DrSclafani answers some questions

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

Postby Cece » Sat Nov 06, 2010 8:15 am

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

We already were (or at least I was); he writes an incredibly good blog.
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Postby NZer1 » Sat Nov 06, 2010 11:19 am

Thanks Dr. the valves make more sense to me now, I was approaching the problem by looking at how to 'fix' it rather than cure the cause of the problem. So the valves are there to stop reverse flow from the heart beating lower down the vein (the on off effect from blood being taken into the heart?), rather than the reverse flow from a restriction in a vein?
Is it possible that the reflux/back flow has a hydraulicking effect because of the pulsing of blood flow?
I am trying to get my head around the way lesions come and go and how they are spread around the brain?
My thought was that waste and de-oxygenated blood could be circulated around the brain because of reflux in no or low pressure, gravity draining areas around the brain, because of this pumping effect.
In situations where there is muscle pinching of veins the amount of restriction would change with muscle use would it not?
Some muscles would be in 'use' and block veins because of its position/posture and that would change its severity of restriction on the vein as the muscle flexes?
Does the BBB breach originating in the clevical spinal cord and then the CSF pumping the breached content around the brain make sense to you?
Again I am trying to find answers to why the RRMS form happens, when the 'truest' form of the disease PPMS is about progression in a less episodic fashion. In the RRMS BBB first breaches then inflammation responds, this seems to happening like the glutamate cascade effect in Strokes, and the disease still has the underlying continuous nature of PPMS. So finding the cause of the RRMS breach would be of value in understanding what is happening to trigger the immune system.
Is it possible that lesions in the vein walls (passages) could 'grow' through to the CSF space and cause the BBB breach?
Thanks Dr. :lol:
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Postby Cece » Sat Nov 06, 2010 2:41 pm

:)
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Postby marcstck » Sat Nov 06, 2010 7:57 pm

Dr. Sclafani, feel free to discuss my case (at least the vascular aspects of it) here on the boards. I've been open about my condition on my blog, so no reason to keep anything hidden here. Sorry if my posts regarding my atypical condition were too public. I can see how such strangeness could confuse the bigger issues being discussed here. I probably should have been more circumspect in my postings.

Also, sorry if some of my assertions regarding reflux and states of stenosis were misguided. Perhaps I'm doing too much thinking, the subject of CCSVI is becoming a more multifaceted subject by the day. It's endlessly fascinating…

As for further review of my case, I'd much prefer to do it in person or via telephone than online. Too many nuances lost when resorting to merely the written word. I understand my vascular issues could go beyond the muscle bundle problem. That one is so darned strange, and seemingly without easy answers, that it keeps me up at night…
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Postby marcstck » Sat Nov 06, 2010 9:24 pm

North52 wrote:
marcstck wrote:
North52 wrote:
marcstck wrote: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.



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


North,

SPMS and PPMS both are notably absent of enhancing lesions, and thus active inflammation. In fact, the lack of inflammation is one of the hallmarks of the progressive forms of the disease, which is why the existing therapies (all anti-inflammatory and/or immuno suppressive in nature) are generally useless in progressive patients. There may still be some underlying systemic inflammation ongoing, but the acute inflammation seen in RRMS is completely absent.

Despite this lack of inflammation, the decline in neurologic function tells of continued nerve damage and death, the mechanism of which continues to be a mystery.

I suppose hypoperfusion could explain an ongoing progression of disability, but why then the dramatic decrease in inflammation when RRMS transitions to SPMS? And why no stage of active inflammation at all in PPMS patients?

I'm also quite certain that patients experiencing plateaus have not run out of tissue to be destroyed. There's plenty of white and gray matter to keep the disease busy for quite some time (limited ultimately by the demise of the patient, caused either by the disease itself or its complications).

Needless to say, there are many questions that need to be answered, both about CCSVI, and MS in general. Hopefully, the investigations into CCSVI will shed light into the many knowledge gaps regarding MS.
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Postby drsclafani » Sat Nov 06, 2010 10:07 pm

marcstck wrote:I misstated in my previous post. I should have said most IRS are treating every stenosis they see, not stenting. There is definitely a lot more ballooning than stenting going on. I'll actually go back and change that through the edit function now.


Marc
i do not know how you can be saying this. There are no data.
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Postby eyesclosed » Sat Nov 06, 2010 10:08 pm

Dr Sclafani,

Thank you so much for the time you spend here!

I went to Barrie Vascular Imaging and I was wondering if you could help me interpret my result.

Findings:

Right and Left (both have exactly the same result)

“The cerebral venous outflow appears patent with no evidence of venous thrombosis. Venous insufficiency was evident with reflux in the internal jugular vein at 0 and 90 degrees. The cross sectional area of the internal jugular vein at 90 degrees is larger than the cross sectional area at 0 degrees resulting in negative delta .”

Conclusion:

“Venous reflux\insufficiency is noted in the internal jugular veins on the right and left at 0 and 90 degrees. Positive values for cross sectional area of the internal jugular veins on the right and left.
Criteria met for CCSVI: 2\5. This is interpreted as an abnormal study“

I know I met the criteria for CCSVi (2\5). However, I am not sure why I have reflux in my internal jugular veins if my veins are open. Essentially, could you please explain this part of the result “the cross sectional area of the internal jugular vein at 90 degrees is larger than the cross sectional area at 0 degree resulting in negative delta (positive result)?”
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Postby drsclafani » Sat Nov 06, 2010 10:18 pm

sbr487 wrote:Dr. S,

The positional statement of SIR came out sometime back. It was then endorsed by the Canadian SIR. How exactly is the SIR hierarchy organized? Does the statement issued by SIR mean that in general there is a consencus around the world on this? Does this need to be carried to local SIR's?

