Lesions and SWI

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby patientx » Sat Sep 19, 2009 9:59 am

cheerleader wrote: Dr. Haacke has found a correlation between iron deposition, hypoxic death and the amount of disability and progression.
cheer


Could you provide a link to the study in which Haacke shows this correlation?
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Postby cheerleader » Sat Sep 19, 2009 11:35 am

Make sure to click on all the links provided in this thread, patient...it wasn't from just one paper. Dr. Haacke used all of his volumes of research using SWIM and BOLD technology in his presentation to present the case. He also showed us new SWI pictures showing iron deposits in PPMS brains. He will have more papers coming out, now that he has found a correlation in CCSVI-

The interesting thing about the particular study below was that they found disease course and disability had no correlation to lesions found on standard MRI....there was actually an inverse correlation. It was the SWI lesions seen that correlated to disease activity and progression. The research team hypothesizes that as inflammation decreases, iron deposition and tissue damage increase. This would correlate to what we see happening as MS becomes progressive.

Google iron deposition and MS for more studies...you'll find alot more info on iron levels and disease course...and then you can post them here-
thanks!
cheer

E. M. Haacke1, M. Makki2, Y. Ge3, M. Maheshwari1, J. Garbern4, O. Khan5, J. Hu1, M. Selvan1, and L. Zahid1
1
Radiology, Wayne State University, Detroit, Mi, United States, 2Radiology and Neurology, Wayne State University, Detroit, Mi, United States,
3
Radiology, New York University, New York, NY, United States, 4Molecular Medicine and Genetics, Wayne State University, Detroit, Mi,
United States, 5Neurology, Wayne State University, Detroit, Mi, United States

Introduction: MRI has been used routinely to diagnose and monitor multiple sclerosis spatially and temporarily. Although T2WI
is highly sensitive in the detection of hyperintensitises in white matter, these studies are not specific to the status of the disease.
Recently, a number of studies have suggested that there is[b] iron deposition
in dentate nucleus, cortex and adjacent subcortical white matter, brain stem, basal ganglia and thalamus. These results showed that hypointensities of T2WI highly related to brain atrophy, disease course and physical disability. For example, nonheme iron deposition has been reported to shorten T2 relaxation time in the basal ganglia [1] as well as in lesions [2] in the cortical and subcortical regions [3] of the brain in multiple sclerosis (MS) patients. These studies were based on conventional or fast-spin-echo T2W imaging, which is not sufficient for detecting a subtle iron component that may be associated with lesion development and progression [4]. The purpose of this study was to
correlate signal intensity loss in lesions seen in conventional T2W images with SWI filtered phase intensity.

Results: Conventional MRI sequences (T2W, FLAIR, T1W pre/post contrast) combined together revealed a total number of 270
lesions (113 on 1.5T, 96 on 3T and 61 on 4T). In comparison, SWI phase and magnitude images revealed more lesions, a total of
387.We found a negative correlation of T2 signal intensity with SWI filtered phase and hence the putative iron content (Figure 1).

The average phase over all lesions was 2186 ± 42 while that in the surrounding normal appearing WM was 2044 ± 20 (Figure 2).
The difference between these two values is 142 units, representing an average iron content of 47μg Fe/g tissue [5,6]. There is a
clear negative correlation between the T2 signal intensity and the putative iron deposition (Table 1).

Conclusions: SWI reveals iron deposition associated with MS lesions both in terms of its presence and characteristics compared to conventional imaging. Further, the SWI data suggests that there is a correlation between T2 signal intensity and phase changes (putative iron content). One may hypothesize that as the inflammatory component decreases, the tissue is compromised and there is an associated increase in iron deposition in the brain. Further work using SWI may provide some insight into the pathogenesis and mechanisms of disability in MS.


http://www.med.nyu.edu/radiology_resear ... /03436.pdf
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Postby cheerleader » Sat Sep 19, 2009 12:09 pm

Also- Dr. Bakshi from SUNY Buffalo has been on the trail for a few years now- and is now working with Dr. Zivadinov, looking at iron deposition in relation to CCSVI, and whether the liberation procedure stops iron deposition as shown on SWMRI.

link
Oct. 22, 2003 -- Iron deposits deep in the brain may cause multiple sclerosis, new imaging studies suggest.

