A History Lesson from Dr. Mark Haacke

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

A History Lesson from Dr. Mark Haacke

Postby cheerleader » Sat Jan 09, 2010 1:55 pm

on venous vascular observations in MS. A good read:
http://www.ms-mri.com/history.php

ALSO...an animal study on CCSVI has already been done....in the 1930s in dogs by Dr. Putnam
(5) Putnam (1935). Studies in multiple sclerosis: encephalitis and sclerotic plaques produced by venular obstruction. Archives of Neurology and Psychiatry. 33: 929-940.

With an ingenious idea, he proceeded to study the effects of obstructed venous flow in the cerebral veins of dogs. These animals developed a number of abnormalities many of them similar to encephalitis or multiple sclerosis. His comment at the end of his paper was as follows (5): "The later stages (up to ten months) of the lesions consist of plaques of demyelinization with practically complete preservation of the axis-cylinders and with dense fibrous gliosis confined to the white matter. The similarity between such lesions and many of those seen in cases of multiple sclerosis in man is so striking that the conclusion appears almost inevitable that venular obstruction is the essential immediate antecedent fo the formation of typical sclerotic plaques.


Let's read Dr. Haacke's research and discuss....

cheer
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Postby ozarkcanoer » Sat Jan 09, 2010 2:00 pm

My first response is if Putnam created an animal model that looked like MS then why wasn't there any follow up ?? The depression ? WWII ? Or just ignored like Gregor Mendel's genetics work.

My second response is, if Putnam created an animal (dog) model then it should be easy for Stanford to make a mouse model. How exciting !!

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Postby CureIous » Sat Jan 09, 2010 2:16 pm

ozarkcanoer wrote:My first response is if Putnam created an animal model that looked like MS then why wasn't there any follow up ?? The depression ? WWII ? Or just ignored like Gregor Mendel's genetics work.

My second response is, if Putnam created an animal (dog) model then it should be easy for Stanford to make a mouse model. How exciting !!

ozarkcanoer


I object to being called a mouse lol. :)
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Postby Johnnymac » Sat Jan 09, 2010 3:44 pm

CureIous wrote:I object to being called a mouse lol. :)

this made me laugh

I think its awesome that there were doctors and scientists so long ago documenting these observations. The evolution of imaging technology is allowing doctors today to actually take those old observations along with new findings and paint a picture that has been in process for I guess 170ish years. It'll be easy for some to question why it took so long to make these connections, I'm just happy they are being made now and am ecstatic there are 170 years of scientific observation and documentation that corroborates this new CCSVI theory. It'll just make things easier to push forward.
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Postby jay123 » Sat Jan 09, 2010 4:01 pm

I did some internet snooping and couldn't find anything (yet), but it would be interesting to see if this research was followed up or ignored.

Do you think references 1 and 5 have wrong dates, or was there 2 Putnams doing research (or was Dr. Putnam over 100 yrs old when she did the dog research(lol - just kidding))?
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Postby Billmeik » Sat Jan 09, 2010 4:11 pm

animal study already done. I like the stuff he calls up from 1836 and such..
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Postby cheerleader » Sat Jan 09, 2010 5:08 pm

jay123 wrote:I did some internet snooping and couldn't find anything (yet), but it would be interesting to see if this research was followed up or ignored.

Do you think references 1 and 5 have wrong dates, or was there 2 Putnams doing research (or was Dr. Putnam over 100 yrs old when she did the dog research(lol - just kidding))?


typos. Dr. Putnam was a he, and it's 1936.
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Postby Vonna » Sat Jan 09, 2010 6:16 pm

Bilmeik and other Woofs... :)
So glad you did it, and I would love a turn!

At least your veins were not restricted on purpose, just so they could watch the liesions and disabilities take place!! Poor dog. 8O
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Re: A History Lesson from Dr. Mark Haacke

Postby CureOrBust » Sat Jan 09, 2010 7:30 pm

cheerleader wrote:ALSO...an animal study on CCSVI has already been done....in the 1930s in dogs by Dr. Putnam
(5) Putnam (1935). Studies in multiple sclerosis: encephalitis and sclerotic plaques produced by venular obstruction. Archives of Neurology and Psychiatry. 33: 929-940.
I am guessing this is the article (first 150 words)
http://archneurpsyc.ama-assn.org/cgi/content/summary/33/5/929
STUDIES IN MULTIPLE SCLEROSIS
VII. SIMILARITIES BETWEEN SOME FORMS OF "ENCEPHALOMYELITIS" AND MULTIPLE SCLEROSIS


TRACY J. PUTNAM, M.D.


Arch Neurol Psychiatry. 1936;35(6):1289-1308.


Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.




