Thoughts on the spreading of lesions and symptoms in CCSVI

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.
radeck
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Thoughts on the spreading of lesions and symptoms in CCSVI

Post by radeck »

CCSVI is not the only problem in MS, but the immune systems response to exposed CNS matter plays a crucial role in beginning a cascade of inflammation that leads to loss of neurological function.

I have a thought about this. Once the blood brain barrier has been perforated (via reflux, edema, leakage caused by hypoxia) and there's an immune system response against the exposed CNS-matter, this might also affect other areas, and cause new lesions by itself, i.e. without stenosis involvement in those areas. A load of T/B-cells and antibodies that have been primed to attack e.g. a lesion around the ventricles could circulate to other areas.

I've never had any neurological symptom until earlier this year, when I came down with symptoms likely emanating from different regions in my CNS. Now it seems an unlikely coincidence for the endothelium of vessels in these different regions to break down around the same time. My only explanation is that one lesion caused an increased number of circulating myelin-reactive T/B-cells and antibodies that facilitated demyelination in a different region. This is comparable to the infection of rodents with EAE in the lab by immunizing them in a location far away from the brain, in the absence of stenoses, where upon administration of MOG or MBP antigenes the immune system causes demyelination in multiple places (I believe there might be a difference in the lesion pattern seen in EAE versus that in MS - it would make sense that the primary lesions in MS are closer to venous outflows, and those in EAE closer to arterial inlets, but I don't know whether this is the case. Anybody?).

This would also help to explain why patients who had the "liberation procedure" didn't experience complete stopping of their MS activity, but that the percentage of them that had new lesions went "only" from 50% to 12%, and relapse rate from 50% to 23% over two years respectively: there were still plenty of circulating myelin-reactive immune cells and antibodies that can cause further damage. However once blood flow has been improved, one may hope that eventually those T-cells die off (if you have been immunized to a certain pathogen you need re-immunization a few years later as well, I don't know about myelin reactive cells. Anybody?), but it could be that some amount of immune suppression may be useful (not just steroids, but longer term suppression, focusing on the Th1 and Th17 channels) to prevent the immune system from creating further lesions and lead to a renewed cascade of increased immune reaction.
Last edited by radeck on Fri Feb 05, 2010 8:54 am, edited 3 times in total.
LR1234
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Post by LR1234 »

Thats a good point Rad, maybe the circulating antibodies that have been created previously need to be curbed to allow healing to take place and there needs to be time for the BBB to heal.

I have always had thyroid antibodies and my neuro has said that those antibodies can attack anything (maybe that is why lowering immune responses whether it be to allergens in foods or other parts of the body can help MS), once the CCSVI is sorted the antibodies hopefully will no longer have access to the nervous system and can stay in the blood stream.

Sounds good to me but I have a very little understaning of how the immune system works compares to some of the medical pros on here!!
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Post by sou »

Hi.

I thought that the only people that had relapses after surgery were the ones that had restenosis. I doubt that the adaptive immune system is the root of all evil. Besides, a stenosis of the jugulars could very well alter haemodynamics across the whole nervous system.

Just my thoughts.

sou
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Post by mrhodes40 »

Hi Rad you are thinking deeply here, may I be devils advocate?

as a comment, BTW, Dr SImka believes there may be some longer term issues with activated leukocytes and microglia too, watch for the next paper to come out. :wink:
Once the blood brain barrier has been perforated (via reflux, edema, leakage caused by a stenosis) and there's an immune system response against the exposed CNS-matter, this might also affect other areas, and cause new lesions by itself
This is an idea that seems a possibility certainly, but there are some reasons to think maybe not, for example in lesions studies very VERY few are anywhere other than on the veins.... (in one study it was one out of hundreds) so almost always on the veins. This is one reason to say it IS venous hypertension/reflux at cause o9f lesions because logically if it is all about the immune system the location of the lesion should be more spread over the brain than that.

