DrSclafani answers some questions

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

Postby NZer1 » Tue Mar 01, 2011 1:17 am

Hi everyone, Dr S I have been doing a catch up on the thread and I have noticed a commonality that has crossed from Dr. F's thread as well.
The bottom line is in regard to age and the veins themselves. Is it possible that the finding of the Hubbard group where a familiaral trend for vein issues such as the findings in the Hubbard family is part of the picture here. If time and all the other factors that de-generate a vein create a worse 'stenosis' effect, one that exists already but not causing symptoms as they have each got, the valve finding may possibly the last cab on the rank when MS symptoms occur like with Devlin.
By improving the vein flows the outcomes have been so wide in result, that said the best standard and the findings from repeating angio treatment finding incomplete treatments are throwing the data as said earlier as well.
I am at risk of waffling here, sorry.
The bottom line of my drift is that the malformation findings are only relevant because of aging effecting the blood flow.
The article Nunzio translated hints at this, as well as some of the less improved outcomes since treatment. Basically the entire vascular system is challenged by age and inherent issues become life effecting with age and poor health practices and diet may have had the greatest detriment and advanced the disease known to us as MS.
In addition if you throw in a trauma to restrict the blood return for sufficient time you will have the same outcome.
Whip lashes and the other accident related injuries that compress or misalign the vascular system have now been shown to predate an MS type onset.
The other clue to my thinking is Marc's compressed my muscle example, although he would have aged with this situation the impact on flow may have also been age and condition of the vein, which lead to collapse, which may have in relative time been resent.
Basically it seems to me that the valves are a bandage fix that may not be sustained.
The flow testing into and out of the brain repeated over time may be a clue for children at risk, such as Cece's. There could be huge learning from a longitudinal test to see what happens for children showing symptoms that are dismissed by current medical people because of the lack of awareness of blood flow restrictions, reflux and the outcome, fatigue to name one symptom.
Regards Nigel
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Postby drsclafani » Tue Mar 01, 2011 6:38 pm

Nigel

i am having difficulty with your commentary. I have to break it down. Sorry if i am not following your thoughts well

NZer1 wrote:Hi everyone, Dr S I have been doing a catch up on the thread and I have noticed a commonality that has crossed from Dr. F's thread as well.
The bottom line is in regard to age and the veins themselves. Is it possible that the finding of the Hubbard group where a familiaral trend for vein issues such as the findings in the Hubbard family is part of the picture here.


i am not following your drift as it relates to age. That family members have ms is not in dispute but i dont i dont understand how age fits it.

If time and all the other factors that de-generate a vein create a worse 'stenosis' effect, one that exists already but not causing symptoms as they have each got, the valve finding may possibly the last cab on the rank when MS symptoms occur like with Devlin.

if i can interpret: are you suggesting that it is established that age makes these findings worse? I may have seen a trend in that direction but i am not saying that i believe it as proven. it is just my own general gut but i wouldnt be so sure.

By improving the vein flows the outcomes have been so wide in result, that said the best standard and the findings from repeating angio treatment finding incomplete treatments are throwing the data as said earlier as well.

i think that a reason that outcomes vary after the same treatment is that there is a damaged brain at the top of that vein. and people have different plasticity (adaption) to that damage. If age has an effect, it may well be the length of time causing brain and spine damage.

Also we do not yet have good measures about what constitutes a good venographic result. Without that assessment of the treatment, how can we compare the outcomes?
I am at risk of waffling here, sorry.


i gather that

The bottom line of my drift is that the malformation findings are only relevant because of aging effecting the blood flow.

i dont think i agree with that. The malformation findings are relevant because they reduce blood flow, possibly from birth.

