Response to Z paper
Posted: Wed Jun 17, 2009 7:21 am
HERE IS A COMMENT on Dr Zamboni's paper published in December.
The author is Steven Brenner MD from the St Louis Veterans hospital neurology department.
The idea that this has to lead to autoimmunity in some way rather than inducing someone to look into how this may be a non autoimmune model is demonstrating how well entrenched the autoimmune idea is.
It takes considerable time studying the venous insufficiency of legs and reading about the changes in the endothelium etc before the pieces fall together for the understanding that there need be no autoimmunity at all in CCSVI for MS lesions to happen in this model....
The author is Steven Brenner MD from the St Louis Veterans hospital neurology department.
This author did not bring anything new to the table in terms of references to support the suppositions and speculation that Dr Zamboni's paper elicited in him, but it is good to see that all the responses to this paper so far have been positive. There are no comments saying "this is not possible and here is why..." as you often see in these comment threads.Dear Editor,
I read the article by Zomboni (1) with interest, with respect to the interaction of the cerebral venous system and central nervous system in development of multiple sclerosis (MS).
An interaction between the central nervous system and venous system has been observed previously in MS lesions by F. A Schelling (2) who initially observed “striking widening of the main venous passageways in the skulls of victims of multiple sclerosis”, and observed venous involvement in the development of cerebral lesions of multiple sclerosis. His supposition was lesions of MS are due to venous back jets from intermittent rises in pressure in the large collecting veins of the neck and especially the chest (2) and noted that Beno Schlessinger, in 1939, while injecting the straight sinus under heavy pressure, noted the extravasations produced around the lateral ventricles “closely stimulate the distribution and even shapes of plaques in multiple sclerosis”.
Certainly venous involvement is distinctive in MS plaques, which usually are perivenous in location, especially in the brain.
The venous outflow obstructions noted by Zamboni (1) appear significant in the development of multiple sclerosis, however their origin remains uncertain. Possibly they are developmental, although an underlying abnormality of the venous wall could also lead to development, especially since MS more commonly develops during adult life, and possibly there is more than one etiology since MS is variable in symptomatology.
Venous obstruction may lead to decreased cerebrospinal fluid reabsorption with subsequent toxicity to neuronal structures from retained CSF components. Additional injury would occur subsequent to breakdown of the blood brain barrier from intermittent elevation of venous pressure injuring capillary and venule endothelium, with secondary development of autoimmunity to brain components following exposure to the systemic immune system, which is ordinarily barred from the central nervous system. After autoimmunization to brain components, MS could transition from a initial abnormality of venous drainage to a secondarily progressive autoimmune disease.
References
The idea that this has to lead to autoimmunity in some way rather than inducing someone to look into how this may be a non autoimmune model is demonstrating how well entrenched the autoimmune idea is.
It takes considerable time studying the venous insufficiency of legs and reading about the changes in the endothelium etc before the pieces fall together for the understanding that there need be no autoimmunity at all in CCSVI for MS lesions to happen in this model....
Maybe scientific world is so slow to change with ideas, that these CCSVI findings just need time in research field.