European journal of anaesthesiology
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We do not know how general anaesthetics cause their desired effects. Contrary to what has been thought until relatively recently, the clinical state of anaesthesia consists of multiple components that are mediated via interaction of the anaesthetic drugs with different targets on the molecular, the cellular, the network and the structural-anatomical levels. The mechanisms by which some of these drugs induce the different components of "anaesthesia" may be rather specific: discrete mutations of single amino acids in specific proteins profoundly affect the ability of certain anaesthetics to achieve specific endpoints. ⋯ This article will focus on evidence for anaesthetic toxicity in the central nervous system, which appears to be susceptible to anaesthetic neurotoxicity primarily at the extremes of ages but via different pathways: in the neonate, during the period of most intense synaptogenesis, anaesthetics can induce excessive apoptosis; in the aging brain subtle cognitive dysfunction can persist long after clearance of the drug and processes resembling neurodegenerative disorders may be accelerated. At all ages, anaesthetics affect gene expression regulating protein synthesis in poorly understood ways. While it seems reasonable to assume that the vast majority of our patients completely restore homeostasis after general anaesthesia, exposure to these drugs probably has more profound and longer-lasting effects on the brain than heretofore imagined.
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The use of inhalation sedation with sub-anaesthetic concentrations of sevoflurane and nitrous oxide mixture is expected to reduce amounts of intravenous sedative drugs needed to produce a balanced sedation with the benefits of having reduced side-effects. ⋯ The use of titrated doses of intravenous sedative drugs for induction of conscious sedation followed by the use of low concentrations (0.1-0.3%) of sevoflurane combined with 40% nitrous oxide for maintenance of conscious sedation in patients requiring endoscopic and/or surgical procedures under local anaesthesia, has the potential advantages of reducing amounts of intravenous sedative drugs, less likelihood of problems from drug side-effects and fast recovery and discharge time. Further investigations to establish the technique are currently in progress.
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Letter Case Reports
Downbeat nystagmus as a manifestation of intrathecal morphine toxicity.