CCVI / CPn

A forum for the discussion of antibiotics as a potential therapy for MS

Postby notasperfectasyou » Mon Jun 08, 2009 7:56 am

Woah!

Sriram is on board with CCSVI? I did not know that. My Goodness, This new learning here at TIMS is beyond compare. WE are seeing Sriram in a month. Please help me with questions. I really don't know how to approach this with him. Ken
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Postby SarahLonglands » Mon Jun 08, 2009 8:12 am

Not on board, he just knows about it and says he is intrigued. Its his job to be intrigued.

Sarah 8O
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 mrhodes40 » Mon Jun 08, 2009 9:04 am

A couple of thing to flesh out
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 true but it bears remembering that I had a complication not normal; abdominal muscle hematoma. My heat tolerance beter and temp regulation better. I have had results from this I did not have from abx, and I feel hopeful about it.

as for the idea that my blockage was congenital, it is. It is not a stenosis, not an area of damage to the vein at all. In my case my anatomy is just such that my jugs were flattened becuase I do not have enough space at the angle of my jaw----you can think of it the same way as a kid whose teeth do not fit and they are crooked and crowded. It is just that some people a have that, others do not.

why can't Marie and Sarah's two different "stories" both be right??
One of our researchers has an interesting theory that allows for two kinds of issues and one is potentially using CPn one not. This theory accounts for many of the findings we have seen in MS, it accounts for my presentation and for CPn presentation. His paper when it comes out will be linked in the CCSVI research thread. More will be learned as time goes on.

I have told everyone I wrote to about the CPn possible connection and asked them all to check any removed tissue from blockage areas for it. I have no idea if any one will, IMHO DW, Stratton or Sriram needs to talk to these people and explain why that is an important idea, not unimportant me. But I've done everything I can to facilitate it.

If you look at stasis ulcers germs like to go in there too, Stratton even did a paper on how CPn might be involved in the development of stasis ulcers. Stasis ulcers are not fully understood even if they know that a blockage caused it. SO the people who know and understand the CPn research need to get involved and help the vascular people understand what might be going on there--those vascular doctors are having a hard time even understanding the whole body of MS research, they can't possibly delve into the CPn stuff to it expects too much of them. They are vascular specialists not MS encyclopedias.

However these stenoses exist. They are not hypothetical, they are real.

It is probably true that a lot of things can get involved after the fact, like even if you have a congenital blockage then there is every reason to think CPn could get in there as well, even if it did not initially "cause" it in that particular individual. But it is possible there are people with no germs at all, just blockage. Time wll hopefully enlighten us. We are speculating about a LOT of unknown things and creating hypotheses right and left here....just trying to tie the two ideas together. We like too speculate here on TIMS!!

There is going to need to be a fantasitc amount of research now that these stenoses have come to light. We are a long way from a totally final answer.
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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Differences in symptoms?

Postby radeck » Wed Sep 23, 2009 4:02 pm

Dear All,

I have a thought and request. If some of us are more affected by the CVI side of things and others more by the Cpn side, wouldn't we also expect the symptoms to be a little different between these two groups? I'm imagining that a clear case of IJV stenosis would lead to more "global" symptoms on average, like heat sensitivity, fatigue, cognitive issues. On the other side I would imagine that localized ulcers that are more directly related to Cpn may lead to symptoms that come from small discrete areas in the brain, like optic neuritis, numbness/weakness in individual limbs, bladder control issues, etc. Does this make any sense?

In any event, perhaps we could do a little survey of:

1) symptoms
2) Cpn/CAP status (Cpn antibodies measured? Abx treatment successful?)
3) CVI status (CVI diagnosed through MRV or Doppler? Ballooning/stents placed? Successful?)

Best regards,
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Postby SarahLonglands » Thu Sep 24, 2009 9:39 am

I'm afraid that with me, when I was 24 I started off with what you assume are more Cpn symptoms but when my disease became progressive, after about fifteen years, the symptoms were what you assume to be more from the CVI side. That is also when I began to notice the enlarged veins above my temples which have now gone. I think this is the case with many people and is more to do with changing from relapsing remitting to progressive disease.

I don't know what you mean by ulcers, though: they are something I have never had.

Sarah
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 radeck » Thu Sep 24, 2009 9:53 am

Nevermind my use of the word ulcers. I simply used the probably wrong word to describe a stenosis caused by Cpn involvement.

