CCSVI&MS Conference, Copenhagen, Nov.3, '10, prof. Simka
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CCSVI&MS Conference, Copenhagen, Nov.3, '10, prof. Simka
http://www.livestream.com/ccsvihoering/ ... m=ui-thumb
His presentation starts at 01:10. There are some new slides.
Erika
His presentation starts at 01:10. There are some new slides.
Erika
Aug. 7, 09 Doppler Ultras. in Poland, left Jugul. valve problem, RRMS since 1996, now SPMS,
- Nov.3,09: one stent in the left jug. vein in Katowice, Poland, LDN, never on DMDs
- Jan. 19, 11: control venography in Katowice - negative but I feel worse
- Nov.3,09: one stent in the left jug. vein in Katowice, Poland, LDN, never on DMDs
- Jan. 19, 11: control venography in Katowice - negative but I feel worse
Thanks Erika,
Among other things, Dr Simka talks about what is the relationship between MS and CCSVI. Are they related or not? (1:15min)
Dr Simka has found CCSVI in the majority of MS patients he has tested 95%. He says that more research is needed to understand why the other 5% of tested MS patients don't present CCSVI. And why some non-MS patients have also been diagnosed with CCSVI.
He said that the first trigger of MS is NOT CCSVI (1.20min). His hypothesis is that there is another (unknown) factor that acts together with CCSVI to trigger MS.
I found this later point the most important of his talk. What is that 'something else' that is acting with CCSVI to trigger MS?
It is perhaps here where neuros and vascular doctors could collaborate to find the answer.
Rox
Among other things, Dr Simka talks about what is the relationship between MS and CCSVI. Are they related or not? (1:15min)
Dr Simka has found CCSVI in the majority of MS patients he has tested 95%. He says that more research is needed to understand why the other 5% of tested MS patients don't present CCSVI. And why some non-MS patients have also been diagnosed with CCSVI.
He said that the first trigger of MS is NOT CCSVI (1.20min). His hypothesis is that there is another (unknown) factor that acts together with CCSVI to trigger MS.
I found this later point the most important of his talk. What is that 'something else' that is acting with CCSVI to trigger MS?
It is perhaps here where neuros and vascular doctors could collaborate to find the answer.
Rox
Diagnosed with Transverse Myelitis in December 2008. Inflammatory demyelination of the spinal cord (c3-c5). No MS, but still CCSVI.
I (with all of my medical "expertise") agree with Dr. Simka. My hypothesis is that chronic bacterial infection is the "(unknown) factor". I am now testing that hypothesis.His hypothesis is that there is another (unknown) factor that acts together with CCSVI to trigger MS.
My name is not really Johnson. MSed up since 1993
Could be a deficiency like vitamin C which causes inflammation in the veins (I read somewhere that Vit C is related to the cardiovascular system)
Before I got diagnosed with MS (when all my brain scans and conduction tests were normal but I was still suffering with major symptoms)
The only tests that ever showed up abnormal were the following:
Thyroid antibodies
IGG/IGM antibodies high (active immune system)
CRP levels high (cardiovascular and inflammation marker)
High Bilirubin levels
I think these had something to do with my veins stenosing.
(I have been thoroughly tested for every bacterial and virus infection (except retro virus which I want to get checked) all were non active but did show evidence of Parvo Virus, Mycoplasma and Epstein Barr)
I tried the abx protocol and had some improvements (I regained some lost sensation) but had to stop due to liver struggling
Before I got diagnosed with MS (when all my brain scans and conduction tests were normal but I was still suffering with major symptoms)
The only tests that ever showed up abnormal were the following:
Thyroid antibodies
IGG/IGM antibodies high (active immune system)
CRP levels high (cardiovascular and inflammation marker)
High Bilirubin levels
I think these had something to do with my veins stenosing.
(I have been thoroughly tested for every bacterial and virus infection (except retro virus which I want to get checked) all were non active but did show evidence of Parvo Virus, Mycoplasma and Epstein Barr)
I tried the abx protocol and had some improvements (I regained some lost sensation) but had to stop due to liver struggling
In a way, the sum of the above observations probably mean that CCSVI for which reflux is a major qualifying factor is not an issue. I find that hard to appreciate.TMrox wrote:
He said that the first trigger of MS is NOT CCSVI (1.20min). His hypothesis is that there is another (unknown) factor that acts together with CCSVI to trigger MS.
I found this later point the most important of his talk. What is that 'something else' that is acting with CCSVI to trigger MS?
So many symptoms are today attributed to MS. Its possible that reflux itself has some standalone symptoms associated with it. And then there are devious MS symptoms associated when immune actions kicks in.
It would have been great if Buffalo too, which found so many 'healthy' people with CCSVI should have tested for fMRI response of these people. And compared the same with fMRI response of healthy controls who did now show CCSVI. I think that would have been such an important data ...
A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die and a new generation grows up that is familiar with it
- Max Planck
- Max Planck
I think this is a smart idea!sbr487 wrote:It would have been great if Buffalo too, which found so many 'healthy' people with CCSVI should have tested for fMRI response of these people. And compared the same with fMRI response of healthy controls who did now show CCSVI. I think that would have been such an important data ...
That is not possible, there are too many. There is also the problem of false negatives/positives; Borreliosis Burgerdorrfi (Lyme spirochete) is almost always shown to be negative when the ELISA test is used, and that is the standard test (at least, in Canada). The test for Lyme is so unreliable that the best way to test is to start an anti-bacterial regimen after a clinical diagnosis. Many other bacteria mutate, shed their cell walls, and hide in macrophages. Others block the VDR (Vitamin D Receptor) and down-regulate the immune system. The VDR is responsible for the transcription of 913 genes...I have been thoroughly tested for every bacterial and virus infection
I'm not claiming to be right, just that I have an hypothesis, and I am testing it.
My name is not really Johnson. MSed up since 1993
Johnson how are you testing your hypothesis?
Unfortunately I got diagnosed for Transverse Myelitis after spending months in Africa. I say unfortunately because that complicated the diagnosis scenario. I was tested for more than 50 viruses (common and weird ones), lymes, bacterial infections, parasites, vitamin levels, autoimmune and metabolic conditions. Since I was negative/normal in everything my neuro re-ordered some tests and again everything came back negative.
I only gave positive for CCSVI. After my treatment I've had further tests that could perhaps tell us what else had upset my immune system.
So far we have found that I have several food intolerances, low omega3. I'm waiting for my vitamin D, minerals levels and metal toxicity results. Calcium level is fine.
Rox
Unfortunately I got diagnosed for Transverse Myelitis after spending months in Africa. I say unfortunately because that complicated the diagnosis scenario. I was tested for more than 50 viruses (common and weird ones), lymes, bacterial infections, parasites, vitamin levels, autoimmune and metabolic conditions. Since I was negative/normal in everything my neuro re-ordered some tests and again everything came back negative.
I only gave positive for CCSVI. After my treatment I've had further tests that could perhaps tell us what else had upset my immune system.
So far we have found that I have several food intolerances, low omega3. I'm waiting for my vitamin D, minerals levels and metal toxicity results. Calcium level is fine.
Rox
Diagnosed with Transverse Myelitis in December 2008. Inflammatory demyelination of the spinal cord (c3-c5). No MS, but still CCSVI.
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