Characterizing brain oxygen metabolism in patients with...

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

Characterizing brain oxygen metabolism in patients with...

Postby ikulo » Sun Jan 22, 2012 10:01 pm

Dr. Grossman is at it again with another fascinating imaging study.

J Cereb Blood Flow Metab. 2012 Jan 18. doi: 10.1038/jcbfm.2011.191. [Epub ahead of print]
Characterizing brain oxygen metabolism in patients with multiple sclerosis with T2-relaxation-under-spin-tagging MRI.
Ge Y, Zhang Z, Lu H, Tang L, Jaggi H, Herbert J, Babb JS, Rusinek H, Grossman RI.
Source
Department of Radiology, Center for Biomedical Imaging, New York University School of Medicine, New York, New York, USA.
Abstract
In this study, venous oxygen saturation and oxygen metabolic changes in multiple sclerosis (MS) patients were assessed using a recently developed T2-relaxation-under-spin-tagging (TRUST) magnetic resonance imaging (MRI), which measures the superior sagittal venous sinus blood oxygenation (Yv) and cerebral metabolic rate of oxygen (CMRO(2)), an index of global oxygen consumption. Thirty patients with relapsing-remitting MS and 30 age-matched healthy controls were studied using TRUST at 3 T MR. The mean expanded disability status scale (EDSS) of the patients was 2.3 (range, 0 to 5.5). We found significantly increased Yv (P<0.0001) and decreased CMRO(2) (P=0.003) in MS patients (mean±s.d.: 65.9%±5.1% and 138.8±35.4 μmol per 100 g per minute) as compared with healthy control subjects (60.2%±4.0% and 180.2±24.8 μmol per 100 g per minute, respectively), implying decrease of oxygen consumption in MS. There was a significant positive correlation between Yv and EDSS and between Yv and lesion load in MS patients (n=30); on the contrary, there was a significant negative correlation between CMRO(2) and EDSS and between CMRO(2) and lesion load (n=12). There was no correlation between Yv and brain atrophy measures. This study showed preliminary evidence of the potential utility of TRUST in global oxygen metabolism. Our results of significant underutilization of oxygen in MS raise important questions regarding mitochondrial respiratory dysfunction and neurodegeneration of the disease.Journal of Cerebral Blood Flow & Metabolism advance online publication, 18 January 2012; doi:10.1038/jcbfm.2011.191.
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Re: Characterizing brain oxygen metabolism in patients with.

Postby MarkW » Mon Jan 23, 2012 2:23 am

Nice find Ikulo,
For me this still suggests that reduced flow increases waste products, which slows the mitochondrial use of O2. It would be great if Dr Grossman would test a few patients undergoing treatment by Dr Sclafani (both around New York). That would be patient focussed research.

MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 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
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Re: Characterizing brain oxygen metabolism in patients with.

Postby Cece » Mon Jan 23, 2012 8:32 am

Our results of significant underutilization of oxygen in MS raise important questions regarding mitochondrial respiratory dysfunction and neurodegeneration of the disease.

This is assuming that there is ample oxygen in the brain, and that our MS brains are simply not using the oxygen that is ample, thus suggesting mitochondrial dysfunction.

CCSVI suggests that there may not be ample oxygen, because of reduced perfusion because of outflow obstructions. And as Mark suggests, reduced removal of waste metabolites might be affecting oxygen use or health of the mitochondria as well.

Question would be if this finding persisted after treatment for CCSVI.
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Re: Characterizing brain oxygen metabolism in patients with.

Postby PointsNorth » Mon Jan 23, 2012 2:04 pm

Sorry if I'm going off course. . . . :?

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Re: Characterizing brain oxygen metabolism in patients with.

Postby cheerleader » Mon Jan 23, 2012 2:12 pm

Agree with all your comments...I think this needs to be correlated to perfusion in order to get the big picture. This study doesn't compare O2 levels available in pwMS compared to normals...it only compares metabolism and consumption of O2. The fact that pwMS had more O2 in the venous sinuses than normals could be a result of hypoperfusion, not just metabolism.

In infants, cerebral hypoperfusion comes first, and that creates reduced O2 metabolism and secondary hypoperfusion...but the first event is asphyxiation, or low O2.

