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PostPosted: Fri Jan 30, 2009 11:13 am
by mrhodes40
I am opening this thread to discuss possible connections between the material on the CCVI thread in the general discussion forum and CPn.

Rather than quote all the material for that 16 page forum thread, I'll assume readers have read the discussion over there, found here

1. Zamboni did blinded research on large numbers of patients in three studies that shows venous abnormalities in 100% of MS patients. There appear to be strictures in the azygous or jugular vein that "back up" blood flow in the same way a stricture in the femoral vein "backs up" blood flow in the leg and causes venous ulcers.
2. Zamboni and Schelling do not say where the strictures that cause the venous back up come from.
3. Several researchers have proposed that MS lesions and venous ulcers are the same kind of injury, supporting the idea venous backups play a role
4. venous ulcers, while they are known to be related to a stricture in the femoral vein, are not well understood. Exactly what causes the minute changes that eventually mean an ulcer is not known, but relieving the femoral stricture helps a lot.

While my personal belief is that MS is a CPn connected problem and that the intriguing results of Zamboni's work shows that MSers have venous problems in the brain, I see these problems as not at all mutually exclusive. Here I paste something I posted on the other thread that shows Dr Stratton's work on venous ulcers in a published paper:

The stratton work on venous ulcers is here ... 0063a.html
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.

That was added to the thread because NAPAY asked for the research Stratton did on venous ulcers and CPn. This shows that Stratton at least has proposed a connection between these venous ulcers and CPn. If venous ulcers are like MS lesions as Zamboni proposes, this is expected isn't it?
There is absolutely every reason to imagine CPn COULD be involved in this pathology (the strictures and the proposed "venous ulcer-like" idea of MS lesions)

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 ... 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.

S with regards to CPn/MS/venous strictures I am thinking that;
1. the strictures might be caused by CPn--atherosclerotic plaques are caused by CPn, why not venous ones?
2. if venous ulcers can be caused by CPn in some research like Stratton and Mitchell's, and we already know MS lesions are caused by CPn in those same minds, there is no reason at all to assume the overall BIG PICTURE pathology is not similar....both a stricture AND a CPn induced lesion at the area of the backup.

It is obvious that some people can, and do, get better with just abx. There is no reason to assume this somehow negates the idea of MS being treatable with abx, obviously Sarah, Katman, Mack and others have had great results. Perhaps they can dissolve the plaque that causes the stricture as well as stopping that "something unknown" :wink: that causes the MS lesion.

But as Stratton mentions above "scarring" is caused by CPn, it is entirely possible that some people have too much scarring so the venous issue remains stubbornly in place in spite of CPn treatment. THUS, BY THIS PROPOSED TOTALLY UNPROVEN MECHANISM BY TOTALL Y SPECULATIVE ME, IT IS POSSIBLE THIS IS THE REASON SOME PEOPLE HAVE TREATMENT FAILURE ON CAP. I am one of those people.

I see the way forward as this:
1 get the venous issue assessed and see if I have a blockage as Zamboni proposed.
2 Get treatment if possible to restore blood flow
3 continue abx and expect a much better outcome with blood flow normal

There is absolutely no way success in my case can prove anything at all: the Zamboni people will see it as success of the venous issue, and any abx I use will be seen as of uncertain value. And I am certain some people will get right in there to remind me that abx are antiinflammatory.....

Empirical treatment is fraught with problems because you can't prove cause by effect: just cause I get better does not mean the reason I am better is what I suppose it is.

But in the end, if I'm better, who cares?! :lol:

I'm following my own lights for MS treatment and my main criteria for doing something is that it is safe, has a resonable and supported hypothesis and its side effects are in line with its PROVEN effectivenss.....That's where the "standard" therapies beyond the first tier CRABS fail. the side effect profile is way to terrible for the minimal results they offer.

While CAP is light on the clinical study side of things because no one has put 100 MSers on either abx or placebo for 4 years to see what happens, it is way high on the safety side.

Plus abx have shown effectiveness in terms of them to ther therapies like Mino to copaxone or doxy to interferon, so there is additional reason to look at it in a positive light.

I hope others will add to the ideas I have offered here.

PostPosted: Sat Jan 31, 2009 1:06 pm
by SarahLonglands
Well, I obviously think that the venous issues are caused, in my case at least and if I had them in the first place, by Cpn because I responded so quickly to the antibiotics.

I will post here what I have told Marie already and which I only rediscovered in myself a few days ago: just above both temples I have a shadow of what was a quite prominent vein. Now it is just about visible, more so on the left side but it looks more like a small stream running in the bottom of a wide gorge, not being at all convex like it once was. It developed shortly before I was at my worst, now it appears to have corrected itself. Since I have usually worn my hair with a longish fringe, its easy to forget about such things, but I am presently growing my fringe out and was experimenting which is the better side to wear my parting and there were the veins, a mere shadow of their former selves.

