CCSVI and BBB

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

CCSVI and BBB

Postby sbr487 » Fri Mar 19, 2010 5:30 am

Most of the MS literatures suggest that healthy people's BBB does not allow the T cells to penetrate CNS. If CCCVI is the cause of MS, how does it explain BBB filtering changes only in MS patients?

Is it that T cells are always capable of entering CNS but in normally people they don't since there is no reason?

Is is that BBB intentionally relaxes filtering in order for T cells to enter CNS?

Also, note that the T cells not only enter the CNS but also attack myelin.
To me it looks like much more synchronized action than just BBB malfunction.

Thoughts?
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Postby JSTCD » Fri Mar 19, 2010 7:26 am

My limited understanding is:

1) CCSVI causes irregualrities in blood flow.
2) irregularity in blood flow cause reflux.
3) reflux means that some percentage of blood is not going allong the perscribed path, heart,lung,kidney,liver,brain etc. and instead is recirculating in the brain withough oxigen replenishment, or removal of metabolic by-products.
4) abnormal buildup of these products, (epecially iron?) leads to inflamation, and iron build up. (Note that at this point the picture IS imunological) T cells are free to do what they want in areas of inflamation.
5) Buildup of these byproducts, or the iron deposits, or the imune system's attempts to clear these products then damages the brain.
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Treat the symptom of CCSVI

Postby MarkW » Fri Mar 19, 2010 7:49 am

sbr487 asks:
If CCCVI is the cause of MS, how does it explain BBB filtering changes only in MS patients?
That is a big IF to start with. I would suggest that MS is multifactorial and one of the factors is probably CCSVI. It is likely to be a 5-10 year horizon to find out how CCSVI is involved in MS.
I recommend to treat the symptom of CCSVI if you have it and wait for the science to catch up. The medical and pharmaceutical worlds have used the approach of 'treat the symptom' for decades so lets stick with it for CCSVI.
Speculation hinders the CCSVI message so why speculate ?

Kind regards,
Mark
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Postby cheerleader » Fri Mar 19, 2010 7:50 am

Dr. Simka has written a wonderful, peer-reviewed paper on the proposed mechanism of the BBB break thru-- we've written about it a few times on here.

Multiple sclerosis is an autoimmune disease characterized by multifocal areas of inflammation and demyelination within the central nervous system. The mechanism that triggers the disease remains elusive. However, recent findings may indicate that multiple sclerosis, at its source, could be a hemodynamic disorder. It has been found that multiple sclerosis patients exhibit significant stenoses in extracranial veins draining the central nervous system (in azygous and internal jugular veins), which are associated with significant pressure gradients measured across strictures. Such anatomic venous abnormalities were not found in the control group of healthy subjects. In this review, it is hypothesized that pathological refluxing venous flow in the cerebral and spinal veins increases the expression of adhesion molecules, particularly intercellular adhesion molecule-1 (ICAM-1), by the cerebrovascular endothelium. This, in turn, could lead to the increased permeability of the blood-brain barrier. Inflamed and activated endothelium could secrete proinflammatory cytokines, including GM-CSF and TGF-beta In these settings, monocytes could transform into antigen-presenting cells and initiate an autoimmune attack against myelin-containing cells. Consequently, a potential therapeutic option for multiple sclerosis could be pharmacotherapy with either substances that strengthen the tight-junctions barrier, or with agents that reduce the expression of adhesion molecules. In addition, surgical correction could be an option in some anatomical variants of pathologic venous outflow. We are optimistic that a hemodynamic approach to the multiple sclerosis pathogenesis can open a new chapter of investigations and treatment of this debilitating neurologic disease.

http://www.ncbi.nlm.nih.gov/pubmed/19442163
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby sbr487 » Fri Mar 19, 2010 8:04 am

cheerleader wrote:Dr. Simka has written a wonderful, peer-reviewed paper on the proposed mechanism of the BBB break thru-- we've written about it a few times on here.

