Chronic Cerebrospinal Venous Insufficiency (CCSVI)-

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

Postby mrhodes40 » Fri Jan 30, 2009 10:02 am

LOL! it is a little technical and it assumes the reader knows some things.

The stratton work on venous ulcers is here
http://www.nature.com/jidsp/journal/v6/ ... 0063a.html
Abstract:
the genus, Chlamydophilia, as obligate intracellular pathogens, induce chronic scarring in humans. Chlamydia pneumoniae, a common cause of pneumonia, infects endothelial cells and circulating macrophages. Evidence that C. pneumoniae is an opportunistic pathogen in chronic skin ulcers and other inflammatory skin conditions analogous to its role in atherosclerosis is reviewed.


There is absolutely every reason to imagine CPn COULD be involved in this pathology.

CPn is present in arterial plaques always and for years has been considered an emerging pathogen in cardiac disease by the CDC.

So CPn is a good candidate for being involved with several known issues in this pathology we are talking about on this thread: endothelium is directly impacted by CPn, CPn is known to be involved with vascular plaques, etc etc. I hope they look for it if they send any removed tissue from the stricture area to pathology if such is needed in an individual case.

NO signaling and CPn and atherosclerotic plaques
from here http://circ.ahajournals.org/cgi/content ... 102/9/1039

Conclusions—C pneumoniae impairs arterial endothelial function, and the NO pathway is principally involved. Cyclooxygenase-dependent vasoconstricting products may also account for the infection-induced impaired relaxation. These findings further support the role of C pneumoniae infection in atherosclerosis development.


The fact that Zamboni has discovered, in his labs at least, he can look at a set of doppler scans and know if the person has MS, and also if they have progressive or RR disease based on scan results because people with MS have these venous drainage problems, does not mean that there are not other co factors involved. Those strictures causing the backup had to get there somehow.....

And on the other side fromt he abxer's point of view, we've always known there must be some co factors in the CPn model too because not everyone gets better on abx, though some have great results. I personally progressed so I have something else going on in addition to any role CPn plays in MS. I hope this is "IT".

I am going to start a thread on the abx forum for exploring the possible connections between CPn and the CCVI.[code][/code]
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Postby cheerleader » Fri Jan 30, 2009 10:53 am

Really want to underline the fact that many other things affect nitric oxide signaling and the endothelium and make veins prone to vasoconstriction and stenoses:
low vitamin D, viral infection, heavy metals, saturated and trans fats, low vitamin B12, arsenic, cadmium, PCBs in plastics, diesel exhaust, and stress. It's a virtual list of life in the 21st century. (all sources are in my paper)

I believe this is why we see vets with Gulf War Syndrome and MS, people living near superfund sites and MS, folks in northern latitudes and MS, people who have had mono and EBV and MS.

Nitric oxide kills pathogens in our bodies, if NO functioning is off, obviously bacteria can flourish.
Here's some more about NO in our bodies-
http://users.rcn.com/jkimball.ma.ultran ... /N/NO.html

Good idea to start the specific cpn and CCVI thread under antiobiotics, Marie.
AC
Last edited by cheerleader on Fri Jan 30, 2009 11:16 am, edited 1 time in total.
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby jimmylegs » Fri Jan 30, 2009 11:12 am

not to mention ... zinc :twisted:

Zinc Deficiency Induces Vascular Pro-Inflammatory Parameters Associated with NF-{kappa}B and PPAR Signaling

In the current study we hypothesized that vascular dysfunction and associated inflammatory events are activated during a zinc deficient state.

Zinc deficiency increased oxidative stress and NF-{kappa}B DNA binding activity, and induced COX-2 and E-selectin gene expression, as well as monocyte adhesion in cultured endothelial cells.

For example, rosiglitazone induced inflammatory genes (e.g., MCP-1) only during zinc deficiency, and adequate zinc was required for rosiglitazone to down-regulate pro-inflammatory markers such as iNOS.


vitamin e gets into it too... i'll find more on that but not this second.
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Postby cheerleader » Fri Jan 30, 2009 11:21 am

Right, JL...
lots of nutritional deficits affect NO functioning, and zinc and E are big ones. I list them in my paper, too...sorry for the oversight above.
I'm just trying to take a giant step back from the specifics, and look at the bigger picture. Off to work,
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby jimmylegs » Fri Jan 30, 2009 12:37 pm

no worries :) did you ever post jeff's last zinc level? i know it's only one among many...
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Postby mrhodes40 » Fri Feb 06, 2009 11:28 am

