Venus,[4] and mentioned him in the book of the series, Cosmos:[5]

"Many hypotheses proposed by scientists as well as non-scientists turn out to be wrong. But science is a self-correcting enterprise. To be accepted, all new ideas must survive rigorous scientific standards of evidence. The worse aspect of the Velikovsky affair is not that his hypotheses were wrong or in contradiction to firmly established facts, but that some who called themselves scientists attempted to suppress Velikovksy's works. Science is generated by and devoted to free enquiry: the idea that any hypothesis, no matter how strange, deserves to be considered on its merits."[6]

Marc's right on---the one thing that's happening now is the doctors are trying to establish what "normal" venous return for the brain looks like in architecture and flow. It's astounding that this hasn't been done already. But it's true. Dr. Haacke has some nice pics of normal veins on his site
http://www.ms-mri.com/ Click thru the pics and you can see the difference. Now, he is measuring flow in normals. Dr. Haacke has tested himself, and said his MRV flow is very different than the pwMS he's tested. More on that in the future. He's also testing healthy students in Detroit now, to get a better idea of normal venous drainage in healthy controls.

There can be anatomical variants, people with one jugular and no MS. Why? Is the flow still OK? This needs further study. What we do know today is that venous reflux and hypoperfusion (slowed blood flow) damages the organ the veins drain. This is why Dr. Dake pointed at Jeff's MRV and said it was not a good situation for his brain....because blood was not leaving the brain in a timely manner and was refluxing back in. Doctors understand this mechanism in Budd Chiari (hepatic venous disease)...because patients' livers start to fail, and they need transplants. But they don't test "normal" hepatic veins...because if the liver isn't failing, why bother? Who knows how many of us have funky liver veins? Is CCSVI analogous? Is the brain starting to fail and is MS the sign? More research ahead.
cheer

http://www.velikovsky.info/Carl_Sagan

The same is said in Sagan's "Broca's brain".

...but wasn't Zamboni and his pals jumping the gun in their claim that people with MS have venuous insuffiency??

Cheer if the blockages in our neck are similar to Budd Chiari(hepatic venuous disease)than from the time we start having syptoms of MS we should be dead in about three years-five years(life expectancy after being diagnosed with hepatic venuous disease). Also in hepatic venuous disease there is no relapsing and remitting but a downward slide from the beginning. Other conditions associated with hepatic venuous disease are bleeding in the esophagus and fluid retention in the abdomen none of which obviousley occur anywhere in the body with MS. So if there is no established "noraml venuous system" please tell me what Zamboni or whomever came up with the term CCSVI based the term on. What this leaves me to believe is that diagnosing CCSVI is completly subjective depending on how each indivdual researcher defines a normal venuous system. I agree that further study of the venuous system is necessary but wasn't Zamboni and his pals jumping the gun in their claim that people with MS have venuous insuffiency??

Fernando

Truncular VM lesions therefore, present either as a hypoplastic or hyperplastic lesion causing obstruction or dilatation (e.g. internal jugular vein aneurysm; azygos vein stenosis), depending on the various defective conditions of the vessel trunk 25-28 (Figure 2 A-D). Intraluminal defects within the vein (e.g. vein webs or membrane) result in stenosis or obstruction.29, 30 More infrequently, truncular VM lesions may also present as a persistent fetal remnant vein that has failed to involute or regress normally (e.g. marginal/sciatic/lat- eral embryonic veins) 31, 32 (Figure 3 A, B).

Truncular VM lesions present with more serious hemodynamic consequences in general due to the direct involvement of the lesion with the truncal venous system (e.g. avalvulosis, marginal veins, popliteal vein aneurysm, IVC steno- sis/occlusion), compared to extratruncular lesions.

As a consequence, chronic venous congestion and hypertension due to venous reflux or occlusion results in more tissue and organ damage along the venous capacitance; membraneous/focal/segmental stenosis of suprahepatic inferior vena cava, known as Primary Budd-Chiari Syndrome has such a profound impact on the liver resulting in severe portal hypertension due to hepatic venous outlet obstruction in addition to chronic venous insufficiency affecting the lower extremities 33, 34 (Figure 4 A-C).

The cerebrospinal venous circulation is not exempt from truncular venous malformations. Cerebrospinal VMs also carry the potential risk of long term of chronic venous hypertension to the brain resulting in various clinical conditions/illnesses such as chronic cerebrospinal venous insufficiency (CCVI) .35-38

An example of CCVI, internal jugular vein valve incompetence (IJVVI) 39 has been postulated to be a cause of transient global amnesia (TGA).40-43 IJVVI is diagnosed when retrograde jugular vein flow is detected by extracranial duplex ultrasound during Valsalva maneuver.

It is believed that IJVVI may produce transient mesiotemporal ischemia by venous congestion. This mechanism requires a patent venous path-
way from the affected IJV through the transverse sinus, confluence, straight sinus, and vein of Galen into the basal vein of Rosenthal and into the internal cerebral veins.

As included in UIP Consensus on the Venous Malformations, 2009 44 further data supporting the role of CCVI in brain function, is found in patients with multiple sclerosis. Truncular VM lesions causing stenosis along the internal jugular, innominate, superior vena cava, and azygos vein system, have been suspected to contribute to the development or exacerbation of multiple sclerosis 45-49 (Figure 5).
Therefore, proper understanding of the evolutional as well as involutional process of embryonic development of the venous system 50-53 is essential for the appropriate management of these truncular VM lesions as a potential cause of var- ious conditions involving chronic cerebrospinal venous hypertension/insufficiency......

This is the best known intrinsic defect to cause varying degree of stenosis and obstruction together with another condition of venectasia and aneurysm causing venous dilatation. Such anomalous condition of the suprahepatic IVC with membraneous obstruction of vena cava (MOVC) along the proximal terminal segment of IVC gives clinically significant hemodynamic impact not only to the lower extremity to cause chronic venous hypertension, but also to the liver resulting in hepatic venous outlet obstruction resulting in portal hypertension.

In view of such profound impact of a relatively simple truncular venous malformation such as a venous web at the hepatic venous outlet causing portal hypertension, a similar condition involv- ing to the head and neck venous system may cause CCSVI and may be involved in the development or exacerbation of multiple sclerosis.

...Please, for those on both sides of the issue, take a deep breath and think for at least 10 seconds before firing off a post that is sure to set off the usual barrage of insults. These inflammatory posts insult the very idea of a forum such as ThisIsMS, where we should be learning from each other, but instead are only displaying the basest aspects of human behavior.

I only know about EuroMedic; I was #515 at the beginning of June, and at the beginning of October, they had done "over 1,000". They are doing 6 per day, 6 days a week.

Jeez, folks, can we give the constant arguing and back-and-forth denigration of each other a rest?

I'm glad my last Wheelchair Kamikaze post was so well received, and that it's generating discussion amongst those interested in CCSVI. Earlier on in the piece, I wrote this paragraph:

At this stage of the game, when very few scientifically valid trials have been conducted, both extreme viewpoints have absolutely no basis in fact, and these vehement arguments only confuse the issue all the more, creating adversarial tensions precisely when a spirit of open-mindedness and cooperation are desperately needed. Furthermore, these loudly voiced conflicting opinions can only work to the detriment of chronically ill patients vainly searching for answers that simply do not yet exist, adding clutter and confusion to an already complicated issue.

It is possible to disagree without being disagreeable. We are all dealing with a very serious, chronic and disabling disease. Why every thread on this board has to turn into some kind of childish tit-for-tat is completely beyond my comprehension.

At the end of the day, we all want the same thing: relief from this terrible disease. A healthy discourse of conflicting ideas can move the conversation forward. Trying to outdo one another in snarky remarks does nothing but make this once valuable forum almost unreadable.

Please, for those on both sides of the issue, take a deep breath and think for at least 10 seconds before firing off a post that is sure to set off the usual barrage of insults. These inflammatory posts insult the very idea of a forum such as ThisIsMS, where we should be learning from each other, but instead are only displaying the basest aspects of human behavior.