Age-dependent electroencephalogram (EEG) patterns during sevoflurane general anesthesia in infants

Laura Cornelissen, Seong-Eun Kim, Patrick L Purdon, Emery N Brown, Charles B Berde, Laura Cornelissen, Seong-Eun Kim, Patrick L Purdon, Emery N Brown, Charles B Berde

Abstract

Electroencephalogram (EEG) approaches may provide important information about developmental changes in brain-state dynamics during general anesthesia. We used multi-electrode EEG, analyzed with multitaper spectral methods and video recording of body movement to characterize the spatio-temporal dynamics of brain activity in 36 infants 0-6 months old when awake, and during maintenance of and emergence from sevoflurane general anesthesia. During maintenance: (1) slow-delta oscillations were present in all ages; (2) theta and alpha oscillations emerged around 4 months; (3) unlike adults, all infants lacked frontal alpha predominance and coherence. Alpha power was greatest during maintenance, compared to awake and emergence in infants at 4-6 months. During emergence, theta and alpha power decreased with decreasing sevoflurane concentration in infants at 4-6 months. These EEG dynamic differences are likely due to developmental factors including regional differences in synaptogenesis, glucose metabolism, and myelination across the cortex. We demonstrate the need to apply age-adjusted analytic approaches to develop neurophysiologic-based strategies for pediatric anesthetic state monitoring.

Keywords: EEG; alpha; anesthesia; computational biology; development; human; infant; neuroscience; sevoflurane; systems biology.

Conflict of interest statement

PLP: PLP has patents pending on brain monitoring during general anesthesia and sedation, and a patent licensing agreement with Masimo Corporation. Application Numbers: 20150080754, 20150011907, 20140323898, 20140323897, 20140316218, 20140316217, 20140187973, 20140180160, 20080306397.

ENB: ENB has patents pending on brain monitoring during general anesthesia and sedation, and a patent licensing agreement with Masimo Corporation. Application Numbers: 20150080754, 20150011907, 20140323898, 20140323897, 20140316218, 20140316217, 20140187973, 20140180160. ENB is a Reviewing Editor for eLife.

The other authors declare that no competing interests exist.

