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• W2763669460 abstract "As animal evidence continues to mount, we face a real dilemma regarding the clinical relevance of anaesthesia-induced developmental neurotoxicity. In December 2016, the US Food and Drug Administration (FDA) issued an announcement stating that commonly used general anaesthetics could potentially be detrimental to very young and rapidly developing brains. This announcement was based on an extensive body of animal research.1Ikonomidou C Bosch F Miksa M et al.Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain.Science. 1999; 283: 70-74Crossref PubMed Scopus (1702) Google Scholar, 2Ikonomidou C Bittigau P Ishimaru MJ et al.Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome.Science. 2000; 287: 1056-1060Crossref PubMed Scopus (1206) Google Scholar, 3Jevtovic-Todorovic V Hartman REY Izumi Y et al.Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits.J Neurosci. 2003; 23: 876-882Crossref PubMed Google Scholar, 4Loepke AW Istaphanous GK McAuliffe 3rd, JJ et al.The effects of neonatal isoflurane exposure in mice on brain cell viability, adult behavior, learning, and memory.Anesth Analg. 2009; 108: 90-104Crossref PubMed Scopus (226) Google Scholar, 5Rizzi S Carter LB Ori C Jevtovic-Todorovic V Clinical anesthesia causes permanent damage to the fetal guinea pig brain.Brain Pathol. 2008; 18: 198-210Crossref PubMed Scopus (164) Google Scholar, 6Yon J-H Daniel-Johnson J Carter LB Jevtovic-Todorovic V Anesthesia induces neuronal cell death in the developing rat brain via the intrinsic and extrinsic apoptotic pathways.Neuroscience. 2005; 35: 815-827Crossref Scopus (55) Google Scholar, 7Boscolo A Starr JA Sanchez V et al.The abolishment of anesthesia-induced cognitive impairment by timely protection of mitochondria in the developing rat brain: the importance of free oxygen radicals and mitochondrial integrity.Neurobiol Dis. 2012; 45: 1031-1041Crossref PubMed Scopus (140) Google Scholar, 8Head BP Patel HH Niesman IR Drummond JC Roth DM Patel PM Inhibition of p75 neurotrophin receptor attenuates isoflurane-mediated neuronal apoptosis in the neonatal central nervous system.Anesthesiology. 2009; 110: 813-825Crossref PubMed Scopus (212) Google Scholar, 9Noguchi KK Johnson SA Kristich LE et al.Lithium protects against anaesthesia neurotoxicity in the infant primate brain.Sci Rep. 2016; 6: 22427Crossref PubMed Scopus (34) Google Scholar, 10Straiko MM Young C Cattano D et al.Lithium protects against anesthesia-induced developmental neuroapoptosis.Anesthesiology. 2009; 110: 862-868Crossref PubMed Scopus (129) Google Scholar, 11Sanchez V Feinstein SD Lunardi N et al.General anesthesia causes long-term impairment of mitochondrial morphogenesis and synaptic transmission in developing rat brain.Anesthesiology. 2011; 115: 992-1002Crossref PubMed Scopus (162) Google Scholar, 12Lunardi N Ori C Erisir A Jevtovic-Todorovic V General anesthesia causes long-lasting disturbances in the ultrastructural properties of developing synapses in young rats.Neurotox Res. 2010; 17: 179-188Crossref PubMed Scopus (150) Google Scholar, 13Briner A De Roo M Dayer A Muller D Habre W Vutskits L Volatile anesthetics rapidly increase dendritic spine density in the rat medial prefrontal cortex during synaptogenesis.Anesthesiology. 2010; 112: 546-556Crossref PubMed Scopus (193) Google Scholar, 14Briner A Nikonenko I De Roo M Dayer A Muller D Vutskits L Developmental stage-dependent persistent impact of propofol anesthesia on dendritic spines in the rat medial prefrontal cortex.Anesthesiology. 2011; 115: 282-293Crossref PubMed Scopus (176) Google Scholar, 15Mintz CD Barrett KM Smith SC Benson DL Harrison NL Anesthetics interfere with axon guidance in developing mouse neocortical neurons in vitro via a γ-aminobutyric acid type A receptor mechanism.Anesthesiology. 2013; 118: 825-833Crossref PubMed Scopus (65) Google Scholar, 16Brambrink AM Evers AS Avidan MS et al.Isoflurane-induced neuroapoptosis in the neonatal rhesus macaque brain.Anesthesiology. 