Effect of analgesics and sedatives on the occurrence of spreading depolarizations accompanying acute brain injury (original) (raw)

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11 Department of Neurosurgery, University of Heidelberg, 69120 Heidelberg, Germany

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22 Department of Experimental Neurology, Charité Berlin, 10117 Berlin, Germany

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33 Department of Neurosurgery, Charité Berlin, 10117 Berlin, Germany

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44 Department of Neurosurgery, University of Cincinnati, Cincinnati, OH 45219, USA

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55 Department of Neurosurgery, University of Miami, Miami, FL 33136, USA

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66 Department of Neurological Surgery, University of Pittsburgh, Pittsburgh, PA 15213, USA

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44 Department of Neurosurgery, University of Cincinnati, Cincinnati, OH 45219, USA

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77 Department of Clinical Neuroscience, King's College London, London, SE5 8AF, UK

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77 Department of Clinical Neuroscience, King's College London, London, SE5 8AF, UK

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88 Department of Neurology, University of Cologne, 50931 Cologne, Germany

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Received:

06 January 2012

Revision received:

08 April 2012

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Daniel N. Hertle, Jens P. Dreier, Johannes Woitzik, Jed A. Hartings, Ross Bullock, David O. Okonkwo, Lori A. Shutter, Steven Vidgeon, Anthony J. Strong, Christina Kowoll, Christian Dohmen, Jennifer Diedler, Roland Veltkamp, Thomas Bruckner, Andreas W. Unterberg, Oliver W. Sakowitz, for the Cooperative Study of Brain Injury Depolarizations (COSBID), Effect of analgesics and sedatives on the occurrence of spreading depolarizations accompanying acute brain injury, Brain, Volume 135, Issue 8, August 2012, Pages 2390–2398, https://doi.org/10.1093/brain/aws152
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Abstract

Spreading depolarizations are waves of mass neuronal and glial depolarization that propagate across the injured human cortex. They can occur with depression of neuronal activity as spreading depressions or isoelectric spreading depolarizations on a background of absent or minimal electroencephalogram activity. Spreading depolarizations are characterized by the loss of neuronal ion homeostasis and are believed to damage functional neurons, leading to neuronal necrosis or neurological degeneration and poor outcome. Analgesics and sedatives influence activity-dependent neuronal ion homeostasis and therefore represent potential modulators of spreading depolarizations. In this exploratory retrospective international multicentre analysis, we investigated the influence of midazolam, propofol, fentanyl, sufentanil, ketamine and morphine on the occurrence of spreading depolarizations in 115 brain-injured patients. A surface electrode strip was placed on the cortex, and continuous electrocorticographical recordings were obtained. We used multivariable binary logistic regression to quantify associations between the investigated drugs and the hours of electrocorticographical recordings with and without spreading depolarizations or clusters of spreading depolarizations. We found that administration of ketamine was associated with a reduction of spreading depolarizations and spreading depolarization clusters (P < 0.05). Midazolam anaesthesia, in contrast, was associated with an increased number of spreading depolarization clusters (P < 0.05). By using a univariate odds ratio analysis, we also found a significant association between ketamine administration and reduced occurrence of isoelectric spreading depolarizations in patients suffering from traumatic brain injury, subarachnoid haemorrhage and malignant hemispheric stroke (P < 0.05). Our findings suggest that ketamine—or another _N_-methyl-d-aspartate receptor antagonist—may represent a viable treatment for patients at risk for spreading depolarizations. This hypothesis will be tested in a prospective study.

© The Author (2012). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com

Topic:

• midazolam
• fentanyl
• morphine
• subarachnoid hemorrhage
• analgesics
• ischemic stroke
• electroencephalography
• traumatic brain injuries
• depressive disorders
• ketamine
• necrosis
• neurons
• propofol
• sufentanil
• brain
• sedatives
• antagonists
• aspartate
• ion homeostasis
• depolarization
• tissue degeneration
• wave - physical agent

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