Dr. Zivadinov finds CCSVI in 100% of pwMS, 0% of controls

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

Re: Let's Be Skeptics

Postby ikulo » Tue Mar 08, 2011 2:14 pm

MarkW wrote:The hypoperfusion may occur early or late in MS progression no one knows.
MarkW


Mark, there have been a few studies noting hypoperfusion in MS as compared to severity of MS. Dr. Grossman has done ncredibly fastinating radiological studies regarding this matter. Here is a quote from one of his papers:

Compared to RR-MS, PP-MS patients showed significantly lower CBF in the periventricular NAWM (p=0.002) and lower CBV in the periventricular and frontal NAWM (p values: 0.0029 and 0.022). EDSS was significantly correlated with the periventricular CBF (r=-0.48, p=0.0016) and with the periventricular and frontal CBV (r=-0.42, p=0.015; r=-0.35, p=0.038, respectively)

http://www.ncbi.nlm.nih.gov/pubmed/16996280
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Postby cheerleader » Tue Mar 08, 2011 2:20 pm

That's a great paper, Ikulo...
here's an entire thread on hypoperfusion. This was the reason I started on the vascular path in the first place. Dr. Haacke has some research coming out on perfusion as well. This is a trememndous piece of the MS puzzle.

http://www.thisisms.com/ftopict-7708.html


Hypoperfusion comes first. We do know this....
http://www.ajnr.org/cgi/content/full/28/4/767

Support for Primary Hypoperfusion in MS

RECENT FINDINGS: Compelling evidence is accumulating for pathological changes in normal-appearing white matter of MS patients, which occur before the actual development of the active demyelinating lesion. Focal disorder has been documented in normal-appearing white matter of MS months to years before the appearance of gadolinium-enhancing lesions.

SUMMARY: Preactive lesions in MS represent early stages in the formation of destructive MS lesions. As many of them spontaneously resolve, they are expected to hold important clues to stop the inflammatory process in MS.


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Postby David1949 » Tue Mar 08, 2011 7:26 pm

This part seems to reconfirm Zamboni's original work, a 100% correlation:
“All 16 MS patients fulfilled the diagnosis of CCSVI (median VH = 4 and
median VHISS = 9) and none of the HC (Table 1) (P < 0.001, Fisher’s exact test). This means a CCSVI prevalence in this small group of MS patients of 100%, with prevalence
of 0% in HC.” (From pg 11)

Not sure what this means though:
“No results for correlation between VHISS and CBV or MTT survived multiple
comparison correction.” (From pg 2)
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Postby cheerleader » Wed Mar 09, 2011 8:40 am

Here is Dr. Zamboni at a conference, explaining this study. It is in Italian, but has been translated by Angela Cleary (our dear Italian friend who now suffers with PML from tysabri).

Dr. Zamboni explains how the participants were selected by Buffalo, and blinded. Buffalo chose 8 normals and 8 with MS and sent them to him. They had the normals act like they had MS, and trained them in the US, by having them meet their MS "twins." Dr. Zamboni was able to find CCSVI in pwMS, not the controls. He then explains the correlation that was found between doppler ultrasound (showing CCSVI) and the lack of cerebral veins, perfusion, iron deposition, slowed mean transit time and slowed cerebral spinal fluid uptake in MS brains when the pwMS were tested with MRI technology. The normals did not have this. It is very illuminating.

link to video

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Postby tzootsi » Wed Mar 09, 2011 9:04 am

Cheer, very interesting video. In addition to blood circulation, Dr. Z talks about the circulation of cerebrospinal fluid. This is something that's rarely discussed by doctors, but is a favorite topic of chiropractors.
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Postby 1eye » Wed Mar 09, 2011 9:43 am

Hypoperfusion comes first. We do know this....
http://www.ajnr.org/cgi/content/full/28/4/767


CONCLUSION: In the normal-appearing corpus callosum of patients with RRMS, decreasing perfusion is correlated with decreasing MD. These findings are more consistent with what would be expected in primary ischemia than in secondary hypoperfusion from WD.


Without having read the whole paper, that conclusion in the abstract sounds significant to me. MD means mean diffusivity, and I can only guess at that.

Primary ischemia, well I believe CCSVI is a form of primary ischemia. It means restrictions in blood flow due to localized problems, I think.

WD means wallerian degeneration, which is severed nerves or axons (also I think).

My diagnosis MRI showed degeneration, atrophy in my corpus callosum. My amateur opinion is that this is improving because I less often have what I was calling 'finger dyslexia' causing me to reverse keys on the keyboard between my left and right hands. I really don't know but I associated this with the piece that connects my two brain halves together. I also reversed digits in speech and maybe that has more to do with improved working memory (see the video Cheerleader linked to).

People have been observed who had broken corpus callosums. Does anybody know if they could type? Or play piano?
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'MS' is over - if you want it
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Postby MrSuccess » Wed Mar 09, 2011 3:22 pm

might I suggest TIMS members take the 10:20 to watch the Professor Zamboni video link posted by Ringleader .

now I'm really looking forward to the soon -to- be published BNAC paper on CCSVI by Dr. Zivadov...

And the upcoming CCSVI conference in Italy - March 13-14th-15th -

and finally ..... some icing on the cake ..... it appears Big Pharma has gotten the message ...... and seem to be moving on to other , more lucrative drug research ..... for other diseases .