ADEM is a disease where a vaccination causes an autoimmune reaction to myelin. Those lesions are not venocentric, they are found diffusely in the brain, MS lesions are very commonly venocentric and periventricular, noting that is a highly vascular area with a high volume of blood flow in the healthy person.
below from HERE
However, T2-weighted images show ADEM lesions
that are more pronounced with poorly defined margins
in deep white matter and periventricular sparing.
If the spinal cord is involved it will show large,
swollen lesions that may extend into the thoracic
region from the cervical region (Dale & Branson,
2005). As a general rule, ADEM lesions in the spinal
cord are continuous lesions affecting multiple levels,
whereas a typical MS lesion is confined to one spinal
cord level. Any single lesion affecting more than one
spinal level should raise suspicion for ADEM in the
appropriate clinical picture. The typical MS lesions
are also posterior in location on axial, cross-sectional
views of the spinal cord, whereas the ADEM lesions
tend to be more diffusely present throughout the
entire cord.
.
So ADEM, a true autoimmune situation where lesions are caused by immune activity not a CCSVI type thing, has a more diffuse expression on MRI than MS.
(e.g. mild optic neuritis) and two weeks later a spinal-cord-based (numbness in left foot) symptoms, to mention just a few
Do you have spinal lesions or are you equating symptoms with lesion location? Because I can tell you from my own situation I have never had any spinal lesions and I definitely have loss of function in my legs and feet including sensory losses. You can have only brain lesions and only jugular issues (as I do) and still have foot numbness and leg dysfunction.

Also if you read the Russian paper they show that severe jugular or brachiocephalic issues can result in both brain and spinal issues by backing up the epidural veins as an after effect of the jug issue. It is probably not correct to say would never be spinal lesions as a result of jugular issues necessarily coonsidering the information they presented, and definitely not true that something like foot tingling is necessarily always a spinal issue.

That having been said, Dr Zamboni did say that his more progressive patients had azygos stenosis, so that suggests some anatomical association, but I suspect maybe we are tending to get a little rigid about that and trying to ascribe individual people's experience of MS to lesions location. More information, such as that in the RUssian paper may show it is a little more variance than that.
This whole idea also would explain, at least in part, why the patients of the liberation procedure didn't experience complete stopping of their MS activity, but that the percentage of them that had new lesions went "only" from 50% to 12%, and relapse rate from 50% to 23% over two years respectively: there are still plenty of circulating myelin-reactive immune cells and antibodies that can cause further damage.
I THINK, but we all need the whole paper, that the relapsing people were the ones that restenosed, based on the preliminary paper found on the research page (liberation prelim results) where the few who relapsed were from the same group that restenosed. Won't it be great to see the whole paper and get all the nitty gritty details? I can't wait :D
However once the root cause of the problem (the stenosis) has been fixed, one may hope that eventually those T-cells die off (if you have been immunized to a certain pathogen you need re-immunization a few years later as well
I agree that it is possible that there is potentially some crossover autoimmunity and I look forward to more research into this aspect.

But I, like you, hope it will resolve with time after the injury stops. Case in point: EAE is self limiting, it goes away if let on its own, and that is a disease of the immune system attacking specifically.
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Post by radeck »

sou wrote:Hi.

I thought that the only people that had relapses after surgery were the ones that had restenosis. I doubt that the adaptive immune system is the root of all evil. Besides, a stenosis of the jugulars could very well alter haemodynamics across the whole nervous system.

Just my thoughts.

sou
I didn't know that the only ones who had relapses were the ones with re-stenosis. Do you know for sure? I guess we'll have to wait for the details of the paper. Fact is, it would be hard to explain onset of brain and spinal symptoms at the same time, unless through spreading of the problem through the immune system.
Last edited by radeck on Tue Sep 13, 2011 8:35 am, edited 1 time in total.
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mrhodes40
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Post by mrhodes40 »

BTW I have urinary retention and I have had 4 spinal MRI's in my 18 years I have never had a spinal lesion or enhancement.....
just my experience....
marie
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Post by radeck »

Hi Marie/mrhodes40,

I agree that your argument, that if most MS lesions are close to veins, that this would be a problem for my theory, if it is true for spinal lesions in patients that started out with brain lesions. Do you know this for a fact?

Fortunately we now have an argument against my theory from the conference notes, that indeed all the patients with relapses seemed to have re-stenoses. I'm looking forward to see this quantified further in the papers.

