DrSclafani answers some questions

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

Re: IVUS measurements

Postby drsclafani » Thu Sep 01, 2011 8:36 pm

MikeInFlorida wrote:
ttucker wrote:The IVUS measurements under discussion are a potentially direct means of determining any haemodynamic standing pressure waves created by venous obstructions. If such pressure waves can measured by IVUS, then through the application of computational fluid dynamics, the amount of hypertension in the area of periventrical lesions could be computed. If this hypertension is sufficiently acute to cause blood-brain barrier breakdown this would provide an explanation for the transport of iron and leukocytes into the cerebral parenchyma. It would also provide a means to estimate the amount of capillary bed ischemia, hence hypoxia, hence loss of oligodendrocytes and hence deterioration of myelin. Leukocytes meet weakened myelin and - voila - MS. If IVUS pressure waveform measurements (systolic and diastolic would suffice) could to be taken at a number of positions going up the vein (IJV?) with a measure of the distance from the obstruction, this could demonstrate that both neurologists and vascular scientists are right. It is an autoimmune disease, but its root cause lies in the venous obstruction causing acute hypertension in the BBB at the venule end of the bed.

Hi ttucker,
If I understand you correctly, you believe that, not only do venous obstructions increase the static venous pressure, but the resultant turbulence (from reflux) creates standing waves, the period of which could be measured with the IVUS equipment. Then using sophisticated mathematics, these wave parameters could be predicted (or translated into) the DCVs?

I love the standing wave idea, but measuring them in the IJV and using that to calculate the DCV wave freq and amp seems... prone to error (but I'm no expert on this).

Regardless, wouldn't it be great if the measurements could be made in or near the DCVs? I wonder how far into the (e.g. straight) sinuses you can safely put the IVUS, using the smallest available catheter sheath? Dr. Sclafani previously said that the sheath used for this patient was 10 french (3.3 mm)... are smaller sheaths available?

(edited: replaced my misuse of the word "harmonic" with "standing". Harmonic and standing waves are related, but not interchangeable.)


There is a pressure wire for the IVUS. I am not going to explore this until i have mastered the IVUS imaging catheter. Maybe in 2012 if i have some funding.
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Re: IVUS measurements

Postby drsclafani » Thu Sep 01, 2011 8:37 pm

Cece wrote:
ttucker wrote:The IVUS measurements under discussion are a potentially direct means of determining any haemodynamic standing pressure waves created by venous obstructions. If such pressure waves can measured by IVUS, then through the application of computational fluid dynamics, the amount of hypertension in the area of periventrical lesions could be computed. If this hypertension is sufficiently acute to cause blood-brain barrier breakdown this would provide an explanation for the transport of iron and leukocytes into the cerebral parenchyma. It would also provide a means to estimate the amount of capillary bed ischemia, hence hypoxia, hence loss of oligodendrocytes and hence deterioration of myelin. Leukocytes meet weakened myelin and - voila - MS. If IVUS pressure waveform measurements (systolic and diastolic would suffice) could to be taken at a number of positions going up the vein (IJV?) with a measure of the distance from the obstruction, this could demonstrate that both neurologists and vascular scientists are right. It is an autoimmune disease, but its root cause lies in the venous obstruction causing acute hypertension in the BBB at the venule end of the bed.

I like the ideas here.

Dr. Sclafani, would IVUS be useful in measuring pressure waveforms as Dr. Tucker is describing?

That last sentence - "It is an autoimmune disease, but its root cause lies in the venous obstruction causing acute hypertension in the BBB at the venule end of the bed" - leaves me hanging for what happens after that root cause (venous obstruction) is treated. Does the autoimmune disease continue or not....


prior response answered this question. There is a pressure wire.
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Re: sigmoid sinus?

