DrSclafani answers some questions

[drsclafani]

Franz schelling thinks that the emissary veins, especially the condylar veins are very important. They may actually be strong contributors to ccsvi by driving venous blood back into the the head from the neck

I never thought of that. Once the jugulars are treated, would the condylar veins no longer be contributors in that way? There is still going to be occasional reflux such as valsalva. My first thought was that these veins could be treated with coil embolization which would get rid of them if sufficient flow was restored through other veins and these were a continuing problem. But it's hard to imagine wanting to get rid of a drainage route.

yes, i tend to agree with you that collaterals are good. Here is what my new mentor has taught me recently:

FLANK FIBROSIS IN MS OF THE SPINAL CORD
· Post mortem studies for MS typically traced fibrous wedges invading the spinal cord’s sides
· No MR expert seems ever to have focused on this point.

Such lesions result in front-to-backwards or longitudinal displacement of the spinal cord. How can these findings be accounted for, through either venous stasis or reflux, relative to CCSVI?

HOW TO PUT CCSVI AND CEREBRAL OR SPINAL MS FINDINGS IN CONTEXT?

This might be done by identifying,
· in MS of the brain, the compartmentalization of venous reflux via or from internal jugular and deep cervical veins to cerebral lesion veins
· in MS of the spinal cord, the compartmentalization of venous reflux from engorged prevertebral veins in the direction of the specifically damaged parts of the spinal cord.

and

---------- Forwarded message ----------
On Thu, Dec 29, 2011 at 5:10 PM, Franz Schelling <> wrote:
Sal, I greatly enjoy your work!
Never having worked with dropbox, please find an additional copy of your paper's edited version in the addendum.

From: salvatore sclafani <ccsviliberation@gmail.com>
Date: 2011/12/29
Subject: Re: suggestions
To: Franz Schelling <xxxxxxxxxxx@gmail.com>


franz, what a great opportunity to have you review my paper and make such important recommendations and corrections!!!

Thank you so much.

Yes, I would like to discuss these phasic narrowing. I fail to see how we can treatment, by interventional techniques. There is never any resitance to balloon inflation and treatments such as surgical releases seem so complicated to me and how can we prove that these phasic narrowings can be clinically impoortant.

I look forward to your educating me on the value of these small veins in the back of the neck

Best wishes for new year

Sal


On Dec 30, 2011 1:36 PM, "Franz Schelling" <xxxxxxxxxxxxx@gmail.com> wrote:
Sal, determining the phasic narrowings' relevance is only possible in elucidating their impact on related lesion developments.
Routine MRI, MRV and even functional IVUS tools hardly enable to this. The phenomena to be studied are probably all too short-lived and exceptional.
The ordinary difference between deep cervical vein and vertebral vein is well shown on page 220, the potential caliber of the deep cervical vein on page 53(-57) of the first volume of Pernkopf E. "Atlas der topographischen und angewandten Anatomie des Menschen", München/Berlin 1963 - and already in considering the diameters of the posterior condylar and mastoid emissary vein shown on Fig. 1 C and on Fig. 3 of Schelling F. "Die Emissarien des menschlichen Schädels", Anat(omischer) Anz(eiger) 1978; 143: 340-382).




from salvatore sclafani ccsviliberation@gmail.com
to Franz Schelling <xxxxxxxxxxx@gmail.com>
date Sun, Jan 1, 2012 at 9:17 AM
subject Condylar veins
mailed-by gmail.com
hide details Jan 1
For the past 100 procedures I begin the venography in the transverse sinus. I have seen condylar veins that are huge, 8mm with many large tributaries. But I have recognized no trend in response, in presentation, or in type of disease. I unfortunately do not have mr data on all of them. What do you think I should be looking for?
Happy new year again my friend
Sal

[drsclafani]

Dr S,
I remember you once mentioned that your IVUS unit can support catheters for pressure gradient measurement. Dr.Schelling has proposed such measurements in jugular bulbs, inferior and superior vena cava as alternative/assisting method for diagnosis of flow problems. Do you consider using these catheters in the future?

yes, but as a pure research tool, i do not want to increase fees to patients. Thus I am looking for some funding: these catheters are very expensive

Would this be fractional flow reserve measurements (FFR) or something different?
Best wishes with obtaining funding! It certainly is deserving of funding.

it would be actual pressure at the probe. I am not sure how useful it iwll be to measure pressures in jugular. i think deep cerebral vein pressures might be more valuable

[mo_en]

Concerning the evolution of abnormal jugular valves: Do you think they obtain their malformed state mostly before birth? Or, is there a somewhat steady rate of progressive malformation? Or, eventually, is there sometime in life, ie puberty, when valves fixate most of their abnormal nature?

[NZer1]

Sal now that the conference is over do you think that there has been interest by other specialties to find what it is that is able to cross the BBB because of CCSVI that is causing these diseases (MS etc)?
Seems that there is now more belief in the capillary bed being effected by back flows, the next big question is finding what is crossing and how to remove it or them. I think from what I am learning at present that there are known virus such as lyme and CPn that are proven to be crossing the BBB and causing symptom groups that have been labeled as MS symptoms, there may be many more.

