Reversing Endothelial Dysfunction

Tell us what you are using to treat your MS-- and how you are doing.

Postby CureOrBust » Tue Dec 16, 2008 4:31 am

cheerleader wrote:I think Dignan should start the thread on the General Board, since Zamboni is his find. (How did he find this????) I'll PM him and ask him to do the honors. But if he doesn't, I'll post it.
Someone has to post this AND someone REALLY has to see/confirm if the results are repeatable. I by chance saw my neuro today and left a copy for him to read. I was a little impressed that he did take it. Tomorrow I see my GP and will be asking for help for referrals on the doppler tests. (PS dignan deserves a Nobel prize, for ALL his work here)

cheerleader wrote:In EVERY single one of the MS patients, there was venous reflux and blockage in the veins. !!!!
I did not see this??? But I did see that the control's were 0. I will read it again now, but if you could point me in the direction of this result (ie 100% MS), that would be appreciated.

cheerleader wrote:I gotta find it locally for Jeff. I'm assuming that vascular docs would have the hand held units Zamboni's team used.
later...
I didn't read that they were "hand held", I remember the use of an ultrasound, and a "tilt bed". But I will be reading it again now.

And tomorrow I will let you know how I go with a arranging the ultrasound referral with my doc.
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Postby cheerleader » Tue Dec 16, 2008 7:35 am

It's up, Cure. I corrected the figures...it was 71% of MS patients and 0% of controls with CCVI. A wee bit over-enthusiastic :)
Glad your neuro was open to reading it.
Keep us posted,
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby CureOrBust » Wed Dec 17, 2008 3:58 am

cheerleader wrote:I corrected the figures...it was 71% of MS patients and 0% of controls with CCVI.
No, I think you were correct the first time. 100% (n=65) of MS patients tested positive on the initial ultrasound tests.

After re-reading the article, I noticed a few things, which would mean 100% of MS patients tested positive in the initial non-invasive ultrasound tests.

Firstly:
"We investigated 65 patients affected by clinically defined MS (CDMS) and diagnosed according to the revised McDonald criteria." pg5

"Our Ethics Committee approved the use of selective venography only in subjects (patients or controls) with abnormal venous ultrasonographic examination. An invasive investigation (potential harmful radiation/catheterization to healthy subject) was felt unnecessary when ECD can is negative at the level of the neck." pg9

"Sixty-five subjects with MS fulfilling the ECD-TCCS screening criteria and 48 controls of the HAV-C group, underwent selective catheterism of the azygous and IJV system via the transfemoral route."

So, as far as I can tell, 65 of the 65 MS patients were found to have an abnormality which justified the invasive test. ie 100%. You will also note in Table III on page 12, they have "categorised" 65 patients.

Also, table III on page 12 adds up to 65; BUT I think it also has a calculation error in the first row (ie the % for "Type A"). They have the numbers of 15 (ie 10 + 5) in total for Type A, but then have 75% for RR where n=10??? it should be 67% (ie 10/15 = 0.666666667 = 67%)

So I did the table again using a spreadsheet and formulae so the calculation would be correct, AND also added the "vertical" % which shows the distribution of the different "Types" (ie A - D) within each type of MS (ie RR, SP. PP). Please check my logic. :?

Image

I have colour coded the numbers to make it easier to read, and added totals for applicable columns to ensure it all resolved back to the original numbers supplied in the text.

The Colours:
Orange: The actual numbers / count. These can be added vertically OR horizontally.
Yellow: % Horizontally. ie Within the A - D "Types". These are what was calculated in the paper (except incorrectly? for "Type A")
Blue: % vertically. ie Within an "MS type"
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Postby gibbledygook » Wed Dec 17, 2008 4:35 am

Cureo, if I ever need a chart doing, I shall employ you!
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 DIM » Wed Dec 17, 2008 5:01 am

So we are sure the above are valid and correspond to the endothelium - iron theories, could then summarize what increases intracranial/cerebrospinal blood flow?
Please add/correct my list:

