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testing mice...

Posted: Thu Jul 02, 2009 8:40 am
by mrhodes40
I boldly asked Dr Simka if we could put sclerosing foam in mice jugular veins and azygos veins to see if they get MS like lesions.

He said no because it is not possible to make an animal model of leg ulcers because the mice do not live long enough for one to develop.

HHHmmmmmmm.

So. that answers the question about how long it takes for these venous stenoses, in legs at least, to result in a lesion: a long time. So the blockage occurs and it takes some years before the person actually gets anything resembling an ulcer.

But with regards to the fact that people with cancer can have jugular veins removed occasionally in a radical neck dissection (throat cancer for example) and that those people, when the venous drainage is checked a month later seem to be "fine" because the vertebral veins have taken the load, are not at all assuring us that people will be fine if they lived another 15 years with the jugulars gone.

I had suspected it would be a long time before these anomalies would result in MS lesions because some lesions such as mine appear to be from birth-just the way I was made. Since my first MS attack was not until 30 years of age and I was my adult size at that point for 15 years, I guessed that it must take some years for these stenoses to result in an MS lesion...and even then I was really fine for another 13 years. If my first attack had not bee so severe that I ended up with MRI I would have gone another bunch of years just feeling bad in general...

Also, a significant number of people are found to have typical MS type lesions on autopsy when in life they had no diagnosis of MS. I bet they got stenoses very late in life too late to end up with a diagnosis because it just did not progress to that level where the person was identified as having a neurological problem before they passed away.

That may explain why it is rarer in older people: unless you are born with the anomaly that results in venous back pressure, it is uncommon to develop one later, therefore the average age some one would notice it is 30-40 when the lesion load reaches beyond plasticity? think so?

Anyway some many years before these lesions develop. I still anticipate the expert commentary that will be used to attempt to debunk this CCSVI model which will offer that jugular removal is known to be "safe and effective".....

Posted: Thu Jul 02, 2009 9:14 am
by guitarguy
Just curious, do you know how hormones might play a part in this? the stats say more females vs males have MS. Also, females seem to do much better MS wise during pregnancy.

to me it doesn't seem to much to do with how big we are but maybe maturity. Our hormones change a lot as we get older. Maybe there is something to that why MS hits most of us in our 20's.

I don't know what I am talking about, just thought Iwould throw that out there. :oops:

Posted: Thu Jul 02, 2009 10:47 am
by cheerleader
Great post, Marie! We can see from CVI in the legs, that is takes about 20 years for damage to start amassing, and then another 10 or so years for diagnosis. You're right about how that massive attack your first time got you into the MRI tube...same thing for Jeff- his was at 42! Although he had been suffering from depression and fatigue for most of his adult life. If it weren't for that week in Salt Lake City, who knows how long his progression would have silently continued?

I actually think more older folks are being diagnosed with MS today, due to better diagnostic healthcare...but in earlier times, their slowing down or motor issues would have been attributed to "old age."

as far as hormones, more women have CVI in the legs- and it's thought this is due to progesterone being a smooth muscle relaxant and the legs not having the oomph to get the blood back to the heart- not the same scenario in CCSVI...but it is an interesting connection. We've talked about pregnancy hormones being vasodilators and labor being vasoconstrictive on here before.
cheer

Re: testing mice

Posted: Thu Jul 02, 2009 6:40 pm
by NHE
mrhodes40 wrote:I boldly asked Dr Simka if we could put sclerosing foam in mice jugular veins and azygos veins to see if they get MS like lesions.

He said no because it is not possible to make an animal model of leg ulcers because the mice do not live long enough for one to develop.
Lately I've been thinking that doing a study in pigs might work. Their lifespan has been reported to be around 12-15 years. It might work if you started with piglets. However, 10 years is still a long time to wait for results. It's certainly not an experiment someone new in research would undertake due to the time it would take to publish anything.

NHE

Posted: Fri Jul 03, 2009 6:28 am
by mrhodes40
NHE I like it! pigs are a lot closer than mice .

however
it might work
That's would be the dilemma what if it did not? would it mean anything? would it mean pigs can't get lesions that way because they have enough drainage otherwise or would it mean it doesn't "cause" MS? And boy that LLOOoooonnggg timeline. Ouch!

I think we are back to saying we need to watch people and see what comes up

1. continue association studies, is this present in the vast majority of MSers? If it is and as more work is elucidated with people weighing in on how these lesions are similar to venous stasis lesions, we may reach a consensus of saying that it is proper to treat these based on physiologic prinicples that we don't leave blocked veins because we know the physical consequences of that.

2. Watch for it in not currently diagnosed people who don't meet the criteria for definite MS but seem to have something going on.... see if they develop typical MS lesions and definite MS with time. I mean if they don't meet the criteria they don't meet it yet and they are not eligible for crabs or anything, they are stuck just waiting... one has only to read the boards to hear of people who swear they must have MS but they keep getting "no not MS". Lynda carol said she had no lesions but was sure she had MS for some years before they finally gave her the diagnosis... such persons having a blockage and developing a typical MS lesion later which would put them in the definite category and qualify them for treatment, at which time they could decide to do stents if they wanted. It would also prove the model. But I assume at some time we have got to run into people with no MS diagnosis yet who have these, especially if they take years to manifest.

You could put out the call to neurologists to ask for people with symptoms but who don't meet the criteria for CDMS that we need people for a study to see if it does develop. Probably such people who are frustrated with the lack of doing something would be glad to have something to do while they wait.

3. and the obvious studies to see if it helps MS to treat it this way

I hope it is enough! I wish we could have mice studies and get an answer in a year or two whether this can cause MS...

Posted: Fri Jul 03, 2009 7:38 am
by cheerleader
Marie...
I think you're right, it's going to have to be determined by watching humans who are pre-MS diagnosis. Only way. Animals will not work for this model. I think the new 7Tesla MRI machines will help in this pursuit. I got a message from Jamie (now heading to Stanford with his Mel.) She just had a 7Tesla done, and he said the level of cerebral damage it showed was much, much more than the 1.5.

If doctors (like Dake) can chart venous flow rates and beginnings of stenosis in the jugulars of younger patients just showing MS symptoms and then use the 7Tesla machine (Stanford has one)...we may be able to see the correlation l-o-n-g before a typical 1.5 diagnosis would pick it up. And then we could see what happens after treatment. In younger patients, a balloon treatment might suffice.
cheer