response to Dr. Bowen

[Cece]

A neurologist from the Swedish Institute in Seattle shares his take on CCSVI:
http://swedish.org/About/Blog/May-2011/ ... -Sclerosis

A patient advocate who runs a Facebook CCSVI advocacy page with over 19,000 members and serves as a founding member of the CCSVI Alliance (ok, yes, it's Cheer) shares her response: <shortened url>

a snippet:

• 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???

[1eye]

remitting: I have believed for some time now, that remissions, so called, are of two kinds: true remission is a return to patency and complete flexibility of the original equipment, without any need for collateral veins, and incomplete remission is a replacement of some, but not all, of the capacity lost to stenosis of the IJV by collateral veins. I have had both types of remission, the former when I was younger. Both took a long time, and were not sudden at all, like the attack was.

Dizziness ensues partly because collateral veins have no valves in them and can carry blood more easily both ways.

JMHO

[1eye]

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.

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.

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

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?

[Cece]

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.

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.

This is not correlated with age, but with severity of MS. Take two thirty-year-olds, one has advanced RR MS of ten years (so was diagnosed at age 20), the other has just had their first event. The one with the advanced MS has more severe or easily found CCSVI; the other has less severe CCSVI or no severe or not easily found CCSVI.

In that Beirut study, they also excluded issues with the valves and they excluded missing jugulars; the first (valve issues) is essentially the definition of CCSVI and the latter (missing jugular) is an undeniable outflow obstruction, also definition CCSVI. The 92% finding is all the more remarkable because of the number of CCSVI abnormalities that were excluded from being counted.

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

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?

I am a little confused by this too.

Dr. Zamboni's plethysmography is specifically measuring the differences in venous volume and congestion, with marked differences in the MS patients upon being sat up suddenly after lying down.

[sou]

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

This is part of the picture. Let us not forget that the skull contains CSF in addition to blood and cerebral tissue. CSF dynamics are heavily altered in MS and it presses the sinuses, shrinking their veins. I think that the Beggs' study presented at the 1st ISNVD in Bologna contains enough information to explain it.

Plethysmography measures the volume of the neck, not the skull. It takes much time for the blood to leave the neck in MS, and thus it would take much time to leave the brain.

[1eye]

OK, so they *are* saying the veins should be dilated, like Dizzy's cheeks, but the CSF and the limiting effect of the bony shell prevent this and things actually go the other way? Have you a reference? I don't have that paper.

[Cece]

http://ccsvism.xoom.it/ISNVD/Other/Abst ... l%20of.pdf
http://ccsvism.xoom.it/ISNVD/Abstract-Beggs.pdf

Dr. Beggs will be at Dr. Sclafani's July symposium.

I don't yet understand how the CSF is impacted by CCSVI in MS. Or how CSF functions in healthy brains. I do remember the phrase 'deadly CSF fluctuations' though!

[sou]

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?

[1eye]

I presume you have actually read papers that these were abstracts of? Where can I see these? They sound fascinating.

[Cece]

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?

really interesting!

[1eye]

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

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.

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.

This means, as I have been thinking all along, that these collateral veins occur because of how you sleep, what position you sleep in. I heard a TV doctor say I should be sleeping on my right side because otherwise, all my internal organs weigh down my heart. I don't know if that's true but I do know I have spent literally decades habitually sleeping on one side or the other, and I would like to know if that is affecting my unilateral disability.

[1eye]

OK wait. Hold the phone. OK. In reality, we are not finding stenoses in the upright veins (non-jugulars). We are finding stenoses in jugulars. So why would rerouting occur if we wouldn't use them anyway? Say you were healthy. Now you get a stenosis in your VV. Rerouting occurs. You measure normal in the prone position. You measure not normal in the upright. That's what was measured. Why?

That must be why it was bothering me. It not only doesn't reflect reality, it is the diametric opposite of what you would expect from reality, and indicates the "MS" cohort had a stenosis in their vertebral veins.

Where is Murphy when you need him? There was no logic error. I just couldn't believe my eyes. Either there was a copying error in a peer-reviewed journal or there were some obviously cooked results designed to discredit and not done in a very competent manner in either case. What price publication? Is any of this true? Or is this one of those dreams I never have at night any more?

[1eye]

These are the results everyone should be clamoring for a repetition of. Say the worst is true. Say CCSVI is proven by some other means to be a figment of millions of imaginations. That means, as we tuck our tails between our legs and crawl back towards the drawing-board, we will realize we have a major clue in these results! These fine researchers have measured a singular difference between people with what we thought was CCSVI but was really "MS", and normal subjects. It is somewhere in their upright veins! Their vertebrals! Hold the presses! We have a eureka here. It must be repeated and explored, as it is obviously the clue we've all been looking for all these years!

[NHE]

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

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.

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.

Isn't this an example of a negative delta cross sectional area (-dCSA) of the jugulars? If I remember correctly, that was one of Dr. Zamboni's diagnostic criteria.


NHE

[1eye]

I don't think this was a CSA measurement. It was flow in upright versus flow in prone postures. That's why it was nonsensical - it actually measured more than just area.