vagus nerve compression in CCSVI in MS

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

Re: vagus nerve compression in CCSVI in MS

Postby drsclafani » Sat Mar 23, 2013 7:55 am

Cece wrote:
drsclafani wrote:Cece, they are talking about the nerves IN the wall of the artery, not on the vagus nerve. They did not look at the vagus itself.

I was trying to decode this: "Vasovagal Therapy- delivery of physical energy to periadventitial autonomic fibers. Not vagal compression"

I thought periadventitial autonomic fibers might mean the nerves within the outer layer of the blood vessel. These nerves within the blood vessel can be damaged by balloon angioplasty. The image above has them labelled as parasympathetic and sympathetic nerves, contained within the tunica adventitia. If they were damaged however it would be very localized. It's possible that I am trying to make sense of something that is nonsensical. I am very uncomfortable with the ballooning of nonobstructed jugulars.


Reading on his website, Synergy says: "We believe this is due to the stimulation of the vagus nerve that generally occurs during the CCSVI procedure."

I understand your reasoning. However in the quote paper, they are referring to nerve fibers in the wall of the artery, although there are autonomic fibers in the wall of the vein as well.

cece, look up renal sympathectomy by ablation of autonomic fibers embedded in the wall of the renal artery as a treatment for essential hypertension. This work is something I do on a randomized trial. In our study this treatment is indicated for uncontrolled hypertension (greater than 160 mm systolic) despite maximum tolerable doses of at least three classes of antihypertensive medications.

There is a distinct feedback between the autonomic fibers in the renal artery and the brain stem that goes awry in essential hypertension. Ablating the fibers by application of radiofrequency derived thermal energy heating the wall of the artery to about 125 degrees fahrenheit damages irrevocably these nerves, cuts the feedback mechanism, causes loss of autonomic overdrive and reduces hypertension an average of 25 points systolic.

If angioplasty actually disrupted autonomic nerve function in jugular veins, would it not have similar effect on renal artery autonomic nerves? Yet angioplasty of renal arteries has not been shown to be of value in patients with essential hypertension. True ablation of these autonomic fibers is required to affect the autonomic function.
Salvatore JA Sclafani MD
Patient contact: ccsviliberation@gmail.com
User avatar
drsclafani
Family Elder
 
Posts: 3103
Joined: Fri Mar 12, 2010 4:00 pm
Location: Brooklyn, New York

Advertisement

Re: vagus nerve compression in CCSVI in MS

Postby Cece » Sat Mar 23, 2013 8:18 am

drsclafani wrote:
Cece wrote:
drsclafani wrote:Cece, they are talking about the nerves IN the wall of the artery, not on the vagus nerve. They did not look at the vagus itself.

I was trying to decode this: "Vasovagal Therapy- delivery of physical energy to periadventitial autonomic fibers. Not vagal compression"

I thought periadventitial autonomic fibers might mean the nerves within the outer layer of the blood vessel. These nerves within the blood vessel can be damaged by balloon angioplasty. The image above has them labelled as parasympathetic and sympathetic nerves, contained within the tunica adventitia. If they were damaged however it would be very localized. It's possible that I am trying to make sense of something that is nonsensical. I am very uncomfortable with the ballooning of nonobstructed jugulars.


Reading on his website, Synergy says: "We believe this is due to the stimulation of the vagus nerve that generally occurs during the CCSVI procedure."

I understand your reasoning. However in the quote paper, they are referring to nerve fibers in the wall of the artery, although there are autonomic fibers in the wall of the vein as well.

cece, look up renal sympathectomy by ablation of autonomic fibers embedded in the wall of the renal artery as a treatment for essential hypertension. This work is something I do on a randomized trial. In our study this treatment is indicated for uncontrolled hypertension (greater than 160 mm systolic) despite maximum tolerable doses of at least three classes of antihypertensive medications.

There is a distinct feedback between the autonomic fibers in the renal artery and the brain stem that goes awry in essential hypertension. Ablating the fibers by application of radiofrequency derived thermal energy heating the wall of the artery to about 125 degrees fahrenheit damages irrevocably these nerves, cuts the feedback mechanism, causes loss of autonomic overdrive and reduces hypertension an average of 25 points systolic.

