IVCC/CCSVI, articles et liens de ce vendredi.

Publié le par Handi@dy

Barre google de traduction indispensable.

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par CCSVI in Multiple Sclerosis, lundi 11 octobre 2010, à 01:41

 For those who are not familiar with this yearly gathering, ECTRIMS stands for European Committe for Treatment and Research in Multiple Sclerosis.  This year the conference in being held in Sweden, and it takes place later this week.   This conference is the big deal in MS research, and is well-attended by neurologists

 

In past years, Dr. Zamboni was allowed to present a poster for display on his research of CCSVI in MS and iron deposition in MS brains, as it related to chronic venous disease.   He has never been invited to speak before.  Dr. Zamboni will be presenting his research along with Dr. Zivadinov  in the Main Auditorium as part of the Charcot Foundation presentation, as they go up against Dr. Omar Khan, co-author of the first negative opinion piece in the Annals of Neurology:  To say that this is a big deal is an understatement.  I've included the schedule of presentations for you all below:

http://www.congrex.ch/ectrims2010/welcome/welcome.html

 

Wednesday, October 13, 2010 12:35 - 12:45 European Charcot Foundation Chronic cerebrospinal venous Insufficiency. Relation to multiple sclerosis? (Main Auditorium) 

 

CCSVI: from hypothesis to reality P. Zamboni (Ferrara, IT) 

 

12:45 - 13:00 European Charcot Foundation Chronic cerebrospinal venous Insufficiency. Relation to multiple sclerosis? (Main Auditorium) CCSVI: relation to multiple sclerosis R. Zivadinov (Buffalo, US) 

 

13:15 - 13:30 European Charcot Foundation Chronic cerebrospinal venous Insufficiency. Relation to multiple sclerosis? (Main Auditorium) Questions on CCSVI in multiple sclerosis O. Kahn (Detroit, US) 

 

On Thursday, Dr. Zivadinov is presenting results from the BNAC MRI studies -

 

Thursday, October 14, 2010 15:30 - 17:00 Imaging 1 MRI results of blinded chronic cerebrospinal venous insufficiency study in patients with multiple sclerosis, healthy controls and patients with other neurologic diseases P 318 

 

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) 

 

Also being presented is the genetics research now completed at BNAC  

 

15:30 - 17:00 Genetics/transcriptomics 1 Associations of HLA DR*1501 status and chronic cerebrospinal venous insufficiency in multiple sclerosis P 265 

 

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) 

 

Dr. Zamboni presents results from his endovascular treatment study-

 

15:30 - 17:00 Therapy disease-modifying - Others 1 Endovascular treatment for chronic cerebrospinal venous insufficiency in multiple sclerosis. A longitudinal pilot study P 508 

 

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) 

 

On Friday, a negative study is being presented by another Italian team who found no CCSVI in CIS patients.

 

Friday, October 15, 2010 09:45 - 10:00 Platform presentation of selected abstracts I (Congress Hall) No evidence of chronic cerebrospinal venous insufficiency in clinically isolated syndrome suggestive of multiple sclerosis 81 

 

C. Baracchini, P. Perini, M. Calabrese, F. Causin, F. Farina, F. Rinaldi, P. Gallo (Padua, IT) 

 

Then Dr. Zivadinov will present on how the visibility of lower brain vasculature ties into CCSVI severity as shown by MRI

 

10:00 - 10:15 Platform presentation of selected abstracts I (Congress Hall) Presence and severity of chronic cerebrospinal venous insufficiency is related to lower brain parenchyma venous vasculature visibility on susceptibility-weighted imaging in patients with multiple sclerosis 82 

 

R. Zivadinov, G. Poloni, C. Schirda, C. Magnano, E. Carl, N. Bergsland, D. Hojnacki, C. Kennedy, F. Parker, M. Dwyer, B. Weinstock-Guttman (Buffalo, US) 

 

Dr. Simka's research on endovascular treatment of CCSVI will be presented

 

15:30 - 17:00 Therapy disease-modifying - Others 2 Safety and complications related to endovascular treatment for chronic cerebrospinal venous insufficiency in multiple sclerosis patients P 914 

 

M. Simka, T. Ludyga, M. Kazibudzki, M. Hartel, M. Swierad, J. Piegza, P. Latacz, L. Sedlak, M. Tochowicz (Katowice, Zabrze, PL) 

 

Dr. Zivadinov's research on utilizing MRV to visualize the jugular veins after angioplasty-

 

15:30 - 17:00 Imaging 2 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 P 773 