PS: I started a new thread over in the CVI section discussing to what extent the stenoses could be congenital, and to what extent not.

http://www.thisisms.com/ftopicp-68843.html#68843

Argument on both sides welcome!
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Postby SarahLonglands » Sat Jan 02, 2010 12:19 pm

Two quotes from CPn Help by my husband, who trained as a pathologist before movIng to microbiology and who has done many post mortems on people with MS, but just before Cpn ws discovered to be a pathogen:


I don’t find this at all convincing, though, and shall not recommend it for Sarah.

There certainly are vascular abnormalities in MSi — this has been recognised since the 1870s — but they are not those of passive venous congestion. Rather, they are angry inflammatory lesions in mid-size and small vessels: a chronic active process is implied. These lesions are characterised by perivascular cuffing with T lymphocytes: later, the affected vessels undergo involution and probably disappear. Parallel vascular lesions can be seen in the eye; both retinitis and ocular episcleritis. These are characterised by abnormal vein construction and new vessel proliferation, and, again, perivascular cuffing. This can be visualized in retinitis. The evidence for C. pneumoniae involvement is now overwhelming; here’s a link to my page on this evidence (now a little out of date.) http://www.davidwheldon.co.uk/peer-review.html

Is there a narrowing of the larger cerebral veins in MS? Dr Zamboni's data certainly suggests so. And if so might it be caused by chronic infection? Or compression by soft tissue swellings in the neck, where space may be limited? — the imaging shows veins which are apparently kinked and flattened. (C. pneumoniae is known to cause lipoma-like lesions in soft tissue: Sarah had a fine example on her right shoulder. It became angry and painful with antibiotic treatment, later shrinking away.)

I wouldn’t like the considerable risks involved in an invasive procedure. Balloon dilatation is likely to be only temporary, I would have thought, particularly if the vein is compressed by external factors. Stenting has further risks. The life of a stent in a mobile area is finite; it may get fatigued and fracture. The neck is highly mobile in many different planes. A stent in a vein might be particularly risky: the direction of the flow of blood is towards the heart: veins are notoriously variable in size. Furthermore, profound anticoagulation is required. It is likely that chronic C. pneumoniae infection is associated with stroke.

I have seen some very good results after the treatment of MS with antibioticsi, antioxidantsi and supplementsi. The truth is that patients and their relatives often forget the severity of the illness at presentation. This is a human attribute: the urge to forget an unpleasant past is quite natural. Sarah, for instance, has no idea how ill she was. And, too, there is a human desire to want a return to perfection. Alas, this does not always occur: brain-damage has taken place and recovery may be limited.




One further point which might be considered is the pathology of chronic venous hypertensioni. Elsewhere in the body chronic venous hypertension gives rise to abnormally dilated veins known as varices. The most common vein to undergo variceal change is the Long Saphenous Vein in the leg. When the valves in the perforating veins fail, great venous pressure is put on the LSV and it becomes dilated and tortuous. Inflammationi is generally not a characteristic unless ulceration has occurred. Another site for varicosities is the submucosal venous plexus in the lower oesophagus; this is most commonly due to portal hypertension.

By analogy, were chronic persistent venous hypertension due to internal jugular compression a factor in the development of MSi, we should expect to see, post-mortem, large, thin-walled, tortuous veins at the base of the brain in this disease. (The venous plexus at the base of the brain consists of remarkably delicate vessels.) I have never seen such changes for myself, and have not seen them described: were this pathology present it would be obvious to the naked eye. I tried finding a reference to the possibility in Oppenheimer’s Diagnostic Neuropathology and found none. There are a couple of photographs of the base of the brain showing surface pontine lesions but normal-appearing vessels. (I studied neuropathology for some time under David Oppenheimer at Oxford: an amazingly idiosyncratic man, he would play the cello to himself while considering diagnostic problems.)

Retinal vasculitisi is by no means universal in MS, Michèle: subtle forms need an expert ophthalmological opinion preferably with fundal photography. My ophthalmoscope is an ancient Keeler I bought as a student 36 years ago. You are absolutely right about MS being a multifactorial disorder, though. Genetic predisposition, infection with CPNi, probable Vitamin Di deficiency, profound oxidative damage, the possible emergence of true auto-immunity due to impaired thymic policing of lymphocytes.