My Vascular guy called back and we are a go. He wants this weekend to get things arranged and I call Mon and make my appointment.
Wow! :D
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Postby Anecdote » Fri Feb 06, 2009 11:39 am

Excellent news, Marie!!!
An Itinerary in Light and Shadow Completed Dr Charles Stratton / Dr David Wheldon abx regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. Can't run but can paint all day.
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Postby CureOrBust » Fri Feb 06, 2009 3:56 pm

That's just outstanding news! :) :D :lol:
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Postby chrishasms » Fri Feb 06, 2009 4:18 pm

Killer!
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Postby CureOrBust » Sun Feb 08, 2009 5:59 am

CureOrBust wrote:this appointment was made with another assistant, and I have a fear that this may just be for an initial consult; she could not confirm either way.

I heard back from my guy, and he said that he will do the TCCD on my first appointment. Meaning, I will get it done the 16th of Feb. He also said it will take some time to analyse the results, so he will either let me know or I may need to see him again, depending on results.

The results will be faxed straight to my GP as soon as he derives them :!:

and I think I will try to get a copy to Zamboni, especially if we do not repeat his results :evil:
(in case we did something wrong of course)
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Postby CureOrBust » Mon Feb 09, 2009 4:34 am

After I looked at the second paper, to see if anything had changed, I noticed possibly a little anomaly, which to my suspicious mind makes me question them. It has slowly been bugging me, so I thought I would type it out, and hopefully get it out of my head. That's the sharing kinda guy I am.

In the first paper published Dec 2008, they had
65 CDMS
187 Healthy(1) controls
48 Sick(2) controls
(1) Healthy in that they had no MS or reason to believe they had any CCVI, but did include OND's
(2) sick in that they were expected to possibly fail one of the exams


They documented that in the Dec trial, the "Healthy Controls" had 0 failures (ie 0% failure), and there were 33 failures between all the "Sick Controls"; ie a 14% failure rate on the tests (33 / (48 * 5) = 14%). When you combine the two "Healthy" populations together, the percentage drops to 3% (33 / (235 * 5) = 3%). To me, that would imply that the % expected from a random sampling of people from the general population, you would expect less than 3%; as its probably reasonable to expect that your average run-of-the-mill candidate does not have an insufficiency (or actually, a reason to get invasive tests performed).

However, in the second article published in Jan 09 we have:
109 CDMS
177 Healthy Controls

Now using logic, I would expect the controls to be a representation of the general public, which I would guess would possibly be a combination of the two control groups in the first trial, but mostly be in the 1st set of healthy controls.

However, the results from the second trial also has a 3% failure rate in the control population. That would imply that if you randomly selected 412 people, you would expect that 20% (48 / (48 + 187) = 20%) should of already been scheduled for an invasive vascular investigation. :?

Yes, I understand that statistics at these small numbers and further projections are questionable, and I have made a few assumptions (which I think are reasonable) or have I completely read it wrong somewhere?
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Postby cheerleader » Mon Feb 09, 2009 8:14 am

Cure-
Here are the TOTAL numbers of tests from the Jan '09 paper. This is where the distinction can be seen. Zamboni sees it in having >2 of the parameters...(which are basically vein distension, reflux, and blockage)

Overall we analyzed 1430 TCSS-ECD parameters. In controls we found 861 normal parameters of cerebral venous return vs. 24 anomalous, whereas in MS 288 parameters were normal and 257 anomalous, respectively. Consequently, each of the considered Doppler haemodynamic parameters, when compared to revised McDonald criteria as a gold standard of MS diagnosis, showed separately a highly significant sensitivity and a noteworthy specificity. However, the detection ≥2 parameters in the same subject, never observed in controls, perfectly overlapped the diagnosis of MS (value, 95%CI: sensitivity 100%, 97–100; specificity 100%, 98–100; positive predictive value 100%, 97–100, negative predictive value 100%, 98–100; p<0.0001)


Yes, you are right, some of the "healthy" controls (which also included ON and other neurological disease) would show one or two of the anomalies. (Not sure how you reached 20%, but I am not a statistician, or very good at math!) Only the MS group showed greater than two. This is why Zamboni wants to do the testing...he's very specific on what should be looked at, and outlines it in this paper, as well as this one-
Doppler Haemodynamics of Cerebral Venous Return

An interesting aside mentioned in this paper...in post mortem studies, 93% of people have jugular valves, the rest are missing valves. Could MS be a combo of a genetic lack of valve and something else? More to come....

AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby mrhodes40 » Mon Feb 09, 2009 12:52 pm

Hi all,
I think I understand your concern about the study, but I do not see a conflict there:

It is important to remember that in a trial the "healthy" cohort is not a cross section of the population, they are screened and designeated as healthy and people with problems will be excluded from study or delegated to another cohort, like anyone showing up for the control group that would be identified as having venous problems in THIS particular study would be sent home or sent to the venous group if they fit the critieria for inclusion over there.

Example: if you were studying osteoarthritis, you would not let the control group include people with inflammatory arhtritis even though the general population would have such persons in it.

The whole point of a scientific study is to control as many factors as possible so the ONE thing you are looking for can be isolated.

Also, the 48 people who were "sick" in the Dec '08 paper had vascular problems specifically and were already scheduled for some doppler exams. This is not your average person, not even an average sick person. This is a person with a specific venous problem/failure to begin with, and since 33 of them failed one exam which seems to me to be a percentage of 33/48=68%. So 68% of people with vascular disease will fail one of these tests.

But to do a good study you need to make sure to exclude those people from later "healthy" cohorts, cause they are not healthy people. They are people with venous problems that you already know will fail one exam. He'd already established that this group does fail one test often.

It's not like he ignored them or is trying to fake something by excluding them, he made a point of comparing the people with vascular problems directly to people with MS using his doppler series and it still showed an important and reproducible difference. As Cheer pointed out, all MSers had 2 or more in the same subject, and that was never true of other people, and even people with venous issues had only one or less.

BTW, that symbol he used is "equal to or greater than" not just "greater than", so

the detection ≥2 parameters in the same subject, never observed in controls, perfectly overlapped the diagnosis of MS

means MSers had two or more and all others had less than 2

He did not change his findings there vs earlier studies. The concordance remains as it was at 100%. MSers have 2 or more, others, even people with known vein issues, only have one or less.

At some point the healthy controls could include some people with MS that are not yet diagnosed if the healthy control cohort gets large enough.
However, keeping that "controlling for all factors" thing in mind, I would expect that they exclude people who "x" the box that asks "Do you ever have numbness tignling clumsiness weakness.....etc" for that reason.

I hope i am not running off at the fingers here and I undestood the concern well............ :oops:
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Postby CureOrBust » Mon Feb 09, 2009 4:36 pm

Cheerleader, yes i think I understand what Zamboni is presenting in the paper regarding MS. However, my point is actually specifically regarding the control populations.

mrhodes, its not necessarily a conflict, but I would like to know why there is a difference.

As for the numbers, I am using the same "numbering" Zamboni uses in reporting his results. He talks of "1430 TCSS-ECD parameters", which is 5 tests on 286 participants = 5 x 286, "109 patients affected by MS, and 177 controls". So when i say 10% failure, I do not mean that 10% of them had a failure, I mean that 10% of the parameters measured registered a fail. was that clear?

Its actually easier to understand where I am coming from if you actually IGNORE the MS participants. Yes, hard to do, but simply look at the controls and their results.

So we now have 2 trials where in the first trial there are
Code: Select all
Trial 1
187  Assumed Healthy Controls
48   Controls suspected of a venous issue

Results of tests failed in each group:
0    Assumed Healthy Controls
33   Controls suspected of a venous issue


Code: Select all
Trial 2
177  Assumed Healthy Controls
0    Controls suspected of a venous issue

Results of tests failed in each group:
24   Assumed Healthy Controls

Now in the first trial, they didn't get any failures from 935 tests (ie 187 x 5 = 935). Not a single one. Yet in the second trial, they manage to find 24.

Its hard to understand that they found none in healthy controls in the first trial, but there were 24 in the second trial, with a smaller population. Yes, I understand the selection criteria could of been different. But what? how?
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Postby cheerleader » Mon Feb 09, 2009 5:22 pm

From an initial cohort of 320 subjects, after application of exclusion criteria, we selected 109 patients affected by MS, and 177 controls respectively composed by age- and sex-matched, healthy aged, and patients affected by other neurological diseases.


Cure...I understand what you're asking. In the second study, The "healthy" controls contained folks w/other neurological disease...they were lumped together under the heading healthy, instead of split out like the first study. Maybe that explains the 24 "healthy" control patients found w/venous issues. I think it's more about semantics than math. You and Marie wanna help me with my taxes???

AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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