EEG performance in the intensive care unit in critically ill patients can be provisionally allocated to a special type of research — EEG of critical states. The article deals with the methodological features of EEG performance in intensive care, as well as general patterns of EEG changes in patients in coma. The analysis of the patterns of the EEG in intensive care unit is described. Parameters of reactivity of the central nervous system are given. An algorithm for describing epileptiform changes is presented. The criteria for the diagnosis of nonconvulsive status epilepticus in patients unconscious are discussed, as well as a prognosis of the outcome of a long unconscious state in the presence of epileptiform changes in the EEG. Data on the parameters of periodic patterns are collected, their description and diagnostic criteria are given. The role and possibilities of EEG in the diagnosis of brain death are considered.

Fifty patients with acute severe ethanol poisoning (depression of consciousness at the time of admission was up to the level of coma) were examined. Based on the purpose of the study, patients were divided into two groups. In the first group, basic etiopathogenetic therapy was supplemented by the intravenous administration of a drug based on reduced glutathione: inosine glycyl-cysteinyl-glutamate disodium (IGCGD). In the second group, only basic therapy was performed. All patients underwent in the intensive care long-term continuous EEG monitoring, which was started at the end of basic resuscitation and stopped when the patient was clearly awake. Based on the nature of spontaneous EEG and reactivity, patients were divided into subgroups: patients with theta coma pattern and patients with delta coma pattern.It was found that the introduction of IGCGD in the treatment of severe ethanol poisoning in the group of patients with a reactive delta pattern significantly increased the rate of formation of awakening in the EEG: in the subgroup with basic therapy, the formation time of the awakening pattern was about 3 hours, and in the subgroup of patients to whom the drug was administered 1,5 hours. In the group of patients with depression of EEG to the level of theta coma, IGCGD had no effect on the time of formation of the EEG pattern of awakening. The inclusion of inosine IGCGD in the treatment of severe alcohol intoxication was not accompanied by more frequent formation of epileptiform activity in the EEG.