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.
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.why can't Marie and Sarah's two different "stories" both be right??
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The evidence for C. pneumoniae involvement is now overwhelming; here’s a link to my page on this evidence (now a little out of date.)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-
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