Multiple sclerosis is an autoimmune disease characterized by multifocal areas of inflammation and demyelination within the central nervous system. The mechanism that triggers the disease remains elusive. However, recent findings may indicate that multiple sclerosis, at its source, could be a hemodynamic disorder. It has been found that multiple sclerosis patients exhibit significant stenoses in extracranial veins draining the central nervous system (in azygous and internal jugular veins), which are associated with significant pressure gradients measured across strictures. Such anatomic venous abnormalities were not found in the control group of healthy subjects. In this review, it is hypothesized that pathological refluxing venous flow in the cerebral and spinal veins increases the expression of adhesion molecules, particularly intercellular adhesion molecule-1 (ICAM-1), by the cerebrovascular endothelium. This, in turn, could lead to the increased permeability of the blood-brain barrier. Inflamed and activated endothelium could secrete proinflammatory cytokines, including GM-CSF and TGF-beta In these settings, monocytes could transform into antigen-presenting cells and initiate an autoimmune attack against myelin-containing cells. Consequently, a potential therapeutic option for multiple sclerosis could be pharmacotherapy with either substances that strengthen the tight-junctions barrier, or with agents that reduce the expression of adhesion molecules. In addition, surgical correction could be an option in some anatomical variants of pathologic venous outflow. We are optimistic that a hemodynamic approach to the multiple sclerosis pathogenesis can open a new chapter of investigations and treatment of this debilitating neurologic disease.

http://www.ncbi.nlm.nih.gov/pubmed/19442163


I make two observations from this:

1) Tsyabri works by manipulation of cells entering BBB. Just the opposite of what Dr. S is suggesting. Neglecting any side effects, both probably do the same. Though Dr. S' suggestion seems to be to fix the issue in BBB which is always the ideal case.

2) I dont know if Tsyabri helps when patients have lesions in Spine but to me it looks like Tsyabri should have no effect whatsoever on the lesions in the spine since it is doing nothing to prevent T cells from entering in that area ...
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Only an hypothesis

Postby MarkW » Fri Mar 19, 2010 8:13 am

Dr Simka, Department of Angiology, Private Healthcare Institution SANA, Pszczyna, Poland wrote:
......................................In this review, it is hypothesized that................
Interesting comment but no evidence as yet.

MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Postby cheerleader » Fri Mar 19, 2010 8:22 am

Mark-
Do wait. No need to follow CCSVI if you're happy with your care.

The question was the mechanism of the breakdown of the BBB- which is still a hypothetical in the autoimmune theory as well. Dr. Dake also addresses this mechanism here-
http://www.youtube.com/watch?v=adbVIR1h7h8
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby sbr487 » Fri Mar 19, 2010 8:39 am

cheerleader wrote:Mark-
Do wait. No need to follow CCSVI if you're happy with your care.

The question was the mechanism of the breakdown of the BBB- which is still a hypothetical in the autoimmune theory as well. Dr. Dake also addresses this mechanism here-
http://www.youtube.com/watch?v=adbVIR1h7h8
cheer


I would like to make one point that CCSVI is more closer to proper explanation than auto immune for the foll reason:

Autoimmune approach tries to say that BBB is compromised but does not still explain why T cells attack myelin. Bring in CCSVI, T cells are not really attacking myelin but are cleaning up the dead cells. Demyelination is just a side effect ...
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CCSVI is worth treating as a symptom of MS

Postby MarkW » Fri Mar 19, 2010 8:53 am

Cheerleader wrote:
Mark-Do wait. No need to follow CCSVI if you're happy with your care.

Joan, I suggest you read my actual comments:

I recommend to treat the symptom of CCSVI if you have it and wait for the science to catch up. The medical and pharmaceutical worlds have used the approach of 'treat the symptom' for decades so lets stick with it for CCSVI.

You seem to want to speculate and so reject my comment 'Speculation hinders the CCSVI message so why speculate ?' Speculation may be entertaining on your chatroom but it allows the neurologists to pick holes in CCSVI. This will slow down CCSVI s acceptance as a symptom of MS which should be treated.

In my view, neither CCSVI nor autoimmunity are complete explanations of MS. They do not cover genetics, environmental and microbial factors so are not complete.

Kind regards,
MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: CCSVI is worth treating as a symptom of MS

Postby cheerleader » Fri Mar 19, 2010 9:33 am

MarkW wrote:
You seem to want to speculate and so reject my comment 'Speculation hinders the CCSVI message so why speculate ?' Speculation may be entertaining on your chatroom but it allows the neurologists to pick holes in CCSVI. This will slow down CCSVI s acceptance as a symptom of MS which should be treated.

In my view, neither CCSVI nor autoimmunity are complete explanations of MS. They do not cover genetics, environmental and microbial factors so are not complete.

Kind regards,
MarkW


All of MS research is speculation. Seeing my husband's 95% occluded jugular veins was real. Seeing him awake again after years of suffering crippling fatigue was real. The only reason I'm on here entertaining, is because I want to help patients see vascular doctors and interventional radiologists.