The findings come from studies of computer-assisted brain scans using a specialized magnetic resonance imaging ( MRI) device. University at Buffalo, N.Y., researchers Rohit Bakshi, MD, and colleagues are the first to use this technique to study multiple sclerosis. Bakshi reported the findings at this week's annual meeting of the American Neurological Association in San Francisco.

Multiple sclerosis has been considered a disease of the white matter in the brain and spinal cord -- the neural pathways that allow areas of gray matter to communicate with one another. But the new findings link iron deposits in the gray matter to movement and thinking impairments in multiple sclerosis.

"If we're going to treat this disease, we have to know where the damage is," Bakshi says in a news release. "Traditionally, we thought MS was strictly a white-matter disease. ... We were able to visualize gray matter structures deep in the brain of MS patients and found some to be atrophied."

These areas of brain damage contained abnormally high levels of iron. It's not yet clear that the iron is the cause of the brain damage. It could be that dying brain cells leave a trail of iron behind.

Walking, Thinking, and Gray Matter
Bakshi's team put 41 multiple sclerosis patients through a walking test. They also gave tests of learning, speed of information processing, and memory to 28 MS patients.

The more unnatural darkness the brain scans saw in a patient's gray matter, the worse the patient's MS symptoms. It was the only factor studied that independently predicted impaired walking and thinking.

"We suspect that MS patients have defective blood-brain barriers, the cell layer that prevents potentially toxic substances from entering the brain," Bakshi says. "Excessive iron entering the brain may damage the deep gray matter structures."

Possible Treatment
If iron is indeed the culprit, it seems possible to do something about it. Bakshi's team is exploring two ideas. The first is simply to remove excess iron from patients' bodies, and then to devise a way to prevent future iron build-up.

If that is impractical, it may be possible to prevent iron from killing brain cells. The excess iron may be causing free radicals -- extremely reactive molecules that damage brain cells. Antioxidants -- such as vitamins C and E, or even more powerful agents -- might mop up free radicals before they do their dirty work.

Even if the iron deposits are the effect, rather than the cause, of brain cell death, the study still offers a way to measure the severity of MS and the efficacy of new treatments.
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Postby mrhodes40 » Sat Sep 19, 2009 12:54 pm

That iron deposits are more useful for predicting level of disability than enhancing lesions deal is actually well known kind of old news....

I have seen papers that suggest iron deposition might be used rather than Gd for studies to show that drugs work---or do not.

Here's a quote from one paper
Conclusions Gray matter T2 hypointensity in MS is associated with brain atrophy and is a stronger predictor of disability and clinical course than are conventional MRI findings. While longitudinal studies are warranted, these results suggest that pathologic iron deposition is a surrogate marker of the destructive disease process.

another paper below:
http://www.springerlink.com/content/tw39jejddtfbfafy/

Pretty easy to see why the idea of checking iron deposits after new therapies is not taken endorsed in spite of the fact that enhancing lesions are well known not to have anything to do with progression: it is virtually guaranteed that anything you do to suppress immunity will alter Gd enhancement, it allows us to continue the myth that by reducing enhancing lesions you are reducing inflammation and that that *will* result in reductions in accumulation of disability.

Never mind scores of people who have had no enhancement for years but progress anyway......... :roll:
I'm not offering medical advice, I am just a patient too! Talk to your doctor about what is best for you...
http://www.thisisms.com/ftopic-7318-0.html This is my regimen thread
http://www.ccsvibook.com Read my book published by McFarland Health topics
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Postby radeck » Sun Sep 20, 2009 8:22 am

cheerleader wrote:There's your assignment, Radeck...
Do some research for us, and find other diseases in the CNS in which the immune system is affected. What happens to the CNS in HIV-AIDS? What causes the immune system to back down in stroke? Do neurologists have any theories as to PPMS and the lack of immune activation?-
get googling and get us some research and answer some of your great questions for us!
cheer


Actually I asked one question, i.e. if anybody had thoughts on why the immune system ceases to attack the CNS at some point, from the viewpoint of CCSVI. When asking this question, I also wrote that "I've been trying to come up with a theory for this but so far with no success". By this I also meant that all I've read about traditional MS auto-immune theory as well as what I've read about CCSVI so far didn't provide me with a good explanation. FYI, I used mostly PubMed, but also google in the process. Sometimes open questions remain like this one, so I asked here as in my understanding the main purpose of this forum is to help each other in our the understanding of CCSVI and MS. I hope that's OK.

