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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.

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

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.

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.
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