DrSclafani answers some questions

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Re: DrSclafani answers some questions

Postby drsclafani » Fri Apr 05, 2013 9:45 pm

Anonymoose wrote:
Cece wrote:Nigel, I've come to the conclusion that Dr. Arata needs the ever elusive superIVUS that has been discussed here before. (A new improved IVUS intravascular ultrasound that is 10 time sharper than old IVUS.) He is ballooning the area of the valves, as are all the IRs, although he is ballooning valves that appear normal, which is different than all IRs. Normal healthy valve leaflets are too thin to show up on regular IVUS. With the new better IVUS, we could get a moving image of these supposedly normal valve leaflets. Either they are indeed normal or they are thickened as is seen in MS or they might be dysregulated so that the flapping is not in sync. This dysregulation of valve leaflet motion could be a result of the dysautonomia and could contribute to flow disruption, which could explain the improvement Dr. Arata has seen when these valves are ballooned. It is at least a way to investigate but the new IVUS is needed.

OK Dr. Sclafani can have his thread back now. Sorry for too many posts!

Do the thickened valves flap around or cause the vein to vacillate on a point? If they do, I wonder if they couldn't disrupt nerve transmissions the same way an artery can when it compresses a nerve. Maybe that's why ballooning functioning valves works...they'd have to be thickened or abnormal in some way though. If this is the case, then it would be the removal of a chronic mechanical stimulation rendering some of the PTA improvements (rather than the addition of mechanical stimulation during the ballooning event).


the thickened valves are pretty much immobile in a fixed closed position. That is what is causing a stenosis.
what do you mean by an artery compressing a nerve. Aneurysms compress nerves but give me an example of an artery that compresses a nerve.

veins are highly complant structures of very low pressure. The idea that they could compress a nerve make no sense to me.
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Re: DrSclafani answers some questions

Postby drsclafani » Fri Apr 05, 2013 9:51 pm

Anonymoose wrote:Not the best example but maybe relevant???
http://circres.ahajournals.org/content/ ... 7.full.pdf
The fundamental natural frequency of the closed cusps of porcine bioprosthetic valves, fabricated from the normal leaflets of pig aortic valves, was estimated using a finite element model. Both normal and stiffened leaflets were considered in the vibrational analysis. The effects of conditions that simulated degeneration, such as stiffening, central perforation, a tear, calcium deposits in the commissural attachments, and combinations of these were determined. The primary frequency of vibration of the normal leaflets was within the range of the dominant frequency of the heart sounds determined clinically by spectral analysis of the recorded phonocardiogram. If only one leaflet was stiffened or calcined, there was only a marginal change of frequency. With stiffening and calcification of the commissures of all 3 leaflets, the frequency of vibration increased. Introduction of a tear in a single leaflet of a stiffened and calcified valve markedly reduced the fundamental frequency. In view of the relation between the frequency content of heart sounds and the frequency of valve vibration, this mathematical simulation establishes a possible basis for the observation of a varying dominant frequency of heart sounds in patients with bioprosthetic valves that are in the process of degenerating. (Circulation Research 1987;61:687-694)

Dr. S,
Do the abnormal valves vibrate?


The answer is yes. Ultrasound is used to detect vibration of vessels.

vi•brate (ˈvaɪ breɪt)

v. -brat•ed, -brat•ing. v.i.
1. to move to and fro, as a pendulum; oscillate.
2. to move to and fro or up and down quickly and repeatedly; quiver; tremble.
3. (of sounds) to produce or have a quivering or vibratory effect; resound.
4. to thrill, as in emotional response.
5. to move between alternatives; vacillate.
v.t.
6. to cause to move to and fro, swing, or oscillate.
7. to cause to quiver or tremble.
8. to give forth or emit by or as if by vibration.
[1610–20; < Latin vibrātus, past participle of vibrāre to move to and fro]


however, that study was speaking about heart valves, different from jugular valves in many ways. Calcification is not something we see often in jugular valves but disease cardiac valves do calcify frequently.
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Re: DrSclafani answers some questions

Postby Cece » Fri Apr 05, 2013 9:52 pm

drsclafani wrote:thanks cece
valves are involuntary structures that do not flap because they have muscles that move. They move because of the flow of blood. there is no dysregulation of the valves. Heart valves are attached to tendinous structures called chorda tendinae to the papillary muscles. That is different

Ohhhhh got it
I discussed this with someone else today. Most patients with MS have bilateral jugular vein valve abnormalities. I treat both jugular veein valves most of the time. i doubt that normal jugular valves exist very often.

