Few if any issues received more attention in the field of pediatric perioperative care over the past decade than developmental anesthesia neurotoxicity. While the possibility of a plausible association between anesthesia and postoperative personality changes in children was first hypothesized more than 60 years ago,1 substantial concern on this subject has been ignited by seminal laboratory work, conducted 50 years later, where exposure of newborn rats to a mixture of anesthetics induced widespread apoptosis and persistent cognitive deficits in these animals.2 The initial mistrust and rejection generated by this publication in the anesthesia community have been rapidly transformed into an important public health concern after the robust confirmation of developmental anesthesia neurotoxicity in a variety of experimental models and, most importantly, with the availability of human epidemiological data suggesting an association between early life anesthesia exposure and subsequent neurocognitive disturbances.
- Prenatal Exposure to General Anesthesia Drug Esketamine Impaired Neurobehavior in Offspring.
- Needle in a Haystack: Localising the Long-Term Neuronal Changes from Early-Life Exposure to General Anaesthesia.
- Toll-Like Receptor 4 Deficiency Ameliorates Propofol-Induced Impairments of Cognitive Function and Synaptic Plasticity in Young Mice.
- Whole-Brain Characterization of Apoptosis after Sevoflurane Anesthesia Reveals Neuronal Cell Death Patterns in the Mouse Neonatal Neocortex.
- Apamin, an SK2 Inhibitor, Attenuated Neonatal Sevoflurane Exposures Caused Cognitive Deficits in Mice through the Regulation of Hippocampal Neuroinflammation.