Update on developmental anesthesia neurotoxicity

@article{Vutskits2017UpdateOD,
  title={Update on developmental anesthesia neurotoxicity},
  author={Laszlo Vutskits and Andrew J Davidson},
  journal={Current Opinion in Anaesthesiology},
  year={2017},
  volume={30},
  pages={337–342}
}
Purpose of review Adverse long-term impact of general anesthesia on the developing brain is a widely discussed and controversial issue with potential public health relevance. The goal of this article is to give insights into the most recent experimental and clinical observations aimed to advance our understanding in this field. Recent findings Recent investigations demonstrate long-term behavioral consequences of early-life anesthesia exposure in nonhuman primates under experimental conditions… 
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77 Citations
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77 Citations

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The findings presented here underscore the importance of invertebrates for research in the field of anesthesiology while highlighting their relevance to both vertebrates and humans.

Can We Really Suggest that Anesthesia Might Cause Attention-deficit/Hyperactivity Disorder?

An association between childhood exposure to multiple anesthetics and increased risk of learning disability and attention-deficit/hyperactivity disorder (ADHD) and the associations were stronger with multiple exposures compared with single exposures.

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The findings suggest that DEX could be an attractive therapeutic for future studies investigating its neuroprotective potential in a translational animal model and SEVO anaesthesia induced widespread apoptosis in infant rat brain.

Implication of microglia in ketamine-induced long-term cognitive impairment in murine pups

It is found that multiple exposures to ketamine in neonatal mice lead to spatiallearning and memory dysfunction and the alterations of microglial development and function are the possible mechanisms of long-term learning and memory impairment.

Maternal sciatic nerve administered bupivacaine induces hippocampal cell apoptosis in offspring

The data suggest that maternal bupivacaine use increases fetal hippocampal cell apoptosis markers such as caspase 8 and cleaved caspases 3, at least in part, via inhibiting the Akt activation.
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