In his best-selling 2011 book entitled “Thinking Fast and Slow”, Nobel laureate Daniel Kahneman elucidates the contrast between two modes of human thought-processing: fast and slow thinking.1 Fast thinking is characterized by rapid and automatic reaction to a simulation or problem, while slow thinking involves a measured and analytical response. This dichotomy epitomises the clash between clinicians and basic scientists on the enigma of anaesthetic neurotoxicity.2 Based on their clinical practise that anaesthetics do not overtly produce neurocognitive deficits, the clinician’s viewpoint relies on instinct and experience, while the scientist’s viewpoint is based on a deliberate analysis of experimental data and its logical extrapolation to the clinical setting.
- Ketamine-induced neurotoxicity in neurodevelopment: A synopsis of main pathways based on recent in vivo experimental findings.
- Ferroptosis contributes to isoflurane-induced neurotoxicity and learning and memory impairment.
- RIPK1/RIPK3-Mediated Necroptosis is Involved in Sevoflurane-Induced Neonatal Neurotoxicity in the Rat Hippocampus.
- lncRNA Xist regulates sevoflurane-induced social and emotional impairment by modulating miR-98-5p/EDEM1 signaling axis in neonatal mice.
- Hypermethylation of EFEMP1 in the Hippocampus May Be Related to the Deficit in Spatial Memory of Rat Neonates Triggered by Repeated Administration of Propofol.