International Society for Neurovascular Disease (March 2011)

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

Postby MrSuccess » Tue Mar 15, 2011 12:04 pm

nice job explaining that CeCe.

once again ..... Professor Zamboni has provided the world with a jaw-dropping revelation....

I also tip my hat to the inventors of such medical devices ..... without them ....where would we be ?

let's see if I understand this correctly ..... so we have two people laying side by side .... each harnessed to a chair ..... a device shaped like a collar ..... is fixed to their necks ...... these neck collars are able to measure blood flow..... BOTH people show good blood flow .... more or less the same ..... then ..... the chairs are slowly risen until the two people are now sitting up ...... now blood flow is vastly different in the two people. One has no change in blood flow ..... it is the same as when they were lying down ..... the other persons bloodflow is much reduced now that they are sitting upright ...... that person has been pre-test diagnosed as having MS.

This discovery is huge.


Bravo Professor Zamboni





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Postby cheerleader » Tue Mar 15, 2011 12:06 pm

Wow, you are fast, Cece :)

Note the research on axonal asphyxial damage...looks like hypoperfusion!

ROLE OF OXYGENATION AND TISSUE DRAINAGE
Among the questions that were answered at the Meeting was also a fundamental one which relates to the observation made by Bruce Trapp from Cleveland (one of the most eminent MS researchers) according to whom nerve cell damage and death are due to an axonal asphyxial phenomenon which has not been yet completely clarified.

Data from a joint study conducted with perfusional MRI by the University of Buffalo, Prof. Zamboni and Dr Salvi (see relevant press release) - soon to be published in the BMC Medicine journal - were presented in Bologna by Prof. Robert Zivadinov, showing that this asphyxial cell phenomenon could be related to severe obstruction of the extracranial veins, thus providing a first substantial answer to asphyxial hypothesis in MS.
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Postby Cece » Tue Mar 15, 2011 12:32 pm

I was 34 minutes slower than you and the Facebook site! :)

Asphyxial axonal injury sounds like the impact on the axons from the hypoxia. This is of particular interest to me. (With my severe bilateral jugular blockages, I had a lot of hypoxia going on.)

MrSuccess wrote:let's see if I understand this correctly ..... so we have two people laying side by side .... each harnessed to a chair ..... a device shaped like a collar ..... is fixed to their necks ...... these neck collars are able to measure blood flow..... BOTH people show good blood flow .... more or less the same ..... then ..... the chairs are slowly risen until the two people are now sitting up ...... now blood flow is vastly different in the two people. One has no change in blood flow ..... it is the same as when they were lying down ..... the other persons bloodflow is much reduced now that they are sitting upright ...... that person has been pre-test diagnosed as having MS.

This discovery is huge.


Bravo Professor Zamboni





Mr. Success

Zamboni and huge discovery - now there are words that go well together. :)

The only correction I'd say is that the neck collar device measures volume, not flow. I don't think we show good blood flow while lying down. (We don't show good blood flow in any position.) I don't know if the supine volume of the MS patient's neck is the same as a healthy patient's.

The measureable difference is when the patient is aggressively sat up. (Not slowly but aggressively.) The healthy patient has a near-immediate decrease in the volume of their neck, as the congestion is swept away, the jugular size decreases, all is well. The MS patient has a very slow decrease, which indicates outflow obstructions, as the volume of blood flow is having a hard time clearing. It is amazing that these things are measureable.

This reminds me of the Zamboni protocol ultrasound, when they are measuring if there is a decrease in the size of the jugulars sitting as compared to lying down. If there is a decrease upon sitting up, that is normal and healthy. If there is no decrease or an increase, that is one of the five criteria that is needed for a CCSVI diagnosis done by doppler sonography.

Hope this helps! I am still working this out myself, I may have some of it wrong.
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Postby MrSuccess » Tue Mar 15, 2011 12:50 pm

i'm just trying to generalize .... to explain a rough outline .... Dr. Zamboni hasn't given me specifics yet :wink:

I can hear the wheels spinning in the naysayers [ Neurologists ] ...... heads .... this will be another procedure they can arrange to have '' muffed up '' ...... and thus refute this wonderful diagnosis tool.

and yes CeCe .... I understand Flow and Pressure .... very well.

It is usually an either / or situation ........


what a great day for CCSVI ...... can tomorrow get even better ?





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Postby Cece » Tue Mar 15, 2011 1:03 pm

I understand flow, I still struggle with pressure. :)

I think we have many better tomorrows ahead of us. :)

ISNVD has been full of the good stuff. There may be some more at SIR in two weeks? Not sure if it can begin to compare.

I looked to see if Dr. Trapp had written about hypoxia and neurons before:

Volume 8, Issue 3, March 2009, Pages 280-291

doi:10.1016/S1474-4422(09)70043-2 | How to Cite or Link Using DOI

Virtual hypoxia and chronic necrosis of demyelinated axons in multiple sclerosis

Bruce D Trapp PhDa, , and Peter K Stys MDb

aDepartment of Neurosciences, Cleveland Clinic, Cleveland, OH, USA

bDepartment of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada


Available online 17 February 2009.

