Chronic Cerebrospinal Venous Insufficiency (CCSVI)-

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

Postby jimmylegs » Fri Jan 09, 2009 9:54 am

exactly i don't see how anyone on mag citrate would ever have to strain. unless you're talking about a sieve 8O
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Postby Loobie » Fri Jan 09, 2009 1:55 pm

I'm on it, but I think I'll find some Natural Calm. It's what everybody talks about and seems to be 'the brand'. I used up an entire bottle of of Carlson Liquid Magnesium (it was Mag. oxide) and also Solgar Mag Citrate and it did nothing for the ol' bowels. So I'll try what seems to be working for others.
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Postby jimmylegs » Fri Jan 09, 2009 2:45 pm

for real loobie? how many mg per day??
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Postby CureOrBust » Fri Jan 09, 2009 7:15 pm

Loobie wrote:I used up an entire bottle of of Carlson Liquid Magnesium (it was Mag. oxide) and also Solgar Mag Citrate and it did nothing for the ol' bowels. So I'll try what seems to be working for others.
I dont see how liquid Mag. Oxide would do the trick, personally. I have used a product called "Homozone", which is a powder. After taking it, you also follow it with fresh lemon juice (acidic). It bubbles up in you stomach, and all through your intestines. The pack has a warning to plan your day around it, as it can be very effective. I do not really notice anything with other forms of mag either.

I use it as a periodic cleanser by taking a single big dose (4-6 tea-spoonfuls) in the evening, with a guaranteed elimination the following day. I do not leave the house until its happened. I read somewhere cancer patients take about 20 spoonfuls of it a day.
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Postby DIM » Sat Jan 10, 2009 2:23 am

I believe constipation/strain isn't as simple as that if not caused by medicine/eating habits, do the "saliva test" the morning for candida overgrowth, take a good probiotic twice daily along with high quantities magnesium (citrate the most bioavailable form) and eat plenty of foods that have fibres and natural oils omega 3 & 9 (stool softeners).
Try also psyllium husk, it is quite effective.
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Postby Loobie » Sat Jan 10, 2009 8:23 am

I do all that stuff. I am always constipated to a degree compared to my old self, but I keep a good eye on it and have products that are effective for me if I get totally locked up. I was just commenting that the Mag. I had taken didn't change my bowel habits whatsoever. I'll also look for the other stuff you're talking about. However, my supplements may be drying up for a while as I really feel like I'm going to get caught in my company's next round of lay offs. We are an automotive supplier, so 'nuff said on that, but paying for Tysabri will become a chore, so I have to come up with the funds for that first.

I think I'll rent the first couple seasons of 'Weeds' for informational purposes................ :lol:
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Postby CureOrBust » Sun Jan 11, 2009 7:28 pm

Another small update.
CureOrBust wrote:For the lab I am referred to, I have spoke to a sonographer (face to face on the 1st Monday they were open for the year), but she would like to speak to one of the Vascular doctors in the clinic. These guys will not be back in the office until next week. So that lab is "on hold" till about mid next week.
I just rung this lab, to see how they were going. I spoke to the receptionist, which knew me as the "MS Guy", which makes me hopeful that it has some visibility within the clinic. She told me that the sonographer is still discussing it with the vascular docs (who would of been back today for the first time). Its 1pm in the afternoon now. She also re-took my contact details, just in case.

I also asked her how long a waiting period it was to see one of the vascular specialists, and she said a couple of weeks.

I asked how long is the waiting period to get some sonography, and she said it was normally possible to get an appointment the next day. :D

So, if all goes well, I should be able to hopefully get the tests done this week. Although, the DCV's tests (i.e. test 2) do appear to be out of reach. I am a bit concerned these may scare them away from even attempting the rest.

CureOrBust wrote:... she said the sonographer at that clinic was very capable. However, after talking a little further, it became clear that they had two sonographers at the clinic, with the other more concerned with cardiac type of doppler investigations.
I also asked / confirmed how many sonographers they had at the practice, and the receptionist said there was only one, not two.

