This Is MS Multiple Sclerosis Community: Knowledge & Support

Sorry, Dr. S....don't mean to blab on your thread, but this hypoperfusion issue is near and dear to me....



Actually, not true, Marc. A reduction in bloodflow, hypoperfusion and low O2 could create demylinating lesions. No need for reflux. People who suffer from diffuse cerebral hypoxia due to low O2 can have demyelination in the brain. It's called delayed cerebral hypoxic demyelination--happens to mountain climbers, divers, folks poisoned by CO2. This is why I continue to urge the doctors to test O2 levels pre and post angioplasty, and why Dr. Haacke is doing just that. I believe Jeff falls into the category of pwMS who had low cerebral O2 levels due to hypoperfusion and CCSVI. He came home from a week at high altitude and soon had an MS diagnosis and seven enhancing lesions. Granted, this is not everyone.

http://neuro.psychiatryonline.org/cgi/c ... l/20/4/473

Hypoperfusion and white matter lesions in rats-
http://www.ncbi.nlm.nih.gov/pubmed/11743996


link

There are many, many discussions on this slowed blood flow detected in MS brains, called hypoperfusion, fogdweller--this has been a very important part of the puzzle--
Here's a good one:
http://www.thisisms.com/ftopict-7708-hypoperfusion.html

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

Dear Marc,

You suggest that "reflux is a key component to the CCSVI hypothesis, in that it explains the breakdown in the blood brain barrier" I really cannot see how reflux can logically break down the blood brain barrier. Reflux is seen in the larger veins using doppper ultrasound. The blood brain barrier, however, is present at the level of much smaller vessels, the capillaries and venules. I have never seen any evidence that reflux occurs at this level and would have a hard time imagining that it would.

There is good evidence that there this hypoperfusion or reduced blood flow in MS brains. You suggest that a simple reduction in blood flow cannot explain the inflammatory reaction that ensues. I would disagree with you here. I would like to propose a mechanism by which this can happen. Slow blood flow results in ischemia and activation of the coagualation cascade with production of fibrin. It is the ischemia and fibrin production that results in the breakdown of the blood brain barrier, compromise of CNS tissue and infilitration of T-lymphocytes. There is good supporting evidence for this type of hypothesis. For a more detailed description of this and supporting evidence for this hypothesis, I will refer you to my next posting "Microvascular Hypercoagulability Model for MS" The first 8 point of this hypothesis are key. What follows is somewhat technical. I also came across a paper that summarizes this process very well: http://www.ncbi.nlm.nih.gov/pubmed/18045138

North

thanks for that, cheer. As I said, I've no doubt that hypoperfusion can cause damage to the CNS, but the papers you cite do not explain the infiltration of immune cells through the BBB. If CCSVI is THE cause of MS, the breakdown of the BBB must be explained by the hypothesis.

My particular case could be the poster child for the fact that hypoperfusion can cause CNS damage, but not immune penetration of the CNS. I definitely have a blockage in my RIJV, caused by a muscle bundle pinching it significantly. My "atypical" presentation of MS is atypical precisely because I've never shown any sign of immune system infiltration into my CNS. No O-bands, no inflammatory lesions, just one big honking lesion that doesn't enhance at the base of my brainstem.

It's for these reasons that my CCSVI dubious neurologist is willing to entertain the notion that my blocked RIJV may indeed play a big part in the pathogenesis of my disease. These very same reasons are cited by the NIH in a determination that I very likely do not suffer from MS.

_________________
Marc
www.wheelchairkamikaze.com

How about:


http://www.medical-hypotheses.com/artic ... 4/abstract

It's the adhesion molecules.

Thanks, North, that's a very interesting hypothesis that appears to have a very substantial basis in fact.

However, much of the discussions surrounding CCSVI have included the notion that the reversal of blood flow through the major vessels does indeed contribute to a breakdown of the BBB. Many pages of discussion on this very forum were spent on this issue in the months before CCSVI hit the mainstream.

If indeed hypoperfusion does result in the breakdown of the BBB, why would the inflammation seen in the relapsing remitting stages of the disease subside after a number of years, as is seen when the disease enters its SPMS phase? Logic would seem to dictate that the continued effects of hypoperfusion would lead to an increase in inflammation, rather than the eventual elimination of it.

As I have stated numerous times before, I do believe that CCSVI plays a significant role in the MS disease process, but I do find certain deficiencies in the hypothesis that lead me to question the idea that CCSVI is a primary cause of what we call MS.

_________________
Marc
www.wheelchairkamikaze.com

very interesting, thanks for that…

_________________
Marc
www.wheelchairkamikaze.com

editing

Dr. Sclafani,
I recently ran across the following pdf PowerPoint presentation that discusses the incidence of stent fracture in the superficial femoral artery (SFA).

