This Is MS Multiple Sclerosis Community: Knowledge & Support

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.

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.

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))?

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.

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. . . .

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

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 . . .