heterogeneity and perivenous MS

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heterogeneity and perivenous MS

Postby frodo » Mon Aug 15, 2011 4:52 am

Several reports have stated that MS is an heterogeneous disease, with more than one source.

I have recently found a statemente here:

www.mscare.org/cmsc/images/pdf/ijmsc-2000-jun.pdf

saying:

"Demyelination can occur independent of perivenous inflammatory changes, supporting the presence of more than one athophysiologic process leading to demyelination in MS"

Should we make a difference between "perivenous MS" and "non-perivenous MS"? Does anybody has an article doing such a distinction?
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Postby Cece » Sun Aug 21, 2011 10:03 pm

Perivenous would mean near the veins, so they are saying that inflammatory changes can occur further from the veins as well? You are suggesting that these could be two different disease processes?
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Postby MegansMom » Mon Aug 22, 2011 4:48 am

The perivenous areas are the ones that seem to have more iron deposits, much like the reflux causes turbulence in that area, but according to SWI MRIs the iron is also higher in the entire brain than normal controls. It's just concentrated at the verivascular areas.

Also there are a few things going on here. Tissue damage due to hypoxia( hypoperfusion), pressure higher, iron deposits and the oxidation it causes.

Venoplasty helps the pressure, and hypoxia but it does not address the iron in the tissues or the oxidation it could cause, which could definitely cause inflammation even after TPA. Macrophages try to remove iron, and iron laden macrophages are seen in MS in the inflammatory areas of the body.

Iron is very caustic and breaks down ( like rusting) through oxidation, it is very irritating to tissues in other areas. Iron is only meant to be in certain areas of the body.

In the future perhaps iron chelation with Desferral will follow TPA to remove this iron?
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Postby frodo » Mon Aug 22, 2011 9:50 am

Cece wrote:Perivenous would mean near the veins, so they are saying that inflammatory changes can occur further from the veins as well? You are suggesting that these could be two different disease processes?


Yes, I really think there could be two or more different processes involved in MS. For example NMO was formerly considered MS and now it is known to be a different condition. There could be more situations like that. And that would explain the different reactions after angioplasties.
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Postby gauchito » Tue Aug 23, 2011 12:43 pm

This takes me back to the issue of demyelination again. Is there conclusive evidence that damage of nerve tissue starts up by loss/breakdown of myelin? Would it be possible that latter ocurrs as part , and among other things, of damage of nerve tisue?
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Re:

Postby frodo » Tue Jun 26, 2012 9:53 am

I am rescuing this old thread just because I am hearing a lot about the all-or-nothing effect of venoplasties. This behaviour would point out to an heterogeneity of MS, being CCSVI-induced-MS just one kind of MS.

Anybody has information about this possibility?
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Re: heterogeneity and perivenous MS

Postby 1eye » Tue Jun 26, 2012 1:11 pm

Venoplasty helps the pressure, and hypoxia but it does not address the iron in the tissues or the oxidation it could cause, which could definitely cause inflammation even after TPA. Macrophages try to remove iron, and iron laden macrophages are seen in MS in the inflammatory areas of the body.

A) Iron oxides get reduced and the oxygen crossed the BBB all alone, leaving the red blood cells with reduced iron. If there are a lot of venous blood cells crossing the barrier too, macrophages swallow them and some leave iron behind, in the tissues and elsewhere. This stops happening if the blood is going through fast enough (after venoplasty) that the red blood will not pass through the BBB (no adhesion molecules).

B) Iron can only oxidize, then contribute to other cells' oxidation if there is lots of free oxygen around. I thought getting rid of hypoxia was a good thing. Are you saying, if iron that shouldn't be there combines with some of the free oxygen that is normally delivered to tissues, it could starve them of free oxygen anyway? Is it now considered to be a free radical because it crossed the BBB as a cell and then became ionized fe, now chemically less stable, and easy to oxidize? That sounds like a reperfusion problem, doesn't it?
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