title: Disruption of frontal-parietal communication by ketamine, propofol, and sevoflurane.
abstract: BACKGROUND
  Directional connectivity from anterior to posterior brain regions (or "feedback" connectivity) has been shown to be inhibited by propofol and sevoflurane. In this study the authors tested the hypothesis that ketamine would also inhibit cortical feedback connectivity in frontoparietal networks.
  
  
  METHODS
  Surgical patients (n = 30) were recruited for induction of anesthesia with intravenous ketamine (2 mg/kg); electroencephalography of the frontal and parietal regions was acquired. The authors used normalized symbolic transfer entropy, a computational method based on information theory, to measure directional connectivity across frontal and parietal regions. Statistical analysis of transfer entropy measures was performed with the permutation test and the time-shift test to exclude false-positive connectivity. For comparison, the authors used normalized symbolic transfer entropy to reanalyze electroencephalographic data gathered from surgical patients receiving either propofol (n = 9) or sevoflurane (n = 9) for anesthetic induction.
  
  
  RESULTS
  Ketamine reduced alpha power and increased gamma power, in contrast to both propofol and sevoflurane. During administration of ketamine, feedback connectivity gradually diminished and was significantly inhibited after loss of consciousness (mean ± SD of baseline and anesthesia: 0.0074 ± 0.003 and 0.0055 ± 0.0027; F(5, 179) = 7.785, P < 0.0001). By contrast, feedforward connectivity was preserved during exposure to ketamine (mean ± SD of baseline and anesthesia: 0.0041 ± 0.0015 and 0.0046 ± 0.0018; F(5, 179) = 2.07; P = 0.072). Like ketamine, propofol and sevoflurane selectively inhibited feedback connectivity after anesthetic induction.
  
  
  CONCLUSIONS
  Diverse anesthetics disrupt frontal-parietal communication, despite molecular and neurophysiologic differences. Analysis of directional connectivity in frontal-parietal networks could provide a common metric of general anesthesia and insight into the cognitive neuroscience of anesthetic-induced unconsciousness.
authors.affiliation: Department of Anesthesiology, University of Michigan Medical School, Ann Arbor, Michigan 48109-5048, USA.
authors.forename: UnCheol
authors.initials: U
authors.lastname: Lee
authors.forename: SeungWoo
authors.initials: S
authors.lastname: Ku
authors.forename: GyuJeong
authors.initials: G
authors.lastname: Noh
authors.forename: SeungHye
authors.initials: S
authors.lastname: Baek
authors.forename: ByungMoon
authors.initials: B
authors.lastname: Choi
authors.forename: George A
authors.initials: GA
authors.lastname: Mashour
mesh_terms: D000328:Adult; D000700:Analgesics / Q000494:pharmacology; D018685:Anesthetics, Inhalation / Q000494:pharmacology; D018686:Anesthetics, Intravenous / Q000494:pharmacology; D004569:Electroencephalography; D005260:Female; D005625:Frontal Lobe / Q000187:drug effects*; D006801:Humans; D007649:Ketamine / Q000494:pharmacology*; D008297:Male; D008738:Methyl Ethers / Q000494:pharmacology*; D008875:Middle Aged; D010296:Parietal Lobe / Q000187:drug effects*; D015742:Propofol / Q000494:pharmacology*; D000077149:Sevoflurane; D055815:Young Adult
chemical_list: D000700:Analgesics; D018685:Anesthetics, Inhalation; D018686:Anesthetics, Intravenous; D008738:Methyl Ethers; D000077149:Sevoflurane; D007649:Ketamine; D015742:Propofol