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Here is my 2 cents worth.
I see a vein obstructing for one of several reasons. Theoretically a vein might constrict as its smooth muscle contracts but I doubt it can constrict in such a focused way and to the degree that it would impair flow. Also, a constricting blood vessel is unlikely to constrict in a "pancake" manner as smooth muscle goes all around the vessel so I do not think this can explain a reversible occlusion.

The other more likely possibility is that the vessel is obstructed from the outside. This seems more consistent with pancaking. But how can we explain a possible reversible compression? My theory is that some of CCSVI is related to reactivation of EBV infection. With reactivation comes lymph node enlargement and worsening compression of the vein. Remember that lymph nodes surround the jugular and vertebral veins. Could it be that rapidly worsening MS coincides with a type of persistent reactivation of EBV infection? We know that steroids can reduce lymph node enlargement in mono, so could this be one reason why steroid can improve ms exacerbations?

North

And with my two cents' worth, we have almost a nickel's worth of "sense."

North, to your statement:

Theoretically a vein might constrict as its smooth muscle contracts but I doubt it can constrict in such a focused way and to the degree that it would impair flow.

I have to wonder WHY muscles could not spasm and block the blood flow. I have very strong muscle spasms in my legs and arms. Couldn't the same happen in my blood vessels? Or... given my preoccupation with insulin which I know thickens and stiffens smooth muscles, could this be the mechanism at work?

Oh, I love brainstorming sessions like this -- mental exercises!

It's a case of Schrodinger's cats...the veins are both open and closed at the same time...although then the imaging should fix them into one reality!

Honestly this case throws me for a loop. Is it that veins are looser and more able to collapse (compared to arteries)? Could it be an issue of blood pressure? The first time blood pressure was lower and not strong enough to hold the jugulars open; the second time blood pressure was higher, maybe due to the excitement/anxiety of having the liberation procedure or differences in any sedation drugs or just plain randomly, and then the blood pressure was high enough to hold the jugulars open?

So: the upper stenosis would be causing the 'downward' pancaking, but that area would come and go based on how high one's blood pressure is at that moment. This would fit with those people with ms who feel better when exercising. (Which is not me: I feel much worse when I exercise.)

I feel seriously hampered by my lack of any years of medical school in trying to decipher all of this.

I also agree that this sheds some light on the stent migration issue. Also it suggests that treatment should be done in a top-down fashion (fix the uppermost stenosis, by stenting, then see if the lower situation resolves itself).

Tense muscles could cause compression on the small blood vessels which in turn could theoretically cause problems with blood flow and cause hypoxia etc. Maybe exercise/muscle relaxents could help in some cases???

While everybody is throwing their money around, here's my two cents...

I've had a number of radiologists (including the radiology team at the NIH) tell me that MRV's are notoriously prone to severe artifacting, and thus false positives, and therefore are not to be trusted as a diagnostic tool. The NIH does not use MRV's for just this will reason.

So, it could be that the initial "stenosis" that showed up on your MRV actually never existed at all, and was merely one of the artifacts that MRV's are notorious for.

As for the relationship between upper and lower stenosis, I spoke with a radiologist who attended the Hamilton conference, and who is familiar with my CT imaging that reveals stenosis very high up in my left internal jugular. He told me that Simka and Zamboni both believe that upper jugular stenosis is secondary to lower jugular stenosis, and that treating lower jugular stenosis, in most cases, rectifies the stenosis seen higher up in the vein.

Of course, there are patients that do only have stenosis higher up in the veins. In my particular case, it appears that the stenosis (as revealed by CT venogram) is caused by the vein being pitched between two bony structures, which, if true, will make it very hard to treat.

That is quite interesting about the possibility of severe artifacting. What does the NIH use instead? Do they go with Doppler, CT scans (despite all the radiation) or just start right away with a venogram (radiation too)? I will certainly ask my doctor about this--I know he has done thousands of scans and procedures--what I don't know is how often his scans are MRV or MRA. In terms of a false positive I could see how that would be very possible especially if you are just looking at the sliced axial pictures starting from say the jawline and moving down. What you are seeing is the two white dots of the jugular veins and the two white dots of the carotid arteries on the sliced image of the skull. But my question would be how could a large extensive web of collateral veins from various side views be a false positive? My understanding was the axial pictures showing narrowing or flattening in combination with pictures of collateral veins would clinch the diagnosis. Without evidence of collateral veins I would be more skeptical of a CCSVI diagnosis, to be honest. What was surprising to Dr. X was my immense collateral system and then suddenly the stenosis was not there. He was just throwing ideas out there--one was maybe there is inflammation that leads to stenosis, in which case it's not congenital. Actually when I asked him about the international group of vascular surgeons headed by the Dr. at Georgetown who listed CCSVI as congenital--his response was "Well how do they REALLY know that?" I look forward to my 2 month follow up Doppler scan. In the meantime I can sit and wonder about my upper left jugular stenosis that needs a stent.

prof8 wrote:That is quite interesting about the possibility of severe artifacting. What does the NIH use instead? Do they go with Doppler, CT scans (despite all the radiation) or just start right away with a venogram (radiation too)? I will certainly ask my doctor about this--I know he has done thousands of scans and procedures--what I don't know is how often his scans are MRV or MRA. In terms of a false positive I could see how that would be very possible especially if you are just looking at the sliced axial pictures starting from say the jawline and moving down. What you are seeing is the two white dots of the jugular veins and the two white dots of the carotid arteries on the sliced image of the skull. But my question would be how could a large extensive web of collateral veins from various side views be a false positive? My understanding was the axial pictures showing narrowing or flattening in combination with pictures of collateral veins would clinch the diagnosis. Without evidence of collateral veins I would be more skeptical of a CCSVI diagnosis, to be honest. What was surprising to Dr. X was my immense collateral system and then suddenly the stenosis was not there. He was just throwing ideas out there--one was maybe there is inflammation that leads to stenosis, in which case it's not congenital. Actually when I asked him about the international group of vascular surgeons headed by the Dr. at Georgetown who listed CCSVI as congenital--his response was "Well how do they REALLY know that?" I look forward to my 2 month follow up Doppler scan. In the meantime I can sit and wonder about my upper left jugular stenosis that needs a stent.

