Rewriting the MS story

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

Rewriting the MS story

Postby Sharon » Thu Jun 11, 2009 8:33 am

Fatigue, brain fog, and heat sensitivity are always at the top of the list of MS symptoms. These symptoms are lumped in with the others, and we have been led to believe the brain lesions are the cause. Jeff and Marie had immediate relief of some of the symptoms. I seriously doubt that a lesion (or two) mysteriously disappeared on the operating table. It seems to me that we now have two groups of symptoms - one group caused by a mechanical failure - another group caused by the lesions. It will be interesting to see how the MS medical community will discuss this.

Here is a link to an article written back in 2005 and published by the Journal of Royal Society of Medicine. Here again is a researcher questioning the autoimmune theory. Nothing about CCSVI but I thought an interesting read anyway. There are neurologists in the medical community that are trying to step "outside the box" - there just are not many in numbers.

Sharon

http://tinyurl.com/lsxz6p
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Postby mrhodes40 » Thu Jun 11, 2009 9:00 am

Cool paper Sharon thanks for posting a general link to it. That's one of my favortie papers, I own a copy of it. In light of CCSVI note this evidence offered as a reason to doubt autoimmune origin (from the table)

Selective anatomical localization, symmetry and sharp margins of plaques


Veins are symmetrical and anatomically predictabl person to person. The veins near the periventricular areas are the same in everyone and they move the most blood of any in the brain, thus would be more vulnerable to blockage. The existance of lesions due to the CCSVI model of causation explains this very well.

I also like that he points out the fact that some MS symptoms re not well explained by autoimmunity and that these are things we seem to be addressing.

I wrote to Dr Chaudhuri about 4 months ago and suggested he might like to check into this model and see if it might be the answer to his questions regarding the possible cause of degeneration in MS. I hope he looked!
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Postby cheerleader » Thu Jun 11, 2009 9:37 am

Thanks for the Chaudhuri paper, Sharon. So many things that do not make sense in the autoimmune model of MS, let alone the fact that EAE in mice is an inappropriate model for this disease- closer to ADEM, which resolves itself, rather than MS, which is a chronic and on-going disease. Hope Chaudhuri responds to the CCSVI research, Marie!

I believe Jeff's brain was oxygen starved for many years, due to the inadequate drainage and slowed perfusion time. The med. term for this is hypoxia. It happens to folks with altitude sickness, diving sickness and those deprived of enough oxygen for the brain...

You're right, Sharon. The immediate relief Jeff has experienced in his levels of fatigue and his newly elevated mood after receiving stents, shows me that his cognitive issues were not due to lesions....however, this hypoxic state may be creating the lesions, as well...and they may heal with new oxygen levels.

Acute hypoxia is experienced by a variety of individuals (neonates to the elderly) and in an assortment of conditions and diseases (terrorist bomb attack to decompensated heart failure). Increasingly, elaboration of inflammatory cytokines appears key to the brain-based response to hypoxia, as evidenced by the biobehaviors of malaise, fatigue, lethargy, and loss of interest in the physical and social environment. These sickness symptoms implicate hypoxia-dependent activation of the neuroimmune system as a key component of acute hypoxia.


http://nro.sagepub.com/cgi/content/abstract/14/3/235

The immune activation is started by hypoxia. Get the brain oxygen, and lesions should heal. No need to shut down the immune system.

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Postby akaheather » Thu Jun 11, 2009 9:47 am

Some see MS as a T-cell-driven autoimmune inflammatory disease, targeting the myelin sheaths in the central nervous system,3 but there is no proof. Unlike autoimmune conditions such as rheumatoid arthritis, systemic lupus erythematosus or myasthenia gravis, MS has no specific immunological marker.2,4


Nice. Is it just me or does "THEIR" science seems a little on the quackery side?

The progressive and global brain and spinal cord atrophy that characterizes the human disease from its earliest stages7 has not been reproduced in animals with EAE.
For basic scientists, the challenge is to develop a new animal model of MS that replicates both demyelination and neurodegeneration.


Okay, I think I can get 100 mice pretty easily. What can I use to clamp down on their jugulars! :lol:


the most neglected aspect of MS research is prevention, and we believe that this again is explained by the erroneous assumption of autoimmunity.


Can I get an Amen?

