In their paper “The role of leukocytes following cerebral ischemia: pathogenic variable or bystander reaction to emerging infarct?” D.F. Emerich et al. review the literature on the involvement of neutrophils in cerebral ischemia:
“We reasoned that if neutrophils play an important pathogenic (i.e., cause-effect) role in the neuronal damage that follows a stroke, then one should expect to find clear evidence that: (1) neutrophils invade the ischemic area prior to terminal stage infarction, (2) greater numbers of early appearing neutrophils are accompanied by evidence of greater neuronal loss, and (3) dose-related inhibition of neutrophil trafficking or activity produces a corresponding decrease in the degree of brain damage following ischemia.”
The authors did not find much evidence for any of the above and speculate that neutrophil recruitment may not be a cause of injury, but rather a response to postischemic necrosis.
Knowledge of the causal and temporal aspects of cerebral ischemia is important to select the right agents to minimize brain injury of cryonics patients. Neuroprotective agents that confer benefits to cardiac arrest and stroke victims may not necessarily offer additional protection during stabilization of cryonics patients if the targets of these interventions are non-causal and/or delayed events in the ischemic cascade.