The article Nunzio translated hints at this, as well as some of the less improved outcomes since treatment. Basically the entire vascular system is challenged by age and inherent issues become life effecting with age and poor health practices and diet may have had the greatest detriment and advanced the disease known to us as MS.
In addition if you throw in a trauma to restrict the blood return for sufficient time you will have the same outcome.
Whip lashes and the other accident related injuries that compress or misalign the vascular system have now been shown to predate an MS type onset.


that is pretty far afield and seems to link everything in life as causative for MS. That could be true, but its a bit too general for me to comment about.

The other clue to my thinking is Marc's compressed my muscle example, although he would have aged with this situation the impact on flow may have also been age and condition of the vein, which lead to collapse, which may have in relative time been resent.


i dont agree that this is a problem of aging. MS becomes symptomatic most of the time before real aging.

Basically it seems to me that the valves are a bandage fix that may not be sustained.

i am betting my career that treating valvular stenosis and annular stenosis is more than a bandaid.

The flow testing into and out of the brain repeated over time may be a clue for children at risk, such as Cece's. There could be huge learning from a longitudinal test to see what happens for children showing symptoms that are dismissed by current medical people because of the lack of awareness of blood flow restrictions, reflux and the outcome, fatigue to name one symptom.
Regards Nigel


no argument there. IT would be good. but it would be pure research.
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Postby NZer1 » Tue Mar 01, 2011 7:54 pm

Hi Dr, sorry about the communication issues, you should hear me in person. Having a bit trouble with stress and its effect on my MS at the moment, I stutter like a machine gun firing now.
The general drift was to be that the veins are effected by age and the patients looking after them eg, diet, smoking etc etc.
As a person ages the effect of the malformed veins is compounded by the diminishing blood flow because of the aging of the patient as well.

In the Hubbard example the family members all have 'issues' with veins, the member with MS has vein problems that became MS. I am thinking that it was more of an event nearer the time of the symptom onset that is the factor rather than the malformations that have been there all along.
The search for an event or lifestyle happening, or diet, who knows what has tipped the already diminished blood flow into the danger zone for MS.
Regards Nigel
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Postby NZer1 » Tue Mar 01, 2011 8:46 pm

In addition to the above.
The RRMS form has the episodic nature that I think helps understand my drift. The factors for slow flow are tipped by an incident such as a trauma to the neck (maybe whip lash and inflammation) that decreases flow even more than the diminished flow from malformations. Stress also commonly effects PwMSers, it may not be stress to the conductivity of nerves, rather to the blood flows from the stress.
Thought 1.. The pregnancy effects on MS symptoms may have answers due to the increase in vascular flows that overcome decreased flow problems from malformations.
Thought 2.. Temperature effects on the nerves is noted and is it possible that blood flow is challenged even more than the malformation slow flow/ reflux with temperature changes from an external source, (in this example though its a little vague with the effects on thalamus and hypothalamus from lesions and flow restrictions pre existing or after disease onset?.) The blood flow to these parts of the CNS is vital and the low flow from malformed valves could simply be tipped by aging and or trauma?
My thought runs to, is still possible that once the CNS is effected there is a cascade effect each time there is the same effect as age related blood flow restrictions, this on top of malformations in RRMS, eg traumas and stresses that step up the MS damage that has begun from the combination of malformations, aging and previous trauma has another insult to the blood flow capability caused another episodic MS event or RRMS attack. Event upon event = RRMS.
We are assuming that the malformations are the primary cause yet there are other possible explanations, eg aging, wearing out, trauma and so on.
So the flow restrictions are not only malformations, they are also the compounding effect on top of malformations and that angio may improve the situation. The amount of improvement from angio is also about the whole vascular picture noted in Nunzios clip. We don't know what the vascular system would be like without the life time of effects of 1. malformations and 2. the aging, body abuse etc and still within the same body (best case scenario).
Turning an unhealthy situation into an MS "stopped" situation may take years of a multi-disciplined approach?
Its almost like the way angio treatment for heart problems (blockages?) is not going to fix issues caused by poor diet, aging and exercise.
Regards Nigel
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Postby Algis » Wed Mar 02, 2011 8:15 am

Doctor: again a wild thought over here:

If blood clotting is leaving markers in the blood; would it be thinkable of a device as people use to monitor sugar-levels in their blood? i.e.: a little quick puncture on the tip of a finger and a result on a small probe inserted?