Postby drsclafani » Thu Sep 01, 2011 8:46 pm

Donnchadh wrote:The following excerpt was from Dr. Sclafani:

:

The catheter was placed in the left transverse sinus.
Dural sinus venography looked like this:

(image was in original post)

These images show that the transverse sinus and the sigmoid sinus had normal diameters. However there was a prominent connection between the transverse sinus inside the skull and the vertebral vein and posterior cervical branches on the outside. These vessels are connected by a very large emissary vein traversing across the skull via the hypoglossal canal. This canal is usually a very small opening in the skull but in this patient it is exceedingly large. I think this suggests that a long standing (perhaps congenital) outflow obstruction of the internal jugular vein has existed



My question is about the sigmoid sinus. I was told that I have bilateral stenosis in this region by three different IR's but this area is untreatable. Is it now possible to treat the sigmoid sinus?

Donnchadh


yes, stenoses of the dural sinuses have been reported. These stenoses may be the result of dural sinus thrombosis with partial recanalization of the sinus.

treatment has been reported as well with stents used.
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Postby drsclafani » Thu Sep 01, 2011 8:56 pm

NZer1 wrote:There has been discussion on other threads about the enlargement of skull drainage passages that is cased by reflux or reverse waves from stenosis further down. I asked Dr. S about this recently on this thread and he said that so far he had not noticed it to be a common problem.
I do wonder though if it was suspected what would be seen.
Regards Nigel


nigel
i am not sure exactly what i wrote and what the context was.

As I have modified my venogram of the dural sinuses, I have noted very prominent emissary veins and these veins provide large conduits increase flow through the spinal veins. I am unclear if there is an association between this emissary vein and symptoms, though.

(I actually emailed dr zamboni about this today!) Wonder what he thinks, although I dont think that dr galleoti routinely images the dural sinuses.
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Postby drsclafani » Thu Sep 01, 2011 8:57 pm

1eye wrote:
I will be in wilderness and unable to read or respond to any email.
If this is a patient inquiry, please email zzz@zzz-zzz.com.
If this is personal, please hold the thought and email me after August 29.


Hope you went somewhere it's not raining!


actually it rained almost every day, and then as we left early to get home before irene, they were looking to get 3-6 feet of rain.
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Postby drsclafani » Thu Sep 01, 2011 9:06 pm

NZer1 wrote:Hi Everyone, I have been talking about the reverse waves and have wondered about the effects of other regions of the body when there is reverse flows.
I am assuming that the blood returning to the heart is, in concept in a pool, and that if there is fluctuations in any system for any reason that pool will 'move' within the veins.
The thought I had was regarding leg veins. Then I thought more about what understanding there is for any movements and functions.

* If the holding of ones breath and unblocking your ears for instance, vasavalar move, directs blood away from the heart, does that mean that many actions in everyday life will send blood back into the brain of someone with CCSVI?

no, actually valsalva causes reflux but the stenotic veins (valves) prevent reflux.

* Is there any way of testing what blood movement is normal?
blood movement is back and forth, highly variable

* Can its transit be tested between normals and PwMS for instance?


dont know

* If we are not aware of what the blood ebbs and tides are, then opening veins is premature?

only if you dont want to have improvements in quality of life now

* The main interest I have is what happens when the lumbar veins are refluxing?

why?
Most patients with PPMS have hypoplastic lumbar veins. They are not going to reflux very much

The source of refluxing blood could be from other sources, such as leg veins, abdominal compression's, and things I have no understanding of.
Regards Nigel


Nigel the vast majority of of refluxing blood comes from the brain, the rest is practically irrelevant, except for renal vein stenosis and possibly to a less extent the may thurner syndrome
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CVI leg veins

Postby Robnl » Thu Sep 01, 2011 11:47 pm

Welcome back doc, well my vacation was also a rainy one..so we have something in common 8)

.....
One should not be surprised that it would be seen in a patient with ccsvi. The incidence of May thurner syndrome is no more common in patients with ccsvi that in healthy controls.

The bottom line is that if you have symptoms of venous disease in the legs, have it looked at by a competent specialist in this area.