2010; 112: 834-841Crossref PubMed Scopus (448) Google Scholar, 17Brambrink AM Back SA Riddle A et al.Isoflurane-induced apoptosis of oligodendrocytes in the neonatal primate brain.Ann Neurol. 2012; 72: 525-535Crossref PubMed Scopus (212) Google Scholar, 18Creeley CE Dikranian KT Dissen GA Back SA Olney JW Brambrink AM Isoflurane-induced apoptosis of neurons and oligodendrocytes in the fetal rhesus macaque brain.Anesthesiology. 2014; 120: 626-638Crossref PubMed Scopus (159) Google Scholar, 19Creeley C Dikranian K Dissen G Martin L Olney J Brambrink A Propofol-induced apoptosis of neurones and oligodendrocytes in fetal and neonatal rhesus macaque brain.Br J Anaesth. 2013; 110: i29-i38Abstract Full Text Full Text PDF PubMed Scopus (282) Google Scholar, 20Schenning KJ Noguchi KK Martin LD et al.Isoflurane exposure leads to apoptosis of neurons and oligodendrocytes in 20- and 40-day old rhesus macaques.Neurotoxicol Teratol. 2017; 60: 63-68Crossref PubMed Scopus (52) Google Scholar, 21Liu F Rainosek SW Frisch-Daiello JL et al.Potential adverse effects of prolonged sevoflurane exposure on developing monkey brain: from abnormal lipid metabolism to neuronal damage.Toxicol Sci. 2015; 147: 562-572Crossref PubMed Scopus (66) Google Scholar, 22Paule MG Li M Allen RR et al.Ketamine anesthesia during the first week of life can cause long-lasting cognitive deficits in rhesus monkeys.Neurotoxicol Teratol. 2011; 33: 220-230Crossref PubMed Scopus (437) Google Scholar, 23Brambrink AM Evers AS Avidan MS et al.Ketamine-induced neuroapoptosis in the fetal and neonatal rhesus macaque brain.Anesthesiology. 2012; 116: 72-84Crossref Scopus (268) Google Scholar, 24Coleman K Robertson ND Dissen GA et al.Isoflurane anesthesia has long-term consequences on motor and behavioral development in infant rhesus macaques.Anesthesiology. 2017; 126: 74-84Crossref PubMed Scopus (107) Google Scholar Now we must grapple with the FDA's official recommendation that potential risks should be balanced with the benefits of appropriate anaesthesia in young children. More importantly, as we deal with the official expectation that potential risks should be discussed with families and heath-care providers, we are reminded how crucial it is to deepen our understanding of the pertinent mechanisms and potential long-lasting behavioural outcomes relating to the exposure of the young brain to anaesthesia. Although initial studies were focused on different rodent models of anaesthesia-induced developmental neurotoxicity, certain limitations were undeniable, thus affecting their translational value. For example, rodent brain development is substantially shorter than human brain development (weeks as opposed to years).25Dobbing J Sands J The brain growth spurt in various mammalian species.Early Hum Dev. 1979; 3: 79-84Abstract Full Text PDF PubMed Scopus (2155) Google Scholar The majority of rodent models used exposures considered to be lengthy (4–6 h).1Ikonomidou C Bosch F Miksa M et al.Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain.Science. 1999; 283: 70-74Crossref PubMed Scopus (1702) Google Scholar, 2Ikonomidou C Bittigau P Ishimaru MJ et al.Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome.Science. 2000; 287: 1056-1060Crossref PubMed Scopus (1206) Google Scholar, 3Jevtovic-Todorovic V Hartman REY Izumi Y et al.Early exposure to common anesthetic agents causes widespread neurodegeneration in the developing rat brain and persistent learning deficits.J Neurosci. 2003; 23: 876-882Crossref PubMed Google Scholar, 4Loepke AW Istaphanous GK McAuliffe 3rd, JJ et al.The effects of neonatal isoflurane exposure in mice on brain cell viability, adult behavior, learning, and memory.Anesth Analg. 2009; 108: 90-104Crossref PubMed Scopus (226) Google Scholar 6Yon J-H Daniel-Johnson J Carter LB Jevtovic-Todorovic V Anesthesia induces neuronal cell death in the developing rat brain via the intrinsic and extrinsic apoptotic pathways.Neuroscience. 