 

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) 15:30 - 17:00 Clinical assessment tools 2 

 

BNAC's correlation of CCSVI to MS

 

Clinical correlates of chronic cerebrospinal venous insufficiency in multiple sclerosis P 653 

 

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) 

 

Dr. Simka's correlation of severity of CCSVI with severity of MS

 

15:30 - 17:00 MS symptoms 2 Correlation of localisation and severity of extracranial venous lesions with clinical status of multiple sclerosis P 641 

 

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

 

A Beirut study that says CCSVI does not cause MS

 

15:30 - 17:00 Pathology 2 Chronic cerebrospinal venous insufficiency is an unlikely cause of multiple sclerosis P 663 

 

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) 

 

Dr. Zivadinov's study showing increase of iron in gray matter of MS/CCSVI

 

15:30 - 17:00 Imaging 2 Multiple sclerosis patients with chronic cerebrospinal venous insufficiency present with increased iron concentration on susceptibility-weighted imaging in deep-grey matter P 774 

 

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) 

 

 

And finally, the German neurological doppler study where they claim they found no CCSVI, but Dr. Zamboni says their results actually PROVE CCSVI.

15:30 - 17:00 Diagnosis & differential diagnosis 2 No evidence for cerebro-cervical venous congestion in patients with multiple sclerosis P 579 

 

F. Doepp, F. Paul, J.M. Valdueza, K. Schmierer, S.J. Schreiber (Berlin, Bad Segeberg, DE; London, UK) 

 

And of course, the pharmaceutical companies will be there, presenting all their positive findings,  sponsoring lectures and discussions and hosting dinners and events.  What fun!

 

I actually wish I could go, but it's too far away, and too much going on at home.  I hope we can get some reports from attendees, and I promise to link to those and any other news that comes out of the conference.  I really wish we could all be flies on the wall as Dr. Omar Khan "questions" Dr. Zamboni.  

Joan

 

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‘Perhaps my advocacy will help to open the doors a little bit more, or will help to break down some of those obstacles that are holding people back from being able to have this treatment in their own country'

MS members pick surgery over waiting ccsvi-new.jpeg

 *Angioplastie veineuse dans la thrombose

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Liberal ladies lobby for ‘liberation’

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IMPORTANT MEDICAL NEWS

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Study by AUBMC faculty disproves theory on cause of Multiple Sclerosis;'Best Research Prize' nominee

IMAGE
Dr. Yamout

A groundbreaking study conducted by Dr. Bassem Yamout, Associate Professor at the American University of Beirut Medical Center and Director of the Multiple Sclerosis Clinic and Research Center, and his colleagues titled "Extracranial Venous Stenosis is an Unlikely Cause of Multiple Sclerosis" has disproved an established theory on the underlying cause of the disease.

Multiple Sclerosis is a debilitating neurological disorder of young people with a presumed autoimmune origin. Recent work from Italy suggested that extracranial venous stenosis inducing cerebrospinal venous congestion, perivenular extravasation of blood, and secondary activation of the immune system leading to demyelination is the underlying cause of the disease. This revolutionary theory swept through the media and generated tremendous interest among patients and within the scientific community. Patients started traveling all over the world undergoing venous angioplasties to "cure" their disease.
To test this theory, venous angiographies were performed on patients with early multiple sclerosis (Less than 5 years duration) and late multiple sclerosis (more than 10 years duration) with the hypothesis that if extracranial venous stenosis is the cause of multiple sclerosis, it should be present early in disease and should affect multiple extracranial veins. The extensive network of anastomoses in the cerebrospinal venous system precludes the possibility of cerebrospinal congestion secondary to a single vein stenosis.

The study showed that multiple venous stenoses were not present early in the disease but could be seen in up to 23% of patients at later stages. Single vein stenosis was rare early in the disease but frequent at later stages. Moreover, anatomic localization of clinical relapses and brain MRI lesions did not correlate with the site of stenosis.
In conclusion, this study showed that extracranial venous stenosis is a late manifestation in multiple sclerosis and unlikely to induce a state of chronic cerebrospinal venous insufficiency since only a minority of patients has a single venous stenosis early in the disease. It is more likely to be a secondary phenomenon, possibly present in other neurological diseases, reflecting chronic brain disease and atrophy.