If angioplasty actually disrupted autonomic nerve function in jugular veins, would it not have similar effect on renal artery autonomic nerves? Yet angioplasty of renal arteries has not been shown to be of value in patients with essential hypertension. True ablation of these autonomic fibers is required to affect the autonomic function.

Ok, that is a very good explanation. Thank you.
Cece
Family Elder
 
Posts: 8956
Joined: Mon Jan 04, 2010 4:00 pm

Re: vagus nerve compression in CCSVI in MS

Postby Cece » Fri Mar 29, 2013 3:51 pm

Now what about this? It's an abstract to be presented at SIR.
http://www.sirmeeting.org/index.cfm?do= ... s&abs=2424
Alterations of Vagus Nerve Electrophysiology in Response to Venoplasty; Towards a Non-Hemodynamic Explanation for Clinical Improvement Following Jugular Venoplasty in Patients with Multiple Sclerosis.
Presented During: Venous Interventions/Thrombolysis and Thrombectomy
Tue, 4/16: 4:26 PM - 4:34 PM
Ernest N. Morial Convention Center
Room: 288

Authors:
A. A. Scappaticci1, G. Soares1, E. A. Prince1, C. Muratore2
Institutions:
1. Diagnostic Imaging, Rhode Island Hospital/Warren Alpert Medical School, Providence, RI, United States. 2. Pediatric Surgery, Hasbro Childrens Hosiptal/Warren Alpert Medical School, Providence, RI, United States.

Purpose:
CCSVI is a controversial entity proposed in the development and treatment of MS. Clinical improvement after Jugular venoplasty has generated debate regarding the etiology of MS. Dysautonomia contributes to a variety of neurologic diseases, including MS. This pilot study evaluates autonomic responses to cervical venoplasty and particular changes in vagus nerve activity with PTA.

Materials:
Experimental model was (NZW) rabbit. Twenty treatments were performed in 5 rabbits under general anesthesia. Cervical vagii were exposed and hook electrodes were attached. A BioLab acquisition system was used to obtain whole nerve recordings. Spike count analysis was performed post hoc. Bilateral supracardinal veins (SCV) were catheterized. A 5mm 3 French balloon catheter ans 4F diagnostic catheter were negotiated into the right and left SCVs. Left SCV catheter served as a control. Four inflations were performed at 60s intervals with the balloon situated at the level of the right SCV adjacent to the ipsilateral upper thoracic vagal nerve. Recordings were performed before, during and after PTA of the right SCV with an average inflation pressure of 14 atm.

Results:
During venoplasty events there was increased bilateral vagus nerve activity when compared to baseline with an average range of 6-15% increase in the number of spikes during treatment. On the right the average increase in spikes ranged from 24.6 -34.7% compared to 13.7-18.7% on the left during balloon PTA.

Conclusions:
Balloon PTA of the SCV in NZW rabbits results in both bilateral increased Vagus Nerve tone and differential increase in the response of the experimental right Vagus Nerve compared to the left control. Cervical venoplasty has a direct mechanical effect on the adjacent nerve manifested as measurable physiologic change in vagus nerve activity. These preliminary data suggest further analysis of a unifying theory to explain clinical change in MS patients following jugular PTA exclusive of or in addition to the current CCSVI model. Specifically, that clinical improvement in MS patients following jugular venoplasty may be due to vagal nerve manipulation.
Cece
Family Elder
 
Posts: 8956
Joined: Mon Jan 04, 2010 4:00 pm

Re: vagus nerve compression in CCSVI in MS

Postby drsclafani » Fri Mar 29, 2013 5:02 pm

Cece wrote:Now what about this? It's an abstract to be presented at SIR.
http://www.sirmeeting.org/index.cfm?do= ... s&abs=2424
Alterations of Vagus Nerve Electrophysiology in Response to Venoplasty; Towards a Non-Hemodynamic Explanation for Clinical Improvement Following Jugular Venoplasty in Patients with Multiple Sclerosis.
Presented During: Venous Interventions/Thrombolysis and Thrombectomy
Tue, 4/16: 4:26 PM - 4:34 PM
Ernest N. Morial Convention Center
Room: 288

Authors:
A. A. Scappaticci1, G. Soares1, E. A. Prince1, C. Muratore2
Institutions:
1. Diagnostic Imaging, Rhode Island Hospital/Warren Alpert Medical School, Providence, RI, United States. 2. Pediatric Surgery, Hasbro Childrens Hosiptal/Warren Alpert Medical School, Providence, RI, United States.