As far as genetics, Dr. BB Lee and a panel of 47 international vascular doctors have already addressed this- finding CCSVI lesions to be congenital truncular venous malformations. This is prevalent in Caucasians:
link to site to purchase paper
Georgetown University- where Dr. Lee is in residence, has gone public with their studies of CCSVI, and the AP will be reporting next week.


As far as environmental and microbial factors, Dr. Zamboni is now studying how cigarette smoking (a known immune system down-regulator) creates endothelial disruption and worsens stenosis....which would finally explain all the studies on smoking and MS progression. In the autoimmune world, this makes no sense. His group is also studying EBV, Cpn, bacterial and viral infections, low vitamin D and the MS hit list as endothelial disrupters. There will be thousands of papers on CCSVI in the next ten years.

But most MS patients do not have 10 years to wait. That's why I'm on chat rooms. Not for researchers, but for patients. I bring the research to universities and let them do the testing and animal models...they can write the papers and share with the neurological community. Not me.
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby hope410 » Fri Mar 19, 2010 9:47 am

And you are a treasure to us, cheer. :)

Your guidance, experience, knowledge, time, efforts, pioneering spirit and "cheerleading" stance are invaluable. And appreciated so much more than you can ever know.

Thank you for all that you're doing and learning and sharing.
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Re: CCSVI is worth treating as a symptom of MS

Postby sbr487 » Fri Mar 19, 2010 10:49 am

MarkW wrote:Cheerleader wrote:
Mark-Do wait. No need to follow CCSVI if you're happy with your care.

Joan, I suggest you read my actual comments:

I recommend to treat the symptom of CCSVI if you have it and wait for the science to catch up. The medical and pharmaceutical worlds have used the approach of 'treat the symptom' for decades so lets stick with it for CCSVI.

You seem to want to speculate and so reject my comment 'Speculation hinders the CCSVI message so why speculate ?' Speculation may be entertaining on your chatroom but it allows the neurologists to pick holes in CCSVI. This will slow down CCSVI s acceptance as a symptom of MS which should be treated.

In my view, neither CCSVI nor autoimmunity are complete explanations of MS. They do not cover genetics, environmental and microbial factors so are not complete.

Kind regards,
MarkW


Mark, I have a different way of looking at what you call speculation.
The reason I have opened up such topics (and I have to credit few people here who are incredible in consciously creating constructive topics) is to bring more understanding among us (starting with me). The better we are informed, the easier it is for us to take an informed decision. If someone takes these topics to some interested researcher, thats good as well.
For example, I was not aware of Dr. S' observations until now.
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Postby ozarkcanoer » Fri Mar 19, 2010 11:31 am

Speculation can be rewarding if it doesn't get contentious. I think speculation is the start of true ideas. Like Dr Zamboni the first time he tried a Doppler wand on an MS patient : "Hmmmm, I wonder what would happen if I look here ????!!!!!".

One story that I love (I don't know if it is true or not) is that Galileo was at church and was bored and he watched the lanterns swaying from the ceiling. Voila, the first real observation of how a pendulum works. But poor Galileo, like many innovators, was stifled by the church for his sun-centered heresy. So let us always speculate !!!!!

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Re: CCSVI is worth treating as a symptom of MS

Postby patientx » Fri Mar 19, 2010 11:34 am

sbr487 wrote:For example, I was not aware of Dr. S' observations until now.


The problem is that these aren't really observations, but hyoptheses.

Autoimmune approach tries to say that BBB is compromised but does not still explain why T cells attack myelin. Bring in CCSVI, T cells are not really attacking myelin but are cleaning up the dead cells. Demyelination is just a side effect ...


Some interesting ideas have been put forth as to how CCSVI can compromise the BBB. But I don't think anyone has suggested why the myelin sheath is being destroyed.

2) I dont know if Tsyabri helps when patients have lesions in Spine but to me it looks like Tsyabri should have no effect whatsoever on the lesions in the spine since it is doing nothing to prevent T cells from entering in that area ...


Do you mean because the blood-brain barrier wouldn't extend to the spinal cord? If so, I asked a neurologist this question. His answer was that the blood vessel walls around the spinal cord also form very tight junctions, similar to those surrounding the brain. So even though it's called the blood-brain barrier, it would aslo apply to the soinal cord.
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Postby Vhoenecke » Fri Mar 19, 2010 11:40 am

Excellent Ozarkcanoer,

I use Galileo all the time in my explanation of Zamboni's hypothesis and how the medical community has rejected it. Galileo went down in the history books and we still mention him today. What were the names of the people that doubted him? Exactly! Keep speculating that's how we and science do things.

Val
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