Kochs E, Schulte am Esch J
Universitätskrankenhaus Hamburg-Eppendorf, Abteilung für Anästhesiologie.
Anasth Intensivther Notfallmed. 1988 Jun;23(3):145-52.
Since the introduction of diazepam, flunitrazepam and midazolam into clinical practice benzodiazepines have been increasingly used for premedication, induction of anesthesia, and long-term sedation in the intensive care unit utilizing their anxiolytic and sedative components. Intraoperative monitoring of central nervous structures has to take into account the effects of benzodiazepines on the electroencephalogram (EEG) and evoked potentials (EP) before their contribution to alterations in brain electrical activity during balanced anesthesia with combination of different drugs can be evaluated. EEG reflects the spontaneous brain electrical activity whereas EP are the averaged time-locked electrical responses to external stimulation. They are thus able to assess the functional integrity of afferent neuronal pathways from peripheral nerves to cortical areas. The specific benzodiazepine antagonist flumazenil binds competitively to benzodiazepine receptors and is able to induce a change in pharmacodynamic parameters, which i.e. can be measured by EEG- and EP-recordings. Characteristical changes in the EEG after benzodiazepine medication consist in an activation of higher EEG-frequencies simultaneous to a decrease in alpha-activity. A facultative increase in delta-activity seems to be dependent on the absolute dose administered and on the speed for intravenous injection. Benzodiazepine-induced EEG-alterations can be reversed by flumazenil almost completely but in the time course will change again in correspondence to the plasma levels of the benzodiazepines and the half-time of flumazenil. Cortical EP-components are suppressed by benzodiazepines whereas subcortical generated potentials are not altered.(ABSTRACT TRUNCATED AT 250 WORDS)