Purpose:
CCSVI is a controversial entity proposed in the development and treatment of MS. Clinical improvement after Jugular venoplasty has generated debate regarding the etiology of MS. Dysautonomia contributes to a variety of neurologic diseases, including MS. This pilot study evaluates autonomic responses to cervical venoplasty and particular changes in vagus nerve activity with PTA.

Materials:
Experimental model was (NZW) rabbit. Twenty treatments were performed in 5 rabbits under general anesthesia. Cervical vagii were exposed and hook electrodes were attached. A BioLab acquisition system was used to obtain whole nerve recordings. Spike count analysis was performed post hoc. Bilateral supracardinal veins (SCV) were catheterized. A 5mm 3 French balloon catheter ans 4F diagnostic catheter were negotiated into the right and left SCVs. Left SCV catheter served as a control. Four inflations were performed at 60s intervals with the balloon situated at the level of the right SCV adjacent to the ipsilateral upper thoracic vagal nerve. Recordings were performed before, during and after PTA of the right SCV with an average inflation pressure of 14 atm.

Results:
During venoplasty events there was increased bilateral vagus nerve activity when compared to baseline with an average range of 6-15% increase in the number of spikes during treatment. On the right the average increase in spikes ranged from 24.6 -34.7% compared to 13.7-18.7% on the left during balloon PTA.

Conclusions:
Balloon PTA of the SCV in NZW rabbits results in both bilateral increased Vagus Nerve tone and differential increase in the response of the experimental right Vagus Nerve compared to the left control. Cervical venoplasty has a direct mechanical effect on the adjacent nerve manifested as measurable physiologic change in vagus nerve activity. These preliminary data suggest further analysis of a unifying theory to explain clinical change in MS patients following jugular PTA exclusive of or in addition to the current CCSVI model. Specifically, that clinical improvement in MS patients following jugular venoplasty may be due to vagal nerve manipulation.


its an interesting paper and I look forward to understanding it more fully. the question in my mind is how long will such an effect last. hows does stimulation of the vagus nerve improve vision, strength, sensation, cognition and memory and balance?
Salvatore JA Sclafani MD
Patient contact: ccsviliberation@gmail.com
User avatar
drsclafani
Family Elder
 
Posts: 3103
Joined: Fri Mar 12, 2010 4:00 pm
Location: Brooklyn, New York

Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Fri Mar 29, 2013 7:32 pm

Cece wrote:Now what about this? It's an abstract to be presented at SIR.
http://www.sirmeeting.org/index.cfm?do= ... s&abs=2424
Alterations of Vagus Nerve Electrophysiology in Response to Venoplasty; Towards a Non-Hemodynamic Explanation for Clinical Improvement Following Jugular Venoplasty in Patients with Multiple Sclerosis.
Presented During: Venous Interventions/Thrombolysis and Thrombectomy
Tue, 4/16: 4:26 PM - 4:34 PM
Ernest N. Morial Convention Center
Room: 288

Authors:
A. A. Scappaticci1, G. Soares1, E. A. Prince1, C. Muratore2
Institutions:
1. Diagnostic Imaging, Rhode Island Hospital/Warren Alpert Medical School, Providence, RI, United States. 2. Pediatric Surgery, Hasbro Childrens Hosiptal/Warren Alpert Medical School, Providence, RI, United States.

Purpose:
CCSVI is a controversial entity proposed in the development and treatment of MS. Clinical improvement after Jugular venoplasty has generated debate regarding the etiology of MS. Dysautonomia contributes to a variety of neurologic diseases, including MS. This pilot study evaluates autonomic responses to cervical venoplasty and particular changes in vagus nerve activity with PTA.

