This Is MS Multiple Sclerosis Community: Knowledge & Support

I agree with Cheer that the title is at odds with the content of the research.

Thanks Cheer. I was puzzling over the results. I read the paper and just couldn't make sense of the conclusion. Very strange logic here.

I don't see what the debate is.

Actually, the title of the paper is "CCSVI is NOT associated with HLA DRB 1501 status in Multiple Sclerosis Patients.". And that is exactly what the authors showed, so the abstract is not misleading. You can't just go by percentages. Using a Fisher's exact test for CCSVI/DRB1*1501 Positive correlation in the MS group, the probability is calculated to be .085. This is greater than the standard cutoff of .05. So, the authors report there is only a trend toward association. They also showed there was no correlation between CCSVI/DRB1*1501 Positive in the control group; the p-value in this case was .41, well above the .05 threshold.

There was a significant association between CCSVI and HLA DRB1*1501 status when the entire study population was considered, but if there was a correlation between CCSVI and this gene, the significance should have held within each group.

Hmmm... seems to me that misleading would be if the title says "not associated..." if what they really mean is that there was no certainty of association from a statistical perspective. "No certainty of" is NOT "not". Ergo, the title was misleading.
...Ted

_________________
Dx SPMS in 2004.  Liberated 29/04/2010.
My blog: www.my-darn-ms.blogspot.com

Hi Patient--
I also had a problem with the conclusions section of the abstract:



It's actual the word caution that bugs me, it reads as a negative. Let me explain what I'm thinking.

If HLA DRB1 1501 is a susceptability gene, which is known to be related to northern European ancestry, acts as an immune system response gene, and also shown to be related to MS vis a vis a three time higher susceptability risk of contracting MS with this gene...how does the lack of "strong associations with CCSVI and HLA DRB1 1501" lead to caution in associating CCSVI in MS?

The HLA DRB1 1501 allele does not cause MS, it does not mean one with this allele will get MS. Having this allele means that the likelihood is increased. Do you see where I'm going with this.....

What if MS is a vascular condition which might secondarily activate this immune response, and people with the allele have more likelihood of this activation becoming MS? Not everyone with MS has HLA DRB 1501---actually, only 53% tested in this study had it. Isn't that an avenue which should be explored? In fact, the body of the paper goes further into the environmental and external factors related to both CCSVI and this allele....and suggests further studies need to be undertaken.



Why does the abstract take such a negative stance, when the full paper is much more neutral? That's my question. The Buffalo doctors wrote the paper....who wrote the abstract? I don't think it was the same author.
Did the editor write the abstract? Editor: Christoph Kleinschnitz, Julius-Maximilians-Universität Würzburg, Germany

Here's the full paper, see if you think the abstract is a bit more negative, patient. Am interested in your take on this--
http://www.plosone.org/article/info:doi ... ne.0016802

Or, I could be completely over-reacting...(but I don't think so)
cheer

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

Cheer, I think what they are trying to say (badly)is if the gene is a causal factor and ccsvi is a causal factor for ms, one would expect there to be a statistical association between the two which there is not ie if the gene is present it should be more likely that ccsvi is present as well, but it is independently associated with ms.

This to me again supports the idea that ccsvi is a symptom of ms.

dreddk, I can see the logic of CCSVI possibly being a cause of many MS symptoms and perhaps a primary cause of the MS "syndrome" itself, but what would be the explanation for MS causing CCSVI? Perhaps I missed some recent discussion about that since I'm not often on here anymore. Early on, just after "experts" stopped insisting that CCSVI didn't exist, some of them began saying "Well, then, maybe MS causes CCSVI", but there was never a logical explanation of how/why that could be. Do you know of something that would explain such a phenomenon?
...Ted

_________________
Dx SPMS in 2004.  Liberated 29/04/2010.
My blog: www.my-darn-ms.blogspot.com

Hi Ted

From the beiruit venography study

"In conclusion, we think that EVS is a late manifestation
in MS, and is unlikely to induce a state of CCSVI
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. The exact mechanism of such process is
unclear, since the extracranial venous system, especially
in the spinal cord, has never been adequately investigated
in chronic neurological diseases. We hypothesize
that chronic degenerative brain diseases resulting in significant
brain atrophy and tissue loss might lead to a
decrease in the volume of venous drainage, resulting
ultimately in venous stenosis. In MS specifically,
chronic perivenous inflammation might hypothetically
lead to release of certain inflammatory mediators that
might alter the venous endothelium or lead to venous
valvulitis resulting in venous stenosis."

Thanks, I hadn't seen that before. Still, it does seem to go against some other results that say that CCSVI is congenital, and a lot of evidence that fixing CCSVI alleviates many MS symptoms. I suppose that could be some kind of vicious circle working.
...Ted

_________________
Dx SPMS in 2004.  Liberated 29/04/2010.
My blog: www.my-darn-ms.blogspot.com

In my case at least, the stenoses were accompanied by a robust network of collateral veins that completely resolved when the stenoses were opened. I don't see any reason to think my venous drainage had decreased.

....and yet my husband had no brain atrophy (and still doesn't) but two severely mangled jugular veins, which his doctors have proclaimed were congenitally malformed. He lost his peripheral vision as a child, no reason ever found until now. So, in his case, his jugular damage came first. Guess he was the only one. Huh. My work is done.
But don't you think other pwMS deserve to know if their veins are malformed?

Anyway...back to the paper at the start of the thread. Does anyone else find the abstract much different from the paper?
cheer

_________________
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
dual stents placed 5/09
CCSVI in MS

This hypothesis might be convincing if you don't understand what CCSVI is.

Makes sense that neurologists do not understand what CCSVI is. It has taken our CCSVI IRs quite some time to understand it as well as they currently do and they do not yet know everything yet.

Phasic venous narrowing as a result of overall reduced blood volume is not what is going on here.

No, I'm not sure I see where you are going with this, but my answer would be along the lines of what dreddk wrote - if past studies showed that MS is significantly associated with that particular gene, and CCSVI is associated with MS, then the authors probably hypothesized that CCSVI should be associated with that particular gene. Statistically they didn't find this to be the case. But the abstract didn't mention expressing "caution in associating CCSVI in MS," as you wrote. The conclusion was

I take this to mean, they aren't saying there isn't an association between CCSVI and MS (the Buffalo doctors have asserted there is, more than once); I believe they are saying that there's not enough evidence to say that CCSVI causes MS (at least based on this one study). Again, this is along the lines of what dreddk wrote.


That was the conclusion the authors reached; I guess you would have to take that up with them. I don't see it as being overly negative.


I asked a few people who have written articles for technical and scientific journals about the publication process. They all told me that one or more of the authors writes the abstract. One thing is almost undoubtedly true - the editor did not write any part of the abstract or paper. The editor of the journal may suggest changes, outright reject a submitted article, or cut the length - but he will not change the content without the author's knowledge.

Dreddk:

I don't know if you've had a chance to read the full article, but you might find this passage interesting: