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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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Citations
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Anesthetic Neurotoxicity — Clinical Implications of Animal Models

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Association between Exposure of Young Children to Procedures Requiring General Anesthesia and Learning and Behavioral Outcomes in a Population-based Birth Cohort.

TL;DR: Findings in children anesthetized with modern techniques largely confirm those found in an older birth cohort and provide additional evidence that children with multiple exposures are more likely to develop adverse outcomes related to learning and attention.
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Executive Function in Children and Adolescents with Critical Cyanotic Congenital Heart Disease

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References
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Journal ArticleDOI

Short-term Memory Impairment after Isoflurane in Mice Is Prevented by the α5 γ-Aminobutyric Acid Type A Receptor Inverse Agonist L-655,708

TL;DR: It is postulated that inhibiting the activity of &agr;5GABAA receptors during isoflurane anesthesia would prevent memory deficits in the early postanesthesia period, suggesting that an isofLurane interaction at &agR;5gabAA receptors contributes to memory impairment during theEarly postanesthetic period.
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Cell Age–Specific Vulnerability of Neurons to Anesthetic Toxicity

TL;DR: Key aspects of the anesthetics phenomenon remain unclear, such as why certain neurons die, whereas immediately adjacent neurons are seemingly unaffected, and why the immature brain is exquisitely vulnerable, whereas the mature brain seems resistant.
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The effects of isoflurane and desflurane on cognitive function in humans.

TL;DR: The findings from this pilot study suggest that isoflurane and desflurane may have different effects on postoperative cognitive function, and additional studies with a larger sample size and longer times of follow-up testing are needed.
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Nociceptive stimuli enhance anesthetic-induced neuroapoptosis in the rat developing brain.

TL;DR: Nociceptive stimulation and prolonged anesthesia produced significantly more apoptosis than prolonged anesthesia alone when administered to neonates during the synaptogenic period.
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Anesthetic-induced preconditioning delays opening of mitochondrial permeability transition pore via protein kinase C-ε mediated pathway

TL;DR: The results point to the connection between cytosolic and mitochondrial components of cardioprotection by isoflurane and the importance of APC-activated PKC in delaying mitochondrial permeability transition pore (mPTP) opening.
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