Editorial Views  |   November 2016
Another Brick in (Some Kind of) Wall
Author Notes
  • From the Department of Anaesthesia, Waikato Clinical School, University of Auckland, Hamilton, New Zealand.
  • Corresponding article on page 861.
    Corresponding article on page 861.×
  • Accepted for publication July 18, 2016.
    Accepted for publication July 18, 2016.×
  • Address correspondence to Dr. Sleigh: jamie.sleigh@waikatodhb.health.nz
Article Information
Editorial Views / Central and Peripheral Nervous Systems / Radiological and Other Imaging
Editorial Views   |   November 2016
Another Brick in (Some Kind of) Wall
Anesthesiology 11 2016, Vol.125, 827-829. doi:10.1097/ALN.0000000000001323
Anesthesiology 11 2016, Vol.125, 827-829. doi:10.1097/ALN.0000000000001323
A COMMON metaphor for the scientific enterprise is that of building an edifice. Understanding of the natural world is painstakingly gained by new observations and interpretations, each of which builds on the foundations of previous work. Over the last decade, we have been quietly living through the construction of a new wing in the research-into-mechanisms-of-anesthesia mansion. This has been largely driven by the development of new experimental techniques in functional brain imaging. Functional magnetic resonance imaging (FMRI)—and at a coarser spatial resolution, the high-density electroencephalogram—have enabled us to see how general anesthetic drugs disturb the activity in precise anatomical regions of the brain. This is somewhat analogous to the impact of ultrasound on cardiology in the 1980s and 1990s. The underlying motivation behind these studies is to see if there are regions in the brain that are preferentially sensitive to and have pivotal roles in generating the state of general anesthesia and also how general anesthetic drugs disrupt the patterns of long-range brain coordination, which are presently believed to be necessary for the various components of normal wakefulness. To date, there are at least nine published FMRI studies and 14 high-density electroencephalogram studies. For practical reasons, most previous work has examined the FMRI effects of propofol. In this issue of Anesthesiology, Ranft et al.1  describe a study looking at how medium (2%) and high concentrations (3%) of sevoflurane disturb the activity and interregional connectivity of the brain, as detected simultaneously by FMRI and high-density electroencephalogram. They found that sevoflurane showed comparable effects to those reported in previous propofol studies, namely, that at 2% concentrations of sevoflurane, there were clear decreases in electroencephalographic measures of information content and interregional information flux. In contrast, when measured by the FMRI, the overall brain connectivity showed surprisingly modest decreases in corticocortical and thalamocortical connectivity (figs. 3 and 4 and table 1, Supplemental Digital Content, in their article). Widespread decreases in brain connectivity only occurred at supra-minimum alveolar concentration (greater than or equal to 3%) concentrations of sevoflurane. This is in agreement with other FMRI studies, which also show that most of the brain carries on business as usual under the usual clinical levels of anesthesia (minimum alveolar concentration, 0.5 to 1.2).2  It is clear that, at these levels, general anesthesia does not dampen down activity in the brain uniformly—the so-called “wet blanket” theory of anesthesia.
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