This Is MS Multiple Sclerosis Community: Knowledge & Support

"In the literature, there have been several re- ports of vaseular malformations that run a long insidious course and simulated multiple sclerosis [Cader and Winer 1999. Honcza- renkoetal. 1995, Stahl etal. 1980, Vrethemet al. 1997].

However, in most published case reports, vaseular malformations were homo- genous and monofoeal.

We would like to demonstrate a case with fluctuating progres- sive neurological deficit and multiple differ- ent vascular malfonnations involving cere- brum, brain stem, cerebellum, spinal cord and spinal roots."

Holy crap.

Have you guys seen this??

http://cat.inist.fr/?aModele=afficheN&cpsidt=18085658

Search google for this:

(Vascular OR Venous) AND Multiple AND Sclerosis

and lots of interesting reading comes up.

They postulate that Vascular malformations usually develop as a result of influence of teratogenic factor(s) acting in the defined embryonic/fetal period.

ATTN: BOB

This (if true and I know I am getting way ahead, think of this as jamming) would tie in all those factors you are talking about. Loose familial connection, natives getting MS when westerners move in (if they brought with them the tetragenic agent) also, clusters. Also this could be an agent that came in around the time MS exploded and be a foetal development thus congenital weakness caused by tetrogenesis.


From Wikipedia:

Teratogenesis
Birth defects are known to occur in 3-5% of all newborns.[1] They are the leading cause of infant mortality in the United States, accounting for more than 20% of all infant deaths. Seven to ten percent of all children will require extensive medical care to diagnose or treat a birth defect.[2] And although significant progress has been made in identifying etiologic causes of some birth defects, approximately 65% have no known or identifiable cause.[3]
It was previously believed that the mammalian embryo developed in the impervious uterus of the mother, protected from all extrinsic factors. However, after the thalidomide disaster of the 1960s, it became apparent and more accepted that the developing embryo could be highly vulnerable to certain environmental agents that have negligible or non-toxic effects to adult individuals.

If that is the case as you've argued a lot of times Bob but not I believe for foetal influence of environmental factors (but it makes sense, not dangerous for adults but would be for baby), vascular weakness introduced - develops slow ischemia (MS).

For some its RR for some its right downhill depending on specific patterns of stenosis that Zamboni believes he's identified.

Nothing before has clicked so well into place in my opinion.

We can nit pick about some stats but I believe the evidence is overwhelming and growing daily.

I couldn't find this on here when I searched.

Look at this:

Immunohistochemical study of vascular injury in acute multiple sclerosis.

http://www.pubmedcentral.nih.gov/articl ... tid=501826

AIMS--To examine the vascular changes occurring in three archival cases of acute multiple sclerosis, and to provide immunohistochemical evidence of early endothelial cell activation and vascular occlusion in this condition. METHODS--Central nervous system tissues from three cases of acute active multiple sclerosis and six non-inflammatory controls were stained using the following methods: haematoxylin and eosin, Luxol fast blue, cresyl violet, Bielschowsky's silver, and reticulin. Tissues were also immunostained with specific antibodies against collagen type IV, factor XIIIa, class II antigens, glial fibrillary acidic protein, and fibrinogen.

RESULTS--Early vascular endothelial cell activation which may progress to vasculitis and vascular occlusion including class II antigen expression and fibrin deposition were identified. The vascular changes were seen prior to cerebral parenchymal reaction and demyelination, and were not seen in control cerebral tissues.

CONCLUSION--It is proposed that vascular endothelial cell activation may be an early and pivotal event in the evolution of multiple sclerosis, and that demyelination may have an ischaemic basis in this condition. The vascular endothelium may contain an early element in the evolution of multiple sclerosis.

Link to Google Books: Multiple Sclerosis, the History of a Disease, T. Jock Murray

http://tinyurl.com/l29unw

Most people may have read this but read that page. In 1882.

good stuff jamie

oo

Holly Crap! Sorry I had to mimic you Jamie...its so appropriate! I have to say after reading all of this I can't help but feel completely disgusted that this has been theorized for many many many years and nothing has come of it. It makes me feel...well...bad for everyone suffering with the disease and for everyone that has had to suffer. Imagine if the theory was tested in the 1800 and proven...Imagine life without the devistating affects of MS...imagine if MS was something you just read about in text books.

