Dr Trevor Tucker with his understanding of CCSVI and flows

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

Dr Trevor Tucker with his understanding of CCSVI and flows

Postby NZer1 » Tue Aug 23, 2011 9:48 pm

This three part presentation gives meaning to the observations made so far in MS and Vascular problems found in CCSVI. It links all of the key theories in Vascular interplay seen in MS by the literature and from the the main Scientists and Doctors and Researchers, enjoy and tell others please,

http://www.youtube.com/watch?v=WriNVSNy6Qw&NR=1
http://www.youtube.com/watch?v=g07XPAA_ ... re=related
http://www.youtube.com/watch?v=ABRD5P8Y ... re=related

Regards Nigel
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Postby cheerleader » Tue Aug 23, 2011 9:58 pm

Hi Nigel-
Many of us have watched these videos and discussed them here:
http://www.thisisms.com/ftopicp-171401- ... tml#171401

cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby NZer1 » Tue Aug 23, 2011 10:12 pm

Thanks Joan, it was, IMO, more of a critique of the Dr.s video skills rather than his mind!
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Postby NZer1 » Tue Aug 23, 2011 10:31 pm

Cece
here is his abstract from ISNVD: http://ccsvism.xoom.it/ISNVD/Other/Abstract-Tucker.pdf

and his post in Dr. Snyder's thread:
www.thisisms.com/ftopicp-171260.html#171260
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Postby NZer1 » Tue Aug 23, 2011 10:47 pm

Quoted from Dr. Snyders thread;
Dr Snyder wrote:
"Dr. Salvi showed a picture of someone with sever edema in the lower extremities that looked just like venous stasis and claimed that they had a complete reduction in the LEG swelling after jugular treatments for CCSVI. This seems hard to explain and I would have liked to see any data to support this."
Cure or Bust wrote:
"Not as obvious, but before my two treatments (both jugular, at different points) I used to get a severely painful leg thing, that originally started out as a superficial thrombosis; however in the last couple of years, the swollen vein was not visible. Since the treatments, this has not happened once. It was getting worse and more frequent, and was starting to occur once every 3 months or so before treatment. They found nothing using ultrasound of my leg. Truly painful, now a memory...please."

Could this be a reverse pressure wave?
It is in the same vein system and the same theory of pressure would apply elsewhere in the same vascular track. Changing the reverse pulse in the neck would change the entire systems flow, legs included, as it is a closed circuit. Maybe a physically weaken area in the legs venous system that is effected by the pulse wave? These lower veins have also been noted as having malfunctioning valves which could be creating their own pulses of pressure in another part of a connected system?

Puzzles, regards Nigel
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Postby fee001 » Wed Aug 24, 2011 1:11 am

Hi!

because of all these changes in blood flow, I can only presume that in some, must affect blood pressure. Mind you I havent a clue which way. Up or down.

I've never understood blood pressure results. I get all confused at all what it means.

Fiona
I do my own research, and find my own answers Its good to talk
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Postby NZer1 » Wed Aug 24, 2011 3:03 am

From Dr. Schelling's site;
http://www.ms-info.net/evo/msmanu/956.htm#level_5_1
(V-1) The Dynamics of Lesion Formation
The development of the pattern of a lesion depends, in the final analysis, on plain mechanical principles. The first clues for determining the cause of a particular kind of injury are thus to be derived from its outer shape and inner organization. In multiple sclerosis, a sober consideration of the patterns of lesion “dissemination", i.e. of the "fibre-borne" extension of patches in the spinal cord's flanks, and the eccentric expansion of homogenous plaques from definite brain veins, will clarify several significant points:
Which forces are capable of bringing about the particular changes via the structures from which the lesions originate and in the observed directions and ranges of spread?
In which ways are the injurious forces transmitted onto the structures and zones from which the lesions arise?
From which sources do the injurious impulses arise?
Which forces control and check the lesion spread?
===============================================
Reading the content of Dr. Schelling's site will give more understanding to the article of Dr. Trevor Tuckers.
Enjoy,
Regards Nigel
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Postby Cece » Wed Aug 24, 2011 8:26 am

It's good to have a thread with all of this. It gets lost so quickly with all the posts here. I've still got to get back and watch his second two videos (I figure I'll have some spare time in the second week of September, that is a ways out!) but the first added to my understanding of how injury can occur in CCSVI.
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Physics and MS

Postby ttucker » Wed Aug 24, 2011 8:42 am

Nigel

Thanks for helping carry this banner. I am in the process of revising a scientific paper that has been accepted for publication in one of the reasonably well known medical journals. It is one thing to put together a youtube presentation and another to put together a scientific paper that it is sufficiently tight that it gets through "peer" review.

I can put up a post when and where it is published after it happens.

