3 ms·

This is super interesting. Links or other sources?

• Udo 11y ago
  https://en.wikipedia.org/wiki/Ischemic_cascade https://en.wikipedia.org/wiki/Ischemic_cascade https://en.wikipedia.org/wiki/Excitotoxicity https://en.wikipedia.org/wiki/Excitotoxicity http://emedicine.medscape.com/article/1161422-overview http://emedicine.medscape.com/article/1161422-overview http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841970/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2841970/ The status quo of efforts basically discards the totally anoxic tissue after a stroke, focussing on protecting the (often large) partially perfused border region. This is what's practical now, but the fight about the totally ischemic core regions is far from over. It's a race between anoxic necrosis (which is the point of no return, where passive cell dissolution happens) and active cell death cascades that are triggered in the fully or partially reperfused cell. The latter one can potentially be halted, the first one leads to irreversible information loss. What the actual timing windows are on both of these in the human brain is subject to active research and the view on them is likely to change over the coming years. I posted links mainly to stroke and TBI-relevant articles, because that's where the research happens. However it's important to keep in mind that the fully dead brain is relatively static, whereas damaged areas in the living brain are subject to internal "cleanup" mechanisms pretty much right away. In this context, prolonged cardiac arrest might turn out to be preferrable to a stroke.
  • joshmarlow 11y ago
    Thanks you for the link!