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CPn infection weakens veins the link to CCSVI treatment is made
http://www.cosmeticcentre.com.au/client ... 043332.pdf

If cPN hurts the vein, then even though I side with the phlebologists in considering most cases of CCSVI to be congenital malformation, what causes what isn't important. If cPN hurts the vein, it would worsen CCSVI. What would be important is that it too be treated.

CPn, EBV etc. must be secondary events in C[CS]VI caused by slowed cerebral drainage or whatever otherwise you would get ADEM/EAE MIR-images (spangled sky) delivered together with your “MS” diagnosis. In C[CS]VI a mechanical trauma must had taken place at first. That’s the only object that can explain the formation of Dawson’s fingers or Steiner’s splashes (direction of flow towards the venule/back jets). ADEM/EAE or other diseases caused by bacteria start IN the venule which means it would just NOT be possible to make MRI images of ‘Dawson’s fingers’- or ‘Steiner’s splashes’...and now let's go to treat it ALL!
-- Thanks dear Dr. Schelling for your book -- “Multiple Sclerosis: The image and its message”. http://www.ms-info.net/evo/msmanu/984

from where i sit, not surprisingly it all comes back to zinc as a lowest common denominator of sorts. maternal zinc status informs whether or not you have congenital malformations, for starters:

Congenital Malformations Resulting from Zinc Deficiency in Rats
http://ebm.rsmjournals.com/content/123/3/692.abstract
A mild but specific zinc deficiency was produced in female rats by the use of a purified diet lacking the element and by stringent elimination of sources of zinc contamination from the environment. Almost all of the full-term fetuses produced under such conditions showed gross congenital malformations encompassing a wide variety of organ systems, including skeletal, brain, eye, heart, lung, and urogenital defects. The fetuses from zinc-deficient females contained less zinc than did their controls, suggesting that the congenital anomalies resulted from a direct effect of lack of zinc in the fetal tissues.

Congenital malformations of the central nervous system in rats produced by maternal zinc deficiency
http://onlinelibrary.wiley.com/doi/10.1 ... 7/abstract
Teratogenic effects of maternal zinc deficiency in rats have been observed, confirming previous reports. The deficient diet differed in several respects from that used by Hurley and coworkers but the results were essentially the same. Special attention was given to malformations of the central nervous system and to tissue anomalies not recognizable by gross inspection of the fetuses.

Maternal zinc status: a determination of central nervous system malformation
http://onlinelibrary.wiley.com/doi/10.1 ... x/abstract
Maternal serum zinc concentrations were estimated during 244 normal pregnancies and 15 abnormal pregnancies. The serum zinc concentrations were lower in the anencephalic pregnancies than in the normal control subjects.

going forward zinc levels help determine genetic expression based on predisposition, zinc levels help determine susceptibility to infection by bacteria and viruses, etc.:

Possible roles of zinc nutriture in the fetal origins of disease
http://www.sciencedirect.com/science/ar ... 6507002288
Risk of diseases of metabolism such as atherosclerosis and adult onset diabetes mellitus is increased by fetal malnutrition. Deficiencies of micronutrients essential for methylation are believed to contribute to the phenomenon in part through epigenetic abnormalities. Zinc is one of the nutrients essential for the epigenome. Because the worldwide prevalence of zinc deficiency is at least 20% (JL: by 'normal' standards), fetal zinc deficiency is common. We suggest fetal zinc deficiency contributes to the pathogenesis of metabolic diseases in adults. In support of our thesis, research in experimental models and humans established the essentiality of zinc at all stages of intrauterine and infant life. Experiments in rodents and/or non-human primates found that fetal and/or suckling zinc deficiency impairs neuropsychological functions of progeny and that the effects persist in spite of nutritional rehabilitation. In addition, maternal zinc deficiency in mice is reported to impair immunity of progeny; effects persist in spite of nutritional rehabilitation into the next generation. We suspect that zinc deficiency is a far greater human health problem than is generally recognized.

i suspect that too

Epidemiological and geographical findings of prevalence of MS indicate the involvement of an infective agent.

There's also no rich countries with mris along the equator. I thought it was vitamin d not infection that proved the epidemiology.This statement needs backup.

CPn Help/pdfs/Cp-MSAssoc.pdf
http://www.davidwheldon.co.uk/ms-treatment.html


Found this test you can do at home using N-acetyl cysteine (NAC)
The NAC Test for CPN

One indirect indicator of chronic infection with this organism is the N-acetyl cysteine test. This relies on the ability of NAC (N-acetyl cysteine) to rupture the extracellular Elementary Body by opening up surface disulphide bonds in the organism’s geodesic coat, as described above. The EB opens and perishes. The release of naked bacterial components causes local inflammatory symptoms. Because EBs are more numerous in primary respiratory infections, the acellular load of EBs is likely to be highest around respiratory structures. In a positive NAC test the daily administration of 2.4 G of NAC will cause, after a few days, sinusitis-like symptoms, with watery mucous; also a cough productive of a clear, moderately viscous sputum. Systemic symptoms — 'NAC flu' — may also occur. If symptoms are severe, the dose of NAC may be cut down to 600mg and slowly built up as may be tolerated. Symptoms wane, sometimes quickly, after a few days if the chlamydial load is small; if the load is large they may continue for a month or more as the EBs are destroyed and their remains removed by the immune system. As far as I am aware, NAC is unlikely to produce die-off reactions with any other genus.