This study has been nominated for "Best Research Prize" at the 26th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) to be held in held in Gothenburg, Sweden from the 13th to the 16th of October, 2010."
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Stopping Natalizumab Causes Inflammatory Rebound in MS

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 VEF Conference organized by Euromedic

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MS patient to discuss liberation therapy in Woodstock

Published Tuesday October 12th, 2010

Treatment | Tim Donovan of Fredericton Junction went to N.Y. for procedure


Click to Enlarge
Click to Enlarge
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Councillor willing to leave country to seek treatment for daughter's MS

Read more: http://www.timescolonist.com/health/Councillor+willing+leave+country+seek+treatment+daughter/3669907/story.html#ixzz12PjUtbT5
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par CCSVI in MS Toronto, jeudi 14 octobre 2010, à 21:23

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

 

Jacobs Neurological Institute (Buffalo, US); University of Alabama (Birmingham, US); Buffalo Neuroimaging Analysis Center (Buffalo, US); Department of Pharmaceutical Sciences (Buffalo, 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).

 

Results:

This study enrolled 499 subjects; 163 HC, 289 MS patients, 21 CIS patients, 26 subjects with other neurological disorders underwent a clinical examination and a combined Doppler and TCD scan of the head and neck. Thirty patients that were defined as borderline (technical limitation for criteria 2 and not meeting definition of CCSVI) were considered negative for this analysis.

 

CCSVI prevalence was significantly higher in more advanced MS disease subtypes:

89.5% in relapsing secondary-progressive (SP), 67.2% in non-relapsing SP, 54.5% in primary-progressive (PP), 49.2% in relapsing- remitting (RR) and 38.1% in CIS (p¼0.033).

 

The mean venous haemodynamic insufficiency severity score (VHISS) was higher for subjects diagnosed with CCSVI (mean VHISS_SD: 4.05_1.4, n¼218) than for subjects without CCSVI (1.20_1.0, n¼281; p<.001). Criteria 2, 4 and 5 showed significant associations with an EDSS_4.0 (Criteria 2: OR of 2.25, p¼0.005; criteria 4: OR: 3.28, p¼0.004 and Criteria 5 OR: 2.67, p¼0.008).

 

MS subjects with CCSVI had significantly higher Pyramidal (p¼0.020), Cerebellar (p¼0.049), and Brain Stem (p¼0.010) EDSS sub-scale score than subjects without CCSVI. Subjects with CCSVI were significantly older than subjects without CCSVI (p¼0.04).

 

However, the mean Multiple Sclerosis Severity Score (MSSS) trended higher for subjects with CCSVI (4.22_2.6, n¼160) than for subjects without CCSVI (3.63_2.4, n¼127), but this difference was not significant (p¼.073).

 

Conclusions:

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

 

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*"Premiers rapports depuis Ectrims, corrélation entre SEP et CCSVI, très positif!
par CCSVI in Multiple Sclerosis, jeudi 14 octobre 2010, à 18:31

Here is the first group of abstracts from the ECTRIMS conference in Sweden this week which we can post:

These are the ones presented by doctors from BNAC (Zivadinov's team) and Ferrara (Zamboni's team)

They are the more "positive" in their findings, and I believe that is because BNAC is working with Zamboni's team to understand how to correctly utilize the technology to study CCSVI--

 

This first study finds a link to brain atrophy (shrinkage) and amount of lesions to presence of CCSVI:

 

Imaging 1

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). Methods: A pre-planned examination of the first 499 consecutively enrolled subjects in the Combined Transcranial and Extracranial Venous Doppler Evaluation (CTEVD) blinded study included 289 MS, 163 HC, 26 OND and 21 CIS subjects. All subjects received extracranial and transcranial Doppler evaluation according to the proposed criteria (Zamboni et al., JNNP 2009). Of these, 20 (95.2%) CIS, 243 (84.1%) MS, 73 (45.6%) HC, and 15 (42.3%) OND received MRI examinations using a standardized protocol. In total, 351 (70.3%) of 499 subjects obtained MRI examination. T2, T1 and gadolinium (Gad) lesion number and volume (LV) were calculated. Normalized measures of global and central brain atrophy were also assessed. Differences in group means were assessed using the Kruskal-Wallis test and all correlations are reported using Kendall's tau. Results: The two venous scales' venous haemodynamic insufficiency severity score (VHISS) and number of venous haemodynamic criteria fulfilled (VH) were both significantly correlated with CCSVI diagnosis (Kendall's tau = .694 for VHISS, tau = .804 for VH, p < .001 for both scales). Subjects diagnosed with CCSVI (i.e. those who met at least 2 of the CCSVI criteria) had a significantly higher mean number of T2 lesions (x= 31.10, sd = 21.3, n = 173) than subjects classified as not having CCSVI (x= 24.96, sd = 22.7, n = 178; p < .001). Subjects diagnosed with CCSVI also had a significantly higher mean T2-LV (x= 20.69, sd = 8.9, n = 173) than those without CCSVI (x= 17.46, sd = 8.8, n = 173; p < .001). There was no significant difference between subjects with and without CCSVI for number orLV of either T1 or Gad lesions. Subjects diagnosed with CCSVI had significantly higher lateral ventricle volume (p < .001) than subjects without CCSVI. Subjects with CCSVI showed significantly lower gray matter volume (p = .023), brain parenchymal volume (p = .025) and cortical volume (p = .023) than subjects without CCSVI. Conclusions: Presence of CCSVI is significantly related to more severe lesion and brain atrophy MRI measures.

