ECTRIMS 2010 (Sweden) List of CCSVI Presentations

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

Postby ikulo » Thu Oct 14, 2010 3:58 pm

MrSuccess wrote:pcakes - '' a smooth sea never made a skilled mariner ''






Mr. Success
love that!
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Postby PCakes » Thu Oct 14, 2010 6:48 pm

MrSuccess wrote:pcakes - '' a smooth sea never made a skilled mariner ''
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:)
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Postby sbr487 » Thu Oct 14, 2010 9:09 pm

The Beirut study concludes that CCSVI is a cause of MS.
So, where does that put German and Swedish studies which found that CCSVI has nothing to do with MS?

Anyway, the question really is not what comes first but whether fixing CCSVI provides relief or not.
A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it
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Postby eric593 » Thu Oct 14, 2010 10:02 pm

sbr487 wrote:The Beirut study concludes that CCSVI is a cause of MS.
So, where does that put German and Swedish studies which found that CCSVI has nothing to do with MS?

Anyway, the question really is not what comes first but whether fixing CCSVI provides relief or not.


The Beirut study concluded that CCSVI was NOT the cause of MS!

Conclusion: CCSVI is an unlikely cause of MS since it is not present in most cases early in the disease, and in only a minority of MS patients affects more than 1 extracranial vein. It is likely to be a late secondary phenomenon, possibly related to chronic central nervous system (CNS) disease and atrophy.


This study resulted in a 'Best Research Prize' nomination for them.

http://www.aub.edu.lb/news/archive/prev ... ?id=111181
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Postby PCakes » Thu Oct 14, 2010 10:12 pm

This NeuroSens synopsis of CCSVI / ECTRIMS paints an aggressive picture.. http://neuro-sens.com/congress-news/3-g ... -justified

Dr Zamboni seems an amazing man. I pray he will find the strength to endure.
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Postby MrSuccess » Thu Oct 14, 2010 10:25 pm

PC - no real suprise that a '' Neuro'' journal was quick to dismiss the CCSVI presentations .

I look forward to getting a different review ...... by other open minded people that attended this conference .

The meer fact that Dr. Zamboni was an invited guest to this conference .... speaks volumes . :idea:


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Postby PCakes » Thu Oct 14, 2010 10:44 pm

MrSuccess wrote:The meer fact that Dr. Zamboni was an invited guest to this conference .... speaks volumes . :idea:

Mr. Success


yes, and i think..the neuro gear shift from 'ccsvi does not exist' to 'okay, ccsvi exists but is a consequence, not the cause of ms'.. is also promising.
Last edited by PCakes on Fri Oct 15, 2010 9:34 am, edited 1 time in total.
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Postby eric593 » Thu Oct 14, 2010 11:44 pm

I too found the substance of the CCSVI content quite disappointing.

I was hoping for something much more substantial and concrete to be presented.

I don't blame anyone for not being excited about CCSVI after reading the content presented at ECTRIMS. It didn't make me want to stand up and give a standing ovation either.
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Postby sbr487 » Fri Oct 15, 2010 12:28 am

eric593 wrote:
sbr487 wrote:The Beirut study concludes that CCSVI is a cause of MS.
So, where does that put German and Swedish studies which found that CCSVI has nothing to do with MS?

Anyway, the question really is not what comes first but whether fixing CCSVI provides relief or not.


The Beirut study concluded that CCSVI was NOT the cause of MS!

Conclusion: CCSVI is an unlikely cause of MS since it is not present in most cases early in the disease, and in only a minority of MS patients affects more than 1 extracranial vein. It is likely to be a late secondary phenomenon, possibly related to chronic central nervous system (CNS) disease and atrophy.


This study resulted in a 'Best Research Prize' nomination for them.

http://www.aub.edu.lb/news/archive/prev ... ?id=111181


I meant -- ccsvi is caused by MS and not other way round ...

Anyway, the beirut study clearly refutes the findings of German and Swedish studies ... so when people were trying to convince everyone that CCSVI does not exist using those studies, can we believe them anymore?