One question I would love to ask a vascular specialist, is that, if a normal, healthy person (ie no MS etc) walked into the office and for some reason had these exact test done, and it showed that they failed two of the tests:
1. What "negative" symptoms / ailments would the Doc be possibly expecting?
2. Would the Doc be possibly considering any intervention? for example, my father had a blocked artery on his heart, but no angina or heart attack, they still did the balloon as a precaution.
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Postby CureOrBust » Mon Jan 12, 2009 4:04 am

for those of you who can't read enough on this topic... :oops:
I found the following two book links when looking up how the 2nd test of the five is performed. maybe. :?
Clinical Sonography By Roger C. Sanders, Thomas Charles Winter
Vascular Diagnosis with Ultrasound By Doris Neuerburg-Heusler
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Postby mrhodes40 » Mon Jan 12, 2009 11:50 am

Boy, that book looks like serious studying for the sonographer, but it seems like it is possible to do.

I like the questions you plan to ask.

Is your comment that the DCV's will be the hardest related to your understanding it is rare and difficult to do in general, or just that it is not done locally?
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Postby CureOrBust » Mon Jan 12, 2009 6:27 pm

mrhodes40 wrote:Boy, that book looks like serious studying for the sonographer, but it seems like it is possible to do.
Interesting to get your "nurses" viewpoint. Although I do not pretend to understand all the text, I felt that it seemed fairly easy and well explained for someone who worked on this day-in-day-out. I am thinking I will get the other 4 tests done (hopefully) then get a copy of this book for my sonographer, if she is interested, and does not know how to do the second test(s).

The tests are obviously "possible", however, reading the published article which almost accompanies Zamboni's one, does not provide too many specifics on exactly how it is physically performed; hence the book search.

mrhodes40 wrote:I like the questions you plan to ask.
My first aim is to get the tests scheduled/done, then see a vascular Dr with my results and the published article. You may end up seeing one first so feel free to use them :) , or if someone else agrees they are interesting questions, and has a vascular doc for a contact :?:

mrhodes40 wrote:Is your comment that the DCV's will be the hardest related to your understanding it is rare and difficult to do in general, or just that it is not done locally?
I am simply going off the fact that the sonographer I spoke to in the hospital appeared very knowledgeable, and she said I may have problems getting the 2nd test performed.
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more evidence of cvi

Postby gibbledygook » Thu Jan 15, 2009 3:59 am

Plasminogen activator inhibitor -1 levels are elevated in MS patients and in patients with chronic venous insufficiency

1: Tohoku J Exp Med. 1999 Dec;189(4):259-65. Links
Elevated plasma level of plasminogen activator inhibitor-1 (PAI-1) in patients with relapsing-remitting multiple sclerosis.Onodera H, Nakashima I, Fujihara K, Nagata T, Itoyama Y.
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan. honodera@neurol.med.tohoku.ac.jp

Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system and one of the earliest changes in inflammatory focus involves the activation of vascular endothelial cells. We determined the plasma level of plasminogen activator inhibitor-1 (PAI-1), a key regulator of fibrinolysis and cell migration, in patients with MS. The level of plasma PAI-1 was significantly higher in active MS cases when compared to stable MS and controls. Plasma concentrations of tissue plasminogen activator, transforming growth factor beta-1, and lipoprotein-a remained normal in spite of disease activity. These results suggested that PAI-1 plasma levels are associated with MS disease activity and is a good marker for MS relapse.