Pycnogenol
Resveratrol
Omega-3
EGCG
Ginkgo Biloba
Horse Chesnut
Quercetin
Nattokinase
Salvia
Vitamin D, E (mainly tocotrienols)
Choline & Phosphatidyle serine
Progesterone/testosterone and estrogens
....
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Postby jimmylegs » Wed Dec 17, 2008 5:55 am

i'm late i can't read it all in detail but i've caught veins, blockage, clear fluid, and liver.

i'm hopping in with zinc, liver function, ammonia, urea(uric acid), ms

biodoc hop in any time.

here are some random pulls from google searches i am SO LATE gotta run just throwing these in the mix:

okay haven't read thoroughly but did i hear, liver, clear liquid, vascular issues...

i'm going to say zinc, ms, liver, ammonia,


http://en.wikipedia.org/wiki/Uric_acid# ... _sclerosis
Lower serum values of uric acid have been associated with Multiple Sclerosis. Multiple sclerosis (MS) patients have been found to have serum levels ~194µmol/L, with patients in relapse averaging ~160µmol/L and patients in remission averaging ~230µmol/L. Serum uric acid in healthy controls was ~290µmol/L.[16] Conversion factor: 1mg/dL=59.48 µmol/L[17]

A 1998 study completed a statistical analysis of 20 million patient records, comparing serum uric acid values in patients with gout and patients with multiple sclerosis. Almost no overlap between the groups was found.[18]

http://diaglab.vet.cornell.edu/clinpath ... mmonia.htm
Gastrointestinal micro-organisms (primarily coliforms and anaerobes in the colon and cecum) convert dietary amino acids and urea into ammonia in the gastrointestinal system. The ammonia is absorbed into the portal circulation, taken up by the liver and converted in the liver, via the urea cycle, into urea.

http://en.wikipedia.org/wiki/Ammonia
Ammonia is a compound with the formula NH3. It is normally encountered as a gas with a characteristic pungent odor. Ammonia contributes significantly to the nutritional needs of terrestrial organisms by serving as a precursor to foodstuffs and fertilizers. Ammonia, either directly or indirectly, is also a building block for the synthesis of many pharmaceuticals. Although in wide use, ammonia is both caustic and hazardous.

http://diaglab.vet.cornell.edu/clinpath ... mmonia.htm
Of the total ammonia produced, 80-90% is shunted into the urea cycle, with the remaining 10-20% metabolised by peripheral tissues, including the kidney, heart, and brain.

http://en.wikipedia.org/wiki/Hepatic_encephalopathy
Hepatic encephalopathy (sometimes hepatoencephalopathy) is a potentially-reversible neuropsychiatric abnormality in the setting of liver failure, whether chronic (as in cirrhosis), or acutely. It can be diagnosed only after exclusion of other neurological, psychiatric, infectious, and metabolic etiologies.

With severe liver impairment, toxic substances normally removed by the liver accumulate in the blood and impair the function of brain cells. If there is also portal hypertension, and subsequent bypassing of the liver filtration system of blood flowing in from the intestines, these toxic substances can travel directly to the brain, without being modified or purified. Signs can include impaired cognition, a flapping tremor (asterixis), and a decreased level of consciousness including coma (hepatic coma or coma hepaticum)

http://www.ncbi.nlm.nih.gov/pubmed/11779097
The mean serum zinc levels in patients with decompensated liver cirrhosis were found to be significantly lower than the levels in controls and patients with compensated liver cirrhosis. The serum zinc levels were inversely correlated with blood ammonia in the fasting state. In the oral zinc-tolerance test, the percent increase in serum zinc levels 120 and 180 min after ingestion was less in cirrhotic patients than in controls. A diuretic administration resulted in a significant reduction in serum zinc levels. An increased uptake of ammonia by and an increased release of glutamine from leg skeletal muscle after oral supplementation of zinc sulfate were evident. Taken together, zinc deficiency in decompensated cirrhotic patients appears to be due to low absorption and to high urinary excretion, for which excessive diuretic administration is, in part, responsible, and zinc supplementation might play an important role in the prevention of hepatic encephalopathy by activating glutamine synthetase.

