DrSclafani answers some questions

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Re: DrSclafani answers some questions

Postby Cece » Thu Dec 01, 2011 7:46 am

drsclafani wrote:Cece
large emissary veins does not prove hypoplasia of J3. obstruction of the more common J1 valve stenoses can also provide a good reason for the persistence of the condular veins.

so my analysis of the condylar veins as discussed was related to trying to differentiate a narrowing of the J3 segment caused hypoplasia from a narrowing caused by a stenosis.

Yes, and it's a brilliant way to distinguish between the two (hypoplastic J3 vs recanalized J3), especially if knowing which one you are looking at will affect treatment choices.
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Re: DrSclafani answers some questions

Postby drsclafani » Thu Dec 01, 2011 8:32 pm

NZer1 wrote:Dr. is it likely that flow rates from all exiting veins (at the point of exit) is the key rather than looking for slow flow areas once the flow has exited. If it isn't getting in or through then what comes out is "so what".
The brain internal flow is known to be different in PwMS, the reason is not.

In my mind looking at this as a plumber would, you have to know what you are starting with before you can expect or improve the outflow?

After that time there would be reason to look at back flows etc.

If it ain't going in, it ain't coming out and when it does it has issues as well?

Regards Nigel


Nigel, if i understand your comments, you are saying that inflow is just as important as outflow. I would agree, even assert that inflow is more important than outflow. If there is no inflow, there is no life.

but it appears to me that the carotid arteries, ie major inflows are not as commonly affected in MS as are the major outflows
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Re: DrSclafani answers some questions

Postby NZer1 » Fri Dec 02, 2011 12:23 am

Thanks, I have the opinion from reading, that there are many abnormalities that congenital malformations will create.

So from that I assume that we need to be looking at the whole picture in these studies.
If it is said that PwMS have a larger amount of blood within the brain we need to know why, what etc?

Is it simply a flow issue or is it something greater than our minds assume at present?

If the brain/skull holds more fluid, what is the 'extra' fluid?

Is it as much about CSF?

Is the added fluid creating the symptoms?

If the added fluid is moved on from PTA treatment and the symptoms also change, and then retuen is it the total fluid of the brain the reason or the flow changes from the PTA?

Get my drift?

The flow is obviously an issue, and changing the pattern is having an effect, is that the answer or is it more about about what Trev T and others are saying that the capillary bed that it is the focus point. The flow from PTA is part of the 'cause/cure' "and" there is more to learn about why the PTA changes symptoms?

We need to know, as you are obviously looking at, what is changing with PTA, and who can confirm the theories.

Thanks Dr,
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Re: DrSclafani answers some questions

Postby drsclafani » Sat Dec 03, 2011 5:24 am

I was asked a question on my facebook account (WWW.FACEBOOK.COM/SAL.SCLAFANI.MD). I answered it there, but don't want to ignore those who read my answers to questions on tims. so i will copy and paste it here.

The question asked my thoughts about thrombosis of the jugular vein that extended into the brain. My answer is as follows:

This is a really complex question and i cannot give anything more than general thoughts

First, I would clarify that the jugular vein does not go into the brain. There are deep cerebral and cortical veins that drain into the dural sinuses. The dural sinuses are the intracranial venous outflow pathways into the jugular vein. So I would suggest that you mean occlusion up into the cranium or skull.

Then I would be skeptical and want to know how that diagnosis was made. Lots of silly diagnoses out there. So I would explore. CTV (or perhaps, depending upon local culture, equipment and expertise, MRV) would be useful to assess whether the dural sinuses were hypoplastic or filled with thrombus.

Then,it would depend upon symptoms. If clinically warranted, I would refer my patient to an interventional neuroradiologist. These IRs specialize in neurological disease treatment, notably intracranial treatments such as embolization and occlusion of intracranial aneurysms and arteriovenous malformations that cause intracranial hemorrhage, thrombolysis of thrombotic emboli to intracranial arteries that cause strokes. The specialized training for intracranial work is beyond the expertise of many IRs.

When I was exploring whether to involve myself with CCSVI, I did my due diligence and found a paper that described two patients who had relatively acute thrombosis of dural sinuses. The patients had pretty severe symptoms: more somnolence, confusion and headaches than that usually experienced in CCSVI. The authors put a catheter up into the dural sinuses through the opposite internal jugular vein and and infused thrombolytic medications that dissolved the clot. They also dissolved the clot in the internal jugular vein. When the clot dissolved, guess what they saw? Yep, a stenosis of the jugular vein at the confluens with the subclavian vein where we typically see stenoses in CCSVI. After angioplasty the patients had good clinical improvement.

