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Neurological deficits caused by tissue hypoxia in neuroinflammatory disease


Senior Member
More Oxygen Please, it'll do wonders for my relapse

Davies AL, Desai RA, Bloomfield PS, McIntosh PR, Chapple KJ, Linington C, Fairless R, Diem R, Kasti M, Murphy MP, Smith KJ.
Neurological deficits caused by tissue hypoxia in neuroinflammatory disease. Ann Neurol. 2013 Aug. doi: 10.1002/ana.24006. [Epub ahead of print]

To explore the presence and consequences of tissue hypoxia in experimental autoimmune encephalomyelitis ((EAE), an animal model of multiple sclerosis (MS)).

EAE was induced in Dark Agouti (DA) rats by immunization with recombinant myelin oligodendrocyte glycoprotein (rMOG) and adjuvant. Tissue hypoxia was assessed in vivo using two independent methods: an immunohistochemical probe administered intravenously, and insertion of a physical, oxygen-sensitive probe into the spinal cord. Indirect markers of tissue hypoxia (e.g. expression of hypoxia-inducible factor-1α (HIF-1α), vessel diameter and number) were also assessed. The effects of brief (one hour) and continued (7 days) normobaric oxygen treatment on function were evaluated in conjunction with other treatments, namely administration of a mitochondrially-targeted antioxidant (MitoQ) and inhibition of inducible nitric oxide synthase (1400W).

Observed neurological deficits were quantitatively, temporally and spatially correlated with spinal white and grey matter hypoxia. The tissue expression of HIF-1α also correlated with loss of function. Spinal microvessels became enlarged during the hypoxic period, and their number increased at relapse. Notably, oxygen administration significantly restored function within one hour, with improvement persisting at least one week with continuous oxygen treatment. MitoQ and 1400W also caused a small but significant improvement.

We present chemical, physical, immunohistochemical and therapeutic evidence that functional deficits caused by neuroinflammation can arise from tissue hypoxia, consistent with an energy crisis in inflamed CNS tissue. The neurological deficit was closely correlated with spinal white and grey matter hypoxia. This realization may indicate new avenues for therapy of neuroinflammatory diseases such as MS.

Dr. Deckoff-Jones uses it in her treament



Senior Member
Great info. In the methods section the listed two adjunct therapies. Mitoq and
something else. Does anyone know what these are ?

Also, I wad reading somewhere else that oxygen alone may cause problems.
Rats .. my brain just died.

Something about the body still having too much carbon dioxide.

It caught my attention because I feel horrible with an oxygen mask but
not with the tubes in my nose.


Senior Member
Im interested in EAE as its the animal model for MS producing an MS "like" illness.Also glial cells are of interest


Senior Member
does loss of myelin production also cause problems like memory loss, attention deficit, incontinence, central sleep apnea?
I've been taking sam-E partly since it's involved in myelin creation and may help central sleep apnea?


Senior Member
South East England, UK
I haven't tried normabaric oxygen but I do use an oxygen concentrator for up to an hour 3 times daily and it has been a fantastic help. I can come home from a short walk with my dog feeling exhausted but after an hour of using my concentrator at 4 litres per minute I get the energy back and then can go on and do a small job like cooking a meal. It will take till the next day before I am fully back to normal.

The other huge benefit I have experienced is that my immune system this past year has been so much stronger than previously. I used to pick up every bug going but that isn't the case anymore. Only last week I was with my daughter in law and son and their kids. There was a lot of sneezing going on and one of them hadn't been feeling well with a cold virus. Two days later I got a sore, dry throat and didn't feel great but within 30 hours all signs were gone.

BTW I was diagnosed with quite severe tissue hypoxia at the Breakspear centre last year by autonomic testing.