Neurophysiologic Mechanisms of Cerebral Ischemia and the EEG

Cerebral ischemia rapidly disturbs neuronal function through failure of synaptic transmission and, with ongoing energy deprivation, loss of ion gradients. Adenosine-mediated inhibition of presynaptic release leads to an early and reversible loss of synaptic transmission, reflected in the EEG by slowing and eventual suppression of rhythmic activity. With more severe or prolonged energy failure, Na + /K + -ATPase failure results in membrane depolarization, cytotoxic swelling, and irreversible injury. Secondary injury mechanisms include spreading depolarizations, inflammation, and oxidative stress. The EEG primarily reflects extracellular currents resulting from synaptic input on pyramidal neurons, providing a real-time readout of cerebral function. Recovery of continuous background activity with physiologic rhythms within 12 to 24 hours indicates preserved and reversible synaptic function, whereas persistent suppression or burst suppression with identical bursts beyond 24 hours is consistently associated with extensive structural injury and poor neurologic outcome.