The new questions you add are also interesting ones. In particular I didn't know that HIV attacked the CNS. The way I understand your response is as a hint that if I google the connection between HIV and the CNS, I will find an answer to my question why the immune system stops attacking the CNS in CCSVI. You also seem to suggest that it is well known why in PPMS the immune system involvement is small, and why in a stroke it backs off. I wasn't aware of this either. Is this what you meant?

Thank you.
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Postby cheerleader » Sun Sep 20, 2009 9:18 am

radeck...

I like Dr. Haacke's hypothesis as to why the immune system eventually stops attacking the CNS in progressive MS-since it correlates directly with the amount of iron deposition.

Conclusions: SWI reveals iron deposition associated with MS lesions both in terms of its presence and characteristics compared to conventional imaging. Further, the SWI data suggests that there is a correlation between T2 signal intensity and phase changes (putative iron content). One may hypothesize that as the inflammatory component decreases, the tissue is compromised and there is an associated increase in iron deposition in the brain. Further work using SWI may provide some insight into the pathogenesis and mechanisms of disability in MS.


my thoughts....
The interesting thing about the particular study below was that they found disease course and disability had no correlation to lesions found on standard MRI....there was actually an inverse correlation. It was the SWI lesions seen that correlated to disease activity and progression. The research team hypothesizes that as inflammation decreases, iron deposition and tissue damage increase. This would correlate to what we see happening as MS becomes progressive.


An inverse correlation between hyperintense lesions showing inflammation and areas of iron deposition. Does the brain tissue eventually "burn out"? Does the communication with the immune system stop? We just don't know.

It's merely their hypothesis, so you'll have to look them up and ask them your questions. Dr. Zivadinov said that there will be tens of thousands of research papers in the next ten year looking at CCSVI in MS. And I'm sure many of those papers will deal with why inflammation stops in progressive MS....
til then !

Back to SWI technology!
cheer
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Postby patientx » Sun Sep 20, 2009 9:31 am

cheerleader wrote:Make sure to click on all the links provided in this thread, patient...it wasn't from just one paper. Dr. Haacke used all of his volumes of research using SWIM and BOLD technology in his presentation to present the case. He also showed us new SWI pictures showing iron deposits in PPMS brains.


I have read through all the papers posted, and they primarily describe Dr. Haacke's method of applying his new filter to the phase of the signal returns to detect iron content in the brain, and comparing the result with those obtained from traditional T1 and T3 weighted images. I didn't see any mention of studying the accumulation of iron over time, and how this correlates to disability progression in MS. Nor did I see any mention of what types of MS (i.e. PPMS, SPMS, RRMS) patients he tested. His primary conclusion, from the paper dated March, 2009 was:

The amount of iron deposition in the brain may serve as a surrogate biomarker for different MS lesion characteristics.


Of course, this is not to find any fault with Dr. Haacke's studies. He is a physicist with expertise in MRI, not an MS researcher. As such, I would expect his interest and expertise to lie in the applications and advancements of MRI technology.[/u]
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Postby cheerleader » Sun Sep 20, 2009 9:48 am

There are many quotes in this thread showing the correlation between iron deposition and disease severity. I am not going to retype them here...I have stated that Dr. Haacke's presentation- which I saw in person- used his research accumulated over the years and from a future paper still unpublished. He also referred to NYU's research and that of SUNY Buffalo. Yes, he is an MRI developer and a brilliant researcher. He is not an MS specialist.

For those interested, Read the whole thread, click on the links
This is from the SUNY Buffalo folks, and part of the reason why they got involved with Dr. Zamboni and CCSVI. A study they conducted in 2003, using SWI MRI to detect iron in MS brains.....

Walking, Thinking, and Gray Matter
Bakshi's team put 41 multiple sclerosis patients through a walking test. They also gave tests of learning, speed of information processing, and memory to 28 MS patients.

The more unnatural darkness the brain scans saw in a patient's gray matter, the worse the patient's MS symptoms. It was the only factor studied that independently predicted impaired walking and thinking.

"We suspect that MS patients have defective blood-brain barriers, the cell layer that prevents potentially toxic substances from entering the brain," Bakshi says. "Excessive iron entering the brain may damage the deep gray matter structures."


Yes, the word "may" is used. Yes, there will be more research in the future. We are at the beginning.
cheer
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lesions and SWI

Postby Inge67 » Sun Oct 04, 2009 4:47 am

Hello all,

I have read the complete post and the articles. It sounds very interesting and logical. It might apply to my personal situation: no changes in regular MRI since 2007, but progressing handicaps since dec 2007 until today.