Aside from this, have a happy New Year-


.............Sarah
Last edited by SarahLonglands on Thu Jan 07, 2010 8:35 am, edited 1 time in total.
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 agatha » Thu Jan 07, 2010 3:36 am

This is all very interesting. I have noticed in the past that if I lie in bed with my neck kinked in a certain way I can feel the beginnings of something unpleasant brewing in my brain - perhaps this position exacerbates a blood flow problem?

What I don't understand from Zamboni's position is why there is evidence of true autoimmunity in many of us MSers - for instance in my own case I also have Sjogren's syndrome and a high level of anti-nuclear antibodies.

Could it be that MS is actually a whole lot of different illnesses with a similar final common pathway - so some people have CPn, others have venous blockage, others true genetic autoimmunity etc? In my own case again, I have long wondered whether a dysregulation of the hypothalamic-pituitary-adrenal axis because of chronic stress in childhood was a predisposing factor as I have had symptoms of adrenal hyperreactivity together with insensitivity to cortisol since early childhood - this kind of problem could disrupt the normal feedback loops which limit autoimmunity in most people.

If MS is actually a number of different illnesses then randomised controlled trials are always going to bring equivocal results.
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Postby notasperfectasyou » Thu Jan 07, 2010 8:06 am

Agatha,

I wouldn't be at all surprised to find that there are many triggers affecting a pathway. I think a key part of the pathology is the breaching of the BBB. This seems to be required and necessary for most spculations to work.

If you think that is interesting, do some Googling with some of the MS terms you know about and add "Atherosclerosis" to the search. If you like reading journal articles, there's some intersting stuff to be found at Google Scholar.

Ken
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Postby SarahLonglands » Thu Jan 07, 2010 11:47 am

My view is that MS is a multifactorial disease, but primarily led by infection, probably Cpn but obviously only in people genetically programmed go get the disease in the first place.

Sriram has found Cpn in the CNS of 93 percent of people with relapsing remitting MS and if you have read what I copied above from David, soft tissue swelling can easily pinch veins, unlike arteries, which are altogether tougher.

I wrote somewhere about two veins above my temple which drain to the internal jugulars. At some point in the disease they became rather enlarged, as though I was suffering from high blood pressure, which I wasn't. After a while on antibiotic treatment, these veins returned to normal, invisible when standing upright, visible when leaning forward.

Also, if you read Zamboni's results, rather than relying on the CCSVI forum, I'm afraid they aren't as wonderful as they first might seem:

http://www.jvascsurg.org/article/SO741-5214(09)01568-7/abstract

Recieved11 June 2009; accepted 23 July 2009.
Objective
Chronic cerebrospinal venous insufficiency (CCSVI) is characterized by combined stenoses of the principal pathways of extracranial venous drainage, including the internal jugular veins (IJVs) and the azygous (AZY) vein, with development of collateral circles and insufficient drainage shown by increased mean transit time in cerebral magnetic resonance (MR) perfusion studies. CCSVI is strongly associated with multiple sclerosis (MS). This study evaluated the safety of CCSVI endovascular treatment and its influence on the clinical outcome of the associated MS.

Methods
Sixty-five consecutive patients with CCSVI, subdivided by MS clinical course into 35 with relapsing remitting (RR), 20 with secondary progressive (SP), and 10 with primary progressive (PP) MS, underwent percutaneous transluminal angioplasty (PTA). Mean follow-up was 18 months. Vascular outcome measures were postoperative complications, venous pressure, and patency rate. Neurologic outcome measures were cognitive and motor function assessment, rate of MS relapse, rate of MR active positive-enhanced gadolinium MS lesions (Gad+), and quality of life (QOL) MS questionnaire.

Results
Outpatient endovascular treatment of CCSVI was feasible, with a minor and negligible complication rate. Postoperative venous pressure was significantly lower in the IJVs and AZY (P < .001). The risk of restenosis was higher in the IJVs compared with the AZY (patency rate: IJV, 53%; AZY, 96%; odds ratio, 16; 95% confidence interval, 3.5-72.5; P < .0001). CCSVI endovascular treatment significantly improved MS clinical outcome measures, especially in the RR group: the rate of relapse-free patients changed from 27% to 50% postoperatively (P < .001) and of MR Gad+ lesions from 50% to 12% (P < .0001). The Multiple Sclerosis Functional Composite at 1 year improved significantly in RR patients (P < .008) but not in PP or SP. Physical QOL improved significantly in RR (P < .01) and in PP patients (P < .03), with a positive trend in SP (P < .08). Mental QOL showed significant improvement in RR (P < .003) and in PP (P < .01), but not in SP.

