This Is MS Multiple Sclerosis Community: Knowledge & Support

http://www.ncbi.nlm.nih.gov/pubmed/20351666

Abstract
AIM: The aim of this open-label study was to assess extracranial Doppler criteria of chronic cerebrospinal venous insufficiency in multiple sclerosis patients. METHODS: Seventy patients were assessed: 49 with relapsing-remitting, 5 with primary progressive and 16 with secondary progressive multiple sclerosis. The patients were aged 15-58 years and they suffered from multiple sclerosis for 0.5-40 years. Sonographic signs of abnormal venous outflow were detected in 64 patients (91.4%). RESULTS: We found at least two of four extracranial criteria in 63 patients (90.0%), confirming that multiple sclerosis is stronghly associated with chronic cerebrospinal venous insufficiency. Additional transcranial investigations may increase the rate of patients found positive in our survey. Reflux in internal jugular and/or vertebral veins was present in 31 cases (42.8%), stenosis of internal jugular veins in 61 cases (87.1%), not detectable flow in internal jugular and/or vertebral veins in 37 cases (52.9%) and negative difference in cross-sectional area of the internal jugular vein assessed in the supine vs. sitting position in 28 cases (40.0%). Flow abnormalities in the vertebral veins were found in 8 patients (11.4%). Pathologic structures (membranaceous or netlike septa, or inverted valves) in the junction of internal jugular vein with brachiocephalic vein were found in 41 patients (58.6%), in 15 patients (21.4%) on one side only and in 26 patients (37.1%) bilaterally. CONCLUSION: Multiple sclerosis is highly correlated with chronic cerebrospinal venous insufficiency. These abnormalities in the extracranial veins draining the central nervous system can exist in various combinations. The most common pathology in our patients was the presence of an inverted valve or another pathologic structure (like membranaceous or netlike septum) in the area of junction of the IJV with the brachiocephalic vein.

This is an important paper by Dr. Simka and his team. It can be placed alongside the BNAC research and Dr. Zamboni's research as showing correlation between extracranial venous abnormalities detected by doppler in pwMS. This was done without use of transcranial doppler, which may have given a higher percentage. But 91.4% is rather high.
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

was this study just out today?...just wondering why it would not make the news like the Buffalo study did....this percentage is very high in comparison.....the skeptics always refer to the Buffalo results to dissuade the CCSVI theory......be hard to do that with these numbers!

This study was presented at the AAN conference in Toronto. Because it does not have a "blinded" segment, and it was done it Poland by a doctor who is currently treating CCSVI, it will not be held up alongside the other blinded studies, or make much news--HOWEVER, it is still more correlation.
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

good to see that jacek kosteki is an author on this paper since im going to be liberated by him in a few weeks.

Open label studies are helpful to investigate where a problem may be found and help other investigators to look in the right places. Neuros will want to dismiss the study but they are not approaching CCSVI with open minds.

0.94 correlation is high but as the sample is small so the standard deviation is likely to be large. The detailed results will tell you this. (Ignore this comment unless you like statistics). To be honest I cannot be bothered to look up the SD on the full paper. All these correlation figures will vary until the testing methodology is refined and agreed, then training given.

Kind regards,
MarkW

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Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 10 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html

Mark, I agree with you. What are your thoughts on how the results should be interpreted in such tests. If I am looking for a suspect element in a patient's body then generally positive is much stronger than negative.
For example, in the process of checking for an infection, a negative is never as strong as positive.

Don't know if I am communicating well here ...

Can someone please correct my line of thought here: The presence of iron overload is manifested by neurological abnormalities...If one presents with abnormal neurological symptoms, could this be a rational for asking for a diagnostic test to measure the iron content in the brain'[ we can do this,,,right?] OK..now once this iron is detected, could the vascular specialist then order a venogram to detect a possible cause for this dangerous situation? And might that test result in the obvious need to open up a stenosed jugular[ or another detected anomaly]
It seems so straightforward. Help me understand where the problem is...please.. Thanks in advance!

Not iron overload-Belsadie....it's iron left from blood.
This is proposed mechanism: Iron is merely the footprint left behind in brain tissue that shows blood has broken thru the blood brain barrier. Nothing to do with amounts of iron in the serum, so it is not called iron overload.

This deposition is created by venous hypoperfusion, slowed drainage, reflux....just like in CVI in the legs. The blood and foreign particles deposited on brain tissue are toxic--they initiate the immune system response. Also deposited are viruses, bacteria, all sorts of things. And the result of hypoperfusion (slower transit time of blood thru the brain) is less oxygen--which can create symptoms like fatigue.

The only test needed is to look at the extracranial veins: the jugulars and azygos. This is where doctors are finding blockage of blood flow. Dr. Haacke and others are using SWI MRI to see if there is a lessening of iron in the brain after correcting venous drainage.
hope that helps, and doesn't confuse more--
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

Very interesting, Dr Kostecki last week said he saw that I had septum's in both jugulars.

I got it...

I've got to make a point re iron overload here Cheer. I appreciate that you don't have to have an iron overload to get the deposits, BUT, if you do have even a slight tendancy to store iron it looks like it speeds up the process. It just makes sense, more iron in the blood and tissue, more iron deposits.

In studies it was found that people who have even one C282Y gene develop MS younger. The C282Y gene causes the body to store more iron. Approximately 1 in 10 people have a C282Y gene, so it should be taken into account. 1 in 3 chance in Ireland. 1 in 7 from Scottish decent.

I have a C282Y gene and I developed my first lesion when I was iron overloaded. I have reduced my iron levels and feel great again, fatigue mostly gone.

It's a side point that should not be overlooked for people who are susceptible, and does not apply to everyone. But it might!

Cheers.........

Breaching of the blood-brain barrier in MS doesn't mean that blood is leaking into the brain. It means that things like white blood cells are getting through the tight junctions between brain tissue and blood vessels.

How very interesting
Bethr how did you find out that you had the C282Y gene ?

poryhyria cutanea was in a paper that talked about, the following,

E80G missense, causeing third enzyme of heme biosynthesis pathway
(hydroxymethlbilane) problems similar to other
iron storage pathologies, especially in lungs and kidneys (difficult
to remove iron from these organs)