The suggestion that multiple sclerosis represents a late stage of a process which is recognized in its acute stage as acute "myelitis" or "encephalomyelitis" of certain types dates well back into the last century.1 The scene of battle has changed somewhat and now centers less about the question whether the lesions of multiple sclerosis are progressive—it appears to be almost universally accepted that they are-than about the more specific point as to whether the disseminated foci of degeneration seen in the group of "demyelinating encephalomyelitides" or encephalomyelopathies most definitely represented by the postvaccinal and postmeasles forms represent an acute form of typical sclerotic plaques. The issue is a difficult one in itself, for it consists in attempting to compare an acute lesion with a chronic one. This difficulty is increased by the fact that several varieties of lesions may often be observed in each case of the same disease. . . .
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Postby bestadmom » Sat Jan 09, 2010 8:56 pm

Joan,

I can't believe you posted this today. I have an email that was sent to my interventional radiologist talking about Putnam's findings with the dog. It blows my mind and I was going to post it!

mb
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Postby SammyJo » Sat Jan 09, 2010 9:07 pm

there are 170 years of scientific observation and documentation that corroborates this new CCSVI theory. It'll just make things easier to push forward.


Is there a scientific standard we can consult, like how much past corroboration needs to pile up before the scientific community can reach a conclusion?

And what is the number of studies required to corroborate Dr. Zamboni's conclusions?

I want to alert the World Health Organization or the UN that we've got a world wide health emergency, as Dr. Haacke terms it. While the studies are going on, there should be planning for immediate patient help, if everything starts confirming the CCSVI theory.
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Postby cheerleader » Sat Jan 09, 2010 9:52 pm

THanks for the paper, Cure...interesting to see that in the 30's MS research was called "The scene of the Battle" by Dr. Putnam. Doctors were lining up on the infectious/encephalitis or vascular sides even then.

SJ- couldn't agree with you more. Here, in Putnam's dogs, we have an actual animal model for MS lesions developed by a neurologist- creating the venocentric lesions we see in MS by blocking outgoing veins and creating venous congestion.

EAE, discovered in the 1930s by a virologist, Dr. Rivers, uses another animal's brain tissue, injects it into a mouse brain and elicits some demyelinating lesions that look more like encephalitis than MS. Yet, we have continued on with the EAE model for 75 years. ( I rant about this on the FB page today.) It is wrong, it doesn't explain MS or hope to cure it, and it needs to stop.

Michelle...Dr. Haacke posted his history of MS yesterday with Putnam's dogs...had to share -even though we both love our dogs as much as our kids:)
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old paper on dog model of CCSVI

Postby msscooter » Sun Jan 10, 2010 12:09 am

This is very exciting. It allows us to advance quickly because an animal model was the next step, of course, and now it's done. I wonder how long it took the dogs to develop lesions and is they were ataxic. I wonder if a mouse model would be good because they don't live long. (BTW they use hamsters to study BSE (madcow) and it has a 50 yr cycle in most people so maybe it works???)

If CCSVI is congenital and most human patients show first signs in their twenties does it take 20 years of iron buildup to trigger the autoimmune response??? Are juvenile MSrs those with the most severe stenosis? OR is there something that leads to stenosis in previously normal veins. It will take a while to figure that out. I wonder if any of the old papers suggested aquired stenosis vs. congennital.
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Postby Leonard » Sun Jan 10, 2010 3:09 am

I knew about the story of the Austrian Dr. Schelling in the 1980's and how his work was frustrated. That is already bad, very bad... But with this new information, it is becoming blatantly clear that here is a systemic failure of unseen proportion.

However firm action to correct the situation is as yet missing. The matter needs gouvernance by states from around the world but so far I fail to see a response.
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Postby Sotiris » Sun Jan 10, 2010 4:00 am

I think CureOrBust has given the correct link but has quoted another paper. The correct one is the following
STUDIES IN MULTIPLE SCLEROSIS
IV. "ENCEPHALITIS" AND SCLEROTIC PLAQUES PRODUCED BY VENULAR OBSTRUCTION


TRACY J. PUTNAM, M.D.


Arch Neurol Psychiatry. 1935;33(5):929-940.


Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.




In previous papers it has been shown that a series of histologic pictures resembling those of "postinfectious encephalomyelitis" may be produced in animals by a variety of agents, such as minute doses of tetanus toxin, carbon monoxide poisoning and certain types of embolism.1 The pathologic alterations ranged, sometimes in a single specimen, from mild perivascular infiltrations with glia and occasional lymphocytic cells through areas of damage to and loss of perivascular myelin to areas of softening and destruction of the axis-cylinders. In one instance, more than a year after the original injection of tetanus toxin, lesions were found which closely simulated those of multiple sclerosis,2 with plaques of loss of myelin, but with almost complete preservation of the axiscylinders and with local gliosis. Multiple sclerosis has been observed as a sequel of "postinfectious encephalomyelitis,"3 and the hypothesis that all of these conditions represent variants of the same . . .
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