Inhibiting Blood To Save The Brain?

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

Inhibiting Blood To Save The Brain?

Postby Ernst » Sun Jul 19, 2009 2:38 am

I found this article couple of yrs ago. What do you think.. does this relate any to CCSVI?

http://www.sciencedaily.com/releases/2007/03/070322105436.htm
My wife's 3 yrs post video: http://www.youtube.com/watch?v=eLeqLps8XR8

Our family: http://www.youtube.com/watch?v=p_QCKxeQAlg
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Postby gibbledygook » Sun Jul 19, 2009 5:50 am

I guess that CCSVI causes gaps in the endothelium to open up under pressure and volume and blood begins to fill the perivascular space and start clotting much as when any blood vessel is damaged. This would be why fibrinogen lands in the CNS. Without the bad heamodynamics of CCSVI then the brain will settle back to the way it was before.

However I'm no doctor!!
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby mrhodes40 » Sun Jul 19, 2009 6:41 am

Hi Ernst ,
I agree with Gibbledegook but I am not doc either. There is leaking of blood components into the brain in CCSVI; in fact it was iron that was first noted to be an inflammatory trigger in MS supporting the idea of blood components leaking out. The big idea paper talks about that.
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Postby Ernst » Sat Jul 25, 2009 1:09 am

Hello all,

Still fascinated by blood :D , especially blood clotting, fibrinogen. Maybe part of my interest relates my wife's (with ms) mother, who had problems with brain circulation (but not ms). She had some abnormal blood values and too low level of B12.

But now back to the point, blood clotting --> Today I red about "hughes syndrome" and this is dx which relates to ms:

"Apparently, Hughes Syndrome can easily be mistaken for Multiple Sclerosis. It shares many of the symptoms and as many as 1 in 3 people diagnosed with MS actually have Hughes Syndrome.

Hughes Syndrome is also known as Sticky Blood Syndrome although it's proper title is Antiphospholipid Syndrome (or APS). Discovered by a Dr. Graham Hughes in 1983 while treating patients for the Lupus condition. Sticky Blood can be easily treated with Aspirin, Heparin or Warfarin but, if left untreated it can be fatal. Sticky blood can lead to the formation of blood clots which can cause Thrombosis or Strokes.

The symptoms of Hughes Syndrome can be uncannily like those of MS. They may include: difficulty with walking, foot drop, double-vision, tingling sensations, slurred speech and loss of balance. I don't know about you, but this is ringing some fairly loud alarm bells with me. Like MS, Hughes Syndrome is an autoimmune deficiency and it's cause is unknown.

Read the MS Resource Centre's article or visit the Hughes Syndrome Foundation Website.

My thanks to the Lady from Port Macquarie in New South Wales for bringing this item to my attention. She would like to see all possible MS diagnosis patients automatically tested for Hughes Syndrome. I promised I would include a piece on the subject and here it is, admittedly short and sweet, but here all the same."

http://www.mymultiplesclerosis.co.uk/hughes-syndrome.html

And some more:

"Hughes syndrome is a condition where clots (thromboses) form in the blood vessels. It is sometimes called "sticky blood", and is also known as antiphospholipid syndrome (APS). The condition is named after Dr Graham Hughes, who discovered it in 1983.

Hughes syndrome is a relatively common cause of recurrent stroke, heart attack, thrombosis and miscarriage. It affects both men and women, but is mainly seen in women.

There are two types of Hughes syndrome:

* primary, where Hughes syndrome develops by itself and is not caused by another condition, and
* secondary, when another condition causes you to develop Hughes syndrome. These conditions are typically autoimmune disorders, such as lupus (a condition where the body develops antibodies that attack healthy tissue)."

http://www.nhs.uk/Conditions/Hughes-syndrome/Pages/Introduction.aspx

Do you have thoughts about this Hughes syndrome and MS/CCSVI connection? I might be in "wrong track" but since my wife's dx I've had some hunt that ms deals with "blood structure", and fibrinogen has been on my mind now and then.
My wife's 3 yrs post video: http://www.youtube.com/watch?v=eLeqLps8XR8

Our family: http://www.youtube.com/watch?v=p_QCKxeQAlg
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Postby mrhodes40 » Sat Jul 25, 2009 8:48 am

I was tested for hughes and did not have anticardoilipid antibodies and also did not have anti phospholipid antibodies but I do have very high thrombin and fibrinogen. These factors are clotting factors and my thrombin which should be about 200 is regularly 1200. I also have a high d-dimer often like 4 when less than one is normal--this test suggests a clot has been made and is now breaking down, not a stretch when the thrombin is so high.

