Editorial Views  |   November 2016
Network-level Mechanisms of Ketamine Anesthesia
Author Notes
  • From the Department of Anesthesiology, Center for Consciousness Science, Neuroscience Graduate Program, University of Michigan Medical School, Ann Arbor, Michigan.
  • Corresponding article on page 873.
    Corresponding article on page 873.×
  • Accepted for publication June 24, 2016.
    Accepted for publication June 24, 2016.×
  • Address correspondence to Dr. Mashour: gmashour@med.umich.edu
Article Information
Editorial Views / Pharmacology
Editorial Views   |   November 2016
Network-level Mechanisms of Ketamine Anesthesia
Anesthesiology 11 2016, Vol.125, 830-831. doi:10.1097/ALN.0000000000001276
Anesthesiology 11 2016, Vol.125, 830-831. doi:10.1097/ALN.0000000000001276
THE first clinical study on ketamine (then known as CI-581) revealed an anesthetic drug that appeared to function like no other, motivating the description of a new state of consciousness.1  Based on behavioral observations and the results of evoked potentials, Corssen and Domino1  also generated prescient insights regarding the state of brain networks during ketamine anesthesia. Recent neurophysiologic data in human and non-human primates confirm that anesthetic doses of ketamine result in a unique constellation: (1) information can still be accurately represented in primary sensory cortex,2  (2) communication patterns between higher-order cortices become disrupted,3  but (3) the complexity and repertoire of brain states are still consistent with disconnected consciousness (such as dreams or hallucinations).4  Although there have been numerous studies of subanesthetic ketamine—as an analgesic, antidepressant, and psychotomimetic—using functional magnetic resonance imaging (fMRI), what has been notably absent is an fMRI investigation of brain networks during ketamine anesthesia. This gap in knowledge has resulted in the inability to compare network alterations induced by drugs such as propofol5,6  and sevoflurane,7  which are thought to act (to varying degrees) through γ-aminobutyric acid (GABA) receptors. Such a comparison could help answer key questions. How do the network-level mechanisms of ketamine differ from more commonly used GABAergic anesthetics? More importantly, what is the “family resemblance” that results in the same functional outcome of general anesthesia? The study by Bonhomme et al.8  addresses these questions, providing insight into how ketamine modulates the mind.
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