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

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

Postby cheerleader » Mon Mar 07, 2011 4:27 pm

Dr. Zivadinov and Dr. Zamboni collaborated on a study of slowed cerebral bloodflow in pwMS, also known as hypoperfusion. They tested 16 pwMS and 8 healthy controls.

All of the pwMS had CCSVI, as noted by doppler ultrasound. All of the healthy controls did not.

They found slowed bloodflow in all of the people with MS...it especially affected cerebral blood flow in the gray matter.

The worse the venous obstructions, the less cerebral bloodflow. Severity of CCSVI was directly related to severity of hypoperfusion in CBF.

This paper will never be published in a neurological journal....so, the doctors kindly published it on an open access site. This research was also presented at ECTRIMS, where it received little fanfare and no press.
Here's the pdf. Enjoy!
http://www.biomedcentral.com/content/pd ... 5-9-22.pdf
cheer
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Re: Dr. Zivadinov finds CCSVI in 100% of pwMS, 0% of control

Postby frodo » Mon Mar 07, 2011 5:44 pm

cheerleader wrote:Dr. Zivadinov and Dr. Zamboni collaborated on a study of slowed cerebral bloodflow in pwMS, also known as hypoperfusion. They tested 16 pwMS and 8 healthy controls.

All of the pwMS had CCSVI, as noted by doppler ultrasound. All of the healthy controls did not.

They found slowed bloodflow in all of the people with MS...it especially affected cerebral blood flow in the gray matter.

The worse the venous obstructions, the less cerebral bloodflow. Severity of CCSVI was directly related to severity of hypoperfusion in CBF.

This paper will never be published in a neurological journal....so, the doctors kindly published it on an open access site. This research was also presented at ECTRIMS, where it received little fanfare and no press.
Here's the pdf. Enjoy!
http://www.biomedcentral.com/content/pd ... 5-9-22.pdf
cheer


Do you mean that this was available at ECTRIMS and the conclusion was "CCSVI is not likely the cause of MS"? What the hell is happening in the medical world?

The first Zamboni study has now been replicated. What else can be done to persuade people?
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Postby orion98665 » Mon Mar 07, 2011 6:32 pm

Cheer, thank you once again. Great info!!


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Postby jackiejay » Mon Mar 07, 2011 8:18 pm

why did it get no fanfare and no press?...I don't understand....give it to the press...perhaps CTV would be interested in following up....
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Postby marcstck » Mon Mar 07, 2011 8:46 pm

Unless I'm reading it completely wrong, this study used 3T MRV imaging, not Doppler Ultrasound.

Just trying to be accurate…

Also, looked at the whole paper, and it was originally presented at the AAN convention in April 2010. So it's about one year old.
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Postby cheerleader » Mon Mar 07, 2011 10:13 pm

marcstck wrote:Unless I'm reading it completely wrong, this study used 3T MRV imaging, not Doppler Ultrasound.


CCSVI was established using blinded doppler ultrasound on 16 pwMS and 8 controls with the Zamboni criteria.

Cerebral venous return was examined using echo-color Doppler equipped with 2.5 and7.5 to 10 MHz transducers (Esaote-Biosound My Lab 25, Genoa, Italy), with the subject positioned on a bed tilted at 90° and 0° as previously described [2]. All subjects were scanned in a blinded manner following the established protocol for diagnosis of CCSVI [2], consisting of transcranial and extracranial echocolor Doppler to measure the following five venous hemodynamic (VH) parameters indicative of CCSVI: (1) reflux in the IJVs and/or in the vertebral veins (VVs) in sitting and in supine positions (90° and 0°), with reflux defined as flow directed toward the brain for a duration of >0.88 seconds; (2) reflux in the intracranial veins with reflux defined as reverse flow for a duration of 0.5 seconds in one of the insonated veins (superior and inferior petrosus sinus, and/or Rosenthal vein); (3) B-mode abnormalities causing absence of flow or significant flow disturbances (vestigial valves, septum, immobile valve leaflets, see Figure 2), or stenoses in IJVs. IJV stenosis was defined as a cross-sectional area of this vein ≤0.3 cm2 ; (4) flow that is not Doppler-detectable in IJVs and/or VVs despite multiple deep breaths; and (5) a wider cross-sectional area of the IJVs in the upright positions respect to supine. A subject was considered CCSVIpositive if at least two VH criteria were fulfilled as previously proposed [2].