http://www.vegsoc.org/info/zinc.html
Zinc has a range of functions. It plays a crucial role in growth and cell division where it is required for protein and DNA synthesis, in insulin activity, in the metabolism of the ovaries and testes, and in liver function. As a component of many enzymes, zinc is involved in the metabolism of proteins, carbohydrates, lipids and energy.
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Postby CureOrBust » Wed Dec 17, 2008 6:01 am

DIM wrote:So we are sure the above are valid and correspond to the endothelium - iron theories, could then summarize what increases intracranial/cerebrospinal blood flow?
My understanding is that , no. This study implicates a physical obstruction.

jimmylegs wrote:i'm late i can't read it all in detail but i've caught veins, blockage, clear fluid, and liver.
Seriously, if these results can be duplicated, its a mind blower. Read it.
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Postby cheerleader » Wed Dec 17, 2008 7:01 am

Cure-
THANK YOU so much...your chart is terrific, and much easier to follow. Really appreciate your time and attention. I'm so glad your medical "team" is interested in this. It appears there was a form of venous reflux in every single person with MS they tested. I had read that the first time, but doubted myself.

Jimmy- Here's the bottom line. In MS patients tested with doppler, the research team found a reverse blood flow (called venous insufficiency) caused by some sort of blockage in the blood vessels. The blood can't get around the blockage (into the brain or spine) so it has to travel back down whence it came. The study does not discuss how this affects MS patients, or what to do about it...it merely points out that EVERY person (65) they tested that had venous insufficiency and vein blockage had MS. None of the controls (healthy people AND people with other neurological diseases) had venous reflux. It is UNIQUE to MS.

I do not feel competent to recommend a regimen based on these findings. All I know is that something is going on in the cerebrospinal vascular system with people who have MS, and this in some way contributes to venous reflux and a breech in the blood brain barrier.

Circumstantial evidence in my home has shown that antioxidant and enzyme therapy with natural anticoagulants has helped Jeff regain some energy and function....but this is bigger than home remedies or postulations. I think everyone needs to find a doc who will listen, and bring in this study. Look for a vascular specialist, talk to your neuro, find a good GP.

Thanks for taking an interest in this study...please all read it line by line for yourselves. This is the first study I have ever read which is true for all of MS, and not true for non-MS.

Here is Zamboni's study...print it out, put a bow on it and give it to your doctor
http://jnnp.bmj.com/cgi/rapidpdf/jnnp.2008.157164v1
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby CureOrBust » Wed Dec 17, 2008 4:27 pm

cheerleader wrote:It appears there was a form of venous reflux in every single person with MS they tested. I had read that the first time, but doubted myself.
More then "appears", its documented. And ironically, I doubted you at first, but my second read made it clear to me also. :oops:

cheerleader wrote:...caused by some sort of blockage in the blood vessels. The blood can't get around the blockage (into the brain or spine) so it has to travel back down whence it came.
If I remember correctly, I think we need to be clear in that it isn't a complete blockage, but a restriction, which causes a "reflux". Also, if I remember it correctly, this restriction and reflux occurs on the "drainage" side, not on the "supply" side. ie the blood gets to the CNS, but can't clear out? as easily as it should.

cheerleader wrote:None of the controls (healthy people AND people with other neurological diseases) had venous reflux. It is UNIQUE to MS.
Again, I think I may of lead partially to this misconception :oops: however, on my second read, I noticed that the people who were previously identified as having some issue:
Zamboni's study wrote:...48 controls not affected by neurological diseases (Tab. Ib), but scheduled for venography (HAV-C) for other pathologies:...

In table II, 7 of the controls failed on test 4, and 25 of the controls failed on test 5. However, only the 48 controls previously scheduled for a HAV-C had the HAV-C, so it is clear that it was only these previously identified as having something wrong with their flow, failed any of the non-invasive tests; apart from ALL the MS patients. Have I read it right?
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Postby cheerleader » Wed Dec 17, 2008 9:05 pm

CureOrBust wrote:In table II, 7 of the controls failed on test 4, and 25 of the controls failed on test 5. However, only the 48 controls previously scheduled for a HAV-C had the HAV-C, so it is clear that it was only these previously identified as having something wrong with their flow, failed any of the non-invasive tests; apart from ALL the MS patients. Have I read it right?


That's what I got, too, Cure. Only 48 controls went ahead w/the invasive testing
In none HAV-C subjects who underwent venographic investigation
with negative ultrasounds, we demonstrated stenotic patterns in the IJVs,
azygous, and lumbar territory (Fig. 2, a-b-c).

The English translation makes it confusing...In none of the controls, (who had failed the ultrasounds and then underwent venography) were there stenotic patterns....meaning none of the controls tested with venography had the venous blockage.

The English trans. is good, but there are some convoluted sentences which make it a bit more confusing than it already is :)
BTW, you have no need to use the embarrassed smiley guys...you're way ahead of me in science class, Cure!
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby DIM » Thu Dec 18, 2008 1:42 am

CureOrBust wrote:
DIM wrote:So we are sure the above are valid and correspond to the endothelium - iron theories, could then summarize what increases intracranial/cerebrospinal blood flow?
My understanding is that , no. This study implicates a physical obstruction.

jimmylegs wrote:i'm late i can't read it all in detail but i've caught veins, blockage, clear fluid, and liver.
Seriously, if these results can be duplicated, its a mind blower. Read it.

Ok Cure, let's say it differently, what increases blood flow in the brain at such levels that overcomes (partially?) the venous reflux blockage problem, is it ok now?
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Postby gibbledygook » Thu Dec 18, 2008 7:05 am

In case the venous stenosis is caused by a build-up of cholesterol and atherosclerotic plaques (venosclerotic anyone?) one might want to add glisodin (superoxide dismutase), pomegranate and other hyperlipidemia appropriate supplements. So keep taking the salvia as that's good for atherosclerosis and reduces endothelin 1 which might be the baddie responsible for the constriction as well.

1: J Neuroophthalmol. 2001 Mar;21(1):37-8. Links
Increased endothelin-1 plasma levels in patients with multiple sclerosis.Haufschild T, Shaw SG, Kesselring J, Flammer J.
University Eye Clinic, Basel, Switzerland.

OBJECTIVE: We tested the hypothesis that the plasma level of endothelin-1 (ET-1) is increased in patients with multiple sclerosis (MS). The peptide ET-1 is one of the most potent known vasoconstrictors. An increased level of endothelin could explain some of the vascular symptoms of these patients. MATERIALS AND METHODS: A specific radioimmunoassay was used to determine ET-1 plasma levels. Twenty patients with MS were compared to 20 age- and sex-pair-matched healthy subjects. RESULTS: The plasma ET-1 levels were, on average, 224% higher in the patients with MS than in the controls (p < 0.005). The mean ET-1 levels (mean +/- standard deviation [SD]) were 3.5 +/- 0.83 pg/mL (min 2.13, max 5.37 pg/mL) in patients with MS and 1.56 +/- 0.3 pg/mL (min 0.9, max 2.13 pg/mL) in healthy volunteers. Neither the different forms nor stages of MS had an influence on the results. The ET-1 level was also not correlated with the duration of the disease. CONCLUSIONS: The plasma ET-1 level is markedly and significantly increased in patients with MS. Neither the cause of such an increase nor the pathogenetic role is known.

PMID: 11315981 [PubMed - indexed for MEDLINE]

Related ArticlesExtraocular blood flow and endothelin-1 plasma levels in patients with multiple sclerosis. [Eur Neurol. 2003] Plasma endothelin-1 concentrations in children with cirrhosis and their relationship to renal function and the severity of portal hypertension. [J Pediatr Gastroenterol Nutr. 2002] Increased circulating endothelin-1 in rheumatic mitral stenosis: irrelevance to left atrial and pulmonary artery pressures. [Chest. 2004] Plasma endothelin and big endothelin concentrations and serum endothelin-converting enzyme activity following aneurysmal subarachnoid hemorrhage. [J Neurosurg. 2002] Blood endothelin-1 levels before and after carotid endoarterectomy for atherosclerotic stenosis. [Atherosclerosis. 2001] » See All...
link



1: Eur Neurol. 2003;49(3):164-8. Links
Extraocular blood flow and endothelin-1 plasma levels in patients with multiple sclerosis.Pache M, Kaiser HJ, Akhalbedashvili N, Lienert C, Dubler B, Kappos L, Flammer J.
University Eye Clinic Basel, University Hospital Basel, Basel, Switzerland.