Figures

Figure 1.. Experiment design.
Figure 1.. Experiment design.
(A) Experiment timeline: schematic time-course of end-tidal sevoflurane concentration during the awake phase, induction, MOSSA (Maintenance of Surgical State of Anesthesia), and emergence phases of general anesthesia. Electroencephalogram (EEG) data from individual recording electrodes were analyzed post hoc for the awake brain state prior to anesthesia (shown in green), and two phases of general anesthesia (i) MOSSA (shown in red), and (ii) emergence from general anesthesia (shown in blue). (B) EEG montage used (modified international 10/20 electrode placement system). DOI:http://dx.doi.org/10.7554/eLife.06513.003
Figure 2.. Study profile.
Figure 2.. Study profile.
Parents of 51 infants were approached and 36 consented. Five EEG recordings were excluded from the final analysis because of technical failures (n = 4) or a clinical event (n = 1; local anesthetic toxicity prior to surgical incision). For MOSSA analysis, data are presented from 30 EEG recordings (0–3 months, n = 11; 4–6 months, n = 19); for awake analysis, 19 infants were included (0–3 months, n = 7; 4–6 months, n = 12); and for emergence from general anesthesia analysis, 24 infants were included (0–3 months, n = 8; 4–6 months, n = 16). DOI:http://dx.doi.org/10.7554/eLife.06513.005
Figure 3.. Frontal spectrograms during MOSSA.
Figure 3.. Frontal spectrograms during MOSSA.
Individual infant EEG spectral power for frequencies from 0 to 30 Hz (left hand axis) during a 5-min period of MOSSA. Frontal spectrograms for infants at 0–3 months of age are shown for (A) individual infants and (B) group-median average. Frontal spectrograms for infants at 4–6 months of age are shown for (C) individual infants and (D) group-median average. F7 used with nearest neighbor Laplacian referencing. DOI:http://dx.doi.org/10.7554/eLife.06513.006
Figure 4.. Frontal EEG power is greater…
Figure 4.. Frontal EEG power is greater in infants 4–6 months of age across all frequencies during MOSSA.
(A) Frontal group-median power spectra (solid line, median; shaded area, 25th–75th percentile) across the 0–30 Hz-frequency band showing increased power in infants 4–6 months of age across all frequencies. (B-E) Differences in frontal group-median power spectra presented with 95% CI from bootstrap analysis (pink line, 97.5th percentile; green line, 2.5th percentile) comparing infants at 0–3 month to 4–6 months of age. (B) Power difference in slow and delta frequency range, 0–4 Hz, (C) theta, 4–8 Hz, (D) alpha, 8–12 Hz, and (E) beta, 12–30 Hz. F7 electrode presented using nearest neighbor Laplacian referencing. DOI:http://dx.doi.org/10.7554/eLife.06513.007
Figure 4—figure supplement 1.. Frontal EEG spectral…
Figure 4—figure supplement 1.. Frontal EEG spectral properties in infants anesthetized under a uniform end-tidal sevoflurance concentration (1.8%).
Group-averaged frontal power spectrograms in infants (A) 0–3 months of age, and (B) 4–6 months of age (C) Frontal group-median power spectra (solid line, median; shaded area, 25th–75th percentile) across 0–30 Hz frequencies. (D–G) Differences in group-averaged frontal power spectra presented with 95% CI from bootstrap analysis (pink line, 97.5th percentile; green line, 2.5th percentile) comparing infants at 0–3 months to infants at 4–6 months of age. F7 electrode presented using nearest neighbour Laplacian referencing. etSEVO: end-tidal sevoflurance concentration. Epoch size of 30 s is used. DOI:http://dx.doi.org/10.7554/eLife.06513.008
Figure 5.. Spatial distribution of spectral power…
Figure 5.. Spatial distribution of spectral power during MOSSA.
Group-median spectrograms at each recording electrode location across the scalp in infants at (A) 0–3 months (n = 11) and (B) 4–6 months (n = 19). DOI:http://dx.doi.org/10.7554/eLife.06513.009
Figure 6.. Topographic EEG maps of spectral…
Figure 6.. Topographic EEG maps of spectral power for distinct frequency bands during MOSSA.
Topographic EEG maps detailing group-averaged power for each EEG frequency band in infants aged (A) 0–3 months (n = 11) and (B) 4–6 months (n = 19). Slow-wave activity is distributed across the scalp in both postnatal age groups, while alpha activity is present to a greater degree in infants 4–6 months postnatal age. Legend for A and B is shown by the color bar. DOI:http://dx.doi.org/10.7554/eLife.06513.010
Figure 7.. Frontal predominance of alpha power…
Figure 7.. Frontal predominance of alpha power is low during MOSSA in infants 0–6 months of age.
Frontal group-median power spectra (solid line, median; shaded area, 25th–75th percentile) showing similar EEG power across all frequencies in frontal and occipital channels in infants aged (A) 0–3 months (n = 11) and (B) 4–6 months (n = 19). Differences in frontal group-median power spectra presented with 95% CI from bootstrap analysis (pink line, 97.5th percentile; green line, 2.5th percentile) between frontal and occipital channels during MOSSA in infants aged (C–F) 0–3 months and (G–J) 4–6 months. A small but significant increase in frontal alpha power compared to occipital alpha power begins to emerge at 4–6 months of age. FPz and Oz electrodes presented using nearest neighbor Laplacian referencing. DOI:http://dx.doi.org/10.7554/eLife.06513.011
Figure 8.. Frontal alpha coherence is absent…
Figure 8.. Frontal alpha coherence is absent during MOSSA in infants from 0 to 6 months postnatal age.
Group-averaged frontal spectrograms in infants aged 0–3 months at (A) Left—F7, and (B) Right—F8, and infants aged 4–6 months (C) F7, and (D) F8. Relative group-averaged frontal coherogram (F7–F8) for infants aged (E) 0–3 months and (F) 4–6 months age. (G) Frontal group-median coherence (solid line, median) showed similar coherence across 0.1–30 Hz frequency bands at all postnatal ages. DOI:http://dx.doi.org/10.7554/eLife.06513.012
Figure 9.. Global coherence is low across…
Figure 9.. Global coherence is low across all frequencies during MOSSA in infants from 0 to 6 months of age.
Topographic EEG maps detailing group-averaged global coherence for each EEG frequency band in infants (A) 0–3 months (n = 11) and (B) 4–6 months (n = 19) of age. (C) Group-median global coherence spectra (solid line, median; shaded area, IQR) show similar low coherence across 0–30 Hz frequency bands at all ages during MOSSA. DOI:http://dx.doi.org/10.7554/eLife.06513.013
Figure 10.. Frontal EEG power changes between…
Figure 10.. Frontal EEG power changes between the awake state and MOSSA.
(A) Group-averaged frontal power spectra (solid line, median; shaded area, 25th–75th percentile) show similar EEG power during the awake state (prior to anesthesia) and MOSSA in infants aged 0–3 months across all frequencies (n = 7). (B) Group-averaged frontal power spectra show increased theta, alpha, and gamma oscillations during MOSSA in infants 4–6 months of age (n = 12). Differences in group-averaged frontal power spectra presented with 95% CI from paired bootstrap analysis (pink line, 97.5th percentile; green line, 2.5th percentile) between Awake and MOSSA in infants (C–F) 0–3 months and (G–J) 4–6 months of age. F7 electrode presented using nearest neighbor Laplacian referencing. Epoch size of 11 s is used for awake and MOSSA states. DOI:http://dx.doi.org/10.7554/eLife.06513.014
Figure 10—figure supplement 1.. Frontal EEG spectral…
Figure 10—figure supplement 1.. Frontal EEG spectral properties in awake infants.
Frontal group-median spectrograms in infants (A) 0–3 months, and (B) 4–6 months of age. (C) Frontal group-median power spectra (solid line, median; shaded area, 25th–75th percentile) across 0–30 Hz frequencies. (D–G) Differences in frontal group-median power spectra presented wtih 95% CI from bootstrap analysis (pink line, 97.5th percentile; green line, 2.5th percentile) comparing infants aged 0–3 months to infants 4–6 months of age. F7 electrode presented using nearest neighbor Laplacian referencing. Epoch size of 11 s is used. DOI:http://dx.doi.org/10.7554/eLife.06513.015
Figure 11.. End-tidal sevoflurane concentration associated spatial…
Figure 11.. End-tidal sevoflurane concentration associated spatial EEG power and body movement during emergence from sevoflurane general anesthesia.
(A) End-tidal sevoflurane concentration increments from MOSSA to emergence from general anesthesia for infants 0–3 months (n = 8), and (B) 4–6 months of age (n = 16), and (C) the corresponding percentage of infants who displayed gross body movement MOSSA. DOI:http://dx.doi.org/10.7554/eLife.06513.016
Figure 12.. Frontal EEG power changes between…
Figure 12.. Frontal EEG power changes between MOSSA and body movement.
(A) Frontal group-median power spectra (solid line, median; shaded area, 25th–75th percentile) show similar EEG power during MOSSA and after first body movement in infants aged 0–3 months across all frequencies. (B) Frontal group-median power spectra show increased theta and alpha oscillations during MOSSA in infants aged 4–6 months. Differences in frontal group-median power spectra presented with 95% CI from bootstrap analysis (pink line, 97.5th percentile; green line, 2.5th percentile) between MOSSA and emergence after first body movement in infants (C–F) 0–3 months and (G–J) 4–6 months of age. F7 electrode presented using nearest neighbor Laplacian referencing. DOI:http://dx.doi.org/10.7554/eLife.06513.017
Author response image 1.. Onset of body…
Author response image 1.. Onset of body movement is not associated with changes in respiration rate.
(A) Mean respiration rate (breaths per min) and (B) heart rate were calculated for all infants over a 20 minute period: 10-min prior to first visible body movement, and 10min after. Time 0 (grey dashed line) indicates where first body movement was observed. Data represented as mean (+/- SD). DOI:http://dx.doi.org/10.7554/eLife.06513.024
Author response image 2
Author response image 2
Midline EEG spectral power is lower compared to temporal regions during MOSSA in all infants.Temporal (T7) electrode comparisons are shown for (A-E) vs. frontal midline (FPz); (F-J ), vertex (Cz); (K-P), occipital midline (Oz); and (Q- U) lateral temporal area (T8). For each electrode pair, a schematic of electrode locations ( A, F, K, Q) are shown with the respective analysis of power spectra in infants aged 0-3 months ( B, G, L, R), and 4-6 months (C, H, M, S), and 95% CI, paired bootstrap analysis for infants 0-3 months (D, I, O, T), and 4-6 months of age (E, J, P, U). DOI:http://dx.doi.org/10.7554/eLife.06513.026