Conclusions
PTA of venous strictures in patients with CCSVI is safe, and especially in patients with RR, the clinical course positively influenced clinical and QOL parameters of the associated MS compared with the preoperative assessment. Restenosis rates are elevated in the IJVs but very promising in the AZY, suggesting the need to improve endovascular techniques in the former. The results of this pilot study warrant a subsequent randomized control study.11 June 2009; accepted 23 July 2009.



Sarah
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 agatha » Fri Jan 08, 2010 3:51 am

Yes, MS does seem to be multifactorial - you need several things out of whack before the body is not able to cope. I guess this makes research horribly complicated.
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Postby tsoft » Thu Jun 03, 2010 6:05 am

Hi everyone,
I just want to share with you the research which i found today.

http://cmr.asm.org/cgi/reprint/15/1/1.pdf

Sounds so relative about CCSVI / Cpn

Regards,
tsoft
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Clarity at last! The Aha Moment!

Postby Notdoneyet » Sat Jun 05, 2010 2:52 am

This post has been edited following a little review over at the CCSVI forum:

I have just returned from Egypt, where I was tested and received three balloon angioplasties to open blocked jugular and azygos veins that the doctor said were the worst he'd seen, so far. I am seven days, post-op and starting to recover from jet lag, sleep deprivation, two thirty hour journeys over three continents and a life changing, but relatively simple medical procedure.

Most of my symptoms and some unexpected ones are returning to normal, at least to some degree, and some seem to have disappeared completely. Here is my symptom report, seven days post-op.


• the ground isn't moving anymore, better balance and no vertigio
• no spasms or shaking anything, my body is at rest
• spasticity mostly gone
• my complexion has changed from bluish to pinkish
• i can breathe properly when I didn't realize how bad my breathing and swallowing is easier and there is less choking
• I am taller and have relaxed neck and shoulders
• I turned the heat up 2º in my house and I am sleeping long and comfortably and amwarm, without sweating or freezng
• walking still isn't that much better, but I am a little weak, though and I'm confident I won't be using the cane much as time goes on. I've also spent so much time trying tocompensate for poor walking that things will have to reorder in my head before I walk better. There are already flashes of brilliant walking
• total clarity of thought, better response from thought to mouth . . .little hesitation, quicker thinking
• Urination problems resolved to a large degree. IP Freely, with less hesitation and i am able to hold it, when I need to, with compete voiding of kidneys
• lots of energy and purpose
and many more things still to come, inshallah

The 24 hours following the procedure was spent resting, staying in, on, or near my bed and watching the American shows on the five available English TV stations. Two movie channels and MTV that promoted war, violence, porn and the American way of life, CNN and Discovery Science, which exhibited the west's vast technological superiority over the Middle East. I digress.

I've been trying to figure out why the antibiotic program that I've been on for the past six years has seemed to arrest the development of my disease progress and weighing that with the CCSVI findings of Zamboni and my own personal experience, then . . .

There was a program about brewing beer in North America and a new Molson's plant, being built in Moncton, New Brunswick. It was explained that $4 million dollars worth of piping had to be sent back to the manufacturer because the inside surface wasn't perfectly smooth. The imperfections trapped bacteria, making for bad beer. And what if the pipes are completely blocked?

It's all about your pipes and keeping them clean! That's why a change of diet, or adding antibiotics early on may reverse, or halt MS progression. As we have developed genetic dispositions and we age, smoke, eat poorly, take birth control pills and pursue other unhealthy vein behaviour, such as poor diet with no real sunlight for Vitamin D, our veins have narrowed and in more women than men and in a worldwide epidemic that is spreading, while we are being urged to preserve the "American" way of life. Read this link on Deep vein thrombosis, explaining the links to vitamin D and vein health. It explains, for me, the heavier weighting that women have towards MS with regards to birth control. <shortened url>

I still am convinced, from my own oersonal experience, that Chlamydia pneumoniae, or something that the Wheldon protocol was fighting, played a major factor in my illness. Even after five years, when I took a long break from my antibiotic regime, my symptoms worsened. I, also, always felt better, sharper when taking flagyl (metronidazole).