Both these papers were presented in the same conference. Its obvious that someone should have noticed such a complete opposite outcomes in 2 studies.
What is the credibility of the these 2 studies?
A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it
- Max Planck
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Postby Billmeik » Fri Oct 15, 2010 6:06 am

MRV has limited value to assess CCSVI for both diagnostic and follow-up purposes


This is an amazing statement coming from a ziv paper. You might as well asy 'all results coming out of buffalo have limited value'
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Postby Billmeik » Fri Oct 15, 2010 6:13 am

It's important to note that it is GOOD news when they start debating chicken or egg with ccsvi. No longer are we subjected to the annoying and persistent claims that 'ccsvi doesn't exist' but now we have to go through a few months of ms causes ccsvi. Really this should be fairly easy to challenge...even if we get time stamped images that prove restenosis comes before new ms problems.

Cheer had a good page on facebook this morning on this. I think it would be useful for patients to collect all the proof known so far and present it to the docs. (cases where the chicken HAD to come before the egg.
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Postby cah » Fri Oct 15, 2010 7:18 am

sbr487 wrote:So, where does that put German and Swedish studies which found that CCSVI has nothing to do with MS?


You know, in germany and sweden there is a system of waste separation for glas, paper, organic waste etc. Every building has several trash cans (in germany).

Maybe another trash can should be set up at neurological clinics, for useless CCSVI studies... :lol:
"There is only one good, knowledge, and one evil, ignorance." Socrates
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Postby PCakes » Fri Oct 15, 2010 9:27 am

MrSuccess wrote: '' a smooth sea never made a skilled mariner ''

Mr. Success


This is all over the internet...must be okay to post now..

Following is a condensed version of the ECTRIMS research 'abstracts' c/w links to the full studies..

Joan/Cheerleader is doing a great dissection over on facebook .. http://www.facebook.com/notes/ccsvi-in- ... 7033472210

<shortened url>

MRI results of blinded chronic cerebrospinal venous insufficiency study in patients with multiple sclerosis, healthy controls and patients with other neurologic diseases

R. Zivadinov, G. Cutter, K. Marr, M. Ramanathan, R.H.B. Benedict, M. Elfadil, N. Bergsland, C. Morgan, E. Carl, D. Hojnacki, E. Yeh, L. Willis, M. Cherneva, S. Hussein, J. Durfee, C. Kennedy, M. Dwyer, B. Weinstock-Guttman (Buffalo, Birmingham, US)

Background: Chronic cerebrospinal venous insufficiency (CCSVI) is a vascular condition characterized by stenoses of the main extracranial veins with hampered cerebral venous outflow.

Objective: To determine the relationship of CCSVI and conventional MRI outcomes in a large cohort of patients with multiple sclerosis (MS), clinically isolated syndrome (CIS), other neurological diseases (OND) and healthy controls (HC).

Conclusions: Presence of CCSVI is significantly related to more severe lesion and brain atrophy MRI measures.

<shortened url>

Associations of HLA DR*1501 status and chronic cerebrospinal venous insufficiency in multiple sclerosis
B. Weinstock-Guttman, R. Zivadinov, G. Cutter, M. Tamano-Blanco, D. Badgett , K. Marr, E. Carl, M. Elfadil, C. Kennedy, M. Ramanathan (Buffalo, Birmingham, US)

Background: Chronic cerebrospinal venous insufficiency (CCSVI) is a vascular condition characterized by anomalies of veins outside the skull (Zamboni et al, JNNP, 2009). The Combined Transcranial and Extracranial Venous Doppler Evaluation (CTEVD) study was designed to independently confirm whether the presence of CCSVI was associated with multiple sclerosis (MS).

Objectives: To evaluate the associations of HLA *1501 status and CCSVI correlates within the CTEVD study.

Conclusions: These cross sectional data support an association between CCSVI and MS progression separate from HLA*DR1501. This association could imply that CCSVI is a risk factor for the progression of disease or that it is a consequence of the progression. Longitudinal studies need to be conducted to decipher the meaning and implications of this association

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Endovascular treatment for chronic cerebrospinal venous insufficiency in multiple sclerosis. A longitudinal pilot study

P. Zamboni, R. Galeotti, B. Weinstock-Guttman, G. Cutter, E. Menegatti, A.M. Malagoni, D. Hojnacki, M. Dwyer, N. Bergsland, M. Hiennen-Brown, A. Salter, C. Kennedy, I. Bartolomei, F. Salvi, R. Zamboni (Ferrara, IT; Buffalo, Birmingham, US; Bologna, IT)

Background: Chronic cerebrospinal venous insufficiency (CCSVI) is a vascular picture characterized by multiple strictures at the level of the main extracranial cerebrospinal venous outflow routes that may interfere with normal venous drainage.

Objective: To evaluate safety and tolerability of minimally invasive endovascular treatment (EVT) for CCSVI associated to MS using MRI, clinical and haemodynamic outcome measures.

Conclusions: Treatment with PTA was safe and well tolerated. Rate of restenosis was low, 0% in the AZY and 29% in the IJV. Further and larger studies are needed to determine the effect of EVT for CCSVI in MS.

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No evidence of chronic cerebrospinal venous insufficiency in clinically isolated syndrome suggestive of multiple sclerosis
C. Baracchini, P. Perini, M. Calabrese, F. Causin, F. Farina, F. Rinaldi, P. Gallo (Padua, IT)

Conclusions: Our findings do not support the hypothesis that cerebral venous congestion plays a causative role in the pathogenesis of MS.

<shortened url>

Safety and complications related to endovascular treatment for chronic cerebrospinal venous insufficiency in multiple sclerosis patients
M. Simka, T. Ludyga, M. Kazibudzki, M. Hartel, M. Swierad, J. Piegza, P. Latacz, L. Sedlak, M. Tochowicz (Katowice, Zabrze, PL)

Purpose: The aim of this report is to assess the safety of endovascular treatment for chronic cerebrospinal venous insufficiency (CCSVI). Although balloon angioplasty and stenting in other vascular territories are already accepted and seem to be safe procedures, there are currently no data on such treatments of a large group of patients with compromised venous outflow in the internal jugular (IJV) and/or the azygous vein (AV).

Methods: A total of 587 endovascular procedures: 414 balloon angioplasties and 173 stent implantations were performed during 361 interventions in 347 CCSVI patients with associated multiple sclerosis.

Conclusion: Regardless of the actual impact of the endovascular treatments for venous pathology on the clinical course of multiple sclerosis, which warrants more clinical studies and long term follow-ups, these procedures appeared to be safe and well tolerated by the patients.

<shortened url>

Use of magnetic resonance venography for visualisation of the internal jugular veins in patients with multiple sclerosis diagnosed with chronic cerebrospinal venous insufficiency and treated with percutaneous angioplasty
A. Lopez-Soriano, R. Zivadinov, R. Galeotti, D. Hojnacki, E. Menegatti, C. Schirda, A.M. Malagoni, K. Marr, C. Kennedy, I. Bartolomei, C. Magnano, F. Salvi, B. Weinstock-Guttman, P. Zamboni (Buffalo, US; Bologna, IT)

Background: Chronic cerebrospinal venous insufficiency (CCSVI) was recently described in patients with multiple sclerosis (MS). CCSVI is diagnosed non-invasively by Doppler sonography (DS) and invasively by selective venography (SV). The role of magnetic resonance venography (MRV) in defining presence of CCSVI is not completely elucidated.

Objective: To assess the role of MRV for visualization of the internal jugular veins in patients with MS diagnosed with CCSVI and in healthy controls (HC) who obtained serial MRV and DS exams over the period of 12 months.

Conclusion: MRV has limited value to assess CCSVI for both diagnostic and follow-up purposes.

<shortened url>

Clinical correlates of chronic cerebrospinal venous insufficiency in multiple sclerosis

B. Weinstock-Guttman, G. Cutter, K. Marr, D. Hojnacki, M. Ramanathan, R.H.B. Benedict, C. Morgan, E.A. Yeh, E. Carl, C. Kennedy, J. Reuther, C. Brooks, M. Elfadil, M. Andrews, R. Zivadinov (Buffalo, Birmingham, US)

Objectives: To evaluate the clinical correlates of chronic cerebrospinal venous insufficiency (CCSVI) in a large cohort of patients with multiple sclerosis (MS).

Background: CCSVI is a complex vascular condition characterized by anomalies of the primary veins outside the skull (Zamboni et al, JNNP, 2009). We previously showed in a pre-planned Combined Transcranial (TCD) and Extracranial Venous Doppler Evaluation (CTEVD) blinded study that the prevalence of CCSVI was significantly higher in the MS cohort vs. healthy controls (HC) (56.1% vs. 22.7%, p< 0.001).