PMID: 10739162 [PubMed - indexed for MEDLINE]
link

1: Vasa. 2001 Jul;30(3):184-7.Links
Coagulation and fibrinolysis in chronic venous insufficiency.Blomgren L, Johansson G, Siegbahn A, Bergqvist D.
Department of Surgery, St Görans Hospital, Stockholm, Sweden. lena@blomgren@stgoran.se

BACKGROUND: Varicose veins (VV) are common, but only some patients will develop chronic venous insufficiency (CVI) with skin changes or venous ulcer. The pathophysiology of venous ulcer development is complex, and may involve abnormalities in coagulation, fibrinolysis and proinflammatory cytokines. The purpose of this study was to correlate plasma markers within these systems and skin pathology. METHOD: A group of twenty consecutive patients with active or recent venous ulcer were matched for sex and age with further three groups of individuals i.e. controls and patients with VV with and without skin changes respectively. Blood samples were analysed for hemoglobin (HB), total platelet count (TPC), C-reactive protein (CRP), activated partial thromboplastin time (APTT), prothrombin complex (PT), fibrinogen, interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha), D-dimer, tissue plasminogen activator (t-PA), plasminogen activator inhibitor 1 (PAI-1), prothrombin fragments 1 and 2 (F1 + 2), and thrombin antithrombin III complex (TAT). RESULTS AND CONCLUSION: There was an increase of systemic levels of PAI-1 activity and tPA with progressive skin pathology in patients with CVI, and in the group with active ulcer there was an elevation of F1 + 2. Those findings could reflect a defect fibrinolysis, a thrombotic potential or a damaged endothelium.

PMID: 11582948 [PubMed - indexed for MEDLINE]
link
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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mmP-2 AND MMP-9 associated with valve damage

Postby gibbledygook » Thu Jan 15, 2009 5:20 am

Those pesky mmp-2 and mmp-9 are associated with valve damage:

1: J Vasc Surg. 2005 Feb;41(2):303-11. Links
An animal model of venous hypertension: the role of inflammation in venous valve failure.Pascarella L, Schmid-Schönbein GW, Bergan J.
Department of Surgery, University of California, San Diego, USA.

BACKGROUND: Clinical observation suggests that chronic venous insufficiency is related to failure of venous valves. Duplex ultrasound studies of lower extremity superficial veins regularly show valve failure and venous reflux. Gross morphologic observation of venous valves in surgical specimens shows tearing, splitting, scarring, and disappearance of valves. HYPOTHESIS: Venous valve damage is acquired, linked with venous hypertension, and affected by inflammation. OBJECTIVE: The objective of this study was to investigate the inflammatory process in valve remodeling associated with acute and chronic venous hypertension. METHODS: A femoral arteriovenous fistula was created in study animals (Wistar rats, n = 60), and animals without an arteriovenous fistula were studied as controls (n = 5). At 1, 7, 21, and 42 days animals with the femoral arteriovenous fistula were anesthetized, and systemic pressure, the pressure in the femoral vein distal to fistula, and the pressure of the femoral vein in the contralateral hind limb were measured. Timed collection of blood backflow after division of the femoral vein distal to the fistula and in the alive, anesthetized animal was collected, measured, and calculated per unit time to be used as an indicator of valve insufficiency. The femoral vein distal to the fistula was harvested; valvular structures were examined and measured. Specimens were processed, and longitudinal sections were made and challenged with immunostaining antibodies against matrix metalloprotease (MMP)-2 and MMP-9. Sections were examined, and expression of molecular markers was determined by light absorption measurements after image digitization. RESULTS: One week after the procedure, all animals exhibited some degree of hind limb edema ipsilateral to the arteriovenous fistula. Pressure in the femoral vein distal to the fistula was markedly increased on average to 96 +/- 9 mm Hg. Reflux was increased in a time-dependent manner, with the 21-day and 42-day groups showing the highest values. Valves just distal to the fistula showed an increased diameter of the valvular annulus and a shortening of the annular height. Venous wall findings included fibrosis and fusion of the media and adventitia and scarring and disappearance of valves principally in the 21- and 42-day specimens. Immunolabeling for MMP-2 showed an increased level in the 21- and 42-day groups. MMP-9 showed an increased level at 1 day, followed by a more marked level in the 21- and 42-day groups. CONCLUSIONS: In this animal model of venous hypertension the findings of limb edema, increasing valvular reflux, and morphologic changes of increased annulus diameter and valve height are seen. Histologic changes included massive fibrosis of media and fusion with adventitia. Inflammatory markers MMP-2 and MMP-9 are strongly represented, and valve disappearance occurs after these markers are present. The gross morphologic changes seen are quite similar to those observed in human surgical specimens removed in treatment of venous insufficiency. CLINICAL RELEVANCE: When observed angioscopically at the time of vein stripping, saphenous vein valves show severe deformities including shortening, scarring, and tearing. The current model of induced venous hypertension demonstrates early venous valve changes that replicate those observed in humans. This observation provides a link from venous hypertension to an induced inflammatory reaction that stimulates the valve damage. Thus the model could be useful for defining the fundamental mechanisms that cause venous valve failure and varicose veins and in pharmacologic testing to prevent or treat venous insufficiency.