 

This next study is a genetic study looking at the frequency of HLA DR 1501 in CCSVI  (this is a human leukocyte antigen which is already known to be highly associated with MS)   This study is rather inconclusive regarding HLA DR and CCSVI, but once again, it shows the relationship between CCSVI and progressive MS....

 

Genetics/transcriptomics 1

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. Results: The CTEVD study enrolled 499 subjects: 163 healthy controls (HC), 289 MS patients, 21 clinically isolated syndrome patients (CIS), 26 controls with other neurological disorders (OND's). Genotyping was obtained for 472 of 499 subjects. All subjects underwent a clinical examination and a combined transcranial and extracranial Doppler scan of the head and neck. The HLA DR*1501 status was obtained by genotyping DNA from peripheral blood for rs3135005, a SNP strongly correlated with DR*1501 status. The controls group consisted of HC and OND's. The MS group was dichotomized into the non-progressive (relapsing remitting, CIS and Devic's disease) and progressive forms (secondary progressive and primary progressive). The frequency of CCSVI was higher (OR = 3.57, p < 0.001) in the MS group 54.8% vs. 25.4% in the controls group and also higher in the progressive MS group 69.6% vs. 48.6% in the non-progressive MS group. The frequency of HLA DR*1501 positivity (HLA+) in the MS group 49.5% was higher compared (OR = 2.15, p < 0.001) to 31.3% in the control group. The frequencies of HLA+ in the non-progressive and progressive MS groups were similar, 48.3% and 52.3% respectively. In the controls group, 53.1% were negative for both HLA DR*1501 and CCSVI (denoted HLA' CCSVI'), 22.3% were HLA+ CCSVI', 15.6% were HLA' CCSVI+ and 8.9% were HLA+ CCSVI+. In the non-progressive MS group, 27.1% were HLA' CCSVI', 23.7% were HLA+ CCSVI', 24.6% were HLA' CCSVI+ and 24.6% were HLA+ CCSVI+. In the progressive MS group, 18.6% were HLA' CCSVI', 11.6% were HLA+ CCSVI', 29.1% were HLA' CCSVI+ and 40.7% were HLA+ CCSVI+. 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

 

 

 

This is Dr. Zamboni's follow-up study in endovascular treatment of CCSVI in MS

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. Methods: We designed an open-label, MRI-blinded, two-center, randomized, EVT intervention parallel-group, 12 month study (EVTMS). Of 16 relapsing-remitting patients who were screened for hemodynamic venous anomalies, 15 (8 from Italy and 7 from the Buffalo) accepted participation in the EVT intervention prospective study (EVTMS). Additional 8 age- and sex-matched healthy controls (HC), 4 from Italy and 4 from Buffalo were followed. All enrolled patients presented with CCSVI and were on disease-modifying therapy. Half of the cohort (immediate treatment group [IEVT], 4 from Buffalo and 4 from Italy) were randomly selected to obtain the EVT procedure (in Italy) immediately after the screening, and half (delayed treatment group [DEVT]) at 6 months. The EVT procedure consisted of selective venography complemented by balloon dilatation (PTA) when significant stenoses were detected. All patients were prospectively evaluated at 0, 3, 6, 9 and 12 months with sonography, MRI (0, 6 and 12 months only), and clinical examinations. Results: No serious adverse events occurred during the study except one transitory vaso-vagal syndrome approximately an hour after intervention.. One subject in DEVT group was lost from the study at 6 month follow-up. Three HC were lost to follow-up. Restenosis occurred in 29% of the study cohort after intervention (2 in DEVT arm at  3-month, 1 in the DEVT at 6-month and 1 in the IEVT arm at 12-month follow-up). There were no significant differences between the 2 groups at 6 months follow-up after the intervention for MRI and clinical outcomes. There was a significant decrease (p=0.0227) in T2 lesion number from the 6 month baseline time period to the 6 months following the intervention in DEVT arm. No significant worsening in mean change for other MRI and clinical metrics was observed in both groups over the follow-up. 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.

