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Joined: Feb 10, 2006 Posts: 768 Location: Northern Virginia
Posted: Mon Jun 08, 2009 8:56 am Post subject:
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 _________________ My Starting Point
Understanding MS 101: Doctor Talk and People Talk<br /><br />
Joined: Jun 18, 2004 Posts: 1707 Location: Bedfordshire UK
Posted: Mon Jun 08, 2009 9:12 am Post subject:
Not on board, he just knows about it and says he is intrigued. Its his job to be intrigued.
Sarah _________________ An Itinerary in Light and Shadow Completed Stratton/Wheldon antibiotic regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. EDSS was 7, now I could pass for perfect most days.
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.
Quote:
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!!
Posted: Wed Sep 23, 2009 5:02 pm Post subject: Differences in symptoms?
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?)
Joined: Jun 18, 2004 Posts: 1707 Location: Bedfordshire UK
Posted: Thu Sep 24, 2009 10:39 am Post subject:
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 Stratton/Wheldon antibiotic regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. EDSS was 7, now I could pass for perfect most days.
Joined: Jun 18, 2004 Posts: 1707 Location: Bedfordshire UK
Posted: Sat Jan 02, 2010 1:19 pm Post subject:
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:
Quote:
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.
Quote:
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 _________________ An Itinerary in Light and Shadow Completed Stratton/Wheldon antibiotic regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. EDSS was 7, now I could pass for perfect most days.
Last edited by Anecdote on Thu Jan 07, 2010 9:35 am; edited 1 time in total
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.
Joined: Feb 10, 2006 Posts: 768 Location: Northern Virginia
Posted: Thu Jan 07, 2010 9:06 am Post subject:
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.
Joined: Jun 18, 2004 Posts: 1707 Location: Bedfordshire UK
Posted: Thu Jan 07, 2010 12:47 pm Post subject:
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:
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 < .0. 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 Stratton/Wheldon antibiotic regime for aggressive secondary progressive MS in June 2007, after four years. Still improving with no relapses since starting. EDSS was 7, now I could pass for perfect most days.
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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. Mental QOL showed significant improvement in RR (P < .003) and in PP (P < .01), but not in SP.