In conclusion, we found that delayed secondary cerebral hypoperfusion following a severe asphyxial insult was associated with marked suppression of cerebral metabolism and a corresponding increase in cortical tPO2 . These data strongly suggest that secondary cerebral hypoperfusion is a consequence of reduced cerebral metabolism. Hypoperfusion was not significantly affected by preceding adenosine A1 receptor blockade. We speculate that this transient suppression of cerebral metabolism may be actively regulated, and that it may help protect the brain from further injury.

http://jp.physoc.org/content/572/1/131.full.pdf

If CCSVI is the original insult, it could lead to secondary lowered O2 utilization. This is the result of hypoperfusion. We really, really need that Hubbard Foundation research on perfusion before and after CCSVI venoplasty. We're getting there.
cheer
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dx dual jugular vein stenosis (CCSVI) 4/09
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Re: Characterizing brain oxygen metabolism in patients with.

Postby MarkW » Tue Jan 24, 2012 2:31 am

cheerleader wrote:If CCSVI is the original insult, it could lead to secondary lowered O2 utilization. This is the result of hypoperfusion. We really, really need that Hubbard Foundation research on perfusion before and after CCSVI venoplasty. We're getting there.
cheer

Hello Cheer,
I realise you started this with "if" but many readers will take your writing to be gospel. I am much more cautious on the causes of MS. I have not seen any research which has found 100% CCSVI in newly diagnosed pwMS which needs to be shown 'if CCSVI is the original insult'.
This research reminds us of mitochondria in the big picture of MS, so more complexity. Mitochondrial DNA is present and those genes could (repeat could) be activated by viruses or bacteria so another set of thoughts on MS etiology are feasible. For background on mitochondrial DNA I suggest: http://ghr.nlm.nih.gov/chromosome/MT.
Thunk - The more I learn, the less I understand................
Kind regards,
MarkW
PS When is Hubbard Foundation work going to be complete ??
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 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
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Re: Characterizing brain oxygen metabolism in patients with.

Postby cheerleader » Tue Jan 24, 2012 9:32 am

Mark--
I use "if" and "could."
And I don't think anyone on this site considers my random thoughts to be gospel.
I know you're smarter and more cautious :-) Bully for you!
(Although I do understand epigenetics and mitochondrial DNA, I agree...it can be confusing.)

The Hubbards are just beginning their study on perfusion before and after venoplasty. They are also testing normals for controls. Although it is not blinded, it will be good to have this information. It should take another year.
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Re: Characterizing brain oxygen metabolism in patients with.

Postby Cece » Tue Jan 24, 2012 10:49 am

Do not take my word as gospel either but it seems intuitive that CCSVI may well be the initial insult in a cascade of events that culminates in what we know as MS. There are other illnesses such as Budd Chiari that lead to failure of an organ and begin with something as seemingly small or minor as a chronic outflow obstruction.

As I've learned from a different Marc (Wheelchair Kamikaze), it would be highly unlikely to see 100% CCSVI in early MS, since 5-10% of people with MS are misdiagnosed and actually have something else. AlmostClever posted in the general forum (what, there's a general forum???) that he had been misdiagnosed and is now being treated for chronic lyme. MS may also be a different disease in different people, so for some CCSVI could be the original insult and for others there could be other processes involved. I agree, though, with the need for more research, and precise ways to image CCSVI, so we can trust the results of research.

Another year for the research from the Hubbards. And there was just some really interesting research presented at ISET and more to come at the next two conferences (SIR and ISNVD).

Mitochondria is inherited from mothers, isn't it? Yet MS is more likely to be passed on if one's father had MS. ( http://www.sciencedaily.com/releases/20 ... 091614.htm ) Wouldn't that argue against MS being a genetic mitochondrial disorder?
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Re: Characterizing brain oxygen metabolism in patients with.

Postby 1eye » Thu Jan 26, 2012 9:00 am

Wonder if anything Dr. Haacke has seen can corroborate that? Maybe global consumption goes down, in response to slowed flow, and it is slow enough that waste is not removed fast enough. In the presence of too much oxygen I would expect the level of free radicals to be higher.

Also, believing the disease not to be fundamentally different, I would like to see similar work done on higher EDSS people. They may hold the keys to what happens earlier on.
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