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Pilot study of propofol-induced slow waves as a pharmacologic test for brain dysfunction after brain injury

Kortelainen, Jukka; Väyrynen, Eero; Huuskonen, Usko; Laurila, Jouko; Koskenkari, Juha; Backman, Janne T.; Alahuhta, Seppo; Tapio , Tapio; Ala-Kokko, Tero (2017-01-31)

 
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URL:
https://doi.org/10.1097/aln.0000000000001385

Kortelainen, Jukka
Väyrynen, Eero
Huuskonen, Usko
Laurila, Jouko
Koskenkari, Juha
Backman, Janne T.
Alahuhta, Seppo
Tapio , Tapio
Ala-Kokko, Tero
Wolters Kluwer
31.01.2017

Kortelainen, J., Väyrynen, E., Huuskonen, U., Laurila, J., Koskenkari, J., Backman, J. T., … Ala-Kokko, T. (2017). Pilot Study of Propofol-induced Slow Waves as a Pharmacologic Test for Brain Dysfunction after Brain Injury. Anesthesiology, 126(1), 94–103. https://doi.org/10.1097/aln.0000000000001385

https://rightsstatements.org/vocab/InC/1.0/
© 2016, the American Society of Anesthesiologists, Inc. Wolters Kluwer Health, Inc. All Rights Reserved. Anesthesiology 2017; 126:94-103. Version of Record can be found at https://doi.org/10.1097/ALN.0000000000001385.
https://rightsstatements.org/vocab/InC/1.0/
doi:https://doi.org/10.1097/ALN.0000000000001385
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Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi-fe2019090627015
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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.

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