I'm not really sure what the NIH uses as their first line for imaging the CNS venous system. Up until now, there really hasn't been much reason to image that particular anatomy, which is why there is so much discussion of what exactly a "normal" system looks like.

I had my CT scan done on the advice of Dr. Dake, since I didn't want to fly out to Stanford without having reason to believe that I had some stenosis. When it did show stenosis, I considered Stanford, but Dakes reading of the scan was different than that of other doctors I consulted, and on the very strong advice from the NIH and another radiologist, decided against it due to their warnings of potentially catastrophic complications associated with putting a stent up that high in the jugular.

I do know that the NIH was considering doing a venogram, but then decided that they don't believe the stenosis in my scan is relevant to my neurologic condition (which they don't believe is MS). They don't have the correct Doppler equipment to do intracranial sonograms. I was told, though, that they will be starting their own investigation into CCSVI...

prof...as you've learned, and we're all learning together, the truth of the matter is that only a venogram can really show what's going on. And that's why it is essential people see IRs/vascular doctors...and not just rely on doppler/MRVs for diagnosis. The proof is only seen once inside, when stenosis and flow can be accurately measured.

Your high upper stenosis is still mild, and so is your MS. May it always be so! Marc's stenosis is pretty severe, and so is his MS. (I am hopeful the docs are going to figure out how to help him.) Jeff's stenosis was somewhere in between you two, as is his MS. The one link we keep coming back to- which the Jacob's research verified- is that the severity of stenosis is linked to the progression of disease. But there's still so much more to learn. Thanks for sharing your experience....more for the research pile!

(as far as the congenital nature of these truncular venous malformations, that came from Dr. Zamboni's research in Sardinia in the 1980's- where he first noticed jugular venous stenosis in several children and followed them into adulthood. 20 years later, 90% of them had MS. Dr. Lee and a panel of 47 vascular experts went over the research and made the congenital ruling. Here's the FB link-
http://www.facebook.com/note.php?note_id=272090457210
cheer

Thanks Cheer, I had forgotten about the Sardinia children research. I'll pass that along to my doc. I had already given him a reference to the inclusion of CCSVI as a VM by the phlebologists. Yes, this is all new evolving research and I hope the vascular and IR docs continue pushing in new and improved directions, building on Zamboni's work. I think I mentioned this before but I've had such great experiences with all the vascular folk I have met and not such great experiences with many of the neurologists over the years! My IR said he could probably fix my upper stenosis with a stent but since my MS is mild we won't go to that yet. And now we will have to follow the jugular (or non-existing) stenosis. I wish both Marc and Jeff good health. Perhaps soon someone will patent a stent specifically for the jugular veins and even high up.

.

Is the guessing game over? I wanna play one more time!

If I understand it correctly, your doctor would of had to push the catheter through the jugulars and up past the stenosis, to release the dye through the stenosis itself. What if the "stenosis" was caused by reduced flow through the Jugulars, and this reduced flow was caused by membranes within the jugulars, which your doctor has inadvertently pierced?

Cure, I like that idea. I had trouble getting pregnant, but after dye passed through and cleared the way, BINGO.

Sound plausible. Maybe another MRV will confirm that a membrane was covering that vein and now it has gone. Good thought Cure:)

I'm looking for the Jacob study that is referenced a couple of times in this topic. Could someone provide a link, please?

Thanks!

I can show tubes expanding and closing by introducing salts to a closed loop suspended 2 meters vertically. Salts flow down one side expanding as gravity draws them down and the pressure from the solvent presses the walls out with a clear bulge using silicone soft walled tubing. While the other side (the return flow side caused by the down flow) is drawn in due to the reduction in pressure as the water id dragged up.

This simple tubular experiment can explain the closure and opening of the veins in the body.

For example: If there is very high humidity, the concentration of salts from respiration is hampered as we breath in moisture rather than dryer air. This alters the evaporation rate so on exhaling there is no concentration of dissolved salts and sugars, resulting in no postural assistance to the circulation, which means the heart / pump has to do all of the work, which means the pressure inside the veins becomes positive instead of the normal tension applied to the return venous flow.

Professor Zamboni argued that Inclined Therapy could not return a stenosis back to a normal venous return flow. I thought then that it would be only a matter of time before we have proof that these veins can alternate between stenosis and normal flow and that maintaining an inclined posture could be shown to affect this flow experimentally.

Now, thanks to Prof8 and a few others reporting differences between 2 scan results on the same person, one showing stenosis and the other not. We must investigate the postural / humidity connection further.

Pauline Phelps reported using an inclined bed together with a dehumidifier while sleeping, she would have no dropped foot problem in the morning on rising from her bed. Yet if she used just the angled bed, her dropped foot problem would be present in the morning and remain so throughout the day.

I have written to Dr Francheschi today in relation to his comment about the answer to CCSVI laying with postural therapy.

Will update as and when I get a reply.

Prof8 thank you for sharing this fascinating observation.

Andrew