My legs were checked last seek, valves are ok and flow is ok
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Postby Cece » Fri Sep 02, 2011 5:50 pm

drsclafani wrote:As I have modified my venogram of the dural sinuses, I have noted very prominent emissary veins and these veins provide large conduits increase flow through the spinal veins. I am unclear if there is an association between this emissary vein and symptoms, though.

(I actually emailed dr zamboni about this today!) Wonder what he thinks, although I dont think that dr galleoti routinely images the dural sinuses.

I wonder too! Might be ok if no azygous blockage but not good if there is azygous blockage because it adds to the flow there. Spinal veins also not meant to carry excess flow?
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Postby NZer1 » Fri Sep 02, 2011 6:11 pm

Quote
"why?
Most patients with PPMS have hypoplastic lumbar veins. They are not going to reflux very much "

Hi Dr. welcome back,

* I am wanting to know/learn why spinal cord lesions occur and why it is more common in PPMS?

I am thinking that there must be an association between lesions on the cord itself and blood flows.
Dr Schelling was quite specific that the lesions appeared to be from an action that looked to him like the veins exploding outwards. I naturally assume that would be from reflux/back flow as Dr. Schelling worded it. Trev T has spoken about reverse wave pressures and it would seem logical that with the information from Dr Schelling, Zamboni, and yourself that we dealing with flow restrictions of some kind effecting the region of the cord near the lesions.
If it was a brain lesion there is more variables.
The cord has less 'possibilities'.
Regards Nigel
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Postby drsclafani » Fri Sep 02, 2011 8:20 pm

Cece wrote:
drsclafani wrote:As I have modified my venogram of the dural sinuses, I have noted very prominent emissary veins and these veins provide large conduits increase flow through the spinal veins. I am unclear if there is an association between this emissary vein and symptoms, though.

(I actually emailed dr zamboni about this today!) Wonder what he thinks, although I dont think that dr galleoti routinely images the dural sinuses.

I wonder too! Might be ok if no azygous blockage but not good if there is azygous blockage because it adds to the flow there. Spinal veins also not meant to carry excess flow?


I have been involved with this since 2009 and no one has ever mentioned the emissary veins. No one!

Well, perhaps that indicates that they are not something worthy of discussion. Or perhaps we have too many people making a buck, or worrying about neurologists objections to ultrasounds in MS patients.

it seems to me that there is much to learn and too few people pushing the envelope....sorry for the rant.

Perhaps its time for patients to expect more from those they go to for treatment. Perhaps they should go to those who are invovled in the pursuits
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Postby drsclafani » Fri Sep 02, 2011 8:25 pm

NZer1 wrote:Quote
"why?
Most patients with PPMS have hypoplastic lumbar veins. They are not going to reflux very much "

Hi Dr. welcome back,

* I am wanting to know/learn why spinal cord lesions occur and why it is more common in PPMS?

I am thinking that there must be an association between lesions on the cord itself and blood flows.
Dr Schelling was quite specific that the lesions appeared to be from an action that looked to him like the veins exploding outwards. I naturally assume that would be from reflux/back flow as Dr. Schelling worded it. Trev T has spoken about reverse wave pressures and it would seem logical that with the information from Dr Schelling, Zamboni, and yourself that we dealing with flow restrictions of some kind effecting the region of the cord near the lesions.
If it was a brain lesion there is more variables.
The cord has less 'possibilities'.
Regards Nigel


nigel
seems like lots of patients, not just those with ppms, have spinal lesions

i see lesions in the spinal cord in patients with normal lumbar veins. I find lumbar hypoplasia in most patients with MS, not just those with ppms.

my question about why? is an impetus to stop asking why but to ask How.
how do we fix this
how do we best image these problems
how do we get all the players to the same table, how do we fund trials
how do we answer aall these really good questions without ending up in asking questions for no endpoint

Sorry nigel

i am ranting
call it frustration
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Postby pklittle » Fri Sep 02, 2011 8:38 pm

drsclafani wrote:
NZer1 wrote:Quote
"why?
Most patients with PPMS have hypoplastic lumbar veins. They are not going to reflux very much "

Hi Dr. welcome back,

* I am wanting to know/learn why spinal cord lesions occur and why it is more common in PPMS?