That could screen candidates?
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anti-restenosis drug coated balloons?

Postby ThisIsMA » Wed Mar 02, 2011 2:09 pm

Hi Dr. Sclafani,

I recently read a reference to using in-vein radiation (I'm sure I'm not using the proper medical term) to prevent coronary artery restenosis. In the process of reading more about that on the web, I came across an article on using drug-coated balloons to prevent restenosis.

Then I found one such balloon that is already on the market. Here is a press release from the balloon manufacturer about the introduction of this balloon:

http://www.biotronik.com/portal/19898/? ... &pid=25913

“We are confident that the Pantera Lux is a solid alternative for in-stent restenosis and possibly for other indications that physicians struggle with where the placement of a permanent device is not optimal.”


And here is a link to an advertisement for this balloon (don't worry, I have no ties to the medical device-making sector!):

http://www.biotronik.de/en/za/24250

Would this balloon or one similar (if there are others out there) be useful in preventing restenosis in CCSVI treatment?

Here is a quote from a more general article on the concept of drug coated balloons to prevent restenosis:

http://www.touchneurology.com/articles/ ... ortunities

Results from several pre-clinical and clinical studies indicate that short-term exposure of injured arteries to paclitaxel delivered from regular angioplasty balloons may be sufficient to reduce late lumen loss and restenosis rates during a critical period of time after the angioplasty of diseased coronary and peripheral arteries. Although the number of published trials and patients treated is still limited, data available seem to prove that restenosis inhibition by immediate drug release is feasible.


I know arteries are quite different from veins. But I am hoping that intimal hyperplasia in a vein and in an artery might have the same cause, and therefore could be prevented by the same treatment? The drug used in the balloon is an anti-cancer drug that limits cell overgrowth.

I would definitely pay more for the use of a drug-coated balloon in a first CCSVI treatment, if there were a reasonable chance it could prevent restenosis. I'm one of those people whose health insurance won't cover CCSVI, and who can't afford to pay for more than one treatment.

Thank you so much for all the amazing work you do!

Mary Ann
DX 6-09 RRMS
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Postby newlywed4ever » Wed Mar 02, 2011 7:58 pm

Since I have a LIJV that is occluded due to 1) scar tissue, 2) blood clot or 3) first angio was not actually in the IJV, I am wondering... does it make any sense to balloon maybe one of the larger collaterals if the IJV can't be treated?
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Postby Cece » Wed Mar 02, 2011 8:12 pm

That's an interesting question. If a hypoplastic vein can be matured, why not a regular vein, even if it wasn't originally the IJV?
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Postby sou » Thu Mar 03, 2011 6:39 am

<deleted -- accidentally posted several times>
Last edited by sou on Thu Mar 03, 2011 7:45 am, edited 1 time in total.
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Postby sou » Thu Mar 03, 2011 6:41 am

<deleted -- accidentally posted several times>
Last edited by sou on Thu Mar 03, 2011 7:45 am, edited 1 time in total.
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Postby sou » Thu Mar 03, 2011 6:53 am

<deleted -- accidentally posted several times>
Last edited by sou on Thu Mar 03, 2011 7:43 am, edited 1 time in total.
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Postby drsclafani » Thu Mar 03, 2011 7:23 am

Algis wrote:Doctor: again a wild thought over here:

If blood clotting is leaving markers in the blood; would it be thinkable of a device as people use to monitor sugar-levels in their blood? i.e.: a little quick puncture on the tip of a finger and a result on a small probe inserted?

That could screen candidates?


algis
you are always thinking outside the box!

