Coma is a state of altered consciousness from which a person cannot be awakened. Although sophisticated brain imaging techniques are now clinically accessible they cannot be readily applicable in the intensive care units so that electroenceplahography (EEG) remains the standard monitoring technique of the comatose patient. With increasing depth of coma the EEG progresses from continuous oscillation to “isoelectric line” through a transitional period during which the EEG activity is discontinuous, consisting of “bursts” of large amplitude oscillations on a “suppressed” electrical background referred to as the burst-suppression pattern (BS). Current methods relating EEG to the depth of coma that rely on statistic quantification of "spontaneous" BS are unsatisfactory. The main objective of our project is to explore the novel approach that the responsiveness of BS to external stimulation (BS reactivity) is more likely to reflect the cortical network dysfunction during coma. Specifically, we aim to explore using clinically applicable neurophysiological methods in rodents: (1) the reactive anesthetic BS behavior to various external stimuli; (2) to which extent BS reactivity of post-ischemic BS can be used to predict the outcome following cerebral ischemic injury and (3) whether the anticonvulsive effect of induced BS coma can be optimized based on BS reactivity. The clinical translation of the BS quantification developed in our study will be will be validated on human data.