Just trying to understand ...

The SIR is the society of interventional radiologists of the united states. there are international members but the society is the leading organization of american IRs. The society works with other societies but this position paper was developed by the research arm of the society. This is not a world view.
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Postby drsclafani » Sat Nov 06, 2010 10:37 pm

Cece wrote:I would think another way for CCSVI to do damage without causing reflux is if the obstructions slow down the flow of blood, reducing the cerebral perfusion of the brain, which is known in MS to be reduced.
possible.

To demolish my earlier point, if an obstruction is low enough down, leaky walls in the collateral or near the obstruction shouldn't matter much, since it wouldn't be leaking onto brain tissue. Hmm.

the collaterals are a sum of flow and conduit capacity. its not like there is one collateral

A question of my own: in CCSVI, why might a jugular have an abnormally high flow velocity?

velocity increases as flow passes a point of obstruction
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Postby marcstck » Sat Nov 06, 2010 10:38 pm

drsclafani wrote:
marcstck wrote:I misstated in my previous post. I should have said most IRS are treating every stenosis they see, not stenting. There is definitely a lot more ballooning than stenting going on. I'll actually go back and change that through the edit function now.


Marc
i do not know how you can be saying this. There are no data.


Dr. S, your absolutely correct, there is no data. Guess I'm guilty of being swayed by lots of anecdotal reports, and the fact that we are starting to see many docs treating (outside of the US) with apparently little or no experience with the procedure. I've heard some (again, strictly anecdotal) disturbing reports out of some of the more recently opened foreign clinics. I made a gross generalization, lumping the good with the bad. Mea culpa.
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Postby fogdweller » Sun Nov 07, 2010 11:41 am

drsclafani wrote:
marcstck wrote:I misstated in my previous post. I should have said most IRS are treating every stenosis they see, not stenting. There is definitely a lot more ballooning than stenting going on. I'll actually go back and change that through the edit function now.


Marc
i do not know how you can be saying this. There are no data.


Any word on when your IRB might allow studies to proceed? Other groups you know of about to go forward? I know you have said that you would telll us when there was something to tell us, but you are on the inside ins some groups and might have some info.
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Postby Drury » Sun Nov 07, 2010 8:19 pm

Dr. Sclafani,

My daughter had a call to schedule a Doppler with Dr. Mandatto at Siskin's office. She had an MRV in August and was told there was no stenosis but that they were not able to see the Azygos properly. Also said she may have reflux but not sure what could be done about it and he basically would have left it at that had we not asked about the Doppler, etc.

Would you suggest she go ahead and have the Doppler? She is on your waiting list and we live in hopes............?

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ccsvi

Postby blossom » Sun Nov 07, 2010 8:30 pm

dr.sclafani, this question may have been answered somewhere already. ?
after angioplasty only how long should i be concerned about clots developing or scar tissue. i know people can get restenosis probably anytime and if so does it seem the restenosis is worse or has that been established?

i got a reg. doppler done here in my hometown "not zambonni type" they say no clots and i have flow. this was done two mo. after procedure as i was concerned because i got a numb leg immediatly after procedure and still persist. any very small improvements have gone. except, a persistent pain that when in bed it would go up the back of my head very often. about 5 days after procedure it was very severe for just a short time and i have not had it since.

anyway, how long should i be concerned? and if i would pursue this again does it look like there are things coming up that will reduce these risks?

it has been 3 mo. since procedure and i actually feel worse and symptoms are worsening.

i had emergency appendix surgery oct 2 and i know it knocked me for a loop too.
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Postby malden » Mon Nov 08, 2010 1:23 am

drsclafani wrote:
A question of my own: in CCSVI, why might a jugular have an abnormally high flow velocity?

velocity increases as flow passes a point of obstruction

Velocity increases after obstruction/narrowing/stenosis?

Then it must be some other case from this basic cardiovascular physiology concept:
http://www.cvphysiology.com/Hemodynamics/H012.htm

Image
" ...
Kinetic energy and pressure energy can be interconverted so that total energy remains unchanged. This is the basis of Bernoulli's Principle. This principle can be illustrated by a blood vessel that is suddenly narrowed then returned to its normal diameter. In the narrowed region, the velocity increases as the diameter decreases (V ∝ 1/D2). If the diameter is reduced by one-half in the region of the stenosis, the velocity increases 4-fold. Because KE ∝ V2, the KE increases 16-fold. If the total energy is conserved, then the 16-fold increase in KE must result in a proportionate decrease in PE. Once past the narrowed segment, the KE and PE will revert back to their original values because the diameter is the same as before the narrowed segment. This simplistic model assumes that there is no loss of total energy along the length of the vessel. In fact, there will be some loss of total energy and pressure (as indicated in the figure) because of the high resistance in the narrowed region and because of turbulence that occurs distal to the narrowed region. To summarize this concept, blood flowing at higher velocities has a higher ratio of kinetic energy to potential (pressure) energy.
... "

Best regards, M.
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Postby fernando » Mon Nov 08, 2010 5:37 am

Malden,

I don't see a contradiction

Dr. S said:

"velocity increases as flow passes a point of obstruction"

You misquoted :

"Velocity increases after obstruction/narrowing/stenosis? "

In fact, the info you posted confirms Dr. S explanation.
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