In order to evaluate whether plasma levels of the potent vasoconstrictor endothelin-1 (ET-1) are increased in patients with multiple sclerosis (MS) and whether these patients exhibit an ET-1-mediated vascular dysregulation, ET-1 plasma levels were measured in 30 patients with MS. Blood flow velocities in the ophthalmic artery, central retinal artery, central retinal vein, short lateral posterior ciliary artery, and short medial posterior ciliary artery were assessed in parallel. ET-1 plasma levels were significantly increased in MS patients when compared to sex- and age-matched healthy controls (2.0 +/- 0.4 pg/ml, range 1.1-2.8 vs. 1.5 +/- 0.2 pg/ml, range 0.9-2.0; p < 0.001). Moreover, the patients exhibited significant alterations of extraocular blood flow. The role of ET-1 in the inflammatory process remains to be clarified. Copyright 2003 S. Karger AG, Basel

PMID: 12646761 [PubMed - indexed for MEDLINE]

Related ArticlesAssessment of blood flow velocity in eyeball arteries in multiple sclerosis patients with past retrobulbar optic neuritis in color Doppler ultrasonography. [Klin Oczna. 2007] Ocular hemodynamics in pseudoexfoliation syndrome and pseudoexfoliation glaucoma. [Ophthalmology. 2001] Color Doppler imaging in optic neuritis with multiple sclerosis. [Graefes Arch Clin Exp Ophthalmol. 2004] ReviewColor Doppler imaging of orbital vessels: personal experience and literature review. [J Clin Ultrasound. 2003] Review[Anatomic diagnostic parallels in ocular vascular and orbital status as shown by color doppler mapping] [Vestn Oftalmol. 2000] » See Reviews... | » See All...
link
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Postby jimmylegs » Thu Dec 18, 2008 8:12 am

okay i went through and tried to put the abstract into everyday language. i imagine there are much better images in the full text but the abstract has eaten my morning as it is! :D

i still think there are some interesting things to be investigated wrt zinc and ammonia and uric acid, but having spent a bit of time on this research i'm not actually making that connection specifically.

here is a first draft for comment.
The veins through which used low-oxygen blood returns from the brain to the heart have never been studied in clinically defined multiple sclerosis (CDMS)

http://www.mult-sclerosis.org/diagnosingms.html
* Clinically definite MS
2 attacks and clinical evidence of 2 separate lesions
2 attacks, clinical evidence of one and paraclinical [JL: like the evoked potential test, MRI and such] evidence of another separate lesion

The researchers tested 300 people. 65 had CDMS. 235 were controls. The 235 controls were divided into four subgroups. Some controls were healthy and either of the same age or younger than the CDMS subjects. Some controls were healthy but older. Some patients had some other neurological disease. Some patients were older and while not suffering from a neurological disease, they were still scheduled to have their blood injected with dye and x-rayed [JL:a procedure usually associated with deep vein thrombosis (blood clot)].

All these folks had their heads and necks scanned with a hand-held doppler device.
http://www.umdnj.edu/uhnetweb/html/comm ... randop.jpg
http://www.gnp-dubai.com/images/ECD.jpg

[JL:doppler scanning is like a better ultrasound. the doppler effect tells you if something is coming towards you or away from you, and how fast. it's noticeable when something loud passes you at high speed, like a car horn, or blaring stereo]

the researchers were looking to find evidence of minimum 2 out of 5 possible problems with blood flow through the brain. in subjects where the researchers did find at least 2 of 5 anomalies, those patients were chosen to undergo a further test in which veins in the spine and neck
http://home.comcast.net/~WNOR/postmediastinumlevel5.jpg
http://home.comcast.net/~WNOR/latpharynx1.jpg
which return used de-oxygenated blood to the heart, were injected with dye and then x-rayed to observe any flow issues.
http://ndt.oxfordjournals.org/content/v ... 569-1.jpeg

