Abstract

Background: Slow waves (< 1 Hz) are the most important electroencephalogram signatures of non-rapid eye movement sleep. While considered to have a substantial importance in, for example, providing conditions for single-cell rest and preventing long-term neural damage, a disturbance in this neurophysiological phenomenon is a potential indicator of brain dysfunction.

Methods: Since, in healthy individuals, slow waves can be induced with anesthetics, we tested the possible association between hypoxic brain injury and slow wave activity in comatose post-cardiac arrest patients (N = 10) using controlled propofol exposure. The slow wave activity was determined by calculating the low-frequency (< 1 Hz) power of the electroencephalograms recorded approximately 48 h after cardiac arrest. To define the association between the slow waves and the potential brain injury, the patients’ neurological recovery was then followed for six months.

Results: In the patients with good neurological outcome (N = 6), the low-frequency power of electroencephalogram representing the slow wave activity was found to substantially increase (190 ± 83%, mean ± SD) due to the administration of propofol. By contrast, the patients with poor neurological outcome (N = 4) were unable to generate propofol-induced slow waves.

Conclusions: In this experimental pilot study, the comatose post-cardiac arrest patients with poor neurological outcome were unable to generate normal propofol-induced electroencephalographic slow wave activity 48 h after cardiac arrest. The finding might offer potential for developing a pharmacological test for prognostication of brain injury by measuring the electroencephalographic response to propofol.