Perioperative Medicine  |   October 2017
Investigation of Slow-wave Activity Saturation during Surgical Anesthesia Reveals a Signature of Neural Inertia in Humans
Author Notes
  • From the Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom (C.E.W., S.J., I.T.); and Department of Anaesthesia, University of Auckland, Waikato Hospital, Hamilton, New Zealand (J.W.S., D.H.).
  • C.E.W. and J.W.S. contributed equally to this article.
    C.E.W. and J.W.S. contributed equally to this article.×
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    Supplemental Digital Content is available for this article. Direct URL citations appear in the printed text and are available in both the HTML and PDF versions of this article. Links to the digital files are provided in the HTML text of this article on the Journal’s Web site (www.anesthesiology.org).×
  • Submitted for publication November 5, 2016. Accepted for publication May 4, 2017.
    Submitted for publication November 5, 2016. Accepted for publication May 4, 2017.×
  • Address correspondence to Dr. Warnaby: FMRIB Centre, John Radcliffe Hospital, Oxford, OX3 9DU, United Kingdom. katie.warnaby@ndcn.ox.ac.uk. Information on purchasing reprints may be found at www.anesthesiology.org or on the masthead page at the beginning of this issue. Anesthesiology’s articles are made freely accessible to all readers, for personal use only, 6 months from the cover date of the issue.
Article Information
Perioperative Medicine / Clinical Science / Central and Peripheral Nervous Systems / Pharmacology
Perioperative Medicine   |   October 2017
Investigation of Slow-wave Activity Saturation during Surgical Anesthesia Reveals a Signature of Neural Inertia in Humans
Anesthesiology 10 2017, Vol.127, 645-657. doi:10.1097/ALN.0000000000001759
Anesthesiology 10 2017, Vol.127, 645-657. doi:10.1097/ALN.0000000000001759
Abstract

Background: Previously, we showed experimentally that saturation of slow-wave activity provides a potentially individualized neurophysiologic endpoint for perception loss during anesthesia. Furthermore, it is clear that induction and emergence from anesthesia are not symmetrically reversible processes. The observed hysteresis is potentially underpinned by a neural inertia mechanism as proposed in animal studies.

Methods: In an advanced secondary analysis of 393 individual electroencephalographic data sets, we used slow-wave activity dose-response relationships to parameterize slow-wave activity saturation during induction and emergence from surgical anesthesia. We determined whether neural inertia exists in humans by comparing slow-wave activity dose responses on induction and emergence.

Results: Slow-wave activity saturation occurs for different anesthetics and when opioids and muscle relaxants are used during surgery. There was wide interpatient variability in the hypnotic concentrations required to achieve slow-wave activity saturation. Age negatively correlated with power at slow-wave activity saturation. On emergence, we observed abrupt decreases in slow-wave activity dose responses coincident with recovery of behavioral responsiveness in ~33% individuals. These patients are more likely to have lower power at slow-wave activity saturation, be older, and suffer from short-term confusion on emergence.

Conclusions: Slow-wave activity saturation during surgical anesthesia implies that large variability in dosing is required to achieve a targeted potential loss of perception in individual patients. A signature for neural inertia in humans is the maintenance of slow-wave activity even in the presence of very-low hypnotic concentrations during emergence from anesthesia.