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.
- Cell cycle activation contributes to isoflurane-induced neurotoxicity in the developing brain and the protective effect of CR8.
- Protective Effects of Xenon on Propofol-Induced Neurotoxicity in Human Neural Stem Cell-Derived Models.
- Neonatal exposure to propofol affects interneuron development in the piriform cortex and causes neurobehavioral deficits in adult mice.
- The expression of glucose transporters and mitochondrial division and fusion proteins in rats exposed to hypoxic preconditioning to attenuate propofol neurotoxicity.
- Inhibition of microRNA-375 ameliorated ketamine-induced neurotoxicity in human embryonic stem cell derived neurons.