Materials:
Experimental model was (NZW) rabbit. Twenty treatments were performed in 5 rabbits under general anesthesia. Cervical vagii were exposed and hook electrodes were attached. A BioLab acquisition system was used to obtain whole nerve recordings. Spike count analysis was performed post hoc. Bilateral supracardinal veins (SCV) were catheterized. A 5mm 3 French balloon catheter ans 4F diagnostic catheter were negotiated into the right and left SCVs. Left SCV catheter served as a control. Four inflations were performed at 60s intervals with the balloon situated at the level of the right SCV adjacent to the ipsilateral upper thoracic vagal nerve. Recordings were performed before, during and after PTA of the right SCV with an average inflation pressure of 14 atm.

Results:
During venoplasty events there was increased bilateral vagus nerve activity when compared to baseline with an average range of 6-15% increase in the number of spikes during treatment. On the right the average increase in spikes ranged from 24.6 -34.7% compared to 13.7-18.7% on the left during balloon PTA.

Conclusions:
Balloon PTA of the SCV in NZW rabbits results in both bilateral increased Vagus Nerve tone and differential increase in the response of the experimental right Vagus Nerve compared to the left control. Cervical venoplasty has a direct mechanical effect on the adjacent nerve manifested as measurable physiologic change in vagus nerve activity. These preliminary data suggest further analysis of a unifying theory to explain clinical change in MS patients following jugular PTA exclusive of or in addition to the current CCSVI model. Specifically, that clinical improvement in MS patients following jugular venoplasty may be due to vagal nerve manipulation.

This reminds me of the depression and vagus nerve stimulation study I posted in this thread months ago. They attached stimulators to the vagus nerves and even without the stimulator turned on depression lifted...was the nerve stimulated just by the contact of the device? I wonder if the same phenomena isn't at play in the bunny study with the sensor they placed. Also, the info you posted says the nerve was stimulated during venoplasty. Did the heightened vagus activity last? Curious as to why activity increased in left vagus when that side wasn't ballooned.
Anonymoose
Family Elder
 
Posts: 976
Joined: Tue Oct 09, 2012 7:33 am

Re: vagus nerve compression in CCSVI in MS

Postby Cece » Sat Mar 30, 2013 10:02 pm

Interesting, anonymoose. That could also have been the dreaded placebo response. I don't think bunnies get placebo?

http://en.wikipedia.org/wiki/Endoscopic ... pathectomy
Was reading about sympathectomy, which sounds awful.
Cece
Family Elder
 
Posts: 8956
Joined: Mon Jan 04, 2010 4:00 pm

Re: vagus nerve compression in CCSVI in MS

Postby blossom » Sun Mar 31, 2013 12:32 am

dr. sclafani, reading this when treating vagus nerve
Cece wrote:Oxygen should be administered via a mask @ 6l/min and the bed tilted to head low position.

you probably don't remember me-i've always maintained that a trauma started my mess. and from the get go if i would lay flat on my back "not the same results if laying on side" i could move better. and from the get go if i tilted my head up standing or sitting positioning i could move better. as i progressed this still is that way only the results are not as dramatic. what does happen is when i lay the back of the electric wheelchair to a position that my head is actually lower than my body i get better movement and laying that way my chest takes in more oxygen. kinda like the treatment for the vagus nerve. i do have cervical spine issues that mainstream has not recognized as being a part of this whole ms thing. the same as mainstream not wanting to recognize the ccsvi connection and the work you are doing. but, none the less, would you see any connection with what i am connecting? could what i'm telling you and the location of the vagus be of interest. i know something throws a switch on and off in my neck area. i was treated for ccsvi with no positive results.

thank you for your time and interest.
User avatar
blossom
Family Elder
 
Posts: 1327
Joined: Thu Dec 03, 2009 4:00 pm
Location: south western pa.

Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Fri Apr 05, 2013 7:02 am

This is waaay out there but I found it interesting in light of the fact that calcification/thickening of the ijv valves *might* cause high frequency vibrations that *might* interfere with vagus nerve impulse transmission.

