Is it possible that there is any exitotoxity (hyper-exitability) after cardiac arrest when there is a flat EEG?
When cardiac arrest occurs, there is an increase in EEG amplitude in the theta range, then there is an increase against as the EEG becomes delta waves. This is followed by no EEG (20 seconds after cardiac arrest).
But because exitotoxicity occurs, I sumised that anoxic respiration would then begin and this would mean that the EEG would increase and neurones would die by over-exiting them-selves.
The only reason that you would not observe the convulsions, is because it is an atonic convulsion.
Is this true?
2007-09-05 16:25:08 · 3 answers · asked by Anonymous in Science & Mathematics ➔ Medicine
no your hypothesis is incorrect
2007-09-08 14:33:17 · answer #1 · answered by belfus 6 · 0⤊ 0⤋
I'd love to see you recruit the study group: "Would you mind wearing these EEG electrodes and letting us monitor while we hope you die?" Heck, I'd like to see you beg the funding!
2007-09-06 00:58:01 · answer #2 · answered by Anonymous · 1⤊ 0⤋
Perhaps you mean excitotoxicity? There isn't any exitotoxicity that I can find.
2007-09-05 23:29:58 · answer #3 · answered by treebird 6 · 1⤊ 0⤋