2005; 35: 815-827Crossref Scopus (55) Google Scholar, 7Boscolo A Starr JA Sanchez V et al.The abolishment of anesthesia-induced cognitive impairment by timely protection of mitochondria in the developing rat brain: the importance of free oxygen radicals and mitochondrial integrity.Neurobiol Dis. 2012; 45: 1031-1041Crossref PubMed Scopus (140) Google Scholar, 8Head BP Patel HH Niesman IR Drummond JC Roth DM Patel PM Inhibition of p75 neurotrophin receptor attenuates isoflurane-mediated neuronal apoptosis in the neonatal central nervous system.Anesthesiology. 2009; 110: 813-825Crossref PubMed Scopus (212) Google Scholar 11Sanchez V Feinstein SD Lunardi N et al.General anesthesia causes long-term impairment of mitochondrial morphogenesis and synaptic transmission in developing rat brain.Anesthesiology. 2011; 115: 992-1002Crossref PubMed Scopus (162) Google Scholar Most importantly, the neuronal networks in rodents are substantially less complex compared with those of primates. This creates a dilemma for practising clinicians: how relevant are these findings to the daily clinical care of children? Are the potentially detrimental histopathological, behavioural, and cognitive outcomes in humans verifiable beyond reasonable doubt? What kind of ethically acceptable studies could be conducted to get us closer to the truth? Can early exposure to anaesthesia and sedatives be linked to poor cognitive outcomes later in life in view of the myriad of socioeconomic and emotional factors throughout life that can shape behavioural and cognitive development? Causation would be perhaps impossible to prove, but could we even attempt to prove association? As we struggle with the possibility that these questions are perhaps not answerable in humans, we simultaneously focus our attention on the rapidly growing body of work being done with non-human primates. Given that their brain development is very similar in timing, duration, and complexity to the development of the human brain,20Schenning KJ Noguchi KK Martin LD et al.Isoflurane exposure leads to apoptosis of neurons and oligodendrocytes in 20- and 40-day old rhesus macaques.Neurotoxicol Teratol. 2017; 60: 63-68Crossref PubMed Scopus (52) Google Scholar studies with non-human primates may be the closest we can get to understanding the true implications of early exposure to anaesthesia in humans. In this issue of the British Journal of Anaesthesia, Dr Noguchi and colleagues26Noguchi KK Johnson SA Dissen GA et al.Isoflurane exposure for three hours triggers apoptotoc cell death in neonatal macaque brain.Br J Anaeth. 2017; 119: 524-531Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar provide an important addition to a growing body of non-human primate studies by focusing on the issue of the clinically relevant duration of anaesthesia exposure. Previous work16Brambrink AM Evers AS Avidan MS et al.Isoflurane-induced neuroapoptosis in the neonatal rhesus macaque brain.Anesthesiology. 2010; 112: 834-841Crossref PubMed Scopus (448) Google Scholar, 17Brambrink AM Back SA Riddle A et al.Isoflurane-induced apoptosis of oligodendrocytes in the neonatal primate brain.Ann Neurol. 2012; 72: 525-535Crossref PubMed Scopus (212) Google Scholar, 18Creeley CE Dikranian KT Dissen GA Back SA Olney JW Brambrink AM Isoflurane-induced apoptosis of neurons and oligodendrocytes in the fetal rhesus macaque brain.Anesthesiology. 2014; 120: 626-638Crossref PubMed Scopus (159) Google Scholar, 19Creeley C Dikranian K Dissen G Martin L Olney J Brambrink A Propofol-induced apoptosis of neurones and oligodendrocytes in fetal and neonatal rhesus macaque brain.Br J Anaesth. 2013; 110: i29-i38Abstract Full Text Full Text PDF PubMed Scopus (282) Google Scholar, 20Schenning KJ Noguchi KK Martin LD et al.Isoflurane exposure leads to apoptosis of neurons and oligodendrocytes in 20- and 40-day old rhesus macaques.Neurotoxicol Teratol. 2017; 60: 63-68Crossref PubMed Scopus (52) Google Scholar, 21Liu F Rainosek SW Frisch-Daiello JL et al.Potential adverse effects of prolonged sevoflurane exposure on developing monkey brain: from abnormal lipid metabolism to neuronal damage.Toxicol Sci. 2015; 147: 562-572Crossref PubMed Scopus (66) Google Scholar, 22Paule MG Li M Allen RR et al.Ketamine anesthesia during the first week of life can cause long-lasting cognitive deficits in rhesus monkeys.Neurotoxicol Teratol. 