Connecting the Dots Between Multiple Sclerosis and CCSVI

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby North52 » Thu Oct 07, 2010 7:11 pm

Lyon wrote:
North52 wrote: but the IR did not want to attempt to balloon the brachiocephalic as this was all very new. I am booked Albany to attempt the ballooning of the brachiocephalic but the chances of success are not likely very good.
The differences between veins and arteries aren't lost on me but it's hard to forget that, back in the 1970's my grandpa had his corotid arteries replaced with veins(?) from his legs with amazing results and no further problems.

Even if things don't turn out favorable in Albany, if stenosis does come to be accepted as having a direct and obvious effect "they" would probably reconsider your situation with it in mind that it would be worth going a little more invasive and replace that stretch of brachiocephalic vein.

Considering shootings and car accident victims, Dr Sclafani has probably already done similar things.


Thanks for the suggestion Lyon btu I already investigated this possibility. My brother in law is a surgical oncologist. He said it was extremely high risk especially with all the collaterals I have. Inadvisable.

North

Thanks
User avatar
North52
Family Member
 
Posts: 55
Joined: Sat Dec 05, 2009 4:00 pm
Location: Montreal, Quebec, Canada

Postby North52 » Thu Oct 07, 2010 7:15 pm

For those of you that might be interested, I updated points 23 and 24. I think you might find them interesting.

Please keep in mind that much of what I am writing is very unscientific and speculative, but has some logic (I hope).

North
User avatar
North52
Family Member
 
Posts: 55
Joined: Sat Dec 05, 2009 4:00 pm
Location: Montreal, Quebec, Canada

Re: Connecting the Dots Between Multiple Sclerosis and CCSVI

Postby malden » Thu Oct 07, 2010 9:32 pm

North52 wrote:...
1) MS is a disease of hypercoagulability that is manifest predominantly at the micro-vascular level (capillaries and post capillary venules) of central nervous system tissue.
2) This local hypercoagulability in the MS population can be a result of numerous factors. The predominant factor is likely venous outflow obstruction from the larger veins that drain the central nervous system.
3) This outflow obstruction of the larger veins results in reduced blood flow and stasis at the microvascular level.
...


You start with "micro-vascular level (capillaries and post capillary venules) of central nervous system tissue" and then you skip a lot of unknown and unexplained steps just to make a conclusion: "outflow obstruction of the larger veins results in reduced blood flow and stasis at the microvascular level"

But you are not alone with that approach. All CCSVI-MS theories start like that: Narowing in large veins...reflux...hypoxia, ischemia...iron deposits...autoimune attack...deth cells...MS.

There is a long trip from large veins to microvascular level. But this trip can be described in detail using the laws of physics and hemodynamic. But no one does. Reflux is the magic word... like absolute truth... it is incontrovertible!

So why is this so? Because the whole CCSVI-MS theory is built on shaky foundations and if you dig some more this house of cards will collapse to the ground.

But I found the rest of your points very interesting and acceptable to my way of thinking about this problem.

Best regards, M.
malden
 

Re: Connecting the Dots Between Multiple Sclerosis and CCSVI

Postby Jugular » Thu Oct 07, 2010 10:37 pm

Malden wrote:There is a long trip from large veins to microvascular level. But this trip can be described in detail using the laws of physics and hemodynamic.
I presume that you posses enough physics and hermodynamics moxie to embark upon such an enterprise, so won't you please?
User avatar
Jugular
Family Elder
 
Posts: 375
Joined: Mon Dec 21, 2009 4:00 pm

Re: Connecting the Dots Between Multiple Sclerosis and CCSVI

Postby North52 » Fri Oct 08, 2010 6:10 am

Malden wrote:
North52 wrote:...
1) MS is a disease of hypercoagulability that is manifest predominantly at the micro-vascular level (capillaries and post capillary venules) of central nervous system tissue.
2) This local hypercoagulability in the MS population can be a result of numerous factors. The predominant factor is likely venous outflow obstruction from the larger veins that drain the central nervous system.
3) This outflow obstruction of the larger veins results in reduced blood flow and stasis at the microvascular level.
...


You start with "micro-vascular level (capillaries and post capillary venules) of central nervous system tissue" and then you skip a lot of unknown and unexplained steps just to make a conclusion: "outflow obstruction of the larger veins results in reduced blood flow and stasis at the microvascular level"

But you are not alone with that approach. All CCSVI-MS theories start like that: Narowing in large veins...reflux...hypoxia, ischemia...iron deposits...autoimune attack...deth cells...MS.

There is a long trip from large veins to microvascular level. But this trip can be described in detail using the laws of physics and hemodynamic. But no one does. Reflux is the magic word... like absolute truth... it is incontrovertible!

So why is this so? Because the whole CCSVI-MS theory is built on shaky foundations and if you dig some more this house of cards will collapse to the ground.

But I found the rest of your points very interesting and acceptable to my way of thinking about this problem.

Best regards, M.


Dear Malden, I am glad to see that you scrutinizing my ideas. I can see why it is a big jump to state that if blood flow is reduced in the large veins, it will be reduced in the samll veins. I will try to explain this to you. First I want try and simplify the venous system. Imagine the venous system as an upside down tree, where blood flows from very small veins to much larger veins. Now block the flow of one of the branches in the tree so that there is no flow. What will happen upstream of this blockage? There will be no flow in the small veins that feed that larger vein. In reality our venous system is much more complex with many other types of connections between veins, so that if a vein is blocked then blood will somehow find a way around it through collaterals or other alternative routes. Flow, however will still likely be decreased upstream of the blockage.