Conclusions: The presence of CCSVI in MS patients was associated with more advanced MS disease subtypes and more severe motor, cerebellar and brainstem involvement.

<shortened url>

Correlation of localisation and severity of extracranial venous lesions with clinical status of multiple sclerosis

M. Simka, T. Ludyga, M. Kazibudzki, A. Adamczyk-Ludyga, J. Wrobel, P. Latacz, J. Piegza, M. Swierad (Katowice, PL)

Purpose: The discovery of chronic cerebrospinal venous insufficiency (CCSVI), which comprises stenoses in the extracranial veins that drain the central nervous system, has shed new light on the potential source of multiple sclerosis (MS). The aim of this report is to assess the correlations between patterns of CCSVI and clinical characteristics of MS.

Conclusion: It has been revealed that at least some elements of clinical characteristics of MS correlated with parameters of CCSVI. These findings indicate that most likely both pathologies are interconnected and CCSVI may play a role in the pathogenesis and progression of MS. Importantly, venous lesions in differently aged patients were comparable, and severity of venous lesions did not correlate with duration of MS. This finding favors the idea of congenital nature of those vascular malformations

<shortened url>

Chronic cerebrospinal venous insufficiency is an unlikely cause of multiple sclerosis

B. Yamout, A. Herlopian, Z. Issa, R.H. Habib, A. Fawaz, J. Salameh, H. Wadih, H. Awdeh, N. Muallem, R. Raad, A. Al-Kutoubi (Beirut, LB)

Introduction: A state of chronic cerebrospinal venous insufficiency (CCSVI) secondary to extracranial venous stenosis (EVS) was suggested as a possible cause of multiple sclerosis (MS).

Conclusion: CCSVI is an unlikely cause of MS since it is not present in most cases early in the disease, and in only a minority of MS patients affects more than 1 extracranial vein. It is likely to be a late secondary phenomenon, possibly related to chronic central nervous system (CNS) disease and atrophy.

<shortened url>

Multiple sclerosis patients with chronic cerebrospinal venous insufficiency present with increased iron concentration on susceptibility-weighted imaging in deep-grey matter
R. Zivadinov, M. Heininen-Brown, C. Schirda, C. Magnano, D. Hojnacki, C. Kennedy, E. Carl, N. Bergsland, S. Hussein, M. Cherneva, L. Willis, M. Dwyer, B. Weinstock-Guttman (Buffalo, US)

Background: Chronic cerebrospinal venous insufficiency (CCSVI) is a vascular phenomenon recently described in multiple sclerosis (MS) that is characterized by stenoses affecting the main extracranial venous outflow pathways that may lead to increased iron concentration (IC) in the brain parenchyma.

Objective: To investigate the relationship between presence of CCSVI and IC, measured on susceptibility-weighted imaging (SWI), in deep-gray matter (DGM) regions of MS patients and age- and sex-matched healthy controls (HC).

Conclusion: This is the first large cohort study suggesting an important association between presence and severity of CCSVI and increased IC in DGM regions of MS patients.


<shortened url>

No evidence for cerebro-cervical venous congestion in patients with multiple sclerosis
F. Doepp, F. Paul, J.M. Valdueza, K. Schmierer, S.J. Schreiber (Berlin, Bad Segeberg, DE; London, UK)

Background: Multiple sclerosis (MS) is characterized by demyelination centered around cerebral veins. Recent studies suggested this topographic pattern may be caused by cerebral venous congestion, a condition termed 'chronic cerebro-spinal venous insufficiency' ('CCSVI'). In a recently published study we were unable to reproduce the reported findings of reflux in the deep cerebral veins and/or the internal jugular and vertebral veins (IJVs and VVs), stenosis of the IJVs, missing flow in IJVs and VVs, and inverse postural response of the cerebral venous drainage (Ann Neurol, in press).

Conclusion: This data confirms in a larger cohort our recently published study challenging the hypothesis that cerebral venous congestion plays a significant role in the pathogenesis of MS. Future studies should elucidate the difference between patients and healthy subjects in BVF regulation.[/b]
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Postby ikulo » Fri Oct 15, 2010 10:55 am

Just wanted to comment on this, the award-winning, paper by Yahmout et al.