My doc callers this variant APA and considers it common to chronic disease, she tests everyone for it. I developed a clot in a superficial vein in my leg while on coumadin after stent surgery... :cry: I am very prone to sticky blood
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Postby Lyon » Sat Jul 25, 2009 9:01 am

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Last edited by Lyon on Sat Nov 26, 2011 11:14 am, edited 1 time in total.
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Postby mrhodes40 » Sat Jul 25, 2009 10:20 am

FYI Dr Dake is testing everyone's d-dimer because mine was high....

I agree after dealing with the clotting factors for the last 4 years it wold be interesting to see if it is consistent to all MSers. it is sort of catch as catch can with this I only know of mine cause I have a doc that is interested in the "variant APA" (antiphospholipid antiboides)
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Postby prof8 » Sat Jul 25, 2009 11:09 am

I'm new to the forum. But wanted to add that when I got diagnosed 2 years ago with MS I had a rheumatologist involved because I had been having low grade fevers for months and months. He thought maybe I had antiphospholipid antibody syndrome (APS). There are two tests he did. One is the standard cardiolipin antibody test. I tested positive on this (although not high positive). They also did a second test for anti-beta 2-glycoprotein which is also an indicator of APA. I tested positive on that too. But, I was diagnosed with MS ultimately because supposedly the lesions caused by APA don't enhance in the brain and mine did, my lesions were in places common for MS, I had Dawson's fingers lesions, I had black holes, and high IgG synthesis and index in my spinal fluid -- no oligoclonal bands though.

Anyhow, I am very curious about myself and whether I have blockages in my jugular etc. I just recently posted another post introducing myself.

By the way my rheumatologist consulted with the top MS doctor in my city. He said the test results were insignificant -- meaning that he has seen positive tests on a variety of things with MS patients but he doesn't think it has any significance.
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Postby mrhodes40 » Sat Jul 25, 2009 7:50 pm

Interesing prof about the odd blood Here's a paper about these coagulation issues specifially in MS and neuro stuff

read this paper you guys and say what you think...it is technical

http://www.pubmedcentral.nih.gov/articl ... d=19154576
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 Rokkit » Sun Jul 26, 2009 1:22 pm

Lyon wrote:Considering all the new testing that is available...and expensive, I sometimes wonder whether someone with the motivation and funding to do exhausting testing on a group of MS'ers at this point could determine what MS "IS" and isn't?


This is what's so exciting to me about CCSVI. If addressing the AI response in MS is barking up the wrong tree, then no wonder the results have been so frustrating. If CCSVI turns out to be the right tree to bark up, as it were, then we can expect the floodgates of research to open like a liberated jugular. Vein stenosis is so mechanical, visible, definable, whatever... it's so different than EAE and mice that we should see a lot of light shed on the subject in a relatively short period of time.

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Postby cheerleader » Sun Jul 26, 2009 5:36 pm

MS is an inflammatory disorder believed to be autoimmune in etiology, and can present with features resembling APS [294-297]. Several reviews of the neurological symptoms of APS/SLE are available [298-300], and many case reports, e.g., cerebral ischemia [301]. However, MS is not thought to involve ischemia, although elements of the coagulation cascade are present in MS lesions, including fibrinogen and recently, tissue factor and protein C inhibitor [302].
In 2000, our collaborative investigation demonstrated elevated endothelial microparticles (EMP) during exacerbations of MS [303,304]. Those findings motivated further investigations, this time of aPL in MS, with the hypothesis that aPL might be involved in endothelial activation in MS. Several prior reports had established that aPL commonly occur in MS, but in most of them the patient population was heterogeneous or inadequately defined, and there was no indication of a relation between aPL and the pathophysiology of MS.


Marie...Much of that paper was over my head, and I don't think I got it :) However...the section quoted above caught my eye.

What I'm wondering is, in the CCSVI model, where stenosis causes reflux and hypoxia.... this is activating the coagulation cascade. In other words, CCSVI could have been responsible for the elevated levels of fibrinogen in your blood. (Also, you've mentioned that you no longer have inflammation...was this in reference to gad-enhancing lesions, or inflammation in your blood? Do you have a high SED rate?)

