Criteria of reversibility of suppression of bioelectric activity of the brain in alcoholic coma: experimental study

Abstract

The aim. The aim of the study is to determine prognostically significant criteria for the reversibility of the suppression of the generation of bioelectrical activity using an experimental model of alcoholic coma. Materials and methods. The work was performed on 27 nonlinear sexually mature rats weighing 340±40 g, which received a 40% solution of ethyl alcohol by the oral route in fractional doses of 12.6 g/kg, which corresponded to LD50. EEG monitoring was performed until there was a definite effect (from 1 to 54 hours). Results. In a favorable outcome of alcoholic coma (11 rats), the EEG results contained the following phase states: 1) a pattern of continuous activity with registration of flashes with intense modulation amplitudes (modulation coefficient 10-12, index 25-35%); 2) a pattern of discrete activity (signal suppression index does not exceed 10%), which was recorded only in the toxicogenic phase; 3) a pattern of awakening. In the lethal outcome of cerebral insufficiency (16 rats), there were the following states of bioelectric activity: 1) weakly modulated continuous activity (modulation coefficient is less than 5); 2) fragmented activity (suppression index is 20-50%); 3) “flash-suppression” pattern; 4) a pattern of periodic discharges; 5) isoelectric silence. The terminal phase of cerebral insufficiency was characterized by the presence of high-amplitude waves with a frequency of 1-1.5 Hz, alternating with 3-4 oscillations decreasing in amplitude. Conclusion. In a case of acute poisoning with ethanol at a dose of LD50, the prognostically favorable EEG sign is the amplitude modulation of continuous activity, which reflects the preservation of synchronizing thalamocortical interactions. In the toxicogenic phase of the poisoning, a pattern of discrete activity can be recorded (modulation index is up to 10%), which reflects the suppressive effect of ethanol rather than the decay of the bioelectrogenesis mechanisms.