Pilot Study of Propofol-induced Slow Waves as a Pharmacologic Test for Brain Dysfunction after Brain Injury
Jukka Kortelainen1, Eero Väyrynen, Usko Huuskonen
1From the Physiological Signal Analysis Team, Center for Machine Vision and Signal Analysis, Medical Research Center Oulu (J.Kortelainen, E.V., T.S.), Department of Clinical Neurophysiology, Medical Research Center Oulu (J.Kortelainen, U.H.), Unit of Surgery, Anaesthesia and Intensive Care, Medical Faculty (J.L., J.Koskenkari, S.A., T.A.-K.), Division of Intensive Care Medicine, Medical Research Center Oulu (J.L., J.Koskenkari, T.A.-K.), and Department of Anaesthesiology, Medical Research Center Oulu (S.A.), University of Oulu and Oulu University Hospital, Oulu, Finland; and Department of Clinical Pharmacology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland (J.T.B.).
Background:
Slow waves (less than 1 Hz) are the most important electroencephalogram signatures of nonrapid 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 neurophysiologic phenomenon is a potential indicator of brain dysfunction.
Methods:
Since, in healthy individuals, slow waves can be induced with anesthetics, the authors tested the possible association between hypoxic brain injury and slow-wave activity in comatose postcardiac arrest patients (n = 10) using controlled propofol exposure. The slow-wave activity was determined by calculating the low-frequency (less than 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' neurologic recovery was then followed up for 6 months.
Results:
In the patients with good neurologic outcome (n = 6), the low-frequency power of electroencephalogram representing the slow-wave activity was found to substantially increase (mean ± SD, 190 ± 83%) due to the administration of propofol. By contrast, the patients with poor neurologic outcome (n = 4) were unable to generate propofol-induced slow waves.
Conclusions:
In this experimental pilot study, the comatose postcardiac arrest patients with poor neurologic 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 pharmacologic test for prognostication of brain injury by measuring the electroencephalographic response to propofol.