they found that the CDMS patients were highly likely to have issues with blood flow according to the doppler scan.
of the patients that went on to have the dye/x-ray vein test, in CDMS patients they found narrowing of the blood vessels that allow de-oxygenated blood to return to the heart.
the narrowing affected the spinal vein, and a slight increase in blood pressure was noted.
the researchers observed four different patterns of vein narrowing locations. [JL:substitute circle *may* refer to alternate flow pathways created by redundancy, similar to the arterial 'circle of willis'].
primary progressive patients showed a much different pattern than other CDMS patients.

CDMS is strongly associated with long term problems with the return of blood through the spinal neck vein to the heart. the problems are caused by constriction of the vein, and the researchers don't know why the constrictions are there. the constrictions show up in different patterns depending what kind of ms you have.

my subsequent random thoughts:
the spinal vein gets used more when upright vs prone (compared to the jugular).
one interesting feature of the spinal vein is that it has no valves to prevent reverse flow.
veins use muscles to squeeze the blood through. perhaps if the muscles don't squeeze right, the blood will have more tendency to stagnate.

run-of-the-mill vein problems in other parts of the body can happen to anyone but chances are higher with:
http://www.vascularweb.org/patients/Nor ... iency.html
family history of varicose veins, being overweight, being pregnant, not exercising enough, smoking, and standing or sitting for long periods of time... age and sex (women older than 50 most often get CVI).

http://en.wikipedia.org/wiki/Neuromuscular_disease
Neuromuscular diseases are those that affect the muscles and/or their nervous control. In general, problems with nervous control can cause spasticity or paralysis, depending on the location and nature of the problem.
Last edited by jimmylegs on Fri Dec 19, 2008 4:22 am, edited 1 time in total.
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Postby DIM » Thu Dec 18, 2008 12:25 pm

Interesting article from David Perlmutter, he mentions that Chlamydia Pneumoniae found in 100% of 37 MS patients studied (Department of Neurology and
Pathology, Vanderbilt School of Medicine, Nashville, Tennessee. Dr. Subramaniam
Sriram).
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Postby cheerleader » Thu Dec 18, 2008 10:05 pm

Jimmy- thanks so much for breaking the abstract down into English. You're absolutely right about the spinal blood vessel being worked harder in an upright position, whereas the jugular builds up pressure when lying down.

I sent the abstract to a vascular doctor I've been corresponding with on my endothelial dysfunction theory. He's been very supportive of the vascular/MS connection. He was quite surprised by the Zamboni study and e-mailed me right back with the following advice-

Have your husband take one baby aspirin daily.
Also, raise the head of the bed, by placing 2 X 4s under the front legs of the bed.The aspirin will reduce the formation of small thrombi if his cerebrovascular veins are abnormal (aspirin isnt the most potent anti-thrombotic, but I would be loathe to start a more potent blood thinner without more evidence). Raising the head of the bed will reduce venous pressure in his head at night. Whenever he is relaxing, he should keep his head elevated, ie. perhaps avoid recumbency on the couch, favoring sitting in a lazy chair for example.

You could get more evidence for cerebral venous abnormalities (I would be particularly concerned about venous stenoses) by MR imaging, with attention to the cerebral veins. If you have the study, you might print out this article for the radiologist, so he/she will know what they are looking for.....


He was most concerned with the cerebral buildup. We've elevated the head of the bed. Won't be able to see a vascular doc for a scan until after the new year.

(Dmitris, Marie (mrhodes40) has written about cpn and hypercoagulation on the boards. Read some of the antibiotic threads and search the author Anecdote (Sarah). Her husband is British physician David Wheldon. Also look into CPn Help.org, a website devoted to helping people follow the antibiotic protocol. Jeff had such an adverse reaction to minocycline that we had to stop. He had vascular headaches with bulging veins and intracranial hypertension. His doc was concerned for his eyesight, since he has optic nerve drusen. But there may be more connections with this study to cpn. I wouldn't count it out.)
how many credits do I get for this course???
AC
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dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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