I'm puzzled by the statement that MS patients have 40% less veins in their brain. It must depend on degree of progression. Wonder how this could related to CCSVI... It seems that if there are so much fewer veins, there would be pressure building up even if the jugulars worked fine. Or could it be that once the jugulars work, the veins will build up again?
Last edited by radeck on Fri Feb 05, 2010 9:07 am, edited 3 times in total.
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Post by Jamie »

40% less visible veins that should be IMO.
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Post by Rokkit »

radeck wrote:Also, one person visiting these threads told me he/she had jugular veins treated and subsequently experienced remission of bladder control problems, which is commonly attributed to a spinal lesion.
The most common bladder problem is spastic bladder: you have to go all the time, and it is typically caused by a lesion in the brain. Less common is flaccid bladder: you can't tell you need to go so you retain urine and your bladder grows bigger and bigger. Flaccid bladder is typically caused by a spinal lesion.

http://www.merck.com/mmpe/sec17/ch228/ch228d.html

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Post by CureOrBust »

radeck wrote:I didn't know that the only ones who had relapses were the ones with re-stenosis. Do you know for sure? I guess we'll have to wait for the details of the paper.
The preliminary results state this, so one can be as sure as much as one trusts that document.
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Post by radeck »

Rokkit wrote:
radeck wrote:Also, one person visiting these threads told me he/she had jugular veins treated and subsequently experienced remission of bladder control problems, which is commonly attributed to a spinal lesion.
The most common bladder problem is spastic bladder: you have to go all the time, and it is typically caused by a lesion in the brain. Less common is flaccid bladder: you can't tell you need to go so you retain urine and your bladder grows bigger and bigger. Flaccid bladder is typically caused by a spinal lesion.

http://www.merck.com/mmpe/sec17/ch228/ch228d.html

Rokkit
Thank you for the clarification. The article states that spastic bladder is caused by brain *or* spinal lesion above T12, i.e. T or C spine. Flaccid bladder stems from sacral nerves all the way at the bottom of the spine. This would be hard to explain by a jugular vein problem. I'd be interested to hear if people have any further thoughts on this.

Just to clarify, I'm not doubting in any way that somebodies bladder function or my foot numbness could get better from fixing jugular veins, I'd just like to understand if this is a possibility at all. Thanks
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Post by catfreak »

marie wrote:
I have never had any spinal lesions and I definitely have loss of function in my legs and feet including sensory losses. You can have only brain lesions and only jugular issues (as I do) and still have foot numbness and leg dysfunction.
I have never had any spinal lesions either (2 MRI's of the spine) and I have lots of numbness and spasms in my feet and legs. I also had a urinary tract infection and felt no pressure or pain also bowel problems.

Cat
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9/3/09 Stanford - Dr Dake - Stent in R-J to unblock Arachnoid Cyst in Sigmoid Sinus. Stent in narrowed L-J. Balloon in narrowing where R & L Jugulars meet.
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Post by radeck »

catfreak wrote:marie wrote:
I have never had any spinal lesions and I definitely have loss of function in my legs and feet including sensory losses. You can have only brain lesions and only jugular issues (as I do) and still have foot numbness and leg dysfunction.
I have never had any spinal lesions either (2 MRI's of the spine) and I have lots of numbness and spasms in my feet and legs. I also had a urinary tract infection and felt no pressure or pain also bowel problems.

Cat
Thanks for sharing this. I take it from your writing that these haven't gotten better yet after the stents?

It seems that either it is just not well enough understood which parts of brain/spine are responsible for which body functions, or MRI's aren't strong enough to detect everything.
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Post by cheerleader »

Some clarification, radeck----
You can have motor issues, bladder issues, numbness in the limbs, etc with only brain lesions. No spinal lesions necessary. In fact, Dr. Elliot Frohman was referring to Normal Pressure Hydocephalus at the conference, which happens in the brain alone, when there is a blockage of cerebrospinal fluid. People have loss of gait, cognitive and bladder issues which resolve once the brain is shunted. He said this was looking alot like MS.

I believe in the coming years we are going to learn that MS is not about lesions or lesion location...that lesions are a sign of microbleeds and iron deposition which activates the immune system. Blood and CSF levels are altered in the CNS. The brain is injured by iron and lack of oxygen. This is seen on SWI- MRIs.

My husband had fatigue, leg spasms, bladder issues, leg pain and 20 cerebral and only one small cervical spinal lesion. In 4 months since stenting, his leg pain has remitted from everyday to once a week, no more urgent bladder, no more fatigue or heat intolerance. Yes, he was newly diagnosed and was RRMS. But I don't think it's about his lesions healing....
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mrhodes40
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Post by mrhodes40 »

Rad, go to the research sticky and look at the second post ---look for the Russian paper and read it. There you will read how in that work spinal issues came from blockages in the jugulars or brachiocephalic....

http://www.thisisms.com/ftopict-7648.html
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
http://www.ccsvibook.com Read my book published by McFarland Health topics
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