Thickened/calcified porcine valves vibrate at high frequency. Tearing a leaflet reduces vibration frequency.
http://circres.ahajournals.org/content/ ... 7.full.pdf

Current pathophysiological views on vibration-induced Raynaud's phenomenon
http://cardiovascres.oxfordjournals.org ... 3/615.full (full text available)
This review attempts to summarize and discuss contemporary pathogenetic views on vibration-induced Raynaud's phenomenon assuming its multifactorial etiology. An increase in central and peripheral sympathetic nervous activity is discussed based on different physiological indicators of autonomic dysfunction and sympathetic hyperactivity. Local acral vasodysregulation is considered. Receptor and nerve endings dysfunction presented with predominance of α2-receptor function in the digital arteries and neuronal loss in those digital cutaneous perivascular nerves containing calcitonin gene-related peptide result in deficiency of endogenous release of this powerful vasodilator. Endothelial damage and dysregulation induced by vibration and increased shear stresses are demonstrated by the elevated plasma level of thrombomodulin and of von Willebrand factor and reduced endothelium-dependent vasodilator responses. The concentrations of endothelin-1 are high, the highest being in most advanced stages. Decreased plasma thiol level, indicating increased production and activity of free radicals, contribute to vasospastic paroxysms in vibration white finger patients. Dysbalance of local vasoactive factors with opposing effects on vascular smooth muscle like endothelin and nitric oxide, endothelin and calcitonin gene-related peptide, nitric oxide and superoxide anion are discussed. Disturbed smooth muscle response is supposed. Changes in hemostasis, fibrinolysis and hemorrheology, activation of blood cells with erythrocyte hyperaggregation and red cell hypodeformability, platelet aggregation with increased release of vasoconstricting thromboxane A2 and serotonin as well as leukocyte activation, entrapment within capillaries and post-capillary venules and increased reactive oxygen species and lysosomal lytic enzymes release might also contribute to digital vasospasms and tissue damage. Elevated soluble intercellular adhesion molecule-1 levels involved in the adherence of leukocytes to endothelium and to other leukocytes have been found in patients with hand–arm vibration syndrome.

Some of that sounds MS'y. I wonder if vibrating valves adjacent to the vagus can cause a similar reaction.
Anonymoose
Family Elder
 
Posts: 976
Joined: Tue Oct 09, 2012 7:33 am

Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Fri Apr 05, 2013 2:26 pm

Apparently the flaps can vibrate. Courtesy of Marie Rhodes. :)
http://books.google.com/books?id=zIXvka ... 8Q6AEwBTgU
Second paragraph.

Can the vibration interfere with vagus function? Still questionable.
Anonymoose
Family Elder
 
Posts: 976
Joined: Tue Oct 09, 2012 7:33 am

Re: vagus nerve compression in CCSVI in MS

Postby Cece » Fri Apr 05, 2013 8:17 pm

The valve leaflets would be vibrating within the jugular vein, which has relatively thick walls (not as thick as an artery).
I am not convinced :)
Cece
Family Elder
 
Posts: 8956
Joined: Mon Jan 04, 2010 4:00 pm

Re: vagus nerve compression in CCSVI in MS

Postby NZer1 » Sat Apr 06, 2013 1:16 am

This is even more out there BUT, the NZW rabbits were also used in studies of CPn infection to understand the tissues that 'can' be infected by the bacteria, and yes nerve tissue was one of many infected.
Intracellular infection disrupts the function and processes of cells. so would testing the nerve also prompt the infection to go into hibernation, as is known to happen, and is this the Arata effect he is quoting?

If there is compression there is likely to be inflammation, one of our main enemies! Inflammation is a magnet for CPn and other opportunistic bacteria and it doesn't take long for chronic infection to deplete ATP and host cell functions.
If there is more and more research results showing infection is a part player in de-generative diseases are we seeing the effects in nerve cells in a new way?
Is stroking inflated nerves actually giving the wrong impression and are we needing to hear from the patients rather than persist with trying to get blood out of the stone? If we are going to progress this angle and Mike doesn't know what is happening then monitoring the patients is more productive?
Are we dealing with too many unknowns at one time?
User avatar
NZer1
Family Elder
 
Posts: 1504
Joined: Thu Feb 18, 2010 4:00 pm
Location: Rotorua New Zealand

Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Sat Apr 06, 2013 6:46 am

Cece wrote:The valve leaflets would be vibrating within the jugular vein, which has relatively thick walls (not as thick as an artery).
I am not convinced :)