I hope that this rather general answer to your question has helped you. If you would like a more personal discussion, send me an email at ccsviliberation@gmail.com.
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Re: DrSclafani answers some questions

Postby Cece » Sun Dec 04, 2011 10:44 am

I wanted to mention before I forgot: in your webcast presentation at the Global Expo, you mentioned the belief that some patients have that CCSVI means they may have venous insufficiency in the legs or elsewhere in the body, and you expressed skepticism at such a connection.

I have been skeptical too but what I see is this: patients with MS are not fully exploring all non-MS solutions to their health issues. We might have symptoms in our legs that we write off as MS symptoms. Even in the absence of a connection between CCSVI and chronic vascular insufficiency in the legs, if we have symptoms of the latter, we should seek treatment. Access to care is irrelevant if we don't get ourselves out there and access the care....
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Re: DrSclafani answers some questions

Postby dania » Sun Dec 04, 2011 11:00 am

Cece wrote:I wanted to mention before I forgot: in your webcast presentation at the Global Expo, you mentioned the belief that some patients have that CCSVI means they may have venous insufficiency in the legs or elsewhere in the body, and you expressed skepticism at such a connection.

I have been skeptical too but what I see is this: patients with MS are not fully exploring all non-MS solutions to their health issues. We might have symptoms in our legs that we write off as MS symptoms. Even in the absence of a connection between CCSVI and chronic vascular insufficiency in the legs, if we have symptoms of the latter, we should seek treatment. Access to care is irrelevant if we don't get ourselves out there and access the care....



With both angioplasties my swollen purple/red foot was 100% normal 5 hours afterwards. And when I restenosed swelling and purple/red colour returned. So, for me there is definitely a connection. How and why I do not know but there is a connection. So many of us report their feet returning to a normal state after the blood is flowing. Swelling disappearing and normal colouring.
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Re: DrSclafani answers some questions

Postby munchkin » Sun Dec 04, 2011 11:08 am

Dr. S

Have you heard of the Turbo Laser that they are using in Briton for arteries? Is this something that might be used for those of us with scar tissue from ballooning? Would you consider using a tool of this nature?

Thank you.
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Re: DrSclafani answers some questions

Postby drsclafani » Sun Dec 04, 2011 9:56 pm

dania wrote:
Cece wrote:I wanted to mention before I forgot: in your webcast presentation at the Global Expo, you mentioned the belief that some patients have that CCSVI means they may have venous insufficiency in the legs or elsewhere in the body, and you expressed skepticism at such a connection.

I have been skeptical too but what I see is this: patients with MS are not fully exploring all non-MS solutions to their health issues. We might have symptoms in our legs that we write off as MS symptoms. Even in the absence of a connection between CCSVI and chronic vascular insufficiency in the legs, if we have symptoms of the latter, we should seek treatment. Access to care is irrelevant if we don't get ourselves out there and access the care....



With both angioplasties my swollen purple/red foot was 100% normal 5 hours afterwards. And when I restenosed swelling and purple/red colour returned. So, for me there is definitely a connection. How and why I do not know but there is a connection. So many of us report their feet returning to a normal state after the blood is flowing. Swelling disappearing and normal colouring.


Dania, my own assessment is that treating CCSVI does something positive for autonomic function. That autonomic function results in improvement vasomotor tone. Also if muscle function is improved, dependent edema may also be improved as muscle function drives blood that has pooled up the legs.

IO want to be clear, I do not discount any symptoms patients may have ESPECIALLY if i cannot explain it. I do have skepticism that the incidence of peripheral venous disease is significantly higher than the general population. I just do not think there will be an association between CCSVI and peripheral venous insufficiency.

be well
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Re: DrSclafani answers some questions

Postby drsclafani » Sun Dec 04, 2011 10:06 pm

munchkin wrote:Dr. S

Have you heard of the Turbo Laser that they are using in Briton for arteries? Is this something that might be used for those of us with scar tissue from ballooning? Would you consider using a tool of this nature?

Thank you.

These lasers can be very useful, although i am concerned about errant direction of the laser energy. The jugular vein is very intimately adjacent to the carotid artery and the inominate artery. I am concerned about injury to those arteries should the energy be misapplied.

I am exploring this but to date have tried to reopen closed jugular veins via a rendevous procedure. I am successful about 50% of the time. I might consider this laser treatment in those that fail. But the thrombosed jugular is a bugger.
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Re: DrSclafani answers some questions

Postby NZer1 » Sun Dec 04, 2011 11:27 pm

http://chiarione.org/symptoms.html

Anyone relate to this symptom list?