I don't think you HAVE to have Cpn to cause the symptoms of MS, but combining the theories of Zamboni with those of Stratton and Wheldon, along with the practicing of good vein health, answers all of the questions I have about the causes, disease process and the treatment protocol in MY exhibition of Multiple Sclerosis. The people over at antibiotics (http://www.thisisms.com/ftopic-6670-15.html) should give themselves a little clap on the back. Instead, they are scratching their heads, because they were getting close and along came Zamboni.

They're all right! Save the folks that are trying to sell us snake oil in the guise of science. This is the Aha! moment for me. Can you think of any aspects of MS that this combination of several theories doesn't explain?

My liberation was a gift from the east to the west and I am SOOOO grateful and happy!

I have a new theme song! http://www.youtube.com/watch?v=dtxuW1cOdTQ. And should I change my name to "almostdone?:

Colin
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Postby SarahLonglands » Tue Jun 08, 2010 10:22 am

Actually, Colin, I for one am not scratching my head because I know that Cpn can cause soft tissue swelling and soft tissue swelling can cause veins to block by pressing on them.

I hope that your improvements last and that you don't restenose.

Sarah
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 dlb » Tue Jun 08, 2010 11:31 am

Hi Everyone,
I would like to ask for some advice here. It appears to me that some of you that have posted are medically trained or much more versed in this topic than I am, so I'd like to know which threads will help me learn more about all this. Secondly, I would like to describe my story and ask for some advice on how I should proceed. Thanks for your help & please feel free to pm if it is repetitious.

I am 51, was dx'd in 2005 RRMS and I have an EDSS score of <1. I take Copaxone & some supplements. I have always said that I know when my immune system went berzerk (when we believed it was soley auto-immune). I have had this gut feeling that my MS is because or somehow related to the worst cold I have ever had in my life the winter before any MS symptoms started appearing. I don't remember the treatment I had for this cold, but I remember being so sick that I never left the house & wouldn't have left the house even if I had felt better because I had such horrible lumps all over my face. I usually have a very clear complexion but I had raised, red lumps on my face - kind of symmetrical and around my eyes. I also had a rash that was treated as eczema (cortizone cream & antibiotic cream, I think). Nothing made it better. Finally my regular GP came back from Africa & he thought I had rosacea & put me on a long round of minocycline, which finally cleared up my skin. Then in the spring, I had my 1st MS symptoms & in July, an MRI that revealed lesions & an MS dx. When I told my story, the neuro was so excited by the fact that I had been on minocycline and made the statement that it was definitely not going to hurt me, very positive about this piece of information. I might be mistaken but, this neuro was in Edmonton, AB & I did hear after that there was a clinical trial underway where they were combining copaxone & minocycline - Edmonton based neuro, but not sure about that??? I have coasted along for the past, taking my daily shot & hoping I stay well until something better comes along. Then last May, I got another cold that I just could not get over. I have moved & had not found a family doctor until my husband took me into emergency one evening in August because I was coughing up blood. I had been so sick with ear infections & coughing & chest congestion pretty much from May until August. I had been seen 4 times, including the very afternoon that he took me to emerg. In the aft, the doc I saw told me there was nothing wrong with my ears & took chest xrays. Finally in emerg, I saw a doc who has taken me as a patient. He was mortified that I had been seen earlier that day because my ears were so infected that he asked my husband - a layman to take a look. He started me on antibiotics & ordered blood work the next day. I had a high sedimentation rate & high reactive protein - both indicators of many things including infection, which I am sure was the case. It took another round of antibiotics until I was finally better last year. The first knocked it down but my ears started up again & he tried another antibiotic & then finally those blood levels improved so he was satisfied that it was the infection. I have been well for the past year so I haven't been in to see this doctor since the knowledge of CCSVI has come on the scene in my life, so I haven't spoken to him about it yet, but I would like to talk to a GP about this. I apologize for the long story, I just want to know if this means anything specific to any of you & where I am best to look for more information & what medical facts I can/should take to my new found GP with a special interest in MS. You see, I believe that things happen for a reason & there was a reason I wound up in emerg with this doc last year. I am on some lists for treatment for CCSVI but when I read threads like this, I think as you seem to, that there is more to the story. I really hope you have comments for me. Thanks....
Deb
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