It seems to me that for people finding that abx alone are not having enough effect, Zamboni's treatment may be the answer, but the abx used here are so harmless if used correctly, they ought to be tried first. If one launches straight into Zamboni's procedure, the infection will still be there and cause the venous issues to reoccur in time.


PostPosted: Sat Jan 31, 2009 3:20 pm
by MacKintosh
Sarah, I could almost duplicate your post.About four to five years ago, my mother wet her fingers and tried to 'smudge' a mark off my face. She rubbed again and I protested. She said I had ink on my face and she was trying to wipe it off. I told her it wasn't ink, it was a vein that had popped, and it really did look like a dark stain, straight down from my temple, across my cheek and down to near the jaw.

Today, I have to look very, very hard to find it. It receded about a year into the abx protocol and I'm very grateful. I rarely wear make-up and it annoyed me that this ugly thing had appeared on my face. Plus, somewhere in the back of my head (before the MS diagnosis) I realized this was not a good omen, medically.

PostPosted: Sat Jan 31, 2009 5:02 pm
by mrhodes40
Wow, veins for both of you? Mack which side of the face was that, the side of the weakness or opposite? And do you know anything about it was it diagnosed at all? Or just a burst vessel that happened one time for some reason? just curious.....

PostPosted: Sun Feb 01, 2009 4:02 pm
by Terry
and it really did look like a dark stain, straight down from my temple, across my cheek and down to near the jaw.

I had to get to the bathroom mirror quickly after reading this. I have had the same EXACTLY since I was a baby, but my mother told me it was from my forceps delivery.
I haven't noticed it for some time- can't see it today. Was for a while showing more when I was tired or not feeling well.

PostPosted: Sun Feb 01, 2009 6:54 pm
by MacKintosh
Marie, I'm sorry. I really meant it when I said carbon copy! It was on the left side and was fairly prominent.

It was REALLY noticeable in flourescent light and I would often get remarks about it at my office. My hair usually covered it, but I knew 'the look' when one of my co-workers noticed it, just before they made their comment. :wink:

PostPosted: Mon Feb 02, 2009 8:46 am
by SarahLonglands
Mack, a question from me: I know you started treatment very quickly, before you had much in the way of residual damage, but where on you MRI scan is most of the damage? With me, the worst vein is on the left, likewise normally hidden by my hair, but most of the MS physical damage is on the right and the worst lesions on MRI are on the left, which kind of all adds up.


PostPosted: Mon Feb 02, 2009 9:31 am
by MacKintosh
Sarah, I'll have to hunt down the paperwork, but I do recall him showing me a spot really in the center/top of the brain and basically saying 'aha, this is why you have weakness in your left hand and foot'. I packed the films and report away when I moved two years ago, but if I can find them, I'll post more.

My inability to hold a glass (or to KNOW I was holding it, more to the point), my initial foot burn, my Bell's palsy, all were on the left side, though the right leg began to drag just before I began abx, and, as you all know, my major gallbladder disease disappeared within ten days of starting the two combined abx.

PostPosted: Fri Jun 05, 2009 9:12 am
by notasperfectasyou
Thanks for grabbing my nose and pointing it here. I did not know this thread was here.

I've been reading about CPn and Alzheimer's a little this week. It's not hard to find interesting articles that link Alzheimer's to CPn just as MS is linked. These articles also discuss the "Infiltration of the Brain" issue. Then I read articles about Atherosclerosis which also involves CPn and how the vascular structure is systematically altered with the involvement of CPn; potentially beginning with ICAM-1.

I think the whole idea of stuff sticking to the vascular structure with follow up inflammation, infiltration and narrowing is the key here.

I don't really want to get bogged down in what happened first or can you have one without the other. I don't think it matters, people are born with different genetic qualities to their vascular system - we know that MS tendencies can run in families.

I think, I believe, I feel that we will find a closer linking between ABX and CCSVI as we go. Marie is the only (correct me if I'm wrong) CCSVI guinea gal who has been on ABX. While pressure and infiltration should help and provide a turn for MS'ers, I'm thinking that those who have had MS for a long time will need to follow up with abx once the vascular damage is corrected.

Final Thought ........ for today

To be more clear about this thought, ICAM-1 induced rolling monocyte infiltrates endothelium causing inflammation and narrowing of veins. Once initiated it becomes easier to repeat the process in the same location because surface becomes more textured and likely to capture infected monocytes. Overtime veins narrow with more inflammation and athero-like build up and reduced blood flow increases the likelihood of even more "sticking" and faster infiltration. Meaning, I suspect that this process starts slowly and builds up exponentially with time, much like the the transition to SPMS to RRMS.