So back to the question, if the BBB can be made secure again by PTA and other methods including vein health if a disease is effecting vein walls and upsetting the healing of PTA, we will need a group of specialists to understand the processes and life time of these invaders, was there any interested people showing their hands at this stage?

Regards Nigel

[drsclafani]

Concerning the evolution of abnormal jugular valves: Do you think they obtain their malformed state mostly before birth? Or, is there a somewhat steady rate of progressive malformation? Or, eventually, is there sometime in life, ie puberty, when valves fixate most of their abnormal nature?

tough question
i think it is a bit of all of this. in my opinion, certainly some of the problems are longstanding and probably congenital. An upside down valve is not going to form later in life, i would think. elongation may occur later but i think that is also very unlikely. The nature of the collagen where there is more collagen 3 in ccsvi veins could certainly change during life. Perhaps this accretes with time, and this may be why such things as thickening are not reported to be seen(note nuance of words) in CIS and RIS and early MS is because collagen thickening occurs over time, obstructions may lead to microthrombus and infections that increase collagen production. But this is all conjecture on my part.

[mo_en]

Thank you Doctor.
Have you ever treated patients diagnosed with Neuromyelitis Optica? Did you notice any peculiarities regarding their ccsvi? They usually have extensive and very long spinal lesions. Well, it is said that NMO differs from MS but then ccsvi is more than MS...

[drsclafani]

Sal now that the conference is over do you think that there has been interest by other specialties to find what it is that is able to cross the BBB because of CCSVI that is causing these diseases (MS etc)?
Seems that there is now more belief in the capillary bed being effected by back flows, the next big question is finding what is crossing and how to remove it or them. I think from what I am learning at present that there are known virus such as lyme and CPn that are proven to be crossing the BBB and causing symptom groups that have been labeled as MS symptoms, there may be many more.

So back to the question, if the BBB can be made secure again by PTA and other methods including vein health if a disease is effecting vein walls and upsetting the healing of PTA, we will need a group of specialists to understand the processes and life time of these invaders, was there any interested people showing their hands at this stage?

Regards Nigel

yes, there were new partners in cell biology and physiology of the endothelium, engineers and physiciests interested in fluid dynamics in the blood vessels and CSF spaces, dentistry, pathology, engineering, a few neurologists too

[drsclafani]

Thank you Doctor.
Have you ever treated patients diagnosed with Neuromyelitis Optica? Did you notice any peculiarities regarding their ccsvi? They usually have extensive and very long spinal lesions. Well, it is said that NMO differs from MS but then ccsvi is more than MS...

i have never treated someone with neuromyelitis optica

[drsclafani]

Thank you Doctor.
Have you ever treated patients diagnosed with Neuromyelitis Optica? Did you notice any peculiarities regarding their ccsvi? They usually have extensive and very long spinal lesions. Well, it is said that NMO differs from MS but then ccsvi is more than MS...

Yes, more than MS. I heard of a neurosurgeon in south america who had treated ccsvi in 11 patients with essential hypertension with improvements.

I told himto publish that data!

[David1949]

DrSchelling has sort of flipped my thinking on so many things this week. Lots of late night over beer with him as i soaked all the ideas he offered

s

Wish I could have been there to soak up the ideas ... and the beer.

[Cece]

FLANK FIBROSIS IN MS OF THE SPINAL CORD
· Post mortem studies for MS typically traced fibrous wedges invading the spinal cord’s sides
· No MR expert seems ever to have focused on this point.

Such lesions result in front-to-backwards or longitudinal displacement of the spinal cord. How can these findings be accounted for, through either venous stasis or reflux, relative to CCSVI?

HOW TO PUT CCSVI AND CEREBRAL OR SPINAL MS FINDINGS IN CONTEXT?

This might be done by identifying,
· in MS of the brain, the compartmentalization of venous reflux via or from internal jugular and deep cervical veins to cerebral lesion veins
· in MS of the spinal cord, the compartmentalization of venous reflux from engorged prevertebral veins in the direction of the specifically damaged parts of the spinal cord.

Is the 'wedge' shape only found in the spinal cord?
At ISNVD Dr. Burks referred to brain lesions in MS as being mostly water. Would that mean that those brain lesions are not fibrous?
What is significant is the directionality of the lesions, such as front-to-backwards, that might point to a directionality of the break in the blood-brain barrier due to the forces of venous reflux and focal hypertension and other effects of CCSVI?

[Cece]

---------- Forwarded message ----------
On Thu, Dec 29, 2011 at 5:10 PM, Franz Schelling <> wrote:
Sal, I greatly enjoy your work!
Never having worked with dropbox, please find an additional copy of your paper's edited version in the addendum.

From: salvatore sclafani <ccsviliberation@gmail.com>
Date: 2011/12/29
Subject: Re: suggestions
To: Franz Schelling <xxxxxxxxxxx@gmail.com>


franz, what a great opportunity to have you review my paper and make such important recommendations and corrections!!!

