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PostPosted: Mon Jan 11, 2010 7:40 am 
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Hi all,

recently I have read about another disease, called TGA (transient global amnesia), also recently suspected to come from venous problems:

http://www.ncbi.nlm.nih.gov/pubmed/1992 ... dinalpos=1

http://www.ncbi.nlm.nih.gov/pubmed/1992 ... dinalpos=2

Somebody has ever heard about an association of MS with TGA?


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PostPosted: Mon Jan 11, 2010 8:37 am 
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The german MS Society (DMSG) noted this and used it as an indicator that CCSVI isn't unique to PwMS. I've translated their statement here:

http://www.thisisms.com/ftopicp-79494.html#79494

their pamphlet suggests that TGA is unrelated to MS.

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PostPosted: Mon Jan 11, 2010 11:23 am 
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cah wrote:

their pamphlet suggests that TGA is unrelated to MS.


Thanks. In fact I started reading about TGA because their statement. I just wanted to know if somebody around here had had that problem. Maybe at the end both diseases will be related.


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PostPosted: Mon Jan 11, 2010 12:15 pm 
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This... thing is just one piece of seeming logic. Not only that TGA is unrelated to MS, they say that their ultrasonic findings are not identical to the ones from Dr. Zamboni. Afterwards they talk only about venous valve insufficiencies. Dr. Schelling said in the german forum that the valves in the veins situated above the heart seem to be not that relevant cause the blood is unlikely to back up simply because of gravity. They are really needed only below the heart (which btw could be an explanation for the effects of inclined bed therapy, but to be honest I haven't really looked into that therapy). Then they talk about studies published only on posters so nobody can investigate them... all in all, there's already much more evidence to the theories of Dr. Zamboni and Dr. Haacke than to their... crap.

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PostPosted: Mon Jan 11, 2010 1:38 pm 
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Here's the deal....neurologists recently have more diagnostic equipment available to them. We were discussing the research linking TGA to jugular scans last year. I don't think TGA or CCSVI are mutually exclusive. TGA looks like a one time whollop to the CNS, while CCSVI is an ongoing problem that creates venous congestion.

Transiant global amnesia happens after stressful situations-

Quote:
In many cases, an episode of transient global amnesia can be traced to a physically or emotionally stressful incident shortly before symptoms began. Among the triggering events commonly reported are:

Sudden immersion in cold or hot water
Strenuous physical activity
Sexual intercourse
Medical procedures, such as angiography or endoscopy
Acute emotional distress, as might be provoked by bad news, conflict or overwork
The underlying cause of transient global amnesia is unknown. There appears to be a link between transient global amnesia and a history of migraines, though the underlying factors that contribute to both conditions aren't fully understood.

from the Mayo Clinic page on TGA

A sudden, hyperacute ischemic change is very different than an ongoing problem. I reiterate, CCSVI and TGA may not be mutually exclusive. Tiny lesions are detected in some patients after TGA-

Quote:
Hakan et al demonstrated tiny increases in signal in the left parahippocampal gyrus and splenium of the corpus callosum on DWI in one patient. This method of imaging allows detection of hyperacute ischemic change. Liang et al and Yang et al have also recently used DWI to document tiny lesions in the hippocampus of patients with acute TGA.1,2 However, Eustache et al reported a PET study consistent with a spreading depression in the left lateral frontal cortex. This case also featured oligemia in the left occipital cortex.3 Strupp et al found mainly medial temporal changes on DWI in 7 of 10 patients with TGA. They suggested that cellular edema or spreading depression could be responsible, not just ischemia.4

http://emedicine.medscape.com/article/1160964-overview

The studies are ongoing. It appears there is substantial evidence that jugular valve malfunctions may play a part in TGA. But that does not nullify CCSVI studies. I think the Germans are wrong to discount CCSVI without researching it.
We have to be really careful about making comments regarding well-established, peer-reviewed research on here, just because it doesn't seem to fit our particular paradigm. We don't know enough about how TGA and CCSVI are different or how they are the same YET, but research will continue to help us understand.

Here is the Chung research I put on the big CCSVI forum last year, Marie has it linked in the research sticky. There is still more to learn regarding jugular venous reflux. Please read this paper-
http://health.elsevier.com/ajws_archive ... 3A4703.pdf
cheer

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


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PostPosted: Wed Jul 20, 2011 2:36 pm 
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sorry to bump an old thread and I don't think it's the most comprehensive one of our discussions of TGA vs MS.

I wanted to add this:
http://ccsvinews.blogspot.com/2010/10/c ... d-tga.html

Quote:
RESULTS: Valve insufficiency was found in at least one jugular vein in 113 of 142 patients with TGA (79.5%) and in 10 of 40 controls (25.0%), P<0.01. The right side was affected more often than the left side, P<0.01, and 26.8% of the patients had bilateral incompetence.

If incompetent valves that let flow through in both directions are found in 25% of the population, then it is a fairly common thing. (Remember that CCSVI valves are incompetent in a different way, they disrupt the flow from going out.)

It is concerning that not having valves might cause TGA or TGA-like symptoms but it was more concerning that having valves was definitely causing CCVSI symptoms.


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