PostPosted: Fri Jun 05, 2009 1:21 pm
by mrhodes40
bogged down with which happened first

I agree. It is almost silly to do so. One problem is correctable with surgery, the other potentially with abx, however I would say that if the stenosis showed in an individual most would do better getting that treated by surgery first because to wait 3 years and see IF abx did dissolve it for you would be risky.

My abx journey resulted in prgression though I had some improvement in energy and clear headedness, so if I'd have gotten surgery first I'd be better off back at a 5.5 or so.

What we need is proof this exists in the stenotic lesions and that it could be the cause, so someone who treats the stenosis needs to test it and find CPn; that would do it....

I have alerted every CCSVI researcher I have contacted to that possibility. Some are interested.............. and one has a novel interest in it connected to the oligodendrocytes dying pre inflammation arriving as shown in the Prineas and Barnett paper of '04 and how that may relate to his opinion happening after the CCSVI fact, although in my mind the stenosis itself is a candidate for CPn involvement to begin with.

We can discuss these things here on this thread, not that many people will find them of interest and they are largely academic anyway since we have no hard data to point to other than the VU CFS with PCR'd CPn in it, and some would argue that is not definitive because not everyone reprouces that (but we know why) and it is likely that most people are carrying CPn whether they have MS or not.

What we need I have always said is a HUMAN brain cell with CPn in it from an MS lesion.........and now with this model a cell drawn from a stenotic area that has CPn in it.

That might spell the whole picture.

As it is right now no one is asking where the azygos loswer jugular stenoses come from (although mine was congential not a plaque of any kind).

SO ther is kind of two ways for CPn to be involved here one is to cause the stenosis and start the entire process, two is to adhere to the endothelial wall in the damaged areas where the endothelium is breaking down and leaking in the brain as a result of the stenosis, thus allowing entry to the lesion area.

So maybe everyone on the planet gets CPn but not everyone gets a plaque in the venous drainage system of the brain, and that is the difference?

Entorely hypothetical, but that never stopped us from specuating before!

PostPosted: Sun Jun 07, 2009 11:25 am
by SarahLonglands
Marie said
I agree. It is almost silly to do so. One problem is correctable with surgery, the other potentially with abx, however I would say that if the stenosis showed in an individual most would do better getting that treated by surgery first because to wait 3 years and see IF abx did dissolve it for you would be risky.

I say:
This is fine if your MS has not become as aggressive as mine had. David decided to put me on doxycycline et al and I responded almost straight away. I don't know if I had any stenoses but I certainly had what turned out to be Cpn infection. I vaguely remember hauling myself up stairs the evening I started treatment but I then became delirious and remember little more until I woke up properly a few mornings later, head and voice clear. as they have remained since. For this reason, even if I was found to have a slightly occluded jugular vein, I would not consider having a stent put in just to be on the safe side because stents are prime areas of new infections.

My abx journey resulted in prgression though I had some improvement in energy and clear headedness, so if I'd have gotten surgery first I'd be better off back at a 5.5 or so.

I can't argue with that and it is a good reason for having a physician who knows all about your health issues to decide which way to go first. In a few years we might have that.

What we need is proof this exists in the stenotic lesions and that it could be the cause, so someone who treats the stenosis needs to test it and find CPn; that would do it....

Here I differ because these stenotic lesions can't be the cause of MS. Yes, the stenoses have aparently been found in everyone with MS who has been tested, but this is not evidence that they caused the MS, even in those with congenital stenoses. There are too many other things being disregarded if someone thinks this. Not even mentioning infection, vitamin D is time and time again shown to be at low levels in people with MS. In your whole body not just your brain and spinal chord. Why is this? Because again, it would appear not to cause the disease. I was taking it in large quantities before I started abx treatment, but I still carried on getting worse.

I still take a minimum of 4000 iu a day of vitamin D because it is so inexpensive, it seems silly not to.

Multiple sclerosis was unknown in the Faroe Islands until British servicemen arrived in 1943. The servicemen were all MS free, but never before had it been seen in Faroe. Although a very northern place, lacking in sunlight, they were protected by their diet high in fish flesh. In 1943 came what is probably a main cause of MS: infection by chlamydia pneumoniae. Now, this is a common pathogen in the Western World and people might well say that very few people get MS, but if you put a genetic tendency together with low levels of vitamin D and the almost inevitable Cpn infection, the numbers start to make sense. Then you add a resultant vascular stenosis, then MS develops.

Many people manage to clear the infection and also the MS just by taking to requisite antibiotics, but a few, like Marie, don't. I did, but I think this is because I had a very healthy and flexible circulatory system: low blood pressure, thin but not too thin blood and very flexible body tissues. Maybe Marie would have done better to have the vascular surgery first, but I certainly did better by taking the antibiotics, making surgery unnecessary.

Sarah (By the way, Marie and I are the best of friends.)