He might very well be seeing normal jugular valves because he is also treating patients who do not have an MS diagnosis (parkinson's, dystonia, dysautonomia).
I definintely think that autonomic functions are affected by MS and CCSVI and that venouos angioplasty somehow improves that function, but this includes other cranial nerves that are components of the autonomic nervous system which do not travel in the carotid sheath.

Can you make that more concise and send it out daily via twitter?
Not seriously. But the opposite viewpoint is getting around that way.
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Re: DrSclafani answers some questions

Postby drsclafani » Fri Apr 05, 2013 10:04 pm

NZer1 wrote:
Anonymoose wrote:Not the best example but maybe relevant???
http://circres.ahajournals.org/content/ ... 7.full.pdf
The fundamental natural frequency of the closed cusps of porcine bioprosthetic valves, fabricated from the normal leaflets of pig aortic valves, was estimated using a finite element model. Both normal and stiffened leaflets were considered in the vibrational analysis. The effects of conditions that simulated degeneration, such as stiffening, central perforation, a tear, calcium deposits in the commissural attachments, and combinations of these were determined. The primary frequency of vibration of the normal leaflets was within the range of the dominant frequency of the heart sounds determined clinically by spectral analysis of the recorded phonocardiogram. If only one leaflet was stiffened or calcined, there was only a marginal change of frequency. With stiffening and calcification of the commissures of all 3 leaflets, the frequency of vibration increased. Introduction of a tear in a single leaflet of a stiffened and calcified valve markedly reduced the fundamental frequency. In view of the relation between the frequency content of heart sounds and the frequency of valve vibration, this mathematical simulation establishes a possible basis for the observation of a varying dominant frequency of heart sounds in patients with bioprosthetic valves that are in the process of degenerating. (Circulation Research 1987;61:687-694)

Dr. S,
Do the abnormal valves vibrate?


Thanks Anonymoose,
It would appear that the nerve sensing at the valves may be multi-faceted and be as much about the body sensing flow and volume as it is about about dysautonomia concept ideas.
The finding from swine aorta studies indicates that the nerves are detecting function as well as rhythm of beating.
Another field of knowledge needed to fathom this aspect!

;)
Nigel

nigel, i do not think that the valves have nerve fibers.
This abstgract is talking about listening to the vibrations coming from the flow through the moving valve These prosthetic pig valve certainly do not have nerve fibers. the findings on this study are only talking about the vibrations that can be heard using a stethescope. There is nothing here that speaks about sensing moving blood
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Re: DrSclafani answers some questions

Postby drsclafani » Fri Apr 05, 2013 10:15 pm

Cece wrote:
drsclafani wrote:thanks cece
valves are involuntary structures that do not flap because they have muscles that move. They move because of the flow of blood. there is no dysregulation of the valves. Heart valves are attached to tendinous structures called chorda tendinae to the papillary muscles. That is different

Ohhhhh got it
I discussed this with someone else today. Most patients with MS have bilateral jugular vein valve abnormalities. I treat both jugular veein valves most of the time. i doubt that normal jugular valves exist very often.

He might very well be seeing normal jugular valves because he is also treating patients who do not have an MS diagnosis (parkinson's, dystonia, dysautonomia).



I definintely think that autonomic functions are affected by MS and CCSVI and that venouos angioplasty somehow improves that function, but this includes other cranial nerves that are components of the autonomic nervous system which do not travel in the carotid sheath.

cece wrote:Can you make that more concise and send it out daily via twitter?
Not seriously. But the opposite viewpoint is getting around that way.

This is very serious. I encourage him to publish his theories and the evidence behind them in a professional journal so they can be properly analyzed. I look forward to it. If his theory is correct, i would jump right in but my simople plumbers mind cannot fathom this.