And my point is that we need to be clear on what is causing our symptoms and not to expect PTA to fix the package we hold. We may have both CM1 and CCSVI.

If we are NOT well dx'ed the data coming from PTA treatment may also not be accurate!!!!!!!!!!!!!!!!!!!

It may be that the Haacke protocol is as much about the wide range of exclusions that these Neurological diseases have.

And many of us will have multiple diseases.

Are the Neurologists up to the task? Do they have the commitment to partner this search?

Regards Nigel
Last edited by NZer1 on Mon Dec 05, 2011 12:09 pm, edited 1 time in total.
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Re: DrSclafani answers some questions

Postby dania » Sun Dec 04, 2011 11:54 pm

drsclafani wrote:
dania wrote:
Cece wrote:I wanted to mention before I forgot: in your webcast presentation at the Global Expo, you mentioned the belief that some patients have that CCSVI means they may have venous insufficiency in the legs or elsewhere in the body, and you expressed skepticism at such a connection.

I have been skeptical too but what I see is this: patients with MS are not fully exploring all non-MS solutions to their health issues. We might have symptoms in our legs that we write off as MS symptoms. Even in the absence of a connection between CCSVI and chronic vascular insufficiency in the legs, if we have symptoms of the latter, we should seek treatment. Access to care is irrelevant if we don't get ourselves out there and access the care....



With both angioplasties my swollen purple/red foot was 100% normal 5 hours afterwards. And when I restenosed swelling and purple/red colour returned. So, for me there is definitely a connection. How and why I do not know but there is a connection. So many of us report their feet returning to a normal state after the blood is flowing. Swelling disappearing and normal colouring.


Dania, my own assessment is that treating CCSVI does something positive for autonomic function. That autonomic function results in improvement vasomotor tone. Also if muscle function is improved, dependent edema may also be improved as muscle function drives blood that has pooled up the legs.

IO want to be clear, I do not discount any symptoms patients may have ESPECIALLY if i cannot explain it. I do have skepticism that the incidence of peripheral venous disease is significantly higher than the general population. I just do not think there will be an association between CCSVI and peripheral venous insufficiency.

be well

Dr S. just to keep you thinking, I am in a wheelchair, cannot walk, and I got a lot of improvements, but none in my legs other than the disappearance of the edema and discoloration of my foot. My foot remained normal until I restenosed. And that happened both times I was treated. Now that all 3 veins are 100% blocked, zero blood flow in the 3 veins, the edema is worse and is now in my right foot also.
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Re: DrSclafani answers some questions

Postby CureOrBust » Mon Dec 05, 2011 12:31 am

drsclafani wrote:I do have skepticism that the incidence of peripheral venous disease is significantly higher than the general population. I just do not think there will be an association between CCSVI and peripheral venous insufficiency.
Do you also have skepticism or any knowledge if affecting the venous blood flow as your treatments do, have any effects on blood flow in the lower extremities? ie no peripheral venous disease as such, but an effect on the flow, aa its a closed loop system?
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Re: DrSclafani answers some questions

Postby ttucker3 » Mon Dec 05, 2011 9:58 am

Sal

Your referring, in several posts on Nov 25, to measuring pressure gradient using a catheter has tickled my brain cell since that time.

The quotes were "I also want to measure pressure gradients so i have to catheterize the vein and i need to see the collaterals." and

"Pressure gradient of more than 3-4 mm, visualization of hemiazygous and gonadal collaterals ..."

While I recognize this was in the context of the renal vein, the reason it captured my attention is that by fluid dynamics the velocity of blood flow and its direction of flow are a direct function of pressure gradient. When you put that in the frame of some of Mark Haacke's MRI flow quantification measurements which show, for an obstructed IJV, venous flow away from the heart for part of a pulsatile cycle, followed by substantially increased flow velocity in the correct direction, toward the heart, for the remainder of the cycle. The increase here refers to the greater flow velocity in the obstructed vein than in the other, unobstructed vein. This means the pressure gradient in the obstructed vein is significantly greater than the pressure gradient in the unobstructed vein for at least part of the cycle. This seems to imply hypertension in the obstructed vein. I have the impression that venous hypertension may be a somewhat unaddressed possible medical condition with perhaps some unknown or uncertain consequences.