Stent Fractures in the SFA - Scheinert.pdf

I know that you are personally against the use of stents in the jugular veins of MS patients. I also know that several doctors are currently using stents and that many patients that have been treated for CCSVI have received stents. Some of these patients have had complications with in-stent stenosis either due to intimal hyperplasia or due to thrombosis. However, one thing that I haven't seen addressed is the expected lifetime of such stents in the jugular vein. The presentation discusses several types of stresses which could lead to fracture and some of these stresses might be found in the jugular vein. For example, axial compression of the stent might occur when one raises or lowers their head in a nodding motion and torsional strain on the stent might occur when one turns their head to look to the side. I realize that many of the stents that have been used in the jugular veins are shorter than the ones discussed for the SFA, however, the presentation still reports a fracture rate of 13.2% for stents shorter than 8 cm. My question is should patients be concerned about stent fracture in stents used for jugular veins? It is still very early in the history of stent use in jugular veins, but could such failures become more common in the not too distant future? Is the possiblity of stent fracture a reason to avoid stents in the jugular veins? The patency rate of Nitinol Smart stents reported in the presentation at only 60% after just 1 year is not very encouraging. Moreover, the patency rate of fractured stents after 20 months is also disturbingly low (around 10%).

Thanks in advance for your response, NHE

]

Marc, while it is acceptable for you to discuss publicly your condition, It is not acceptable for me to do so (which i would love to do) without your explicit permission. It would be a HIPPA violation. So, let me know and we can discuss your blockages on this site. Let's just say that i disagree with your synopsis of your condition and leave it at that for the moment. At the very least, you and I have to have another review of your case to clarify some issues. We can do that in person or on line privately if you wish


in other words you are saying cause without effect is not important. Sort of like the tree falling in a forest with no one to hear it fall. Theoretically I can agree with that. HOwever, if we are finding outflow obstructions (i would rather use this all encompassing term rather than stenosis) predominantly in symptomatic patients, I would consider it a problem leading to another problem.



I lost your logic there. Dr Sinan is not dilating obstructed veins in patients without symptoms...thus an indication to treat outflow obstructions is symptomatic patients. Moreover, i believe that Dr Sinan is testing for CCSVI by ultrasound, is he not? Does that not indicate that he is looking for outflow obstructions in patients who DO have evidence of reflux. So I would not think that looking for outflow obstructions by "compliant balloon inflation" is overkill. Remember these malformations are not easily visible on venography because the septations might isolate areas of the vein from the contrast media column.


Marc, the statement, that some of these stenoses have negligible impact on blood flow, is unfounded. While it might be true, the statement is not based upon fact.

I think we have to take these internet accounts with a grain of salt. We are unclear from these accounts what stenoses were present, what the logic was for the IR to do the angioplasty, what flow looked like on the live fluoroscopy images, and many more considerations .


I wish i could tell you what degree of narrowing results in significant blood flow disturbance, but i cannot yet. In many circumstances, that narrowing is rather dynamic actually. Veins are highly compliant, in essence that have great capacities to distend or collapse depending upon blood flow. When the vein is less compliant, as happens in CCSVI, the capacity to distend may be reduced. Also if there is an outflow obstruction, blood flow is diverted to paths of less resistance, so the normal parts of the vein might not distend as much. So the % of narrowing (diameter or area the narrowed segment divided by the diameter or area of the normal vein) might be a gross underestimation.

Furthermore, the veins are low pressure systems. while 70% stenosis is considered significant in an artery, smaller percentages of narrowing are significant in veins because the pressure driving blood across the narrowing is so much lower.



Marc, that muscle is something that is a special case. I dont want to speak about it here, without your permission.

I am inclined to treat stenoses in the 30% range, but this might not be aggressive enough. of course other factors, such as turbulence, collaterals,symptoms, progression of disease, etc will factor into that decision.



you are never off the marc

Dear Marc,

I will take stab at this. Is there really less inflammation in the SPMS phase? In SPMS patients with continued progressive worsening, I would suspect continued hypoperfusion and inflammation. Some patients do plateau, however. In these patients, I suspect inflammation may have subsided as all the tissue that could be destroyed has been destroyed. Why have inflammation if there is no more viable tissue? The underlying hypoperfusion would still, however, be present.

North

ok, now I know for certain I have not only restenosed but my vein is a lot worse. I am pm'ing you Dr.

Just a note to point out to those reading that even if you are treated and see no symptomatic benefits, you STILL should have followup because your vein(s) may protest by getting worse, and ms symptoms can become worse.

i think i answered this above.

it is difficult to interpret such reports. sometimes the doppler ultrasound is done and interpreted incorrectly for ccsvi. other times the report is interpreted incorrectly by patients.

write your report accurately on here and we can have a look at it together, if you would like

marc
you have the entire world of ms now wondering about your condition.

yes, we need more evidence