PostPosted: Sun Jun 07, 2009 2:32 pm
by notasperfectasyou
Do I ever feel like the third wheel.

I see where both of you are coming from and I know and respect that both of you have been at this longer than I have.

For me cause is a squishy word. I promise not to write paragraphs about what I mean by that. Do we have to know how the CPn got in the CNS in order to go about giving someone ABX to rid themselves of the problem? I don't think we must, are required to know - just take these pills and lets get started killing the bacteria. Well, I don't think we need to know more than that there is a dangerous condition in the veins in order to get stents. I see this as identical arguments. Cause is squishily unnecessary to know in both cases.

4 MS'ers we know here at TIMS have gone out, gotten tested in follow up to a study in which 100% of the MS'ers had this condition and 100% of the non-MS'ers did not. Now we are 4 of 4 in our little community here. Cause or effect, I don't care right now. Kim's MS is similar to Marie's. Kim is responding to ABX, but that don't mean that we should not be concerned about the possibility that, whether cause or effect, Kim might have vascular blockage. I have learned that 2 of Kim's sups that she takes in large quantiites are both vascular dialators. NAC 5gm/dau and Ascorbic acid 5 gm/day.

But, at the end of the day, I don't think it really does much to help bantering about this right now. I think we need to see how everyone does in about 3-6 months and then we'll have objective measurable documented results to talk about. When I learned of Sarah's ABX, I had a million questions. I needed info, I needed to understand. I have a million questions about this too. In the case of ABX, I was able to see how folks were getting results in 3 or so months or reading, we got Kim to Vanderbilt as soon as a confluence of events made that path clear. I think others like Mac, Rica and Sarah improved faster than Kim is, I wonder if, whether cause or effect, I have to wonder if, CCSVI is part of what's impacting Kim. But, Like I said, I think I have a few months to wonder about this and I think Kim is doing really well and if I could wish this summer away for everyone and get us straight to the fall I would.

Putting this more simply, a combined Bacterial Venous pathology makes way more sense than an autoimmune one. Ken

PostPosted: Sun Jun 07, 2009 6:20 pm
by SarahLonglands
Agreed! :)

PostPosted: Sun Jun 07, 2009 7:44 pm
by cheerleader
Just to be devil's advocate(and balance out Ken's third wheel)...why can't Marie and Sarah's two different "stories" both be right?? Why do we need only ONE way?

Maybe some stenosis are created by cpn, maybe some are congenital. (Jeff was born with tight jugs which were constricted by his anatomy. He had pseudodrusen all his life...)
The endothelial wall is further damaged by low vitamin D, bad fats, toxins, heavy metals or stress (all disrupters of nitric oxide) and flares occur. Jeff never had colds or flus. He got his first flare after a week at high altitude in Salt Lake City. Now we know why. His brain was starved for oxygen.

Why does it need to be either/or? With all the varieties of presentation of MS, it doesn't seem like a one size fits all disease. If MS is tied to venous reflux and slowed perfusion, it may be created by a vast number of's up to the MS patient/doctor to figure out the puzzle.

I have no doubt that Sarah's MS was due to her cpn infection...she and her husband have proven that beyond doubt. I know there are many whose lives have been changed because of their diligence in teaching the antibiotic protocol. But I also know it hasn't cured everyone...and there is an obvious reason for that. Not that people didn't try hard enough, or had thicker blood...but that their venous issues were created by another scenario. I'm not being disrespectful to all of the research I will never completely understand, and I hope I don't come off that way, because I am out-classed by the antibiotic crew :)

In any event, Ken is right...our words here are moot. Let the future MRIs, and MRVs and upcoming studies be our words and let's keep fighting this dreadful disease together. The combined brain power here can do alot!

PostPosted: Mon Jun 08, 2009 7:31 am
by SarahLonglands
Cheer, we don't need only one way. I think we probably have two, but I think the infection comes first and even before that comes the genetic propensity for MS: Most people first develop MS in their twenties, soon after seroconcversion of Cpn first takes place. Some people manage to clear both the infection and vascular blockage more easily than others.

Your husband cleared the blockage very easily, I cleared the infection and I guess also the blockage which it seems I must have had. My first MS attack was definitely not of a vascular nature yet Zamboni found blockages in 100% of MS people he tested so I guess it was either there or came very soon after. Marie didn't have a great deal of success with just abx and is now finding her stent surgery not as easy as she thought. This is presumably just like some people taking much longer to respond to antibiotics than others. Kaman, for instance spent months just getting worse before she stopped progression and now she is wonderfully well. Marie will be as well.

Kim will be also and she will have the advantage of being able to question Prof. Sriram about this at her next appointment. I know he is looking into the vascular findings because I sent him Marie's notes a few months ago, which he finds most intriguing. Now, as Professor in Experimental Neurology at Vanderbilt, he definitely is not an autoimmune adherent.