 

 

And here is Dr. Zivadinov's study on decreased grey matter in MS brains as associated with increased disability.  Once again, more proof that it's not about white matter lesions, it's about what is going on deep inside the brain---

Increased iron concentration and decreased volume of deep-grey matter are associated with increased disability in patients with multiple sclerosis

R. Zivadinov, M. Heininen-Brown, C. Schirda, N. Bergsland, C. Magnano, D. Hojnacki, D. Ramasamy, C. Kennedy, E. Carl, M. Dwyer, B. Weinstock-Guttman (Buffalo, US)

 

Background: MRI lesion-related measures account for only part of clinical disability in patients with multiple sclerosis (MS). New studies suggest that measurement of gray matter (GM) atrophy is clinically relevant, and is not entirely linked to white matter (WM) lesion formation. In particular, measurement of deep-gray matter (DGM) atrophy, which occurs from the earliest stages in the clinical course of MS, is under intense investigation. Objective: To investigate the relationship between iron concentration (IC), measured on susceptibility-weighted imaging (SWI), and volumes of the DGM with clinical outcomes in MS patients. Methods: Eighty-four (84) consecutive MS patients [58 relapsing-remitting (RR) and 26 secondary-progressive (SP]  were imaged on a 3T GE scanner using SWI. All patients were assessed with clinical and MRI outcomes. Disability was measured by Expanded Disability Status Scale (EDSS). Mean age in MS patients was 46.7 yrs, mean disease duration 14.6 yrs and median EDSS 2.5. High-iron tissue mean IC (HITMIC) was determined for the total DGM, caudate, putamen, globus pallidus, thalamus, pulvinar nucleus of the thalamus, hippocampus, amygdala, nucleus accumbens, red nucleus and substantia nigra. Volumes of the same DGM structures were calculated. T2, T1, Gadolinium (Gad) lesion volumes (LV) and global and central brain atrophy measures were also obtained. Results: Both increased IC (r=0.42, p<0.001) and decreased volume (r=0.31, p<0.01) of the total DGM were related to higher disability and longer disease duration. The relationship was stronger in SP compared to RR MS patients, particularly for IC measures. Of all examined DGM structures, caudate, putamen and thalamus showed the strongest correlations. In multivariate regression analysis, when all lesion, atrophy and IC measures that showed significant correlations in univariate analyses were entered, the only independent predictors of disability remained decreased total DGM IC (p=0.001) and increased T2-LV (p<0.001). Similar analysis selected normalized brain volume (p=0.006) for disease duration. Conclusions: Increased IC and decreased volume of DGM showed an important relationship to increased disability and longer disease duration. Measurement of IC and volume of DGM structures may become an important biomarker of disease progression in MS. Follow-up studies are needed to determine clinical relevance of the evolution of these MRI measures over mid-to long-term.

 

 

And here is another study looking at hypoperfusion in MS brains---literally, slowed blood flow--

 

 

Relation between quantitative venous vasculature assessment on susceptibility-weighted imaging and haemodynamic MRI metrics in multiple sclerosis patients</span>

G. Poloni, M. Dwyer, F. Parker, C. Magnano, C. Schirda, N. Bergsland, R. Zivadinov (Buffalo, US)

 