I'm not convinced either. But...the vein, with a thinner wall, is in a sheath with the vagus. Maybe that makes it easier for the valve vibrations to affect the nerve? Weak...I know. lol Also, in the link above to Marie's book, the vein wasn't completely blocked. It just had a valve leaflet vibrating. Repairing the leaflet caused improvements. Was this due to change in flow or elimination of vibrating parts? Arata seems pretty convinced about the impact of ballooning on the vagus in the sheath...there has to be a reason for that so I'm trying to have a little faith and work with his theory (in a way).

I still think the far greater impact has to be from the reduction of CSF pressure on the brain stem and cranial nerve roots but even that hasn't fully panned out to make sense to me. If PTA doesn't reduce pressure in the sinuses, how does CSF flow improve so quickly?? The improved perfusion also strikes me as more important as it likely causes regeneration of atrophied glands essential to autonomic function. The vagus, in Arata's context, is just a sidenote for me. :P
Anonymoose
Family Elder
 
Posts: 976
Joined: Tue Oct 09, 2012 7:33 am

Re: vagus nerve compression in CCSVI in MS

Postby Cece » Sat Apr 06, 2013 9:15 am

Dr. Dake did a venogram with the assistance of an intravascular ultrasound. He discovered a flap inside Mark's right jugular vein at the clavicle/valve level that was completely invisible to the venogram and MRV. This flap was vibrating with the pulise and was very long. High above this area, there was a stenosed area with the pressure gradient of 4 mm/Hg. When Dr. Dake repaired the flap, the upper area opened up and the pressure gradient disappeared, along with the collateral network.

This was an extra long valve leaflet that was not seen on venogram or MRV, but was seen on IVUS. (Go IVUS!) When the lower jugular stenosis (the valve leaflet) was ballooned, the upper jugular opened up. An indication back in 2010 that those upper jugular stenoses may appear to be in need of treating when they shouldn't be.

I do see the word vibrating there. If it's an immobilized fixed valve leaflet, it might move incidentally with each pulse beat but not open up and close as it should. Vibrating with the pulse might mean less vibration than if it was vibrating constantly.

If the sheath had any amplification effect, then maybe?
NZer1 wrote:Are we dealing with too many unknowns at one time?

Fewer unknowns now, I think, then there were back in 2010?
If Dr. Sclafani is not seeing evidence of an infectious process when he looks at the veins, then I trust that.
Cece
Family Elder
 
Posts: 8956
Joined: Mon Jan 04, 2010 4:00 pm

Re: vagus nerve compression in CCSVI in MS

Postby Anonymoose » Sat Apr 06, 2013 9:40 am

Cece wrote:
Dr. Dake did a venogram with the assistance of an intravascular ultrasound. He discovered a flap inside Mark's right jugular vein at the clavicle/valve level that was completely invisible to the venogram and MRV. This flap was vibrating with the pulise and was very long. High above this area, there was a stenosed area with the pressure gradient of 4 mm/Hg. When Dr. Dake repaired the flap, the upper area opened up and the pressure gradient disappeared, along with the collateral network.

This was an extra long valve leaflet that was not seen on venogram or MRV, but was seen on IVUS. (Go IVUS!) When the lower jugular stenosis (the valve leaflet) was ballooned, the upper jugular opened up. An indication back in 2010 that those upper jugular stenoses may appear to be in need of treating when they shouldn't be.

I do see the word vibrating there. If it's an immobilized fixed valve leaflet, it might move incidentally with each pulse beat but not open up and close as it should. Vibrating with the pulse might mean less vibration than if it was vibrating constantly.

If the sheath had any amplification effect, then maybe?
NZer1 wrote:Are we dealing with too many unknowns at one time?

Fewer unknowns now, I think, then there were back in 2010?
If Dr. Sclafani is not seeing evidence of an infectious process when he looks at the veins, then I trust that.