Friday, October 15, 2010, 15:30 - 17:00

Chronic cerebrospinal venous insufficiency is an unlikely cause of multiple sclerosis

B. Yamout, A. Herlopian, Z. Issa, R.H. Habib, A. Fawaz, J. Salameh, H. Wadih, H. Awdeh, N. Muallem, R. Raad, A. Al-Kutoubi (Beirut, LB)



Introduction: A state of chronic cerebrospinal venous insufficiency (CCSVI) secondary to extracranial venous stenosis (EVS) was suggested as a possible cause of multiple sclerosis (MS). Methods: In this study we performed selective extracranial venous angiography (SV) on 42 patents with early MS (EMS): clinically isolated syndrome (CIS) or relapsing remitting MS (RRMS) of less than 5 years duration, and late MS (LMS): RRMS of more than 10 years duration. We also reviewed available MRI and clinical relapse data in patients with documented EVS.



Results: EVS was present in 7/29 (24%) patients with EMS and 12/13(92%) patients with LMS, a highly significant statistical difference (p<0.0001). Only 3/42 (7%) patients (all in the LMS group) had 2 vessel stenosis, while the rest had only 1 vessel involved. The incidence of EVS in CIS was 9% compared to 33% in RRMS of less than 5 years duration.



The most important factor in determining presence of EVS was disease duration: mean=9.4±6.8 years in 19 patients with EVS compared to 3.2±4.1 years in patients without (p<0.005), which stayed significant after controlling for age at disease onset and gender (p<0.002). Within the EMS group, patients with (n=7) and without (n=22) EVS had similar EDSS (1.43±2.13 and 0.8±0.008, p=0.85) and disease duration (mean =2.1 and 2.4 years, p=0.521), suggesting similar disease severity. The 7 EMS patients with stenosis had a total of 14 relapses since disease onset. No clear correlation could be found between site of EVS and relapse anatomical localization. A total of 97 spine and brain MRIs available since disease onset on all 19 patients with stenosis were reviewed. Again no clear correlation could be seen between the location of gadolinium enhancing (Gd+) lesions and site of EVS. Conclusion: CCSVI is an unlikely cause of MS since it is not present in most cases early in the disease, and in only a minority of MS patients affects more than 1 extracranial vein. It is likely to be a late secondary phenomenon, possibly related to chronic central nervous system (CNS) disease and atrophy.


These findings are extraordinary -- 92% of late MS had stenosis and 24% of early MS had stenosis. First, stenosis isn't exactly the only factor in CCSVI since we've seen cases of webs, etc. Nevertheless, it's good to see an unbiased *cough* paper come out acknowledging that CCSVI does exist. Second, I think this paper may disprove that CCSVI is a congenital phenomenon, but it doesn't necessarily disprove that CCSVI causes MS. Yahmout relies on the assumption that stenosis is a constant and static phenomenon. However, we still don't know whether stenosis is a condition that is static, progressive, or whether it fluctuates (for example, maybe in RRMS there is another factor that makes the veins stenos during relapses? -- viral/bacterial..?). Hopefully Yahmout et al continue more award-winning research into CCSVI since there is, at the very least, an association! *holding breath*
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Postby PCakes » Fri Oct 15, 2010 8:58 pm

PCakes wrote:This NeuroSens synopsis of CCSVI / ECTRIMS paints an aggressive picture.. http://neuro-sens.com/congress-news/3-g ... -justified

Dr Zamboni seems an amazing man. I pray he will find the strength to endure.


Although disheartening to read such a report.. I tell myself to remember how far CCSVI has come in a very short time.

ECTRIMS 2010 has CCSVI on centre stage .. last year CCSVI was an 'upcoming attraction' poster.

There is no longer outright denial of CCSVI. CCSVI now exists but only as a consequence of MS. (Can someone please tell me the when/how/where of that neurological jump? Somewhere - In the minutes... "noted, burial is not working.. next step, camouflage?")

I am saddened to see valuable time is being wasted in debate over the term 'Liberation' .. seems petty but, to me, reflects a clear lack of solid evidence to refute Zamboni's theory. If they had proof to the contrary, wouldn't now be the time to share it?

I believe that Dr Paolo Zamboni is an ethical, compassionate, gifted man driven by his passion for life, science and family. I believe that his research will touch many lives in many ways. I believe that this man will, one day soon, enjoy the professional respect and acclaim he so deserves.

If I met him, and if he let me, I would give him a big hug.
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