Ok, sure, we could call it neuroptocrosis. Good a name as any. Sometimes I like to call it ischemic neurolysis. Some people just call it ischemic neuronal death. Either way, what we're talking about is a spectrum of cell death phenotypes initiated by ischemia. We've seen, for example, how extremely complex interactions between Bcl-2 proteins can lead to varying outcomes--like the outcome of a throw of the dice or a chaotic shootout in Tombstone. We've seen how the Four Horsemen interact with each other. Which one is more responsible for cell death? Nobody can answer that question.

And so one could make the argument that the final death phenotype--classically apoptotic or classically necrotic--is not nearly as important as important as the lethal events that occur early in ischemia--loss of high energy phosphate, surges in glutamate, Ca2+ flux, elaboration of reactive oxygen species, activation of proteases, phosphorylation of eIF2α, and interruption of translation initiation. And the ultimate death phenotpe is not as important as as events that come some time later--dysfunction of organelles, abnormal genetic responses, calpain-mediated proteolysis, release of cytochrome c, and complex Bcl-2 interactions.

We do know that, given a particular insult, a given population of cells will usually assume a particular range of death phenotypes. But I think this is a little like knowing that, given a particular set of circumstances, a storm will probably brew today and not tomorrow, or an electron will probably be here and not there. As with the weather pattern and the electron's position, the final fate of a particular cell after a particular insult isn't so much a deterministic fate as a statistical one.