Editorial Views  |   August 2018
Targeting Microglia: A New Avenue for Anesthesia Neuroprotection after Brain Injury?
Author Notes
  • From the Department of Anesthesiology, Pharmacology and Intensive Care, University Hospitals of Geneva, Switzerland (L.V.); and Department of Anesthesia and Perioperative Care, University of California, San Francisco, California (J.W.S.).
  • Corresponding article on page 278.
    Corresponding article on page 278.×
  • Accepted for publication April 11, 2018.
    Accepted for publication April 11, 2018.×
  • Address correspondence to Dr. Vutskits: laszlo.vutskits@unige.ch
Article Information
Editorial Views / Central and Peripheral Nervous Systems / Trauma / Burn Care
Editorial Views   |   August 2018
Targeting Microglia: A New Avenue for Anesthesia Neuroprotection after Brain Injury?
Anesthesiology 8 2018, Vol.129, 232-234. doi:10.1097/ALN.0000000000002272
Anesthesiology 8 2018, Vol.129, 232-234. doi:10.1097/ALN.0000000000002272
The concept of pharmacologic neuroprotection by general anesthetics has attracted a considerable amount of interest during the past few decades.1 Via their actions on neuronal metabolism and signaling, general anesthetics are plausible candidates to protect the brain after injury. In line with this possibility, laboratory studies have revealed some neuroprotective properties of anesthetic agents in experimental models of both ischemic and traumatic brain lesions. However, clinical evidence of the relevance or benefit of these observations is lacking. Despite years of laboratory investigations and clinical trials, neither anesthetics nor any other drugs have been shown to improve outcome after brain injury in humans.2  Hence, preserving neuronal networks, or enhancing their functional recovery after deleterious insults to the central nervous system (CNS), remains a major unsolved challenge in clinical medicine. Among the numerous variables hindering extrapolation of laboratory results to clinical practice in this domain is the extraordinary complexity of molecular and cellular events initiated by either ischemic or traumatic insults. Research aimed to better understand how these lesion-induced pathologic cascades are linked to each other over time is a prerequisite for understanding how future clinical trials should be designed to target neuroprotection.