Background: The venous vasculature of the brain parenchyma is significantly less visible on susceptibility-weighted         imaging (SWI) in patients with multiple sclerosis (MS) compared to healthy controls (HC), as previously described. Objective: To investigate the relation between the altered venous vasculature visibility in the brain parenchyma and  Cerebrospinal Fluid (CSF) Imaging and Perfusion Weighted Imaging (PWI) MRI metrics in patients with relapsing-remitting (RR) and secondary-progressive (SP) MS disease course, and HC. Methods: Fifty nine (59) MS patients [41 RR and 18 SP] and thirty three (33) age- and sex-matched HC were scanned on a 3T GE scanner using CSF imaging, PWI and SWI. Mean age at scan was 44.3 yrs, mean disease duration 13.2 yrs and median EDSS 2.5. CSF flow rates (positive, negative and net), Mean Transit Time (MTT), Cerebral Blood Flow (CBF) maps and Cerebral Blood Volume (CBV) maps were calculated. 3D multi-scale line filter was used to extract the venous vasculature from SWI images. Absolute venous volume (AVV) was estimated in milliliters (ml); relative venous intracranial fraction (VIF) was calculated to correct for head size and amount of brain atrophy. Vein volumes were classified by vein radius: <0.3mm, 0.3-0.6mm, 0.6-0.9mm and >0.9 mm. Voxel brain average distance-from-vein (DFV) maps were calculated. Results: MS patients showed reduced AVV, volume of veins with diameter <0.3mm and VIF (p< .05) and increased DFV (all p< .001) with respect to HC. In MS patients lower AVV, volume of veins with diameter <0.3mm and VIF, and higher DVF were strongly related to lower net negative flow (Spearman r = .48 to .61, p< .001) and higher net positive flow (r = .53 to .64, p< .001). A similar relation was found with an increased MTT (gray matter: r = .36 to .43, p< .01; white matter: r = .40 to .46, p< .001) and a decreased CBF (gray matter: r = .38 to .45, p< .01; white matter: r = .37 to .49, p< .001). The relationships were consistently stronger in RR than SP MS patients. No significances where found for HC. Conclusions: This study showed that lower brain parenchyma venous vasculature visibility on SWI is related to altered hemodynamic CSF flow and hypoperfusion in patients with MS. The events contributing to these findings are probably occurring early in the disease process. Further studies are needed to elucidate relationship between reduction of venous vasculature and the hemodynamic MRI parameters in MS patients.

 

 

 

 

 

 

 

 

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*Toujours basé sur Ectrims, analyse des deux études négatives sur la théorie de Zamboni, toutes deux mal menées, sans protocole correct:
par CCSVI in Multiple Sclerosis, jeudi 14 octobre 2010, à 23:25

Tomorrow I'll be posting the negative studies presented at ECTRIMS.  There are two new studies that are approaching CCSVI from a new angle...that of proving that CCSVI is not the cause MS.  They both look at clinically isolated syndrome (CIS) and early MS are conclude there is no CCSVI.  Both studies appear to be doing the doppler and venography testing incorrectly, and we'll get into more specifics tomorrow...but what I found interesting is that these studies actually found CCSVI in more progressed or later-stage MS.  They do not deny CCSVI exists...but they are trying a new tactic.  They are saying CCSVI is created DUE TO brain damage from MS.  It's the old chicken and egg switcheroo.

 

Here's why this is interesting.  It is obvious that the correlation to CCSVI and MS is undeniable.  More and more patients are coming forward with positive venograms showing stenosis and reflux in the central veins.  It is becoming impossible to ignore or deny.  So, the neurologists and MS specialists are going to re-write the script and say, Yes...you do have CCSVI.  But it's because you have MS.  MS causes CCSVI.  Let us treat your MS with our drugs, and your CCSVI won't progress.

 

Now,  this was the question raised by the Alberta document (maybe MS causes CCSVI?)  and I think those who hope to disprove CCSVI were very smart to pick up on this line of logic.  Problem is...CCSVI exists.  And it exists early in the MS disease process.   Other doctors are finding it in early MS and clinically isolated syndrome.  I've told the story of Dr. Dake testing the daughter of one of his first patients, and finding she had occluded veins, even though she did not have an MS diagnosis.  She later had an MRI, and there were the white matter lesions.  Dr. Dake treated her with angioplasty, even before she ever had an official MS diagnosis.  The other daughter had great veins, no CCSVI and no MS.   And Dr. Zivadinov told a similar story in Bologna, about the daughter of an MS patient in his study who was part of the healthy control group.  Sure enough, she had CCSVI and it was a few months later she showed white matter lesions on MRI and received an MS diagnosis.  And this is happening world wide.

 

Those who've been following this page already know that Dr. Byung B. Lee and a panel of international vascular experts have classified CCSVI stenosis as truncular venous malformations, formed in utero.  Here's Dr. Lee's paper.

http://www.fondazionehilarescere.org/pdf/03-2518-ANGY.pdf

 

And we also know that these truncular venous malformations grow with the body, and get progressively worse with age.  And yes, as inflammation in the body increases, the stenotic lesion will worsen as well.  MS is a chronic disease which progresses over the duration of the disease...and venous malformations get worse as the body ages and disturbed blood flow continues to damage the veins.  Chronic venous disease gets worse.  CCSVI gets worse.

 

So, be prepared for the neurologists' new tactic...telling you that your MS has created your CCSVI.   It's getting more interesting all the time....til tomorrow---

Joan

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