You mention pressure gradient of more than 3-4 mm, which I take it to mean 3-4 mmHg. However, for the units to be correct this should probably be something like mmHg/cm where the gradient is the slope of pressure drop per unit length. So, is your 3-4 mm perhaps a pressure measurement, not a gradient measurement? Irrespective of the answer if it is a pressure measurement it means, if you can measure pressure at two points in the vein, then you can calculate the gradient. The over-riding question, however, is this: is the measurement an average over a number of pulses, systolic pressure, diastolic or something else? In order to compare your pressure measurement results to Mark Haacke's flow velocity measurement, the pressure measurement will need to be within one pulse cycle, perhaps systolic and diatolic. Is this intrapulse measurement doable with your catheter? Have to talked to Mark about comparing notes on flow vs pressure? If you would like to take this offline drop me a note at ttucker@tti-ecm.com

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Re: DrSclafani answers some questions

Postby drsclafani » Mon Dec 05, 2011 6:41 pm

dania wrote:
With both angioplasties my swollen purple/red foot was 100% normal 5 hours afterwards. And when I restenosed swelling and purple/red colour returned. So, for me there is definitely a connection. How and why I do not know but there is a connection. So many of us report their feet returning to a normal state after the blood is flowing. Swelling disappearing and normal colouring.


Dania, my own assessment is that treating CCSVI does something positive for autonomic function. That autonomic function results in improvement vasomotor tone. Also if muscle function is improved, dependent edema may also be improved as muscle function drives blood that has pooled up the legs.

Dr S. just to keep you thinking, I am in a wheelchair, cannot walk, and I got a lot of improvements, but none in my legs other than the disappearance of the edema and discoloration of my foot. My foot remained normal until I restenosed. And that happened both times I was treated. Now that all 3 veins are 100% blocked, zero blood flow in the 3 veins, the edema is worse and is now in my right foot also.


This certainly does not sound like venous problem of the legs,
it sure sounds like an autonomic thing to me. This can be seen in ccsvi and in ms
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Re: DrSclafani answers some questions

Postby drsclafani » Wed Dec 07, 2011 12:04 am

SIR Abstract

TITLE: High pressure balloon angioplasty to treat internal jugular vein stenoses in patients wlth CCSVl
AUTHORS: Sclafani Salvatore JA, Zhang, Karl
INSTITUTIONS: 1. American Access Care, Brooklyn, NY, United States. 2. Radiology, SUNY Downstate Medical Center, Brooklyn, NY, Umted States.
PRESENTATION TYPE: Original Scientific Research - Oral
CURRENT CATEGORY: Venous Interventions: Other
KEYWORDS: Venopiasty, multiple sclerosis , veins.
ABSTRACT BODY:
Purpose
The nature of Internal Juguiar Vein (IJV) obstructions associated with chronic cerebrospinal venous insufficiency (CCSVI) is not well established, but it appears to be different from those stenoses caused by thrombosis,recanalization, scarring, tumor encasement and access intimal hyperplasia. We sought to determine the balloon sizes and pressures that were necessary to attain complete distension of IJV obstructions due to CCSVI.
Materials and Methods
The records of all patients undergoing endovascular treatment of CCSVI were reviewed. Angioplasty was based upon venographic findings such as stenosis >50%, stasis, reflux, collaterals or upon intravascular ultrasound (IVUS) findings, such as cross sectional area stenoses (CSA)>50%, immobile valves, septum, membranes or webs
Balloon sizing was initially calculated by vlsual estlmatlon, but converled to IVUS measurement of CSA. . lnflatlon endpolnts were ellmlnalion of balloon waist wlthout recoll or exceedlng rated burst pressure. Balloon size and maxlmum pressure were recorded. Compllcatlons were revlewed.
Results :
93% of 150 treated patients underwent angioplasty of 239 lJVs. 82% recelved bllateral angloplasty. Balloons used were sllghtly larger ln dlameter on the rlght (avg. 15.8mm, range 10-20mm) than on the left (avg 14.4mm range 8-20 mm). Endpoint pressure requlrements averaged 12.7 Atmospheres (range 4-25 atm) on the rlght slde and 13.2 atm (range 6-23 atm) on the left slde.
There were three balloon ruptures, two occurred during removal from the sheath.There were three dissections, two perforations and ten thromboses (6.3% of treated veins). All but one dissection and one thrombosis occurred prior to using IVUS CSA for balloon selection. Complication rate of 16% using visual estimation was reduced to 1.3% using IVUS CSA measurements.
Conclusion :
1. Hlgh pressures are requlred to completely dilate the lesions of CCSVI.
2. IVUS reduces rlsk of veln lnjury during angioplasty.


Any questions?
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