I have one question: once the iron is deposited in your brain and attacking gray matter, is this permanent? Or can the ironbe removed, either by medications or by solving stenosis?

regarding medicine:
I read only a few remarks about supplements like Ginko Biloba, IP6, pycnogenol etc. Are those it? Or should I as my doctor for subscrition medicine?

regarding stenosis:
Once the stenosis is solved, will the iron deposed be slowly removed by the increased blood flow (e.g. flushed away?) and will disabilities slowly recover or has that not been researched yet?

Hopefully you can help me with this question.
Thanks.
Inge
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Re: lesions and SWI

Postby NHE » Sun Oct 04, 2009 10:42 pm

Green tea might help to chelate excess iron.

Effect of green tea on iron status and oxidative stress in iron-loaded rats.
Med Chem. 2008 Jul;4(4):365-70.
    Plasma non-transferrin bound iron (NTBI) is potentially toxic and contributes to the generation of reactive oxygen species (ROS), consequently leading to tissue damage and organ dysfunction. Iron chelators and antioxidants are used for treatment of thalassemia patients. Green tea (GT) contains catechins derivatives that have many biological activities. The purpose of this study was to investigate the iron-chelating and free-radical scavenging capacities of green tea extract in vivo. Rats were injected ip with ferric citrate together with orally administered GT extract (GTE) for 4 months. Blood was collected monthly for measurement of iron overload and oxidative stress indicators. Plasma iron (PI) and total iron-binding capacity (TIBC) were quantified using bathophenanthroline method. Plasma NTBI was assayed with NTA chelation/HPLC. Plasma malonyldialdehyde (MDA) was determined by using the TBARS method. Erythrocyte oxidative stress was assessed using flow cytometry. Levels of PI, TIBC, NTBI and MDA, and erythrocyte ROS increased in the iron-loaded rats. Intervention with GT extract markedly decreased the PI and TIBC concentrations. It also lowered the transferrin saturation and effectively inhibited formation of NTBI. It also decreased the levels of erythrocyte ROS in week 4, 12 and 16. Therefore, green tea extract can decrease iron in plasma as well as eliminate lipid peroxidation in plasma, and destroy formation of erythrocyte ROS in the rats challenged with iron. The bifunctional effects could be beneficial in alleviating the iron and oxidative stress toxicity. In prospective, these GTE activities should be further examined in thalassemic animals or humans.

NHE
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Lesions and SWI

Postby Inge67 » Mon Oct 05, 2009 2:16 am

Thank you!

I will increase my green tea intake as of now. If I understand it correctly, green tea extracts might even be better. I will try to find a place where they sell this.

thanks,
Inge
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Postby Needled » Mon Oct 05, 2009 6:02 am

Thanks NHE. I got the gist of it all. Now I need to know how much, how often, and if there are extracts, what are the best ones? I bet I know someone who could help. Oh, Jimmylegs, are you around? I think we need you over here for a lesson on green tea...
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Postby cheerleader » Mon Oct 05, 2009 7:33 am

EGCG (green tea) info-
http://www.thisisms.com/ftopic-3600-day ... gcg-0.html
Jeff's been on 600mg capsules for over a year. There's a trial for MS and EGCG in Germany...Ursula had been posting for awhile. Good stuff, and probably why asian populations have less endothelial dysfunction.

cheer
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Postby radeck » Mon Oct 05, 2009 8:03 am

The caffeine in green tea (extract) is also a vasoconstrictor though. I am under the impression that that affects arteries mostly. However as I understood other posts here vasodilators should be preferred for CCSVI?
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Postby cheerleader » Mon Oct 05, 2009 8:34 am

radeck wrote:The caffeine in green tea (extract) is also a vasoconstrictor though. I am under the impression that that affects arteries mostly. However as I understood other posts here vasodilators should be preferred for CCSVI?


They make decaf...that's what Jeff takes



HEY EVERYONE...THIS THREAD IS A MOOT POINT! Dr. Haacke has come out and set up a website of his own (he don't need me to explain it!- he's much smarter, and a doctor and stuff. Plus he has movies and pictures!)

He is asking technicians to test MS patients and submit their results...he is coming forward as saying that the CCSVI paradigm brings together all the MRI/SWI research.
Take Dr. Haacke's website to your doctors-

http://www.ms-mri.com/

check it out and bring it to your docs-
cheer
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