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 Isoflurane Anesthesia or Disruption of Postsynaptic Density-95 Protein Interactions Change Dendritic Spine Densities and Cognitive Function in Juvenile Mice.
- Autophagic Network Analysis of the Dual Effect of Sevoflurane on Neurons Associated with GABARAPL1 and 2.
- Effects of ketamine on neurogenesis, extracellular matrix homeostasis and proliferation in hypoxia-exposed HT22 murine hippocampal neurons.
- LncRNA Rik-203 Contributes to Sevoflurane Induced Neurotoxicity?
- Upregulation of miR-215 attenuates propofol-induced apoptosis and oxidative stress in developing neurons by targeting LATS2.