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http://www.ncbi.nlm.nih.gov/pubmed/21849656


Neurology.

2011 Aug 17. [Epub ahead of print]

Progressive multiple sclerosis is not associated with chronic cerebrospinal venous insufficiency.

Baracchini C, Perini P, Causin F, Calabrese M, Rinaldi F, Gallo P.Source

From the First Neurology Clinic (C.B., P.P., M.C., F.R., P.G.), Multiple Sclerosis Centre of The Veneto Region (P.P., M.C., F.R., P.G.), and Neuroradiology Unit (F.C.), Department of Neurosciences, University Hospital, Padova, Italy.

Abstract

OBJECTIVE:
Chronic cerebrospinal venous insufficiency (CCSVI) had been suggested to play a major pathogenetic role in multiple sclerosis (MS), but recent data on early stages of MS have not confirmed this theory. Nonetheless, CCSVI could represent a late phenomenon of MS or be associated with progression of disability. Thus, we studied CCSVI prevalence in primary progressive (PP) and secondary progressive (SP) MS, to clarify whether CCSVI characterizes the progressive forms of this disease.

METHODS:

A total of 35 patients with SPMS, 25 patients with PPMS, and 60 age- and gender-matched normal controls (NC) were enrolled into a cross-sectional study. Extracranial and transcranial high-resolution venous echo color Doppler sonography (ECDS-TCDS) was performed in all patients and NC. Those patients having any abnormal ultrasound finding were asked to undergo selective venography (VGF).

RESULTS:

Patients with PPMS (11 women, 14 men; mean age 47 ± 11 years) had a disease duration of 11 ± 7 years and Expanded Disability Status Scale (EDSS) score of 6.0 ± 0.5. Patients with SPMS (22 women, 13 men; mean age 45 ± 14.5 years) had a disease duration of 18 ± 14 years and EDSS score of 6.0 ± 0.8. TCDS was normal in all patients. ECDS showed one or more abnormal findings in 9/60 (15.0%) patients (7/35 [20.0%] SPMS, 2/25 [8.0%] PPMS) and in 14/60 (23.3%) NC (p not significant for all comparisons). CCSVI criteria were fulfilled in 0 NC and 4 (6.7%) patients with MS: 3 SPMS and 1 PPMS. VGF, performed in 6/9 patients, was abnormal only in one case who had bilateral internal jugular vein stenosis.

CONCLUSION:

Our findings indicate that CCSVI is not a late secondary phenomenon of MS and is not associated with disability.

PMID: 21849656 [PubMed - as supplied by publisher]

Another study with statistically very meaningful results for the 75,000 people with MS in Canada, done by neurologists. And another one which has the lesson: further study is not required. When will we learn?

_________________
"Try - Just A Little Bit Harder" - Janis Joplin
CCSVI procedure Albany Aug 2010
'_MS' is over - if you want it
Patients sans/without patience

for myself, the EDSS score didn't change, but after CCSVI treatment, the change was remarkable.

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PPMS. Liberated Katowice, Poland
06/05/10 angioplasty RJV-re-stenodsed
26/08/10 stent RJV
28/12/10 follow-up ultrasound intimal hyperplasia

studies are always welcome reading ........ but I really like the real life story's of CCSVI pioneer patients.

and more first-hand reports coming everyday....



Mr.Success

If you look even at this so-called negative study, it found 7% of people with MS had CCSVI and that 0% of people without MS had it. This was by echo doppler, but it did not hold up under catheter venogram; there it was one person with MS who had CCSVI, if I understand correctly.

A 7% association between CCSVI and MS is of interest. This would be attention-grabbing if it was the first study ever done and if no expectations of extremely high associations were in play.

According to this study, CCSVI is found to a greater extent in people with MS. Toss this into the meta-analysis and let's see what we get.

(I am much more interested in the recent Zamboni/Zivadinov endovascular treatment study with follow-up MRIs of brain lesions. I did not know if they'd see results like that but they did.)

I'm keying in on the "0% in normal controls" part. It is my understanding that some of the arguments used by the anti-ccsvi camp are that what passes for ccsvi is merely abnormalities that can be found in the general populace, yet out of 60 nc's they found NONE.

Perhaps someone could fwd this to CR so he can start poo-pooing the neuros too.

I always question tcd in the hands of untrained sonos when it comes to detection. My own ut was pronounced clean as a whistle and just look at what was missed on my video.

Remember, they only venogramed those with ut anomalies, not the entire cohort, who knows what has been missed? Dearth of information can be argued both ways, always. Plus without IVUS to rule OUT that which cannot be seen even with the so-called venography, we'll never get the Big Picture.

Toss it in the rest of the "neuros finding what they're looking for" pile, sometimes it pays handsomely to be ahead of those tasked with securing my help, as I placebically enjoy my third straight blistering summer in a row and STILL have lesions on the brain...

Now, if we can somehow get these austere neuros to contact their colleagues at Stanford, and pass on this very message, to wit: Dear colleagues, all is well, CCSVI is a non-contender, please see our recent study, and as such, we highly recommend you enjoin yourselves to Dr. Dakes treatment study, as it poses no threat, and we can put this matter to bed once and for all, and earn accolades beyond that, no IR will ever again want to risk crossing our paths again...

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RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap