This Is MS Multiple Sclerosis Community: Knowledge & Support

The prevalence of internal jugular vein (IJV) valve incompetence, as assessed by ultrasound, was found to be more prevalent in patients with TGA [transient global amnesia] than in controls. In all of these studies, IJV valve incompetence was detected in 97 of 131 [TGA] patients (74%) and in 65 of 191 controls (34%).

That one used valsalva to assess for reflux, not the test Z uses so the 45% controls is not the same. But notice that the difference between so called healthy normal controls and patients with TGA is small in terms of pressure. This to me suggets the brain can't take a lot of difference here, reflux is hard on it (BTW, these TGA patients do not have abnormal white spots on MRI, I looked) But note that the TGA issue is often one of a post valsalva problem. The valsalva is the thing you do if --ahem!--constipated and you hold your breath and push..got it?

If you have TGA it appears the mechanism may be that your jugular valve is not competant and that "push" results in backflow into the brain briefly--Wham!--you get transient amnesia. It goes away, perhaps not to happen again for months.

But, accepting Z work, MSers have reflux that happens all the time not just with valsalva. Even though the times are smaller it is with every breath all the time. It is not at all hard to understand that this constant whirl and chaotic blood flow might cause an the issue we call MS esp when you realize that it is these specific veins that are attached to those specific lesion area that are affected.

As to the theorie on CCSVI.
Hi Julie, i have been following the principle behind CCSVI very closely. But i am also a bit sceptical. So i had a look at medical publication out on the web. An interresting studie that i came across, and it is not one there are a couple dating back as far as 2000.
Dr Zamboni indicates that all of the ms patient had jugular insifiecancys and none of his control group. He also state that he did not find that in any other neurological disease. How ever, i found the above mentioned studies was done on Transient global amnesia. 86% of all the patient had jugular vein reflux in the brain. Also nearly 30% of the healthy controls who do not suffer from tga also had jugular insufieciency. This is clearly describe by dr Schreiber in 2005 in a leading german institution. It was also studied in italy and the result were the same. And as far back as 2000 Dr Sander came to similar conclusion. Furher evidence is that this is is also found in certain lung disease as well. As well as in TIS. Even certain studies done on megraines point to jugular reflux in the brain.So it is hard for me to see that CCSVI is the cause of ms but rathe another symptom of Ms.

In TGA, the reflux is minimal and associated with a stressful event compounded by a valsalva manuever (forced reflux). It is temporary, thus the transient nature. In CCSVI, the reflux is continual, found in a variety of positions, and not created by valsalva, thus the name "chronic".

We've discussed this many times on here.
http://www.thisisms.com/ftopicp-53518-tga.html#53518
http://www.thisisms.com/ftopict-9698-tga.html

cheer

Transiant global amnesia happens after stressful situations-

From the Mayo Clinic-
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.


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-

"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."

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

You should post that in the comments section of Julie's article so people can know. Or I can if you want. I just know that I was discouraged when first reading that comment but what you say makes a lot of sense.