A d-dimer screening tool?
interesting

all we need now is clinical need, enough patients needing, a venture capitalist willing to invest, a research lab and a research team, and a willing public
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Postby sou » Thu Mar 03, 2011 7:42 am

Perhaps this is a question for sonographers, but anyway, I shall ask:

Supposing a patient has only azygos (or hemiazygos) stenosis/membranes/etc, what is the sonographic evidence that an ultrasound examination may provide? Can these people be erroneously diagnosed as "healthy"?
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Re: anti-restenosis drug coated balloons?

Postby drsclafani » Thu Mar 03, 2011 7:57 am

ThisIsMA wrote:Hi Dr. Sclafani,

I recently read a reference to using in-vein radiation (I'm sure I'm not using the proper medical term) to prevent coronary artery restenosis. In the process of reading more about that on the web, I came across an article on using drug-coated balloons to prevent restenosis.

Then I found one such balloon that is already on the market. Here is a press release from the balloon manufacturer about the introduction of this balloon:

http://www.biotronik.com/portal/19898/? ... &pid=25913

“We are confident that the Pantera Lux is a solid alternative for in-stent restenosis and possibly for other indications that physicians struggle with where the placement of a permanent device is not optimal.”


And here is a link to an advertisement for this balloon (don't worry, I have no ties to the medical device-making sector!):

http://www.biotronik.de/en/za/24250

Would this balloon or one similar (if there are others out there) be useful in preventing restenosis in CCSVI treatment?

Here is a quote from a more general article on the concept of drug coated balloons to prevent restenosis:

http://www.touchneurology.com/articles/ ... ortunities

Results from several pre-clinical and clinical studies indicate that short-term exposure of injured arteries to paclitaxel delivered from regular angioplasty balloons may be sufficient to reduce late lumen loss and restenosis rates during a critical period of time after the angioplasty of diseased coronary and peripheral arteries. Although the number of published trials and patients treated is still limited, data available seem to prove that restenosis inhibition by immediate drug release is feasible.


I know arteries are quite different from veins. But I am hoping that intimal hyperplasia in a vein and in an artery might have the same cause, and therefore could be prevented by the same treatment? The drug used in the balloon is an anti-cancer drug that limits cell overgrowth.

I would definitely pay more for the use of a drug-coated balloon in a first CCSVI treatment, if there were a reasonable chance it could prevent restenosis. I'm one of those people whose health insurance won't cover CCSVI, and who can't afford to pay for more than one treatment.

Thank you so much for all the amazing work you do!

Mary Ann


MA
you certainly have done your homework. Yes, inhibition of intimal hyperplasia wither by coating the balloon or the stent has promise and we look forward to progress in this regard. the company you mention is a european one and we are several years away from such devices here in the US. but demand directs research and the use of stents in the doronary arteries is the primary focus of this research and where the funding is directed. Those blood vessels are in the range of 2-4 mm,, well below the diameter of the jugular veins. So when these devices are approved by the FDA they will be indicated for coronary work. Alas, they will be too small to use in the IJVs as an off label device and we will have to prove to FDA that they have value in the IJVs for PsMS. Hoperfuly by then we will have proved that venoplasty with and without stenting has value.

in the meantime, we need to focus on other techniques of treating without stents and other techniques of reducing intimal hyperplasia when stents are used.
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Postby drsclafani » Thu Mar 03, 2011 8:00 am

newlywed4ever wrote:Since I have a LIJV that is occluded due to 1) scar tissue, 2) blood clot or 3) first angio was not actually in the IJV, I am wondering... does it make any sense to balloon maybe one of the larger collaterals if the IJV can't be treated?


if they are stenotic, it might make sense to improve the collateral veins. this is the reason for looking for the may thurner syndrome as an alternative pathway for drainage in the presence of azygous stenosis.

IT might make sense to look at your vertebral veins the next time you undergo venography.

But remember that the vertebral veins are small and vulnerable. the external jugular veins may also be collaterals but there are so many of them it would be quite challenging to figure this out.
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