But i am not going to twitter about this. My goal is to educate what people do not understand about things i know or can research about.
there is a lot of misinformation being bandied about here on tims about the autonomic nervous system, and its relationshiip to jugular valves.
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Re: DrSclafani answers some questions

Postby NZer1 » Fri Apr 05, 2013 10:17 pm

I appreciate what you are saying thanks Dr., could it be that we are observing the 'other sense' of nerve transmission that researchers are finding? Electrical nerve conduction speeds have been known to be too slow for some time and they are experimenting and finding there is another method with sound or light transmission. A work in progress.

What do you think of the Simka paper?
Dr M Simka's paper is very balanced and well thought through, imo

Discussion;
A review of literature suggests that MS may be triggered
by an infectious factor (Murrell et al., 1991; Thibault, 2012;
Kurland and Reed, 1964; Kurtzke, 2000a; Kurtzke, 2000b).
It is tempting to speculate that MS may actually result from
chronic infection associated with autoimmune response
against CNS antigens (Von Herrath et al., 2003) and an
altered venous drainage caused by CCSVI. We suggest that
future research should focus on such hypothetical pathogenetic scenario.

Just thought I would throw in the link to Paul Thibault's paper,
on CPn, Multiple sclerosis: a chronic infective cerebrospinal venulitis?

http://koti.mbnet.fi/hiihoo/ccsvi/thiba ... tkimus.pdf

Did I mention I am on day 195 of Paul Thibault/David Wheldons Protocol?
I'm definitely feeling the effects of treatment from the die off endo-toxins and the secondary porphyria and I do have some little gains in 'MS' symptoms eg sensory feeling my feet, but I am also more disabled by the side effects of the protocol. So I have another 6-12 months before I have real answers and then need to have another doppler to see what has changed.

;)
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Re: DrSclafani answers some questions

Postby Anonymoose » Sat Apr 06, 2013 7:10 am

drsclafani wrote:
Anonymoose wrote:
Cece wrote:Nigel, I've come to the conclusion that Dr. Arata needs the ever elusive superIVUS that has been discussed here before. (A new improved IVUS intravascular ultrasound that is 10 time sharper than old IVUS.) He is ballooning the area of the valves, as are all the IRs, although he is ballooning valves that appear normal, which is different than all IRs. Normal healthy valve leaflets are too thin to show up on regular IVUS. With the new better IVUS, we could get a moving image of these supposedly normal valve leaflets. Either they are indeed normal or they are thickened as is seen in MS or they might be dysregulated so that the flapping is not in sync. This dysregulation of valve leaflet motion could be a result of the dysautonomia and could contribute to flow disruption, which could explain the improvement Dr. Arata has seen when these valves are ballooned. It is at least a way to investigate but the new IVUS is needed.

OK Dr. Sclafani can have his thread back now. Sorry for too many posts!

Do the thickened valves flap around or cause the vein to vacillate on a point? If they do, I wonder if they couldn't disrupt nerve transmissions the same way an artery can when it compresses a nerve. Maybe that's why ballooning functioning valves works...they'd have to be thickened or abnormal in some way though. If this is the case, then it would be the removal of a chronic mechanical stimulation rendering some of the PTA improvements (rather than the addition of mechanical stimulation during the ballooning event).


the thickened valves are pretty much immobile in a fixed closed position. That is what is causing a stenosis.
what do you mean by an artery compressing a nerve. Aneurysms compress nerves but give me an example of an artery that compresses a nerve.

veins are highly complant structures of very low pressure. The idea that they could compress a nerve make no sense to me.


Here's an example of neurovascular compression.
http://radiology.rsna.org/content/early ... 00477.full

I no longer have the misguided idea that veins can compress a nerve (ty)...I'm working with a new misguided idea. Could the higher frequency vibrations of the thickened (if they behave like stiffened/calcified) valves travel through to the vagus and impact nerve transmission or tone?? Would it be a bit like a tuning fork on the nerve?? (I don't think this would be a major player in PTA...but maybe a sidenote, something to look for if room for improvement remains? Trying to make sideways sense of Arata's focus on the vagus at the valves.)

Edit:
Vibration and vasospasm??? chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic20130-75.html#p207530 When you balloon valves, do surrounding stenosi typically resolve? Is zamboni having better results with his valve clipping tool?