Thanks for the great info Jamie!

_________________
javaneen

No it is not holly crap although when I do it is a holy crap

hehehe...Jamie fell down the rabbit hole today. Nice work! Hadn't seen the vascular injury paper...that's terrific!!!!

Dr. Dake's office is full of these studies now, piles and piles of them...he wanted to talk about all of the vascular research that got scrapped for the AI model when we saw him last month. He was flummoxed and a bit angry...

I really think it's just because the vascular model could not be monetized. Plain and simple. Doctors tried anticoagulants, no luck. End of story. There's an MS doc in Scotland who theorized that fat embolisms in the blood were to blame and uses HBOT for his patients. Jonez, Swank...were seen as quacks, but they saw the connection. The vascular connection was made to seem "fringe." The only doc who took me seriously when I sent out my endothelial paper last fall was Dr. Cooke at Stanford...he wrote me back and we began corresponding. Here's what he said to me after reading the paper...."I quite like the hypothesis that MS is secondary to a derangement of the endothelium of the cerebrovasculature, that results in inflammation and local damage." It made sense to him, but Jeff's neuro thought I was nuts.

well, at least we're getting somewhere now.
cheer

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

Bob,

That's what I am thinking, yes.

Jamie

If you think about this logically it would explain the infuriating vague but real 'pattern' of MS distribution.

Why Mel has it but I don't considering we've shared the same environment for years.

Why hypoxia causes ischemic lesions and MS like symptoms (proven, not conjecture).

It would explain why when westerners invade an ecosystem native rates go up.

The pathology I think is clear, studies of fresh lesions days old show no immune activation until later on.

Are the MS lesions and symptoms caused by venous blockages? I think yes, they are. I am almost certain, I understand why others aren't though.

However that still doesn't answer the WHY? The blocked veins are a symptom of SOMETHING in of itself.

With the malformites and twisting seen in a lot of people, some with multiple jugulars like Mel as well as narrowing/occlusion does that not point to a conjenital fault rather than caused by inflamation etc (malformed twisted jugs surely not caused by a late life onset disease).

So if congenital then why? We've just shifted the mystery (with of course the bonus of an ability (if all proven in the end) to judge course of MS, to definitively diagnose MS, and most wonderful of all to intervene.

So if congenital then a foetal development issue causing weakened vascular system that causes slow progression and/or relapsing symptoms (depending on level of reflux and associated hypoxia) to show up later in life when either the condition degenerates or plasticity stops hiding the damage (probably both). If that development issue is caused by an environmental toxin or even a virus or bacterial infection whilst still in the womb then a lot of dots are connected.

And in a way, we're ALL right. The jigsaw always seems easy once its done.

I mean its well know that veins dilate in pregnancy, and women get relief from MS during pregnancy. Additionally after they stop nursing the veins shrink again, lots of women then have a 'bad' relapse after the relief of pregnancy.

This is just my thinking along with you guys but I don't think any of that is a massive stretch logically.

Imagine in 20 years if with new super duper scanning equipment this was a standard pregnancy scan or new born scan and early intervention could happen or life long monitoring or at least a note in their fricken EMR to watch out.

Or even better imagine all this data was collected in a massive global database of EMR's with advance AI pattern searching happening to sift correlation and severely narrow down potential causes for not just this but all disease.

The technology is almost there, how about the will/cash? Maybe a slice of the hundreds of billions the banks have got ??!

Anyway, I've put south park on, Mary has come round for a visit and I'm going to rest what passes for my brain.

Cheers all.

Wow seems like an understatement, but wow and thanks for the links. Guess putting the puzzle pieces together has been left to the patients or their loved ones.

_________________
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

check out this thread, cureious...some good discussion/research on vitamin D and hypoxic preconditioning from Sharon at the bottom of the page...
http://www.thisisms.com/ftopict-7542.html

cool, huh?
cheer

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