Hmmmm....... I wonder why .... :twisted:



I like twins . :wink:



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Postby Cece » Wed Mar 09, 2011 3:59 pm

MrSuccess wrote:now I'm really looking forward to the soon -to- be published BNAC paper on CCSVI by Dr. Zivadov...

And the upcoming CCSVI conference in Italy - March 13-14th-15th -

I am looking forward to these too. ISNVD starts this weekend. :)
and finally ..... some icing on the cake ..... it appears Big Pharma has gotten the message ...... and seem to be moving on to other , more lucrative drug research ..... for other diseases .

We might also see them speed up the release of the oral MS drugs (if it can be sped up) so as to maximize the gain from them, if indeed in five or ten years CCSVI venoplasty will be the standard of care and the immune suppressing drugs will be a secondary treatment for people who do not respond to the venoplasty.
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Postby MrSuccess » Wed Mar 09, 2011 5:18 pm

better remind me CeCe .... ISNVD ..... where , when .... I know why :wink:



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Postby Cece » Wed Mar 09, 2011 5:20 pm

It's the conference this weekend in Italy. ISNVD = International Society of Neuro Vascular Disorders. Dr. Zamboni is the president, now that is high Society!
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Postby MrSuccess » Wed Mar 09, 2011 7:57 pm

grazie


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Postby Jugular » Wed Mar 09, 2011 8:21 pm

cheerleader wrote:Dr. Zamboni explains how the participants were selected by Buffalo, and blinded. Buffalo chose 8 normals and 8 with MS and sent them to him. They had the normals act like they had MS, and trained them in the US, by having them meet their MS "twins." Dr. Zamboni was able to find CCSVI in pwMS, not the controls. He then explains the correlation that was found between doppler ultrasound (showing CCSVI) and the lack of cerebral veins, perfusion, iron deposition, slowed mean transit time and slowed cerebral spinal fluid uptake in MS brains when the pwMS were tested with MRI technology. The normals did not have this. It is very illuminating.

Could Buffalo have sent Zamboni pre-screened textbook MS patients with CCSVI and controls without? Allso, no matter how brilliant the acting, it would be pretty easy for a doctor (especially one personally familiar with neurological impairment) to spot MS pretenders - for instance someone pretending to hobble along with nice juicy symmetrical calve muscles.
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Postby cheerleader » Wed Mar 09, 2011 10:20 pm

Jugular wrote:Could Buffalo have sent Zamboni pre-screened textbook MS patients with CCSVI and controls without? Allso, no matter how brilliant the acting, it would be pretty easy for a doctor (especially one personally familiar with neurological impairment) to spot MS pretenders - for instance someone pretending to hobble along with nice juicy symmetrical calve muscles.


I don't know jug...maybe it's all smoke and mirrors. All I know is that in this study, pwMS have slowed bloodflow, iron deposition and it related to how severely their venous return is hampered. And the normals didn't. And Dr. Zivadinov participated in this study, and is speaking about it in Bologna in a cuppla weeks.
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Postby Cece » Thu Mar 10, 2011 7:40 am

WD means wallerian degeneration, which is severed nerves or axons (also I think).

Wallerian degeneration? Yes...axons as you know are the long branches out from a nerve cell. If an axon gets severed, the branch that is out on its own is no longer able to get food and nutrients from the nerve cell, so that branch shrivels up and dies. In the peripepheral nervous system, the nerve puts out a new axon branch, things reconnect, all is well. In the brain, glial cells often get in the way and form a blockage and the neuron is not able to grow a new branch.

Why is wallerian degeneration seen in MS? There would be no point of severage. I assume it means the axonal damage or axons dying from the outmost point inward. If we look at what CCSVI might mean in this context, my guess is that the neurons are not receiving enough nutrients and glucose, and what nutrients and glucose they get are not enough to feed the entire nerve cell all the way out to the end of the axons, so the axon goes unfed and undernourished and eventually begins to die from the outmost point inward.

So, to me, wallerian degeneration means that pre-CCSVI treatment, we should keep the level of nutrients in our body high and our glucose levels steady. Post-CCSVI treatment, if the wallerian degeneration process has already started, unfortunately it may continue, if the damage is already too great. This is my best understanding of this. The name "Wallerian" comes from the guy (Waller?) who discovered the phenomenon, but it's specifically most commonly in reference to severed axons, so it's odd that we see the same process in MS where the axons are not severed.
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Postby Jugular » Thu Mar 10, 2011 9:06 am

cheerleader wrote:I don't know jug...maybe it's all smoke and mirrors. All I know is that in this study, pwMS have slowed bloodflow, iron deposition and it related to how severely their venous return is hampered. And the normals didn't. And Dr. Zivadinov participated in this study, and is speaking about it in Bologna in a cuppla weeks.
cheer
Hardly smoke and mirrors Cheer.

I'm just pointing out the obvious hard questions that are going to be asked about this study since it is saying once again that an US can reliably detect CCCVI and CCSVI is 100% in MS patients and 0% in controls.

It would be better, I think, if someone other than Zamboni interacted with the patients and employed the US while Zamboni was restricted to interpreting the results. This would remove all doubt and the need for the controls having to feign disability.

Like it or not, Zamboni's credibility has been under attack from the beginning and he needs to better insulate himself from this sort of negative scrutiny in order for his claims about the effectiveness of US as a detection tool and the prevalence of CCSVI in MS patients to gain acceptance.

The other part of the study mentioned by you is very encouraging though
!
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