Edit 2:
Could some restenosi be caused by leftover valve parts starting to vibrate again?
Last edited by Anonymoose on Sat Apr 06, 2013 2:13 pm, edited 2 times in total.
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Re: DrSclafani answers some questions

Postby Cece » Sat Apr 06, 2013 8:52 am

Anonymoose wrote:I no longer have the misguided idea that veins can compress a nerve (ty)...I'm working with a new misguided idea.

That made me laugh :)
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Re: DrSclafani answers some questions

Postby dlynn » Mon Apr 08, 2013 11:08 am

Dr. Sclafani,
Is it possible to stent an IJV at the location of scar tissue if it is causing reflux?
or even if it's just stenosed (because of scar tissue) without reflux?
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Re: DrSclafani answers some questions

Postby drsclafani » Mon Apr 08, 2013 10:46 pm

Nigel, I've come to the conclusion that Dr. Arata needs the ever elusive superIVUS that has been discussed here before. (A new improved IVUS intravascular ultrasound that is 10 time sharper than old IVUS.) He is ballooning the area of the valves, as are all the IRs, although he is ballooning valves that appear normal, which is different than all IRs. Normal healthy valve leaflets are too thin to show up on regular IVUS. With the new better IVUS, we could get a moving image of these supposedly normal valve leaflets. Either they are indeed normal or they are thickened as is seen in MS or they might be dysregulated so that the flapping is not in sync. This dysregulation of valve leaflet motion could be a result of the dysautonomia and could contribute to flow disruption, which could explain the improvement Dr. Arata has seen when these valves are ballooned. It is at least a way to investigate but the new IVUS is needed.

OK Dr. Sclafani can have his thread back now. Sorry for too many posts!

Do the thickened valves flap around or cause the vein to vacillate on a point? If they do, I wonder if they couldn't disrupt nerve transmissions the same way an artery can when it compresses a nerve. Maybe that's why ballooning functioning valves works...they'd have to be thickened or abnormal in some way though. If this is the case, then it would be the removal of a chronic mechanical stimulation rendering some of the PTA improvements (rather than the addition of mechanical stimulation during the ballooning event).


the thickened valves are pretty much immobile in a fixed closed position. That is what is causing a stenosis.
what do you mean by an artery compressing a nerve. Aneurysms compress nerves but give me an example of an artery that compresses a nerve.

veins are highly complant structures of very low pressure. The idea that they could compress a nerve make no sense to me.


Here's an example of neurovascular compression.
http://radiology.rsna.org/content/early ... 00477.full

I no longer have the misguided idea that veins can compress a nerve (ty)...I'm working with a new misguided idea. Could the higher frequency vibrations of the thickened (if they behave like stiffened/calcified) valves travel through to the vagus and impact nerve transmission or tone?? Would it be a bit like a tuning fork on the nerve?? (I don't think this would be a major player in PTA...but maybe a sidenote, something to look for if room for improvement remains? Trying to make sideways sense of Arata's focus on the vagus at the valves.)

Edit:
Vibration and vasospasm??? chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic20130-75.html#p207530 When you balloon valves, do surrounding stenosi typically resolve? Is zamboni having better results with his valve clipping tool?

Edit 2:
Could some restenosi be caused by leftover valve parts starting to vibrate again?


The valve IS the stenosis. The surrounding vein is almost always normal. the "vibrations" are not like your power toothbrush. They arent vibrating like that. I think oscillation might be a better term, but lots of our body vibrate, the hairs in our nose, the valves ini the heart and other valves as well,
i think this vibration thing is another out of control urban legend waiting to happen :sad:

The restenosis is just adhesions at the sites where the valve was torn or stretched.
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Re: DrSclafani answers some questions

Postby drsclafani » Mon Apr 08, 2013 10:48 pm

dlynn wrote:Dr. Sclafani,
Is it possible to stent an IJV at the location of scar tissue if it is causing reflux?
or even if it's just stenosed (because of scar tissue) without reflux?


if the stenosis is bad enough there will be reflux (or more properly, reversal of flow) above the stenosis.

stents are often used at sites of scar tissue, but scar tissue is rarely the cause of the stenosis unless an angioplasty resulted in a tear of the wall. Hematoma outside the vein may cause scarring
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Re: DrSclafani answers some questions

Postby NZer1 » Mon Apr 08, 2013 10:58 pm

Dr S is Endothelin-1 something that IR's are concious of and therefore have tactics for dealing with the increases when doing PTA?

