Cortical veins under 7 tesla MRI

[frodo]

It seems that they are able to detect oxygen percentages and to use it as biomarker.

Edit: I had a bad link. This is the right one.
http://www.ncbi.nlm.nih.gov/pubmed/25352043

Quantitative oxygen extraction fraction from 7-Tesla MRI phase: reproducibility and application in multiple sclerosis.

Abstract
Quantitative oxygen extraction fraction (OEF) in cortical veins was studied in patients with multiple sclerosis (MS) and healthy subjects via magnetic resonance imaging (MRI) phase images at 7 Tesla (7 T).

Flow-compensated, three-dimensional gradient-echo scans were acquired for absolute OEF quantification in 23 patients with MS and 14 age-matched controls. In patients, we collected T2*-weighted images for characterization of white matter, deep gray matter, and cortical lesions, and also assessed cognitive function. Variability of OEF across readers and scan sessions was evaluated in a subset of volunteers. OEF was averaged from 2 to 3 pial veins in the sensorimotor, parietal, and prefrontal cortical regions for each subject (total of ~10 vessels).

We observed good reproducibility of mean OEF, with intraobserver coefficient of variation (COV)=2.1%, interobserver COV=5.2%, and scan-rescan COV=5.9%. Patients exhibited a 3.4% reduction in cortical OEF relative to controls (P=0.0025), which was not different across brain regions. Although oxygenation did not relate with measures of structural tissue damage, mean OEF correlated with a global measure of information processing speed.

These findings suggest that cortical OEF from 7-T MRI phase is a reproducible metabolic biomarker that may be sensitive to different pathologic processes than structural MRI in patients with MS.

Journal of Cerebral Blood Flow & Metabolism advance online publication, 29 October 2014; doi:10.1038/jcbfm.2014.187

[cheerleader]

Thanks, Frodo-
interesting to see this research continue, and be considered as a biomarker. Here's the correct link to abstract:
http://www.ncbi.nlm.nih.gov/pubmed/25352043

Dr. Yulin Ge of the ISNVD has been looking at the underutilization of O2 in pwMS--
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3293125/

[1eye]

It seems commonly found (by various means including 7-tesla, ordinary-strength MRI, and others) and agreed that there is under-utilization of oxygen in the "MS" brain. This seems counter-intuitive if there is slow flow as well. It is speculated (with some evidence) that there is over-production of NO, which interferes with oxygen utilization by interfering with mitochondrial respiration. There seems to be evidence of a direct relationship between disability, lesion load, and oxygen under-use. This set of facts seems to go against the whole theory that better production of NO by increased sun exposure will lead to better endothelial health, vascular tone and increased overall health. In fact, we might already have too much NO, perhaps due to inflammation.

It would seem to me that if there is a problem with perfusion that might explain the under-use of oxygen, since blood must pass through capillary beds to get the oxygen into the tissues. Here it might make sense to have a cause-and-effect assessment. Is there overall slow flow of blood through the entire "MS" head, and if so, how does that affect oxygen use? On the surface, if the blood is going through more slowly, there should be more oxygen-use, not less.

Judging by my energy level, especially when I'm hot, something is interfering with my mitochondria...

So many questions, so little understanding, on my part anyway...

[cheerleader]

Many issues could be behind the underutilization of O2 in MS. Like metabolic issues from ischemia, or It could be mitichondrial disease, or brain atrophy. Hard to know.
Traumatic brain injury is another cause of underutilization of O2 in children.
http://www.nature.com/jcbfm/journal/v33 ... 2130a.html

Not to go to OT too far, but wanted to help clarify. There are different types of NO, 1eye. Here's an earlier thread.
http://www.thisisms.com/forum/chronic-c ... 19264.html

eNOS controls perfusion, is vasodilating and strenghtens the BBB. It comes from a healthy endothelium, which has shear stress and good tight junctions.
iNOS is induced by cytokines, is inflammatory and damaging to the BBB.

Here's a recent paper from Dr. Alexander--
‎www.direct-ms.org/sites/default/files/M ... n%2003.pdf

eNOS, which is induced from the endothelium by exercise, sunshine, and whole foods full of antioxidants--will strengthen our blood vessels and balance the inflammatory cascade. iNOS, which is induced by ischemia and resultant cytokines, creates inflammation. Dr. Alexander spoke about this difference at ISNVD, when discussing NO with Dr. Ge.

Endothelial nitric oxide synthase (eNOS) is emerging as a key target in molecular stroke research. eNOS ameliorates acute ischemic injury and promotes recovery following cerebral ischemia
http://www.medscape.com/viewarticle/580254

HTH,
cheer