PointsNorth wrote:Hey 1eye, I ain't no expert in fluid dynamics, but wouldn't a narrowing just cause blood to flow faster thru a narrowing but not necessarily affect total volume of blood? From a presentation that Dr. Arata recently gave he said that vein architecture doesn't necessarily result in reflux or limit volume of flow. I remember BourNouelli's theory (more Italians!).
MS appears to be related to venous flow abnormality of the brain with secondary brain autoimmunity
Steven R Brenner, physician
Dept. Neurology St. Louis VA Medical Center and Dept. Neurology & Psychiatry at St. Louis University
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.
Secondary development of autoimmunity can occur, as the weakened capillary endothelium allows leukocytes gain access to the brain. The blood brain barrier is there for a reason, it is not by chance that the endothelium of the capillaries of the brain has those extreme tight junctions, and we get to live the results of that BBB being weakened. Dr. Brenner uses the words 'secondarily progressive' autoimmune disease, does that mean he is suggesting that this secondarily acquired autoimmunity marks the change from relapsing-remitting MS to secondarily progressive MS? I don't think this quite fits. Relapsing-remitting has a strong role for the immune system; secondarily progressive does not much involve the immune system, since the DMDs no longer do much for SP the way they do for RR. I find it more likely that SP is a result of the accumulation of axonal damage and the natural consequences of aging meaning that the brain can no longer heal and recover the way it could when we were twenty.
I believe what the author is referring to is the fact that once such an autoimmune engine has been started, eliminating the key that started it will no longer relieve the disease.
During chronic inflammation, immune effectors progressively organize themselves into a functional tertiary lymphoid tissue (TLT) within the targeted organ. TLT has been observed in a wide range of chronic inflammatory conditions but its pathophysiological significance remains unknown. We used the rat aortic interposition model in which a TLT has been evidenced in the adventitia of chronically rejected allografts one month after transplantation. The immune responses elicited in adventitial TLT and those taking place in spleen and draining lymph nodes (LN) were compared in terms of antibody production, T cell activation and repertoire perturbations. The anti-MHC humoral response was more intense and more diverse in TLT. This difference was associated with an increased percentage of activated CD4+ T cells and a symmetric reduction of regulatory T cell subsets. Moreover, TCR repertoire perturbations in TLT were not only increased and different from the common pattern observed in spleen and LN but also “stochastic,” since each recipient displayed a specific pattern. We propose that the abnormal activation of CD4+ T cells promotes the development of an exaggerated pathogenic immune humoral response in TLT. Preliminary findings suggest that this phenomenon i) is due to a defective immune regulation in this non-professional inflammatory-induced lymphoid tissue, and ii) also occurs in human chronically rejected grafts.
Nasti wrote:Definition of the scientific revolution. Plus, it doesn't happen over night (unless all the old proponents die pretty fast) and it is completely and utterly different from the old definition (Galileo's Sun completely switched places with the Earth in the rotation who around who). And this is how progress happens. And we, the suffering, in this theory switching time, are just warriors (some veterans, some casualties) paving the way for the future not as unfortunate generations.
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