2011; 33: 220-230Crossref PubMed Scopus (437) Google Scholar, 23Brambrink AM Evers AS Avidan MS et al.Ketamine-induced neuroapoptosis in the fetal and neonatal rhesus macaque brain.Anesthesiology. 2012; 116: 72-84Crossref Scopus (268) Google Scholar, 24Coleman K Robertson ND Dissen GA et al.Isoflurane anesthesia has long-term consequences on motor and behavioral development in infant rhesus macaques.Anesthesiology. 2017; 126: 74-84Crossref PubMed Scopus (107) Google Scholar has focused on examining outcomes of anesthesia exposure of 5–24 h, which were often considered to be of limited clinical relevance because clinical exposures are commonly shorter. This prompted Noguchi and colleagues26Noguchi KK Johnson SA Dissen GA et al.Isoflurane exposure for three hours triggers apoptotoc cell death in neonatal macaque brain.Br J Anaeth. 2017; 119: 524-531Abstract Full Text Full Text PDF PubMed Scopus (63) Google Scholar to focus on a 3 h anaesthesia exposure, which is particularly timely considering that the recently issued FDA warning focused on exposures of 3 h or longer. The authors also reviewed clinical data from two US children's hospitals to show that ∼30% of infants and 10% of children <3 yr of age are exposed to general anaesthesia lasting 3 h or longer. They remind us that this translates into several hundred thousand young children undergoing general anaesthesia every year in the USA alone. In a systematic morphological study, they examined the neurotoxic potential of the inhaled anaesthetic isoflurane administered for 3 h to 6-day-old infant rhesus macaques. Infant monkeys were intubated and mechanically ventilated during anaesthesia, and the inhaled isoflurane concentration was tightly controlled to maintain a surgical plane of anaesthesia while physiological homeostasis was closely monitored. The histopathological findings were compared with those from animals in a control group that were not anaesthetized but underwent a mock anaesthesia procedure, such as ‘insertion of an i.v. catheter, physiological measurements, and a period of handling to simulate the environment of the experimental animals'. Using activated caspase-3 staining, a well-established method for detecting neurones and glia undergoing apoptotic cell death, they reported that a 3 h exposure to isoflurane significantly increased both neuronal and oligodendroglial apoptosis by four-fold compared with controls. Although the apoptosis in oligodendrocytes was evenly distributed throughout the white matter, neuronal apoptosis was more brain region specific, including all regions of the cerebral cortex, caudate nucleus, putamen, and thalamus. Given that a substantial number of surgical procedures in children last 3 h or longer, they concluded that this protocol is relevant to clinical medicine. Based on their previous findings with longer exposure to isoflurane (5 h) they concluded that there is a direct correlation between the duration of exposure and degree of apoptotic activation. Although a similar pattern of widespread apoptotic neurodegeneration was noted, the intensity of apoptosis after a 5 h exposure was higher compared with the 3 h exposure. Moreover, this study solidifies earlier observations that monitoring and maintenance of proper homeostasis during general anaesthesia has no impact on the severity of anaesthesia-induced neuronal damage when exposure occurs at the peak of brain development. Oligodendrocytes are responsible for myelination of axons and, as such, are crucially important for normal neuronal development and function. Their vulnerability to anaesthesia-induced apoptotic degeneration coincides with the critical time of myelination, thus suggesting that anaesthesia could be causing damage to developing neurons not only by triggering their apoptotic death but also by disturbing timely axonal myelination. Although the focus of the present study was not on long-term behavioural and cognitive sequelae, recent evidence suggests that a single 5 h exposure to isoflurane, unlike multiple exposures (a total of three times), of infant rhesus macaques did not result in motor reflex deficits at 1 month of age and did not lead to an increased anxiety response to a new social environment.24Coleman K Robertson ND Dissen GA et al.Isoflurane anesthesia has long-term consequences on motor and behavioral development in infant rhesus macaques.Anesthesiology. 