I am thinking that there must be an association between lesions on the cord itself and blood flows.
Dr Schelling was quite specific that the lesions appeared to be from an action that looked to him like the veins exploding outwards. I naturally assume t

hat would be from reflux/back flow as Dr. Schelling worded it. Trev T has spoken about reverse wave pressures and it would seem logical that with the information from Dr Schelling, Zamboni, and yourself that we dealing with flow restrictions of some kind effecting the region of the cord near the lesions.
If it was a brain lesion there is more variables.
The cord has less 'possibilities'.
Regards Nigel


nigel
seems like lots of patients, not just those with ppms, have spinal lesions

i see lesions in the spinal cord in patients with normal lumbar veins. I find lumbar hypoplasia in most patients with MS, not just those with ppms.

my question about why? is an impetus to stop asking why but to ask How.
how do we fix this
how do we best image these problems
how do we get all the players to the same table, how do we fund trials
how do we answer aall these really good questions without ending up in asking questions for no endpoint

Sorry nigel

i am ranting
call it frustration


I received my ms diagnosis based on spinal lesions seen on an mri I had for another reason (back pain).

Good evening Dr. :)
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Postby cheerleader » Fri Sep 02, 2011 11:39 pm

drsclafani wrote:
I have been involved with this since 2009 and no one has ever mentioned the emissary veins. No one!


Hi Dr. S..welcome home! Actually, Marie and I were writing about emissary veins on here in relationship to heat intolerence in MS. And Dr. Flanagan was writing about it, too...although we hadn't read him at that time.
Here's me rambling....
Jugular vein stenosis will probably affect all of the "tributary" veins surrounding them--and those include the emissary veins, which control the body's temperature regulation, and the thyroid veins, which control the release of thyroid hormone. I even postulated on another thread that vitamin D may be getting screwed up because the HPA axis (hypothalmic/pituitary/adrenal) pathway was being messed up, do to delayed signaling and slowed flow....but there are no studies on that yet. The neck veins are responsible for CSF, hormones and blood flow from the brain. Lots going on in there--



Marie linked this study on emissary veins from 3/09
http://www.ajnr.org/cgi/content/figsonly/23/9/1500

I remain convinced that it's the overuse of the emissary veins messing up the brain's cooling mechnism in CCSVI.
Here's Dr. Flanagan on this very topic....he explains it quite well.
http://uprightdoctor.wordpress.com/2010 ... n-cooling/
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby NZer1 » Sat Sep 03, 2011 12:02 am

Thanks Dr., you are sounding more like 'us' and you have just had a break.lol.
If we know more of the why then we can push for treatment in countries like mine. The Mr. Fixit's are doing a fantastic job, sure there is now concern about people making money of us PwMS from a new angle, at least this time we have you.

Dr its good to hear your passion :D

My point about cord lesions has for years been that it will be the 'place' that we can learn the most about the disease. The other areas that lesions form have too many variables. The studies of pathology have been the most progressive for MS and the ones by Dr Schelling are the direction that needs to be picked up by a bright researcher. If that researcher was to pick your brains for info imagine what could happen!

So finding the fix for cord lesions will find the cause as much as finding the cause of lesions will find the fix. It is such a confined area to understand and then expand that knowledge.

But you already know all of this, share the load Dr.

Regards Nigel
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Postby dania » Sat Sep 03, 2011 6:17 am

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PostPosted: Sat Sep 03, 2011 4:35 am Post subject: Reply with quote
Dr Sclafani what is your opinion of Daflon 500? Apparently it is used to medically treat venous insufficiency, although not specifically CCSVI. http://www.thisisms.com/ftopict-17751.html
Is it possible it might provide a means of treating CCSVI medically rather than surgically in some cases?
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