Thank you so much.

Yes, I would like to discuss these phasic narrowing. I fail to see how we can treatment, by interventional techniques. There is never any resitance to balloon inflation and treatments such as surgical releases seem so complicated to me and how can we prove that these phasic narrowings can be clinically impoortant.

I look forward to your educating me on the value of these small veins in the back of the neck

Best wishes for new year

Sal


On Dec 30, 2011 1:36 PM, "Franz Schelling" <xxxxxxxxxxxxx@gmail.com> wrote:
Sal, determining the phasic narrowings' relevance is only possible in elucidating their impact on related lesion developments.
Routine MRI, MRV and even functional IVUS tools hardly enable to this. The phenomena to be studied are probably all too short-lived and exceptional.
The ordinary difference between deep cervical vein and vertebral vein is well shown on page 220, the potential caliber of the deep cervical vein on page 53(-57) of the first volume of Pernkopf E. "Atlas der topographischen und angewandten Anatomie des Menschen", München/Berlin 1963 - and already in considering the diameters of the posterior condylar and mastoid emissary vein shown on Fig. 1 C and on Fig. 3 of Schelling F. "Die Emissarien des menschlichen Schädels", Anat(omischer) Anz(eiger) 1978; 143: 340-382).




from salvatore sclafani ccsviliberation@gmail.com
to Franz Schelling <xxxxxxxxxxx@gmail.com>
date Sun, Jan 1, 2012 at 9:17 AM
subject Condylar veins
mailed-by gmail.com
hide details Jan 1
For the past 100 procedures I begin the venography in the transverse sinus. I have seen condylar veins that are huge, 8mm with many large tributaries. But I have recognized no trend in response, in presentation, or in type of disease. I unfortunately do not have mr data on all of them. What do you think I should be looking for?
Happy new year again my friend
Sal

There are patients who have all their CCSVI treated except for phasic narrowings. In these patients, if you are confident that all other CCSVI is addressed, then any further brain or spinal lesion development might be due to the phasic narrowing? First it would need to be established that CCSVI treatment stops new MS lesions from forming, as seen on MRIs, before it could be further investigated if there is continuing damage in patients with phasic narrowing. We are not there yet...

Are phasic narrowings short-lived and exceptional, making them hard to study? If a phasic narrowing occurs every time the head is turned to the left, that would be reproducible and, hence, more amenable to studying.

Dr. Schelling was writing about emissary veins back in 1978? Amazing. Have you had a chance to look at the figures or images he referenced?

You could do a retrospective study of MRIs of patients who had phasic narrowings, to see if there is anything different about their brain lesions compared to those of patients who did not have phasic narrowings. You've never had a patient who only had phasic narrowings, have you? Wouldn't that be interesting. The very lack of such a patient suggests that on their own, in the absence of jugular or azygous or renal lesions, phasic narrowings are not promoters of MS. A retrospective study of MRIs of patients with abnormal condylar emissary veins would also be possible.

Sorry if any of my commentary and questions miss the mark! I am still learning, and not as familiar with Dr. Schelling's work as I would like to be.

[mo_en]

Dr.Schelling in a nutshell:
Brain lesions form out of massive blood flow reversals (back-jets) that commence from thorax, pass the (left) jugular and exert pressure inside periventricular veins (formation of Dawson's fingers). Blocked right jugular helps in building up of stagnant blood volume.
Spinal lesions form because of swift displacement of CSF due to sudden and massive filling of epidural veins with blood from the lumbar area. The spinal cord is forced into stressful up-down movements and gets injured around the denticulate ligaments anchoring points, which hold it still inside the vertebral column.

I hope i haven't got it all wrong!

[milesap]

a worth a look the Canadian video

[drsclafani]

FLANK FIBROSIS IN MS OF THE SPINAL CORD
· Post mortem studies for MS typically traced fibrous wedges invading the spinal cord’s sides
· No MR expert seems ever to have focused on this point.

Such lesions result in front-to-backwards or longitudinal displacement of the spinal cord. How can these findings be accounted for, through either venous stasis or reflux, relative to CCSVI?

HOW TO PUT CCSVI AND CEREBRAL OR SPINAL MS FINDINGS IN CONTEXT?

This might be done by identifying,
· in MS of the brain, the compartmentalization of venous reflux via or from internal jugular and deep cervical veins to cerebral lesion veins
· in MS of the spinal cord, the compartmentalization of venous reflux from engorged prevertebral veins in the direction of the specifically damaged parts of the spinal cord.

Is the 'wedge' shape only found in the spinal cord?
At ISNVD Dr. Burks referred to brain lesions in MS as being mostly water. Would that mean that those brain lesions are not fibrous?
What is significant is the directionality of the lesions, such as front-to-backwards, that might point to a directionality of the break in the blood-brain barrier due to the forces of venous reflux and focal hypertension and other effects of CCSVI?

Dr Burke was speaking about inflammatory lesions. They are filled with edema which is water.

Franz is suggesting that there are shear forces that impact on ligamentous attachments and cause fibrotic scar, possibly due to traction.