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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.

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.

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 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.

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.

Cece wrote: Oxygen should be administered via a mask @ 6l/min and the bed tilted to head low position.

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.

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

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.

NZer1 wrote:Are we dealing with too many unknowns at one time?

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.

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.