Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, January 6, 2013

The neuroprotective actions of hypoxic preconditioning and postconditioning in a neonatal rat model of hypoxic ischemic brain injury

This is a fascinating idea, treat your recently oxygen starved brain with more reduced oxygen supply. Completely opposite of the HBOT theories.
http://www.ncbi.nlm.nih.gov/pubmed/23274537

Abstract

Perinatal hypoxic-ischemic (HI) brain injury remains a major contributing factor to newborn mortality and morbidity. Preconditioning with mild hypoxia has been shown to protect the brain against HI insults and it has recently been shown that mild hypoxia administered after a brain injury, termed 'postconditioning' can protect the adult mouse brain. Here, we have investigated the neuroprotective effects of hypoxic pre- and postconditioning in a neonatal rat model of HI brain injury. 7-day-old Sprague-Dawley rat pups underwent unilateral common carotid artery ligation in combination with 3h at 8% oxygen. Hypoxic treatments consisted of either 3h of 5.5% oxygen performed 24h prior to injury (preconditioning); or 1h of 8% oxygen 24h post-injury, performed once a day for 5 days (postconditioning). Brains were removed 1 week post-injury for histological analysis. HI caused an increase in lesion volume compared to controls and both hypoxic pre- and postconditioning reduced the degree of brain damage following HI injury. To specifically examine neuronal loss, NeuN immunohistochemistry and regional brain area analysis was performed. HI injury caused a loss in NeuN staining in all brain regions examined. Preconditioning with hypoxia resulted in a significant reduction in cortical, hippocampal and striatal neuronal loss, compared with HI alone. Hypoxic postconditioning resulted in a reduction in cortical and striatal neuronal loss, compared to HI alone. Our results further support the clinical potential for mild hypoxia in the treatment of brain injuries, either as a pre- or post-injury treatment strategy.

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