This Is MS Multiple Sclerosis Community: Knowledge & Support

• CCSVI does not seem to explain the distribution of white matter lesions or the relapsing and remitting course that most patients experience
-If we hold CCSVI to this measure, perhaps we should hold the autoimmune theory to this as well?

CCSVI does explain the lesion distribution, since white matter lesions are perivenous (along the veins in the brain), which would certainly be in line with venous reflux and slowed venous drainage. In fact, Rindfleisch noted the tiny, engorged veins inside each white matter lesion while looking thru a microscope at an MS brain in 1863. Dr. Alfons Schelling writes of venous back pressure and the location of MS lesions in his book. http://www.ms-info.net/evo/msmanu/839.htm

Here is research from 2011 showing MS white matter lesions are perivenous in over 80% of those with MS:

http://www.ncbi.nlm.nih.gov/pubmed/21300968

-The relapsing-remitting nature of MS has NEVER been explained by MS specialists. As a matter of fact, the animal model of MS, EAE, is NOT relapsing and remitting, but constant, and more like ADEM in humans. That said, venous stenosis and reflux can be worsened in CCSVI by increases in hypoxic environments caused by viruses, colds, stress, high altitude, smoking--all situations which are known to exacerbate MS and possibly lead to relapses. How does the EAE model of MS explain relapses???

A study from London, Ontario, found that venous blockage increased with age in both MS and controls. A study from Beirut, Lebanon, found venous changes in only 9 percent of patients after their first MS attack, increasing to 92 percent with advanced MS, possibly suggesting a late finding that is unrelated to the cause of the disease.

This group found a decrease in cerebral venous volume in MS patients compared to normal, whereas blockage in venous flow would be expected to induce vascular dilation and increased venous volume

ridiculous to imagine anything else happening with age. The 92 percent is the most damning evidence of all, not "possibly suggesting a late finding that is unrelated to the cause of the disease", whatever that may be supposed to mean.

I need more info on this, as all the pictures I have seen show something entirely different above the stenoses. It seems counter-intuitive to me that someone with a blockage would have "increased venous volume" anyway, unless that meant only capacity, like Dizzy Gillespie's cheeks. I need details. How did anyone else respond to that?

This group found a decrease in cerebral venous volume in MS patients compared to normal, whereas blockage in venous flow would be expected to induce vascular dilation and increased venous volume

Imagine CSF as if it were a spring/coil. It absorbs energy by the pulse of the incoming arterial blood, stores it by moving towards the spinal column and pressing soft tissues and then gives it back, pushing venous blood out of the skull.

If there is a blockage to the venous outflow, the energy will be stored (thus the soft tissues pressed) until its pressure manages to overcome the obstruction and push the blood out (as if milking a cow). However, this will make it flow towards the "easiest route" which is upwards the aqueduct of Silvious and finally "hit" the walls of the lateral ventricles, compressing their veins. (Do the Dawson's fingers come to anybody's mind?)

Dr Begg's mathematical model is one of the most exciting research I have ever seen that can accurately predict the anomalous hydrodynamics observed in MS.

What's next? Some research that tiny T cells are strong enough to compress the nervous system?

When supine, the IJVs generally act as the principle route by which blood drains from the brain, whereas when upright, their role becomes minimal, with the vast majority of the blood traveling either down the VVs or through other venous pathways [13, 14]. In Doepp et al’s study both cohorts conformed to this norm when supine, whereas only the healthy controls did when upright – a situation that is highly unusual. Doepp et al’s results therefore suggest that, rather than any autonomic cause, the rerouting of blood in MS patients occurs as a result of stenosis which primarily affects the venous pathways that are normally used to transport blood back to the heart when upright.

References: (1) Zamboni et al. J Neurol Neurosurg Psychiatry 80:392, 2209. (2) Doepp et al. Ann
Neurol 68:173, 2010. (3) Beggs. Ann Neurol 68:560, 2010. (4) Zamboni et al. Curr Neurovasc Res 6:204,
2009. (5) Law et al. Radiology 231:645, 2004. (6) Varga et al. J Neurol Sci 282:28, 2009. (7) Adhya et al.
Neuroimage 33:1029, 2006. (8) Zamboni et al. J Vasc Surg 50:1348, 2009. (9) Zamboni et al. Funct
Neurol 24:133, 2009. (10) Saari et al. Clin Neurophysiol 115:1473, 2004. (11) Kanjwal et al. Int J Med Sci 10:62, 2010. (12) Flachenecker et al. Neurology 61:851, 2003. (13) Valdueza et al. Lancet 355:200,
2000. (14) Alperin et al. Acta Neurochir Suppl 95:129, 2005.

This text, from one of the references above, has been bothering me:





I realized that this is just an error of logic in the same binary way that used to foul me up with TTL logic all the time. One guy said of me: if you had a 50% chance of getting it right you'd be wrong every time. I think he got that from Murphy. Anyway, since "only the healthy cohort conformed to [the] norm" when upright, the unusual situation, and the one which is responsible for the rerouting, is the supine posture.