Cerebral perfusion was measured by MRI ---since that's the only way to measure blood flow inside the gray matter.


Also, looked at the whole paper, and it was originally present]ed at the AAN convention in April 2010. So it's about one year old.


This paper was presented in the poster session of
the American Academy of Neurology annual meeting, Toronto, ON, Canada, 10 to 17 April 2010.


Correction...you're right, Marc, it wasn't ECTRIMS. It was presented as a poster at the AAN meeting.
It is published in an open access journal today. And that is the full paper I linked, for the first time available. Many papers take a year or more to go from poster/abstract to publication...although you wouldn't know that reading the CCSVI studies in the Annals of Neurology :)
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Postby marcstck » Tue Mar 08, 2011 12:33 am

cheerleader wrote:
marcstck wrote:Unless I'm reading it completely wrong, this study used 3T MRV imaging, not Doppler Ultrasound.


CCSVI was established using blinded doppler ultrasound on 16 pwMS and 8 controls with the Zamboni criteria.

Cerebral venous return was examined using echo-color Doppler equipped with 2.5 and7.5 to 10 MHz transducers (Esaote-Biosound My Lab 25, Genoa, Italy), with the subject positioned on a bed tilted at 90° and 0° as previously described [2]. All subjects were scanned in a blinded manner following the established protocol for diagnosis of CCSVI [2], consisting of transcranial and extracranial echocolor Doppler to measure the following five venous hemodynamic (VH) parameters indicative of CCSVI: (1) reflux in the IJVs and/or in the vertebral veins (VVs) in sitting and in supine positions (90° and 0°), with reflux defined as flow directed toward the brain for a duration of >0.88 seconds; (2) reflux in the intracranial veins with reflux defined as reverse flow for a duration of 0.5 seconds in one of the insonated veins (superior and inferior petrosus sinus, and/or Rosenthal vein); (3) B-mode abnormalities causing absence of flow or significant flow disturbances (vestigial valves, septum, immobile valve leaflets, see Figure 2), or stenoses in IJVs. IJV stenosis was defined as a cross-sectional area of this vein ≤0.3 cm2 ; (4) flow that is not Doppler-detectable in IJVs and/or VVs despite multiple deep breaths; and (5) a wider cross-sectional area of the IJVs in the upright positions respect to supine. A subject was considered CCSVIpositive if at least two VH criteria were fulfilled as previously proposed [2].


Cerebral perfusion was measured by MRI ---since that's the only way to measure blood flow inside the gray matter.


Also, looked at the whole paper, and it was originally present]ed at the AAN convention in April 2010. So it's about one year old.


This paper was presented in the poster session of
the American Academy of Neurology annual meeting, Toronto, ON, Canada, 10 to 17 April 2010.


Correction...you're right, Marc, it wasn't ECTRIMS. It was presented as a poster at the AAN meeting.
It is published in an open access journal today. And that is the full paper I linked, for the first time available. Many papers take a year or more to go from poster/abstract to publication...although you wouldn't know that reading the CCSVI studies in the Annals of Neurology :)
cheer


Thanks for the clarification, Joan. The Doppler Ultrasound wasn't mentioned in the abstract, mea culpa.
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Postby Ernst » Tue Mar 08, 2011 4:23 am

I red the whole reserch this morning and it was most interesting. I understood that Italian team made doppler and Buffalo team clinical and MRI examinations. There was some lovely brain images at the end, which showed clearly the differences with CBF.
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Postby Sotiris » Tue Mar 08, 2011 5:00 am

It looks as a continuation of http://www.fondazionehilarescere.org/pdf/VHISS-CSF.pdf
We knew that the CSF was affected by CCSVI and now, with this new study, we see that there is hypoperfusion in the brain parenchyma.
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Let's Be Skeptics

Postby MarkW » Tue Mar 08, 2011 5:19 am

Let's be skeptics as all scientists are trained to be. It was a study on 16 pwMS so it gets a 'maybe' interesting. The hypoperfusion may occur early or late in MS progression no one knows. That is a critical question to answer in order to say if CCSVI maybe a causitive factor in MS or a secondary event.

However, even this eventually proves to be a secondary event in MS etiology, that is no reason to stop pwMS from treating CCSVI syndrome. Also note these pwMS are still on immune regulators.

Pretty pictures (no idea what they really show) and some really hard science to take in.

MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Postby sou » Tue Mar 08, 2011 5:52 am

And the big question rises, once again:

Who can guarantee that leaving CCSVI untreated is, in the long term, perfectly safe for a person with or without MS?

Edit: Allow me 1 more thought: The doppler scan is operator dependent, so somebody could say that it is Zamboni who only finds 100%. How about the MR scanner, which is a heartless machine?
Last edited by sou on Tue Mar 08, 2011 9:42 am, edited 1 time in total.
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Postby cheerleader » Tue Mar 08, 2011 9:30 am

I heartily recommend that everyone read the full paper. It's rare we get the whole enchilada for free--

http://www.biomedcentral.com/content/pd ... 5-9-22.pdf

It was a blinded study. The doctors did not know who had MS, and who was a healthy control. All had doppler ultrasound to first establish CCSVI. 100% of the pwMS had it, the eight controls did not. Then, perfusion was measured.

All subjects were examined on a 3-T GE Signa Excite scanner (General Electric,Milwaukee, WI, USA). The following sequences were acquired: two-dimensional (2-D)multiplanar dual fast spin-echo proton density and T2-weighted images, fluid-attenuatedinversion recovery (FLAIR) images, a 3-D high-resolution (HIRES) fast spoiledgradient echo (FSPGR) with magnetization-prepared inversion recovery (IR) pulse- and
perfusion-weighted imaging (PWI).


The two things I hate most about reading research papers are math and acronyms. I can't help with the math, but here are some acronyms they use:

VHISS is a venous insufficiency score derived by timing perfusion and correlating it with CCSVI severity. (it involves math....) GM is gray matter. WM is white matter. CBV is cerebral blood volume, CBF is cerebral blood flow. MTT is mean transit time (the time it takes blood to go in and out of the brain.) HC is healthy controls

There was a significant association between increased VHISS and decreased CBF in the majority of examined regions of the brain parenchyma in MS patients (Figures 3 to 5 and Table 2). The most robust correlations were observed for GM (Figure 3) and WM (Figure 4) (r = -0.70 to -0.71, P < 0.002, Q = 0.022) and for the putamen, thalamus, pulvinar nucleus of thalamus, globus pallidus and hippocampus (r = -0.59 to -0.71, P < 0.01, Q < 0.05). No results for correlation between VHISS and CBVor MTT survived multiple comparison correction (Figures 3 and 4 and Table 2). No significant relationship was observed between VHISS and PWI outcomes in HC.

This pilot study demonstrates that the presence and severity of CCSVI are associated with hypoperfusion of the brain parenchyma in patients with MS. In particular, a strong relationship was found between increased VHISS and decreased CBF in the GM, SGM and WM regions of the brain. No significant association was found in HC.

It has previously been demonstrated that MS patients show abnormal blood flow PWI patterns. These include increased MTT and decreased CBF and CBV within normal appearing WM and GM [4, 11-15]. Perfusion abnormalities in the normal appearing WM are present from the earliest stages of the disease. The GM perfusion changes seem to appear somewhat later in the disease [4, 13] and involve the thalamus,
putamen and other SGM structures. PWI indices are also altered in both enhancing and nonenhancing lesions [12]. The severity of the perfusion changes is more pronounced in progressive MS compared to relapsing forms of the disease [11, 13, 15].


Hope that helps explain a bit....
cheer
Last edited by cheerleader on Tue Mar 08, 2011 9:46 am, edited 1 time in total.
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Postby prairiegirl » Tue Mar 08, 2011 9:41 am

Thanks for posting the link to the paper, Cheer. I look forward to reading it today; looks very interesting.
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Postby Rokkit » Tue Mar 08, 2011 12:34 pm

Can anyone help me understand the significance of this form of publishing? Does it go through a peer review process? Does it have the cache of something published in a journal or would it be panned by the medical community?
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Postby Sotiris » Tue Mar 08, 2011 1:04 pm

Rokkit wrote:Can anyone help me understand the significance of this form of publishing? Does it go through a peer review process? Does it have the cache of something published in a journal or would it be panned by the medical community?
The article was peer-reviewed. The significance has to do with the credibility of the journal. The study is a continuation of a previous one (same cohort of patients and controls as in http://www.fondazionehilarescere.org/pdf/VHISS-CSF.pdf). They made more tests and showed a correlation of increased VHISS and hypoperfusion in the brain parenchyma.
Last edited by Sotiris on Tue Mar 08, 2011 1:07 pm, edited 1 time in total.
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