Newly Published
Perioperative Medicine  |   October 2017
Propofol-induced Changes in α-β Sensorimotor Cortical Connectivity
Author Notes
  • From the Department of Neurosurgery (M.M., N.A., C.M.P., E.T., N.P.), Department of Bioengineering (N.P.), Neuroscience Interdepartmental Program (N.P.), Brain Research Institute (N.P.); and Department of Anesthesiology (A.E.H.), University of California, Los Angeles, California.
  • 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).
    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 May 23, 2017. Accepted for publication September 22, 2017.
    Submitted for publication May 23, 2017. Accepted for publication September 22, 2017.×
  • Acknowledgments: The authors would like to thank the patients who consented to participate in this study, without whom recording of local field potentials would not be possible.
    Acknowledgments: The authors would like to thank the patients who consented to participate in this study, without whom recording of local field potentials would not be possible.×
  • Research Support: This work was supported by the National Institute of Biomedical Imaging and Bioengineering (Bethesda, Maryland; grant No. K23 EB014326), National Institute of Neurological Disorders and Stroke (Bethesda, Maryland; grant No. R01NS097782), and philanthropic support from Casa Colina Centers for Rehabilitation (Pomona, California). Dr. Malekmohammadi also was supported by a postdoctoral fellowship from American Parkinson Disease Association (New York, New York).
    Research Support: This work was supported by the National Institute of Biomedical Imaging and Bioengineering (Bethesda, Maryland; grant No. K23 EB014326), National Institute of Neurological Disorders and Stroke (Bethesda, Maryland; grant No. R01NS097782), and philanthropic support from Casa Colina Centers for Rehabilitation (Pomona, California). Dr. Malekmohammadi also was supported by a postdoctoral fellowship from American Parkinson Disease Association (New York, New York).×
  • Competing Interests: The authors declare no competing interests.
    Competing Interests: The authors declare no competing interests.×
  • Correspondence: Address correspondence to Dr. Malekmohammadi: UCLA Neurosurgery, 635 Charles Young Drive South, Suite 225, Los Angeles, California 90095. mmalekmohammadi@mednet.ucla.edu. 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 / Pharmacology
Perioperative Medicine   |   October 2017
Propofol-induced Changes in α-β Sensorimotor Cortical Connectivity
Anesthesiology Newly Published on October 26, 2017. doi:10.1097/ALN.0000000000001940
Anesthesiology Newly Published on October 26, 2017. doi:10.1097/ALN.0000000000001940
Abstract

Background: Anesthetics are believed to alter functional connectivity across brain regions. However, network-level analyses of anesthesia, particularly in humans, are sparse. The authors hypothesized that propofol-induced loss of consciousness results in functional disconnection of human sensorimotor cortices underlying the loss of volitional motor responses.

Methods: The authors recorded local field potentials from sensorimotor cortices in patients with Parkinson disease (N = 12) and essential tremor (N = 7) undergoing deep brain stimulation surgery, before and after propofol-induced loss of consciousness. Local spectral power and interregional connectivity (coherence and imaginary coherence) were evaluated separately across conditions for the two populations.

Results: Propofol anesthesia caused power increases for frequencies between 2 and 100 Hz across the sensorimotor cortices and a shift of the dominant spectral peak in α and β frequencies toward lower frequencies (median ± SD peak frequency: 24.5 ± 2.6 Hz to 12.8 ± 2.3 Hz in Parkinson disease; 13.8 ± 2.1 Hz to 12.1 ± 1.0 Hz in essential tremor). Despite local increases in power, sensorimotor cortical coherence was suppressed with propofol in both cohorts, specifically in β frequencies (18 to 29 Hz) for Parkinson disease and α and β (10 to 48 Hz) in essential tremor.

Conclusions: The decrease in functional connectivity between sensory and motor cortices, despite an increase in local spectral power, suggests that propofol causes a functional disconnection of cortices with increases in autonomous activity within cortical regions. This pattern occurs across diseases evaluated, suggesting that these may be generalizable effects of propofol in patients with movement disorders and beyond. Sensorimotor network disruption may underlie anesthetic-induced loss of volitional control.