I have been learning heaps on the thread and notice it is also being looked at by Dr's involved with ABx Protocols, aka Paul Thibault when I asked him yesterday!

;)
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Re: DrSclafani answers some questions

Postby drsclafani » Tue Apr 09, 2013 1:12 am

NZer1 wrote:Dr S is Endothelin-1 something that IR's are concious of and therefore have tactics for dealing with the increases when doing PTA?

I have been learning heaps on the thread and notice it is also being looked at by Dr's involved with ABx Protocols, aka Paul Thibault when I asked him yesterday!

;)
Nigel


Nigel
endothelin-1 may have an important role in the development of myointimal hyperplasia after angioplasty. However most of the trials of Endotheln receptor antagonists have not been positive so far because of complications, and difficulties in establshing doses. ERAs, to the best of my knowledge have only found clinical indications for pulmonary hypertension and digital ulcers.

I certainly keep an open mind and a hopeful attitude that this will be something that will help us. But EARs do not appear ready for prime time yet

DrS
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Re: DrSclafani answers some questions

Postby NZer1 » Tue Apr 09, 2013 1:50 am

Dr S the thread
chronic-cerebrospinal-venous-insufficiency-ccsvi-f40/topic15731.html
has got me thinking in all sorts of directions and the 'levelness of ET-1 across the board' in PwMSers gets my attention most of all. It stands out and is almost unusual, which may be the reason I need to consider this learning with an open mind,imo. I wonder most of all if it is an indication of a process that is separate to the CCSVI phenomenon and may be related to the infection status with Lyme or CPn or micoplasmas and their bio-films.

Dr S do you think that high levels of ET-1 are significant in MS or other de-generative diseases, and if so why, and of course if not why?

The figure 224% higher in PwMS gets attention, but is it something that is 'ground breaking must learn more' news?

The endothelial layer whether in the gut or the veins is going to get attention because of CCSVI awareness and I sometimes wonder if the normal processes of the body, especially healing processes, send us off on wild goose chases. Do you think that the levels found in the study are learning edges?

Thanks,
Nigel

http://journals.lww.com/jneuro-ophthalm ... ts.11.aspx
"Increased Endothelin-1 Plasma Levels in Patients With
Multiple Sclerosis
Timo Haufschild, MD, Sidney G. Shaw, PhD, Jürg Kesselring, MD, and Josef Flammer, MD
Objective: We tested the hypothesis that the plasma level of
endothelin-1 (ET-1) is increased in patients with multiple sclerosis
(MS). The peptide ET-1 is one of the most potent known
vasoconstrictors. An increased level of endothelin could explain
some of the vascular symptoms of these patients.
Materials and Methods: A specific radioimmunoassay was
used to determine ET-1 plasma levels. Twenty patients with
MS were compared to 20 age- and sex-pair-matched healthy
subjects.
Results: The plasma ET-1 levels were, on average, 224%
higher in the patients with MS than in the controls (p < 0.005).
The mean ET-1 levels (mean ± standard deviation [SD]) were
3.5 ± 0.83 pg/mL (min 2.13, max 5.37 pg/mL) in patients with
MS and 1.56 ± 0.3 pg/mL (min 0.9, max 2.13 pg/mL) in healthy
volunteers. Neither the different forms nor stages of MS had an
influence on the results. The ET-1 level was also not correlated
with the duration of the disease.
Conclusions: The plasma ET-1 level is markedly and significantly
increased in patients with MS. Neither the cause of such
an increase nor the pathogenetic role is known."
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Re: DrSclafani answers some questions

Postby drsclafani » Tue Apr 09, 2013 6:33 am

Nigel
I don't think that study is a smoking gun merely a single ale of uncertain significance at this point. The test would need to be validated by large numbers and cpntrolled for numerous variables and meds and supplements.

Way to early to make any conclusions
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