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Open AccessJournal ArticleDOI

Anaesthetic neurotoxicity and neuroplasticity: an expert group report and statement based on the BJA Salzburg Seminar

TLDR
mounting evidence from preclinical studies reveals general anaesthetics to be powerful modulators of neuronal development and function, which could contribute to detrimental behavioural outcomes, however, definitive clinical data remain elusive.
Abstract
Although previously considered entirely reversible, general anaesthesia is now being viewed as a potentially significant risk to cognitive performance at both extremes of age. A large body of preclinical as well as some retrospective clinical evidence suggest that exposure to general anaesthesia could be detrimental to cognitive development in young subjects, and might also contribute to accelerated cognitive decline in the elderly. A group of experts in anaesthetic neuropharmacology and neurotoxicity convened in Salzburg, Austria for the BJA Salzburg Seminar on Anaesthetic Neurotoxicity and Neuroplasticity. This focused workshop was sponsored by the British Journal of Anaesthesia to review and critically assess currently available evidence from animal and human studies, and to consider the direction of future research. It was concluded that mounting evidence from preclinical studies reveals general anaesthetics to be powerful modulators of neuronal development and function, which could contribute to detrimental behavioural outcomes. However, definitive clinical data remain elusive. Since general anaesthesia often cannot be avoided regardless of patient age, it is important to understand the complex mechanisms and effects involved in anaesthesia-induced neurotoxicity, and to develop strategies for avoiding or limiting potential brain injury through evidence-based approaches.

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Mild hypothermia ameliorates anesthesia toxicity in the neonatal macaque brain.

TL;DR: Investigation of protective potential of hypothermia against histological toxicity of the anesthetic sevoflurane in the developing nonhuman primate brain found it ameliorates anesthesia-induced apoptosis in the neonatal primatebrain within a narrow temperature window (35-36.5 °C).
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Sevoflurane Induces Exaggerated and Persistent Cognitive Decline in a Type II Diabetic Rat Model by Aggregating Hippocampal Inflammation.

TL;DR: The results suggest that diabetic GK rats exhibit cognitive dysfunction probably due to increased hippocampusal inflammation, and that sevoflurane induces exaggerated and persistent cognitive decline in GK rat by aggregating hippocampal inflammation.
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Long-Term Neurobehavioral Consequences of a Single Ketamine Neonatal Exposure in Rats: Effects on Cellular Viability and Glutamate Transport in Frontal Cortex and Hippocampus

TL;DR: Findings indicate that a single neonatal ketamine exposure induces a short-term reduction in the hippocampal, but not in cortical, cellular viability, and long-term alterations in hippocampal glutamate transport, improvement on motor performance, and short- term recognition memory impairment.
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Neuroimaging young children and associations with neurocognitive development in a South African birth cohort study.

TL;DR: Overall, this study demonstrates the feasibility of carrying out a neuroimaging study of young children during natural sleep in sub-Saharan Africa and indicates that dynamic morphological changes in heteromodal association regions are associated with cognitive and language development at this young age.
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Sevoflurane exposure has minimal effect on cognitive function and does not alter microglial activation in adult monkeys.

TL;DR: The data suggest that exposure to anesthesia alone may not be sufficient to cause persistent POCD in adult populations and that general anesthesia appears to be less neurotoxic then in young animals.
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