Trev. Tucker
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Postby NZer1 » Wed Aug 24, 2011 2:30 pm

Thanks Trev.

I have been spreading the videos all over the place on Face Book to try and get some dialogue going that will give people an opportunity to challenge why there are so many following the cellular 'chemical' dysfunction trail.
It seems that the Pharmacuticle Industry would prefer that MS be drug modulated so there is much work to do to 'arrange' the details of these findings so that there is more impact from a news release that connects as many of the dots as possible in one place/document.

Thank you for making time to present this to us, it will be important for people to understand that there is a physical component in the BBB break through!

Regards Nigel
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Postby Cece » Wed Aug 24, 2011 2:41 pm

I am in the process of revising a scientific paper that has been accepted for publication in one of the reasonably well known medical journals.

Congrats! That is an accomplishment. Yes, please post when it is published. We like to scrutinize such papers, when we can. :)
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Postby 1eye » Wed Aug 24, 2011 8:06 pm

I am more comfortable considering standing waves and other wave phenomena in brain vessels, where there are no valves. The presence of asynchronous muscle movements and valves actively interrupting flow I would think makes any kind of frequency or wave analysis impossible. It might be significant that lesions are not found where there are any valves or smooth muscles. Or are they? How do frequency, appearance, locations etc. of brain lesions differ from spinal ones? Or are they the same?
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Postby NZer1 » Wed Aug 24, 2011 10:56 pm

I'm with you Ieye on the 'how' of cord lesions.

The cord lesions are the one that has the most interest to me as it is within the BBB and also the veins are probably inaccessible. So, is the stenosis within the cord region or in the veins exiting the spinal column? or the veins elsewhere in the return system creating the waves and slow flow?
All of this cord flow is likely to be associated with the CSF flow and its creation from the arteries, and what if this whole system of blood in and out is effected by the wave pattern and slowing flow in general both in and out? A long time ago I asked the question of Dr. S about total volume through the brain and if it was measurable, it is still an unanswered question that would no doubt be a challenge to measure, although it appears that the MR programming Dr. Haacke has done is achieving results that are being calculated against normals.

Trev did you have any feed back from Dr. Schelling or Dr. Zamboni on this?

It would seem to be the learning area on MS because of the progressive nature of disability involved with cord lesions and the pathology definition of lesions that has been done by Dr. Schelling and others.
Regards all,
Nigel
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Postby 1eye » Thu Aug 25, 2011 6:46 am

I don't think we have any problem imaging lesions or flow, except it will likely be somewhat unconventional. I got MRIs of my spine, and they are done with jugular flow, in prone position. No veins on mine.

Are spinal lesions perivenous? We must know that much, even if it is from corpses. What you would need there, for a standing reflection, is a long run of valve-free vein, downstream from the from the last valve. and upstream of the reflection, or stenosis. Note that if this is the mechanism that causes spinal lesions to form, they would be inside that area, and if they are caused by pressure waves, there would have to be places where the blood is coming from some place where there are new additions to the flow, like rib veins, or spinal ones, to be perivenous in the same way as brain lesions. I really don't see how similar they can be, since there is no brain matter for them to form on.

Given the influence of gravity I can't see them being on both the uphill and the downhill sides of the heart, though their formation may be posture-dependent. Is sleeping time an influence? Is this partly because as we age we spend more time upright? A key factor might be exercise, which would tend to disrupt waves. The lesions would only appear if we spent a long time sitting still. More of that, as you age?
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Postby ttucker » Thu Aug 25, 2011 7:42 am

A comment to 1eye - my perception is that your observation that "muscle movements and valves actively interrupting flow I would think makes any kind of frequency or wave analysis impossible" might be a bit of overstatement. I would say it makes it more difficult and is why I propose the discipline of "Computational Fluid Dynamics" be applied. This could incorporate the kinds of complex "boundary conditions" that you describe in a more complete and accurate fluid dynamics analysis. Because there are so many correlations between the observables in MS and the predictions of even my simple analysis, it seems worthy of further study. I suspect perhaps 8 or 10 PhD theses lurking here - any CFD grad students out there interested in cardio-vascular flow looking for a good thesis topic? (Some day, 1eye, we should discuss over lunch at the Swan in Carp, or perhaps the Cheshire Cat)

To NZer - I have not communicated with Dr. Zamboni, but had a good discussion with Dr. Schelling while in Bologna in Feb. Also, good feedback from Dr. Simka. I strongly suspect the breakdown of the blood brain barrier (which might be a consequence of reflux in any of the cerebral capillary bed's drainage vessels) is a consequence of chronic, persistent hypertension (over the years causing fatigue failure, like the slab of roof that came off that Northwestern Airlines 737 a few months ago). However, I also suspect that sudden acute traumatic hypertension may, in some instances, also be a contributor.

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