PMID: 15768014 [PubMed - indexed for MEDLINE
link
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 CureOrBust » Thu Jan 15, 2009 6:48 am

another quick update. On wednesday I heard back from the sonographer. she informed me that she had spoken with the vascular doctors, and that they would recommend I get the tests done at the lab at the hospital. They also recomended I go through the neurologists connected with the labs.

DOH!!! :( :x :evil: arrrrgggghHH!

Ok, so that made me take a "day off" from chasing it.

She did say she wished to discuss it with her counterpart at the recommended hospital lab also, and will get back to me with how that went, tomorrow (ie Friday).

Tomorrow, I will be calling the hospital, and try to talk with the sonographer about getting the tests done. I think I already spoke to her the other day, and she said i should wait for the response from the other lab before we discussed it further. The lab that finally said no, were not comfortable with doing any of the tests when I suggested that we could do just the non cranial exams.
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Postby mrhodes40 » Thu Jan 15, 2009 10:31 am

Gibbles interesting papers! I notice that one reason for plasminogen activator inhibitor and TPa to be active is endothelial dysfunction there's a real which came first question with that in my mind, but it seems clear that there are issues here that have not been taken seriously into consideration in the mainstream MS literature. I really like the first paper that shows how similar the MS profile and the venous insufficiency really are when regarding this.

CUr-o said

neurologists connected with the labs.

DOH!!! arrrrgggghHH! :cry: :x :evil:


BROTHER! man! I'm with you on that. You'll negotiate this little detour, but I can't wait to hear how....

It never ceases to amaze me how a disease of unknown origin can be so well known as a hypothetical (autoimmune) that everyone everywhere assumes the hypothesis is the only choice and any other thought shows a complete lack of intelligent understanding. My neurologist told me once that MS has to be autoimmune or else the drugs wouldn't work "so well" 8O ........enough said.

I still have no feedback from my chosen vascular guy who now I have contacted both through his university email and through his online appointment request......tick..... tock...... tick.....tock.....

Thanks for putting info here!
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Postby cheerleader » Thu Jan 15, 2009 11:12 am

Keep going, Cure. Stay on those wily sonographers!

Oh, this is taking too long for old, impatient me. Our vascular doc is out of town, but answering e-mails. His dept. is still mulling the research over. This is going to be a harder route to follow...but I still think we can get the docs to look into venous insufficiency.

Here's part of the problem...the cerebrovascular system is pretty much a valveless system (which explains most docs confusion over reflux) EXCEPT for the jugular and azygous veins. It is only in the last 3-5 years that radiologists and researchers have put together the fact that valve failure and reflux can create neurological problems like global amnesia and seizures. Unless doctors have been keeping up on the research (like we obsessive thisisms folks) they will look at you like you just told them the space aliens have landed. We will have to be clear and unrelenting in our requests for vascular screening.

This observation provides a link from venous hypertension to an induced inflammatory reaction that stimulates the valve damage.


Thanks for the research, Alex. Hard to know what comes first in this unrelenting cycle of inflammation and damage, but we're starting to see some familiar culprits in mmp-2 and 9 and endothelial dysfunction.
ArGHH....think I'm gonna go buy me some doppler scanners at the hardware store....
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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