Thanks for the post Sharon.
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Postby akaheather » Thu Jun 11, 2009 10:42 am

2004: Barnett Michael H; Prineas John W
Relapsing and remitting multiple sclerosis: pathology of the newly forming lesion.
Annals of neurology 2004;55(4):458-68.
The study describes the clinical and pathological findings in 12 patients with relapsing and remitting multiple sclerosis, who died during or shortly after the onset of a relapse. Pathological changes not previously associated with the formation of new symptomatic lesions were observed in seven cases namely, extensive oligodendrocyte apoptosis and microglial activation in myelinated tissue containing few or no lymphocytes or myelin phagocytes. No current laboratory model of multiple sclerosis, in particular, experimental allergic encephalomyelitis, is known with these features, which raises the possibility of some novel process underlying new lesion formation in multiple sclerosis.
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Postby cheerleader » Thu Jun 11, 2009 11:02 am

akaheather wrote:
2004: Barnett Michael H; Prineas John W
Relapsing and remitting multiple sclerosis: pathology of the newly forming lesion.
Annals of neurology 2004;55(4):458-68.
The study describes the clinical and pathological findings in 12 patients with relapsing and remitting multiple sclerosis, who died during or shortly after the onset of a relapse. Pathological changes not previously associated with the formation of new symptomatic lesions were observed in seven cases namely, extensive oligodendrocyte apoptosis and microglial activation in myelinated tissue containing few or no lymphocytes or myelin phagocytes. No current laboratory model of multiple sclerosis, in particular, experimental allergic encephalomyelitis, is known with these features, which raises the possibility of some novel process underlying new lesion formation in multiple sclerosis.


Yup...Prineas and Barnett...them's Marie's favorites. Oligodendrocytes die and microglials are activated in brain tissue that is suffering from oxygen deprivation-Hypoxia/ischemia- or stroke. Marie...I'm lobbing this one up for you :)

AMEN on the mouse-throttling, Heather. Paper-clips? Mouse-sized Bolo ties?
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Postby MaggieMae » Thu Jun 11, 2009 11:13 am

Cheer,

You wrote "I believe Jeff's brain was oxygen starved for many years, due to the inadequate drainage and slowed perfusion time."

Could this be why Hyperbaric Oxygen Therapy is known to help with MS symptoms and is used quite often in Europe for the treatment of MS?
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Postby IHateMS » Thu Jun 11, 2009 12:52 pm

Fatigue, brain fog, and heat sensitivity are always at the top of the list of MS symptoms. These symptoms are lumped in with the others, and we have been led to believe the brain lesions are the cause


Sorry docs, I don't think so.

I have extreme heat sensitivity so much that I sit under a ceiling fan all year. Guess what? Yep, after 10 years, no brain lesions. Just those two pesky c-spine lesions.
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Postby mrhodes40 » Thu Jun 11, 2009 1:50 pm

THe Barnett and Prineas paper is my favorite. I was leaning in the way of "MS is not AI" before that but when that paper came out overnight I was completely convinced. If you read it and understand it, it shows that MS CAN"T be AI...although the Luccinetti camp tried to argue that the fact the person had died somehow stopped the immune system from being there in the normal way.................uh that doesn't work though :lol:

ALso HERE is a paper that compares EAE to MS and shows very plainly why these are not at all similar on a cytokine level. Since EAE is a AI disease, this is problematic if MS is not showing with the same type of cellular activation.

Second
Some see MS as a T-cell-driven autoimmune inflammatory disease, targeting the myelin sheaths in the central nervous system,3 but there is no proof.


People who believe that AI model ignore this fact and explain it away with a lot of talk about how complex MS is, how difficult to work with, etc. Really they take it on faith that MS is AI because they believe it. SO it is AI because they believe it is AI not because it is proven to be.

But the bottom line fact is that for a disease to be autoimmune it has to have a "PRIMED" immune system, there has to be an antigen in the body that the immune system has been programmed to attack, even though it is healthy...and it has to go to this healthy area and start breaking down perfectly healthy, perfectly functional cells that express that antigen and otherwise would have been working correctly had they been left alone.

The lab is good at finding these kinds of cells we have identified them over and over in all kinds of diseases like rheumatic fever. They've looked for 60 years and can't find one in MS. The fact they can't find this cell in MS is damning for the theory that it is autoimmune.

If the immune cells are going there because the tissue is hurt and damaged, it is not autoimmune. Period. The cure, in that case, is to stop the hurting a damaging from happening in the first place.

I don't know if CCSVI is the cause of this damage that brings the immune system in or not, but it sure is a decent candidate...............

considering the same problem CVI in legs causes cell damage and destruction in that leg that looks just like an MS lesion from a cellular standpoint as shown in this table comparing MS and stasis ulcers both have these same features(the numbers are references). From Zamboni '06 Big Idea
Perivenous inflammation + 2,4,5,9,10 + 17–25
erythrocyte extra-vasation + 4–9 + 18–21,24
Haemosiderin deposits + 4–9 + 20,21
Adhesion molecules and white cells activation+ 10–12 + 26,27
Macrophage migration-infiltration + 4–6,12 + 26,27,30
T cell migration-infiltration + 12 + 26,27,30
Iron laden-macrophage + 4–6 + 20,21
MMPs hyper-activation + 4–7,15 + 30
TIMPs hypo-expression + 4–7,15 + 30
Local iron overload + 4–9 + 18,20,21,28
Urine haemosiderin test + 9 + Personal unpublished
data
HFE mutation + 5,6 + 29
Fibrin cuff (on going reparative process)


I've said it before but it bears repeating that these immune cells listed above are seen as proof MS is autoimmune..........but these same cells are there in leg ucers in order to clean up the hurt and amaged cells, so how does that compute?
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
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Postby cheerleader » Thu Jun 11, 2009 2:39 pm

Right, Marie..

