can ccsvi explain these?

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

can ccsvi explain these?

Postby Cece » Sun Jun 05, 2011 7:17 pm

J R Soc Med 2005;98:303-306
Multiple sclerosis: looking beyond autoimmunity
Abhijit Chaudhuri PhD FRCP 1 Peter O Behan DSc FRCP 2
Box 1 Important facts about MS that cannot be explained by the concept of myelin-specific autoimmunity

Age effect of migration

Geographic variation (higher prevalence in most northern latitudes)

Maternal contribution to disease risk (Ref. 5)

Early and extensive grey matter involvement (estimated number of deep grey matter lesions per gram wet weight is higher than in any other brain structure [Ref. 6])

Progressive brain and spinal cord atrophy, beginning at the stage of clinically isolated demyelinating syndromes (Ref. 7)

Selective anatomical localization, symmetry and sharp margins of plaques

Absence of specific immunological marker

Effect of stress

General failure of immunotherapies that are highly successful in other organ-specific autoimmune diseases and transplant rejection

Associations with Charcot-Marie-Tooth disease and neurofibromatosis-1 (Ref. 2)

These are ten things about MS that cannot be explained by the autoimmune theory. How many can be explained by CCSVI? I am hoping for all ten. :)

great paper, well worth a read: http://tinyurl.com/6jxo78e
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Postby newlywed4ever » Sun Jun 05, 2011 7:33 pm

Thanks for more great info, Cece!
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Postby Thekla » Thu Jun 09, 2011 5:58 am

Age effect of migration always fascinated me. It also prompted our sudden relocation to tropical latitudes with our boys in 2005. I haven't seen reverse migration data anywhere--hoping that the protective influence is more lasting since we had to move back north.
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Postby frodo » Thu Jun 09, 2011 6:27 am

Thekla wrote:Age effect of migration always fascinated me. It also prompted our sudden relocation to tropical latitudes with our boys in 2005. I haven't seen reverse migration data anywhere--hoping that the protective influence is more lasting since we had to move back north.


I am not sure how reliable are those studies. I have heard only about only one study with a small population
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Postby se1956 » Thu Jun 09, 2011 7:00 am

One should always be careful about what is "known" about MS.

Here another example:

I think these numbers should be reliable
(and are different from most other numbers)

8401 children in MS-families
798 children had MS
Father and mother passed MS to the children with the same risk of nearly 10%

http://www.msrc.co.uk/printable.cfm?pageid=1891

R.
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Postby ThisIsMA » Fri Jun 10, 2011 10:24 am

O.K. Here's my amateur attempt at explaining a few of these:

Age effect of migration

Geographic variation (higher prevalence in most northern latitudes)


Protective effect of Vitamin D on endothelial health. Vitamin D is a vasodilator.

Maternal contribution to disease risk (Ref. 5)


Maternal genetic influence on venous '"birth defects"

Early and extensive grey matter involvement


Effect of hypoperfusion?

Progressive brain and spinal cord atrophy, beginning at the stage of clinically isolated demyelinating syndromes


Effect of hypoperfusion? And it might start at birth, since no one's looking before symptoms of CIS appear

Selective anatomical localization, symmetry and sharp margins of plaques


I wonder if this is another way of saying that the lesions are centered around a vein?

Absence of specific immunological marker
An indicator that this may not be an autoimmune disease, but a vascular disease with immune system activation to clean up the mess!

Effect of stress
Stress causes vasoconstriction.

General failure of immunotherapies that are highly successful in other organ-specific autoimmune diseases and transplant rejection
I love this one! Researchers admitting that the DMD's don't work. I think big pharma chose the name "disease MODIFYING drug" very carefully. No false promises that their drugs might actually treat the disease or improve the symptoms... If immunotherapies don't work, maybe its not an autoimmune disease? Makes sense to me...

Associations with Charcot-Marie-Tooth disease and neurofibromatosis-1


This one stumped me, maybe someone else has a clue...
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