What I'm thinking is that as the hypoxia is healed- after returning oxygen to the brain and spine- then the coagulation cascade should STOP. Right? Maybe ending CCSVI with your stents will end the blood issues for you and others? Maybe your coag numbers will normalize now?

The coagulation/microparticle numbers are highest during a relapse...when hypoxia is occurring. Jeff's SED rate was thru the roof when he was diagnosed. Veins are shut down, deoxyginated blood floods brain and spine, hypoxia occurs...coagulation cascade begins. Perhaps progressive MS is like a continuing relapse...where slow and unremitting hypoxia activates the coagulation cascade...

Here's a paper showing how cerebral ischemia and hypoxia changes the coagulation cascade and increases fibrin accumulation-
http://ajp.amjpathol.org/cgi/content/full/169/2/566
The combination of hypoxia to ischemia may trigger pathological events that are not induced by ischemia alone. One potential pathological event is hypoxia-induced fibrin deposition that results from altered anti-coagulant properties of endothelial cells as demonstrated in pulmonary vessels.3,4 Thus, the reduction of CBF in conjunction with hypoxia may induce spontaneous thrombus formation to reduce blood perfusion further. This ischemia/hypoxia-induced microvascular thrombosis may also prevent cerebral reperfusion after the release of the large artery occlusion, similar to the previously described no-reflow phenomenon after brain and cardiac ischemia.5,6


just some random thoughts,
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby Terry » Sun Jul 26, 2009 8:12 pm

What I'm thinking is that as the hypoxia is healed- after returning oxygen to the brain and spine- then the coagulation cascade should STOP. Right? Maybe ending CCSVI with your stents will end the blood issues for you and others? Maybe your coag numbers will normalize now?


This is my hope.

I have been unconvinced that we all have a congenital issue. But, for those who do, this could be the answer.
A family friend is an MSer. She had a car accident with injury a few years back and had neck surgeries to repair. MS followed. Her neuro told her that many people who have MS have been victims of accidents with injuries such as hers. I don't know where he got that info, but I was interested in that thought. For those, this could be the answer.
For the rest of us, it seems to me that we are left with all the questions we have always had. What causes this? Virus, bacteria, coagulation issues, thyroid, nutrition, you know the list.
It would be amazing if it could be proven that our coagulation issues are caused by CCSVI, and restoring flow makes them go away. Same with D issues, liver issues, and on and on.
Until then, I am still reading the same things we have always read, only now, I search it all with things like "vascular" or "veins". I'm getting the same place I always got, and that is EVERYWHERE. So many possibilities.
My selfish prayers are with the docs who are dedicating themselves to this idea. I hope they are looking at the blood coagulation and viruses and bacteria and nutrition and the thyroid and the liver ....
If they are not, I hope they will soon. Am I asking too much?
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Postby prof8 » Sun Jul 26, 2009 9:29 pm

Marie, thanks for sharing the paper on antiphospholipid antibodies. I remember when the docs were talking about MS v. APS (sticky blood) with me 2 years ago I did a lot of research on it. Of course I was hoping I had APS and not MS since I would just have to take blood thinners. I knew then that APS is often linked to lupus as a secondary condition. And yeah it can mimic MS. But I'm sure more has been discovered as is clear by this article. It looks like they now have other tests they can do for APS as indicators. By the way, I don't think they were even aware of APS until the 1980s, if I remember correctly. Anyhow, I'm usually pretty good at reading through dense medical stuff but this was a slog!

However, I couldn't just help but say "hmmmmmm" when I read through it. Here is why. Remember how I said my rheumatologist consulted with the bigwig MS expert he knew about my case? And the expert said that even though I tested positive on cadiolipin test and anti-beta 2-glycoprotein that it didn't mean I had APS/sticky blood because lots of MSers sometimes have weird somewhat abnormal tests? (like SED rate, APS tests, CBC etc.) Well, I happened to look at the program for the conference in Bologna in Sept. (right place??) There are a small group of doctors going like Zamboni and Drake. Well, the MS expert my rheumatologist called is one of the participants!!!!!!!! Holy cow. I wonder if he had a change of heart? Or is he merely curious about a new paradigm?
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Postby mrhodes40 » Mon Jul 27, 2009 9:32 am

Wow good people are getting involved that is great news!