We have THREE known medical models for immune system activation in CCSVI/ MS-

1. Chronic Venous Insufficiency in the legs-
2. Congestive Venous Myelopathy in the Spine
3. Ischemic/hypoxic attack of the brain

In each of these models, injury to tissue and cell death created by venous blockage and lack of oxygen activates the immune system. The INJURY comes first, then the immune system follows.

After all this time and money spent, an antigen has never been found in MS, yet it is still purported to be an autoimmune disease. And we're the ones with a crazy theory? There's no need for an antigen if you acknowledge the immune system is responding to injury. And yes, I think this is why some folks find relief from HBOT therapy, Maggie...but it won't heal the veins. Only surgical/endovascular repair can do that.
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Postby Loobie » Thu Jun 11, 2009 3:21 pm

I just love when I read you guys bantering and it just fits with everything that's happened to me to date. You guys may never know how thankful some of us who almost get it but don't have the time to research all the details are. Just what I DO understand is enough to make me voluntarily go into debt on the 13th of next month 8O , but your keeping on connecting dots and making corralaries (sp?) is just incredible to me. I love you guys, you are the best.
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Postby Sharon » Thu Jun 11, 2009 4:38 pm

Cheer wrote
"I believe Jeff's brain was oxygen starved for many years, due to the inadequate drainage and slowed perfusion time."


This brings up a good point - Colorado has one of the highest incidences of MS in the United States....it also has some of the highest altitude averages within the state compated to other states. Denver is at 5280 ft (the Mile High City) above sea level. Could it be less oxygen that is affecting us?- an interesting query and I am not even going to hazard a guess that there is a relationship.
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Postby cheerleader » Thu Jun 11, 2009 5:16 pm

Sharon wrote:This brings up a good point - Colorado has one of the highest incidences of MS in the United States....it also has some of the highest altitude averages within the state compated to other states. Denver is at 5280 ft (the Mile High City) above sea level. Could it be less oxygen that is affecting us?- an interesting query and I am not even going to hazard a guess that there is a relationship.


Absolutely, Sharon....this was one of the issues I brought up months ago regarding altitude's effect on nitric oxide and oxygen and the endothelial cells in blood vessels. I think less oxygen and vasoconstriction at high altitude exacerbates MS for many people. And I think it's part of the higher MS rates in Colorado.
I've often wondered why MS rates are high in higher altitude locales like Colorado and the alps...especially since UV rays and vitamin D levels are higher in these places. Came across some articles on brain changes in mountain climbers, and then found some research on endothelial changes at high altitudes.

For people not born at high altitude, a move or relocation to a higher altitude can stress the endothelial structure...an extreme example of this reaction is high altitude pulmonary edema-

Quote:
"Conclusions: Hypoxia markedly impairs vascular endothelial function in the systemic circulation in HAPE-S subjects due to a decreased bioavailability of NO. Impairment of the NO pathway could contribute to the enhanced hypoxic pulmonary vasoconstriction that is central to the pathogenesis of HAPE."

There is vasoconstriction at high altitudes- for people who are not native to the locale. Sherpas and Tibetans have been shown to have a different genetic makeup which allows them to synthesize more NO- and reduce vasoconstriction-

Genetic contribution of the endothelial nitric oxide synthase gene to high altitude adaptation in sherpas.
http://www.ncbi.nlm.nih.gov/pubmed/16978133

I wonder if people who move to higher altitudes may experience more severe MS symptoms and flares, and be more likely diagnosed as MS, because of the stress on their endothelial structure.
Jeff was in Salt Lake City for a week before his first major flare....
AC

http://www.thisisms.com/ftopic-6318-day ... sc-15.html

This makes so much more sense to me since CCSVI. Another puzzle piece, if you will.
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http://ccsviinms.blogspot.com
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Postby mrhodes40 » Thu Jun 11, 2009 5:23 pm

I was thinking about the blockages earlier today and it occured to me that they are not 100% so perhaps that is why it we get by ....maybe losing only 50% of the lumen is manageable for the body, but beyond that it starts to get ahead of the body's ability to compensate.

Then these other things are a bigger deal than they would be like NO issues or vasocontrictive things, fats in the diet ball up there a little bit etc. Thus it may be true that it is an issue of degree and intermittant lifestyle issues may make the difference.
think so?
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
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Postby javaneen » Thu Jun 11, 2009 5:33 pm

I agree with you Loobie...I love to read all the bantering...its facinating and really does make sense. I am so truly thankful for all the work you guys put into this topic. Its amazing and very much appreciated by so many of us.

So I agree with Loobie...you guys are the best!
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