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.
- Neonatal general anesthesia causes lasting alterations in excitatory and inhibitory synaptic transmission in the ventrobasal thalamus of adolescent female rats
- Mild hypothermia ameliorates anesthesia toxicity in the neonatal macaque brain
- Using animal models to evaluate the functional consequences of anesthesia during early neurodevelopment
- microRNA‐124 attenuates isoflurane‐induced neurological deficits in neonatal rats via binding to EGR1
- Hemin treatment protects neonatal rats from sevoflurane-induced neurotoxicity via the phosphoinositide 3-kinase/Akt pathway