Summary
Multiple sclerosis (MS), an inflammatory demyelinating disease, is a major cause of neurological disability in young adults in the developed world. Although the progressive neurological disability that most patients with MS eventually experience results from axonal degeneration, little is known about the mechanisms of axonal injury in MS. Accumulating evidence suggests that the increased energy demand of impulse conduction along excitable demyelinated axons and reduced axonal ATP production induce a chronic state of virtual hypoxia in chronically demyelinated axons. In response to such a state, key alterations that contribute to chronic necrosis of axons might include mitochondrial dysfunction (due to defective oxidative phosphorylation or nitric oxide production), Na+ influx through voltage-gated Na+ channels and axonal AMPA receptors, release of toxic Ca2+ from the axoplasmic reticulum, overactivation of ionotropic and metabotropic axonal glutamate receptors, and activation of voltage-gated Ca2+ channels, ultimately leading to excessive stimulation of Ca2+-dependent degradative pathways. The development of neuroprotective therapies that target these mechanisms might constitute effective adjuncts to currently used immune-modifying agents.

http://tinyurl.com/4maxxeq

He's using a different explanation to come up with why the axons would have lowered oxygen levels, but everything from that point fits with CCSVI and axonal asphyxia and what consequence hypoxia has on the axons.

Dr. Trapp is another of the neurologists who presented at ISNVD, that is what set this conference apart from ISET and upcoming SIR, as those are all just for the vascular guys and this one succeeded in its mission to be both neuro and vascular.
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Postby cheerleader » Tue Mar 15, 2011 2:06 pm

Another neurologist who was keynote speaker at ISNVD was Dr. Berislov Zlokovic of the University of Rochester who spoke on the connection of the endothelium, BBB, vasculature, and neurodegeneration. I first contacted Dr. Zlokovic in 2008, when I was sending out my endothelial paper to different universities. I had included some of Dr. Zlokovic's research in the original endothelial health paper. Jeff and I are alumni from the University of Rochester's Eastman School of Music, and I was hoping to get a meeting with Dr. Zlokovic when we were in town for masterclasses....but we were never able to meet. And now, to see him speaking at the CCSVI conference in Bologna was incredibly gratifying.

Here are Dr. Zlokovic's CV and publications:
http://www.urmc.rochester.edu/people/?u ... esearchers

An interesting aside, Dr. Zlokovic dedicated his research to neurodegeneration after a dear friend developed ALS....he is a very well-respected researcher.
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Postby zinamaria » Tue Mar 15, 2011 3:10 pm

Wow, my head is spinning (that's while sitting upright! oh oh, better watch flow!!), but really this is so astonishing, and although I am connecting the dots, you sure help me out cece and cheer!

Sou, you're like our private detective, getting it all as it's happening, again molto grazie!
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Postby cheerleader » Tue Mar 15, 2011 4:16 pm

Just posted on the plethysmography collar on Facebook (wow! What an incredible use of current technology by Dr. Zamboni!) and realized it was probably the Doepp study that pointed him in this direction. Remember how they found increased blood volume in pwMS in the upright position!! Voila! The collar shows the difference between normals and pwCCSVI/MS....slowed venous drainage thru the extracranial veins. Brilliant.
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Postby MrSuccess » Tue Mar 15, 2011 4:22 pm

I don't think they spelled '' dope'' right. :wink:




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Postby Cece » Wed Mar 16, 2011 5:57 pm

cheerleader wrote:
Data from a joint study conducted with perfusional MRI by the University of Buffalo, Prof. Zamboni and Dr Salvi (see relevant press release) - soon to be published in the BMC Medicine journal - were presented in Bologna by Prof. Robert Zivadinov, showing that this asphyxial cell phenomenon could be related to severe obstruction of the extracranial veins, thus providing a first substantial answer to asphyxial hypothesis in MS.

Is this the study that was just published or is it a different one? I didn't know there was anything about the "asphyxial cell phenomenon" in there. Very interested in this.

I am encouraged by everything coming out of ISNVD. So many different directions that are being explored. Our researchers have been busy and I think we'll be keeping them busy for the foreseeable future as well. :D
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Postby Drury » Wed Mar 16, 2011 7:56 pm

Thanks everyone for all the new info. Brilliant!
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Postby Cece » Thu Mar 17, 2011 4:14 pm

Cece wrote:I looked to see if Dr. Trapp had written about hypoxia and neurons before:

Volume 8, Issue 3, March 2009, Pages 280-291

doi:10.1016/S1474-4422(09)70043-2 | How to Cite or Link Using DOI

Virtual hypoxia and chronic necrosis of demyelinated axons in multiple sclerosis

Bruce D Trapp PhDa, , and Peter K Stys MDb

aDepartment of Neurosciences, Cleveland Clinic, Cleveland, OH, USA

bDepartment of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Calgary, Alberta, Canada


Available online 17 February 2009.

Summary
Multiple sclerosis (MS), an inflammatory demyelinating disease, is a major cause of neurological disability in young adults in the developed world. Although the progressive neurological disability that most patients with MS eventually experience results from axonal degeneration, little is known about the mechanisms of axonal injury in MS. Accumulating evidence suggests that the increased energy demand of impulse conduction along excitable demyelinated axons and reduced axonal ATP production induce a chronic state of virtual hypoxia in chronically demyelinated axons. In response to such a state, key alterations that contribute to chronic necrosis of axons might include mitochondrial dysfunction (due to defective oxidative phosphorylation or nitric oxide production), Na+ influx through voltage-gated Na+ channels and axonal AMPA receptors, release of toxic Ca2+ from the axoplasmic reticulum, overactivation of ionotropic and metabotropic axonal glutamate receptors, and activation of voltage-gated Ca2+ channels, ultimately leading to excessive stimulation of Ca2+-dependent degradative pathways. The development of neuroprotective therapies that target these mechanisms might constitute effective adjuncts to currently used immune-modifying agents.

http://tinyurl.com/4maxxeq

What he said at ISNVD is almost identical to this previous work:
Hypoxic-like Aspects of MS
Bruce D Trapp, Department of Neurosciences,
Lerner Research Institute, Cleveland Clinic
Multiple sclerosis (MS), an inflammatory demyelinating disease, is a major cause of
neurological disability in young adults in the developed world. Although the
progressive neurological disability that most patients with MS eventually experience
results from axonal degeneration, little is known about the mechanisms of axonal injury
in MS. Accumulating evidence supports the concept that the increased energy demand
of impulse conduction along excitable demyelinated axons and reduced axonal ATP
production induce a chronic state of virtual hypoxia in chronically demyelinated axons.
In response to such a state, key alterations that contribute to chronic necrosis of axons
include mitochondrial dysfunction (due to defective oxidative phosphorylation or nitric
oxide production), Na influx through voltage-gated Na channels and axonal AMPA
receptors, release of toxic Ca from the axoplasmic reticulum, and activation of voltagegated
Ca channels, ultimately leading to excessive stimulation of Ca-dependent
degradative pathways. The development of neuroprotective therapies that target these
mechanisms constitute effective adjuncts to currently used immune modifying agents.
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Postby Cece » Thu Mar 17, 2011 11:07 pm

So much information coming out now! here is Arlene Hubbard on Facebook:
http://www.facebook.com/notes/arlene-pe ... 6662914970
Neurovascular Mechanisms in Neurodegenerative Diseases-B Zlokovic

Dr Zlokovic was the keynote speaker and is a world renowned scientist and (opera singer!).He described the triad of .: Neuro,inflammatory, and vascular...the perfect storm. He suggested that new pharmaceuticals would address the vascular component. He reviewed the literature showing abnormal perfusion, damaged endothelium including micro hemorrhage, periocyte loss in humans and animals. He is studying novel pharmaceuticals that will target inflammation and endothelial pathology.

(much more through the link)

Novel pharmaceuticals that will target inflammation and endothelial pathology! I like some pharma, like the Arixtra and aspirin and nuvigil. Perhaps there will be something for us. I like the description of the triad (neurological, inflammatory & vascular) as the perfect storm. That feels about right.
The pathology of the extracranial venous wall in MS- G Gabbiani

He showed abnormalities in the vein wall in MS which could not be explained by traditional atherosclerotic disease.

Are these the collagen differences? Dr. Zamboni had some very interesting slides on this at ISET.
Plethysmography and multiple sclerosis: analysis of novel data-S.J. Shepherd

Dr Shepherd, an engineer showed that neck venous flow could be modeled with simple mathmatical algorithms.

Simple! Or at least, simple to an engineer.

There are just so many presentations, so many ideas, so much ground-breaking.

MRI in treatment planning- M Haacke

Dr Haacke, the acknowledged expert in MR explained the superiority of MR. MR is the gold standard for describing MS lesions, it's the only technology that describes iron accumulation,it's the only technology that visualizes small veins, and it's the only technology that describes and objectively quantifies venous flow independent of operator expertise, which allows objective pre and post treatment comparison.

There's the argument in favor of MRV.
4D Magnetic Resonance Velocity Measurements in the Internal Jugular veins-CJ Elkins

Dr Dake presented for Dr Elkins. Catheter venography is a"tarnished" gold standard. CNS venous flow,not anatomy ,is the key to pathophysiology. New MR venous flow techniques show abnormal flow amplitude and phase in MS patients. New MRV technique provides detailed information on venous flow.

Catheter venogram as a tarnished gold standard? MRV is better? Abnormal flow amplitude and phase: are these in the haacke protocol or is this new?

Flow not anatomy is the key. But the anatomy is what can be treated directly, then resulting in changes in the flow. Much to think about here. It has definitely been a candy store, a feast, more than I expected.
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