2017; 126: 74-84Crossref PubMed Scopus (107) Google Scholar Furthermore, unlike repeated exposures, a single exposure of 5 h did not result in affiliative or appeasement behaviour at 12 months of age. These early repeated exposures to isoflurane result in long-lasting and detrimental effects on socioemotional development.24Coleman K Robertson ND Dissen GA et al.Isoflurane anesthesia has long-term consequences on motor and behavioral development in infant rhesus macaques.Anesthesiology. 2017; 126: 74-84Crossref PubMed Scopus (107) Google Scholar The relevance of a single 3 h exposure to long-term behavioural outcomes remains to be examined using a wide array of sensitive behavioural approaches. Elsewhere in this issue of the Bristish Journal of Anaesthesia, Alvarado and colleagues27Alvardo MC Murphy KL Baxter MG Visual recognition memory is impaired in rhesus monkeys repeatedly exposed to sevoflurane in infancy.Br J Anaesth. 2017; (10.1093/bja/aex270)Abstract Full Text Full Text PDF Scopus (65) Google Scholar show that repeated exposures to sevoflurane also lead to neurocognitive deficits in macaques. With such a large body of animal evidence, including this recent study, the question of the clinical relevance of such convincing scientific evidence gathered from several mammalian species of different phylogenic complexity remains. Is it possible that findings reported in >300 original manuscripts by numerous groups throughout the last 25 yr are not applicable to human children? The scientific community has spent a great deal of time, resources, and intellectual acumen not only on describing and understanding the phenomenon of anaesthesia-induced developmental neurotoxicity but, rightfully so, on challenging and scrutinizing every aspect of it. In the true spirit of scientific rigour and inquiry, we search for weaknesses, shortcomings, and logical explanations for the observed phenomena. As the medical community is faced with the warning issued by the FDA, we continue to struggle with the best and most responsible course of action. As we move from doubting the relevance of an extensive body of research to perhaps accepting that our clinically used general anaesthetics might not be as innocuous as we once believed, we are reminded of Kuhn's,28Kuhn T The Structure of Scientific Revolutions. 1st ed. University of Chicago Press, Chicago, IL1962Google Scholar in which he described three stages of a paradigm shift in science: (i) first it is ridiculed; (ii) then it is resisted; and (iii) finally, it is considered self-evident. The recent warning by the FDA may be challenging us to re-evaluate our position in this particular paradigm shift. Ultimately, we must leave it up to the scientific community and clinicians to decide the best course of action. Further studies of non-human primates will continue to help us evaluate the complex issues posed to our daily anaesthesia practice in very young children. V.J.-T. is an Established Investigator of the American Heart Association. V.J.-T. would like to thank Dr James Bennett for introducing her to The Structure of Scientific Revolutions by Thomas Kuhn. V.J.-T. is on the Associate Editorial Boards of the British Journal of Anaesthesia, Anesthesiology, and the Journal of Neurosurgical Anesthesiology. National Institutes of Health (NIH)/National Institute of Child Health and Human Development (NICHD)(R0144517, R0144517-S and R21 HD080281; NIH/National Institue of General Medical Science (NIGMS) (R01 GM118197); NIH John E. Fogarty Award (007423-128322); March of Dimes National Award, USA (to V.J.-T.)." @default.
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• W2763669460 title "Anaesthesia-induced developmental neurotoxicity: reality or fiction?" @default.
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