And the expert said that even though I tested positive on cadiolipin test and anti-beta 2-glycoprotein that it didn't mean I had APS/sticky blood because lots of MSers sometimes have weird somewhat abnormal t
I agree there is something going on here and it ties in. I too am very hopeful for a new line of research.

I have been unconvinced that we all have a congenital issue. But, for those who do, this could be the answer
I also don't think all of us have congenital issues that block the veins, I think it will be many different issues but the common thread is blocked veins from the head

A family friend is an MSer. She had a car accident with injury a few years back and had neck surgeries to repair]


I KNEW IT!! I just knew that there would be cases where this was true.

Here's why: the medical community thinks it is acceptable to remove the jugulrs in cases of cancer or trauma where the neck is damaged. The thought is that the vertebral veins take up the slack adequately, and the reason they think this is because if they take out your jugs this week and test next week, the vertebral veins seem to take the load. It seems to work. Yet other work suggests the vertebral veins are not adequate on their own after all, the Russian paper is one such that says directly the medical community needs to rethink that point of view because it is not true: if the jugs are damaged it reroutes bloood to the vertebral plexuses and refluxes into the cerebral veins...which causes myelopathy.

This is of course CCSVI.

The biggest problem with finding people who've had such trauma or cancer and later discovering they actually have MS is that it takes YEARS for actual MS lesions to show up, and the two are not associated in the mind of the person then. Also in many cases like cancer people do not live long enough to develop lesions necessarily, and if they do develop neuro symptoms i t is often blamed on the chemo and not necessarily investigated In my case my issue is probably congenital and I was 30 before my first big exacerbation, so you can see why a person would not necessrily see their neck thing as associated with their MS if ithappened that way

However, if you still know of this person she may be able to provide a critical clue to this if it can be shown that the neck trauma caused alterations in cerebral drainage and it appears she had no MS prior. Maybe she would be interested in seeing Dr Dake?

additionally, I think a lot of times MS diagnosis is associated with accidents but not necessarily neck trauma directly The old idea was that this somehow caused wacky function of the immune system, but with CCSVI it would be more the stress and increased cortisol causing issues that sets the CCSVI off, ie upregulation of clotting factors etc

n the CCSVI model, where stenosis causes reflux and hypoxia.... this is activating the coagulation cascade. In other words, CCSVI could have been responsible for the elevated levels of fibrinogen in your blood. (Also, you've mentioned that you no longer have inflammation...was this in reference to gad-enhancing lesions, or inflammation in your blood? Do you have a high SED rate?)
]
I meant my Gd enhancement is gone and no inflammation in my MRI. I have RA so my sed rate is always up. AND my reg doc is a chronic disease specialist and she sees coagulation problems in the blood of people with chronic disease all the time and that is why I was tested and knew that my blood was sticky. I regularly test for fibrin manometer and thrombin with numbers so high occasionally they can't even quantify it. My d-dimer which is a little non specific but which can mean that a clot is breaking down, is usually high. 4 days before I left for stanford it was 4 when1 or less is normal. It was this that brought it to Dr D's radar he does expect it may drop into normal ranges he said.
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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Postby Newman » Wed May 12, 2010 9:59 pm

What a great thread... I have been telling my GP that this is a blood disorder I have not MS. I started coming to this conclusion when I did a routine blood test and my left arm would NOT bleed, 3 tiny specks bled out. Last May I started taking blood pressure medication (norvasc), oddly my MS symptoms were significantly reduced within days and my BP returned to normal and I felt great. Norvasc works by opening the capillaries in the legs to reduce blood pressure. This casued my legs to swell, I discontinued norvasc and my symptoms returned

An interesting bit of info. MS affects women in ratios reported between 2:1 to 5:1 and there is no explanation for this. Or is there. Blood clotting is linked to the X chromosome and women have XX were men have XY. Estrogen has also been proven to play a factor in blood clotting. The more I dig into this the more sense it makes that this is a blood related disorder. Blood flow is probably the MOST important body function, we can hold our breath but impairment of blood flow of any kind is unhealthy.

If you google Alemtuzumab you will fid that it is a lukemia drug now being used on MS patients with a 75% success rate of halting remissions. The first listed side effect is "unsual" bleeding... which sounds to me like hemophilia.. thinning of the blood... which would let it flow through veins better.
I am glad I foundthis thread.. thanks..!!!!
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