This Is MS Multiple Sclerosis Community: Knowledge & Support

What are the implications of this? If we've had our jugulars ballooned, should we be avoiding coughing and 'acute increases in intrathoracic pressure' (whatever that means)?

I come away with the thought that this is all assumed. If we were able to measure the pressure or vacuum changes inside the veins of normals and MSers we would be moving ahead.

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

kind of fell flat

had a funny thought, kind of fell flat

Based upon what I learned in the other thread , it would seem that valves with truncular malformations (stuck closed) are associated with CCSVI and MS, whereas valves that are insufficient (stuck open) are associated with TGA.

I'm still not sure that it is a "pick your poison" dichotomy. Firstly, trying to balloon veins upstream from valvular malformations seems to be at best a temporary fix (clinics focused on valves have markedly lower restenosis rates). Secondly, there have been no reported cases of TGA in the ever growing population of patients having undergone valvular angioplasty.

A few other things to keep in mind. TGA does not seem to cause any lasting damage, patiients who have experienced it once, tend not to again, and (as 1eye) points out, collaterals have no valves. So patients with valvular malformations have the worst of both worlds and patients having undergone valve "opening" have the best of one and an unproven risk of the other (which they had anyway).

28 patients with transient global amnesia (TGA) were followed for a mean period of 73 months. The patients fell into 3 diagnostic groups: a group where patients had associated symptoms and signs of transient focal cerebral ischemia (TIA), a migraine group and a miscellaneous group. 22 patients had evidence of cerebrovascular disease or risk factors for cerebrovascular disease, and a vascular basis for the amnesic attack was highly suggestive in 25 patients. During the follow-up period 2 patients died, 3 had recurrent TGA and 13 developed a completed stroke or suffered from further TIA's. Permanent memory impairment was encountered in 9 cases. An unfavourable course was related to the presence of other TIA manifestations and/or risk factors for cerebrovascular disease. The study indicates that TGA is probably due to transient ischemia in the vertebrobasilar arterial distribution area. TGA per se has a good prognosis, but the coexistence of risk factor or manifest cerebrovascular disease implies a high rate of a subsequent completed stroke or permanent memory impairment.

Repeated attacks of TGA are not rare and with each attack the likelihood increases of permanent memory deficits and progressive dementia. A rarer outcome is cerebral infarction in the territory of posterior cerebral arteries commonly referred to as "amnesic stroke."

In my case; I have noticed no ill effect from repeated valsalva maneuvering. Knock on wood.

This type of internet rumor about restenosis rates is what got people going to Bulgaria to get LARGER Balloons....they thought it lead to lower restenosis rates, and now they have NO FLOW. People with valvupasty have just as many restenoses...here's a guy in Las Vegas who went to Arata's clinic NINE times, due to restenosis. He needed a vein transplant--
http://msmikejuices.blogspot.com/search ... results=29

The study indicates that TGA is probably due to transient ischemia in the vertebrobasilar arterial distribution area. TGA per se has a good prognosis, but the coexistence of risk factor or manifest cerebrovascular disease implies a high rate of a subsequent completed stroke or permanent memory impairment.