As for reflux, it does definitely exist and it fits in very well with the theory I am proposing. If an outflow route is blocked, blood will try to find a way past this obstruction. Sometimes this may mean backtracking and going in the reverse direction. I do not think that reflux is the cause of ms symptoms. I think is just a manifestation of CCSVI and perhaps more severe CCSVI. Thank you for this comment as I had not previously thought about how reflux fits into the picture.
North
User avatar
North52
Family Member
 
Posts: 55
Joined: Sat Dec 05, 2009 4:00 pm
Location: Montreal, Quebec, Canada

Re: Connecting the Dots Between Multiple Sclerosis and CCSVI

Postby malden » Sun Oct 10, 2010 11:53 am

North52 wrote:I am glad to see that you scrutinizing my ideas. I can see why it is a big jump to state that if blood flow is reduced in the large veins, it will be reduced in the samll veins. I will try to explain this to you. First I want try and simplify the venous system. Imagine the venous system as an upside down tree, where blood flows from very small veins to much larger veins. Now block the flow of one of the branches in the tree so that there is no flow. What will happen upstream of this blockage? There will be no flow in the small veins that feed that larger vein. In reality our venous system is much more complex with many other types of connections between veins, so that if a vein is blocked then blood will somehow find a way around it through collaterals or other alternative routes. Flow, however will still likely be decreased upstream of the blockage.

As for reflux, it does definitely exist and it fits in very well with the theory I am proposing. If an outflow route is blocked, blood will try to find a way past this obstruction. Sometimes this may mean backtracking and going in the reverse direction. I do not think that reflux is the cause of ms symptoms. I think is just a manifestation of CCSVI and perhaps more severe CCSVI. Thank you for this comment as I had not previously thought about how reflux fits into the picture.
North


Reductin of cross section in a large veins (if it realy exists !?) is not the same as blocking. Blood still flows in arteries, hart is pumping, brain capilaries are full of blood... no problem at all. Possible effect of narrowing at the big vain level is just faster velocity at the place of narrowing... but no blood stop or "reflux" - no change in preasure sign.

"Reverse direction" is non documented prejudice, fabricated as a suport to CSVI theory. Non venography, non colour doppler can show that (colour doppler artifacts in nonexperianced/malicious hands can ;).

Best regards, M.
malden
 

Postby North52 » Sun Oct 10, 2010 12:25 pm

North52 wrote:Thank you for your responses.

Regarding heparin, I came across an old article. Because it was scanned it is very difficult to cut and past. Here is a portion of it. Part of it talks about ms and heparin. Look at the bottom as well. There are 3 articles/studies about heparin treatment in ms. There is no text, though. It would be very interesting to track these down. I will see what I can do. I may not be able to respond for a day or 2, as I will likely be admitted to the hospital tomorrow

patients with autoimmune hemolytic anemia.
Donzelot and Kaufmann34 found that heparin
ameliorated bad cases of rheumatism, supposedly
by an antiexudative action. But Burkls5
suggested that it acts by the inhibition of hyaluronidase
activity. The action of heparin
in rheumatism is an example of its antiinflammatory
influence on connective tissue. Other
such examples are its ameliorating effect in
thrombophlebitis36 and its action in interstitial
cystitis.37
Heparin has been used with some success
in multiple sclerosis,3840 and the authors suggest
that this may be due to its action on lipid
metabolism.
Heparin was also...

References:

COURVILLE, C. B. The effects of heparin in acute
exacerbations of multiple sclerosis. Observations
and deductions. Bull. Los Angeles Neural. Sod., 24:
187,1959.

MASCHMEYER, J., SHEARER, R., LONSER, E. and
SPINDLE, D. K. Heparin potassium in the treatment
of chronic multiple sclerosis. Bull. Los
Angeles Neural. Sot., 26: 165, 1961.

28. PARROT, J. L., NICOT, G. and LABORDE, C. Capta- 42. SIKORSKI, H. Hyaluronidase und Heparinoide bei
tion de l’histamine par I’heparine. Influence du der Behandlung entzuendlicher Stauungen.
PH., Compt. rend Sot. biol., 154: 1426, 1960. Ztschr. bout. Geschlechtskr., 31 : 225, 1961.

Jimmy


I was able to obtain these articles on heparin use in MS. One study uses subcutaneous heparin and results seem quite remarkable, almost like the Liberation procedure. Another is in German, which I do not understand and the third uses sublingual (under the tongue) heparin with interesing but marginal results. I have these just in PDF form. Does anyone know how I can post these on this site?

Sorry for not answering recently. I have have been in the hospital receiving IV antibiotics for a severe cellulitis (skin infection) of my left shin. I am presently on a day pass and will make sure to buy a wireless USB key before I reutrn. I found out some very interesting things. I will communicate this to you in my next few posts today or tomorrow.

North

Jimmy
User avatar
North52
Family Member
 
Posts: 55
Joined: Sat Dec 05, 2009 4:00 pm
Location: Montreal, Quebec, Canada

Postby Billmeik » Sun Oct 10, 2010 6:25 pm

good to have you aboard north.
User avatar
Billmeik
Family Elder
 
Posts: 694
Joined: Fri Nov 27, 2009 4:00 pm

Previous

Return to Chronic Cerebrospinal Venous Insufficiency (CCSVI)

 


  • Related topics
    Replies
    Views
    Last post

Who is online

Users browsing this forum: No registered users


Contact us | Terms of Service