I wonder if his tinnitus was pulsatile...pulsing with the vibration. Also got sidetracked when you pointed out upper stenosis corrected when the valve part was repaired (abolished?). Vibration and vasospasm. Pick a study. http://scholar.google.com/scholar?q=vib ... CCgQgQMwAA I woooonnnndeeerr. Lol
Anonymoose
Family Elder
 
Posts: 976
Joined: Tue Oct 09, 2012 7:33 am

Re: vagus nerve compression in CCSVI in MS

Postby NZer1 » Sat Apr 06, 2013 1:04 pm

Cece wrote:
Dr. Dake did a venogram with the assistance of an intravascular ultrasound. He discovered a flap inside Mark's right jugular vein at the clavicle/valve level that was completely invisible to the venogram and MRV. This flap was vibrating with the pulise and was very long. High above this area, there was a stenosed area with the pressure gradient of 4 mm/Hg. When Dr. Dake repaired the flap, the upper area opened up and the pressure gradient disappeared, along with the collateral network.

This was an extra long valve leaflet that was not seen on venogram or MRV, but was seen on IVUS. (Go IVUS!) When the lower jugular stenosis (the valve leaflet) was ballooned, the upper jugular opened up. An indication back in 2010 that those upper jugular stenoses may appear to be in need of treating when they shouldn't be.

I do see the word vibrating there. If it's an immobilized fixed valve leaflet, it might move incidentally with each pulse beat but not open up and close as it should. Vibrating with the pulse might mean less vibration than if it was vibrating constantly.

If the sheath had any amplification effect, then maybe?
NZer1 wrote:Are we dealing with too many unknowns at one time?

Fewer unknowns now, I think, then there were back in 2010?
If Dr. Sclafani is not seeing evidence of an infectious process when he looks at the veins, then I trust that.


Great waking up to these posts :)
I have some other thoughts.
Cece the infection is not always on the inside of the veins! There can be wall only infection or artery/vein internal only infection or both. Macrophages are carriers of the intracellular infection, the CPn has modified the DNA of the host cells and is 'invisible' to the immune system, hence the name 'Stealth Bacteria'.
So I wouldn't write off infection having a part to play somewhere, the findings of CPn cells on brain autopsy by Stratton in 95/98% of PwMS are hard to dismiss.
The second thought is regarding the 'fixed' valve statement and is doppler or IVUS technology actually able to indicate what has frequency and what doesn't, are we needing another mode of measurement? eg sound or pulse measurement at higher frequency.
The Arata findings may be a body warning system that there is an issue with blood and CSF flows and the symptom group that crosses nearly all de-generative diseases aka dysautonomia is simply a warning to change lifestyle, diet, stresses and mindfullness?
If Terry Wahls/ George Jelinek can achieve the same outcomes (overtime) with their methods as Mike Arata's PTA then is that actually the link between dysautonomia and Vagus stroking and Lifestyle, diet etc?

Paulo's (Zamboni) leaflet removal tool he is Patenting is probably another hint that there are oscillation frequency disruption of the nerve conduction methods.

When we hear the term valve leaflet thickening is that proven? Is it also possible what we are seeing is the valve oscillation and the doppler and IVUS are working at a different frequency and make the moving leaves look thickened?

In autopsy study are the valve leaves flexible at all? Are there indications of possible movement at a set rate that could be the frequency required for the signal type that is 'dysautonomic'?

Almost all de-generative diseases have dysautonomia as a symptom and when you look at lists of symptoms across the board there are only a few 'extra' symptoms that define the choice of dx label.
When you look at the methods of Wahls/Jelineck I believe there is a need to look at the differences in the diseases and see what the fine points or 'extra' symptoms indicate.
If the base symptom group can be managed by one method then can the symptoms that differentiate dx categories give us HOPE for finding causes to diseases such as 'MS'? Another way to word this is 'MS' equals dysautonomia plus vascular reflux/back flow into the brain causing Dawsons Fingers from sources such as the spinal veins (Franz Schelling)?
User avatar
NZer1
Family Elder
 
Posts: 1504
Joined: Thu Feb 18, 2010 4:00 pm
Location: Rotorua New Zealand

PreviousNext

Return to Chronic Cerebrospinal Venous Insufficiency (CCSVI)

 


  • Related topics
    Replies
    Views
    Last post

Who is online

Users browsing this forum: No registered users