References

    1. Akeju O, Loggia ML, Catana C, Pavone KJ, Vazquez R, Rhee J, Contreras Ramirez V, Chonde DB, Izquierdo-Garcia D, Arabasz G, Hsu S, Habeeb K, Hooker JM, Napadow V, Brown EN, Purdon PL. Disruption of thalamic functional connectivity is a neural correlate of dexmedetomidine-induced unconsciousness. eLife. 2014a;4:e04499. doi: 10.7554/eLife.04499.
    1. Akeju O, Pavone KJ, Westover MB, Vazquez R, Prerau MJ, Harrell PG, Hartnack KE, Rhee J, Sampson AL, Habeeb K, Gao L, Pierce ET, Walsh JL, Brown EN, Purdon PL. A comparison of propofol- and dexmedetomidine-induced electroencephalogram dynamics using spectral and coherence analysis. Anesthesiology. 2014b;121:978–989. doi: 10.1097/ALN.0000000000000419.
    1. Akeju O, Westover MB, Pavone KJ, Sampson AL, Hartnack KE, Brown EN, Purdon PL. Effects of sevoflurane and propofol on frontal electroencephalogram power and coherence. Anesthesiology. 2014c;121:990–998. doi: 10.1097/ALN.0000000000000436.
    1. Bokil H, Andrews P, Kulkarni JE, Mehta S, Mitra PP. Chronux: a platform for analyzing neural signals. Journal of Neuroscience Methods. 2010;192:146–151. doi: 10.1016/j.jneumeth.2010.06.020.
    1. Boly M, Moran R, Murphy M, Boveroux P, Bruno MA, Noirhomme Q, Ledoux D, Bonhomme V, Brichant JF, Tononi G, Laureys S, Friston K. Connectivity changes underlying spectral EEG changes during propofol-induced loss of consciousness. The Journal of Neuroscience. 2012;32:7082–7090. doi: 10.1523/JNEUROSCI.3769-11.2012.
    1. Boveroux P, Vanhaudenhuyse A, Bruno MA, Noirhomme Q, Lauwick S, Luxen A, Degueldre C, Plenevaux A, Schnakers C, Phillips C, Brichant JF, Bonhomme V, Maquet P, Greicius MD, Laureys S, Boly M. Breakdown of within- and between-network resting state functional magnetic resonance imaging connectivity during propofol-induced loss of consciousness. Anesthesiology. 2010;113:1038–1053. doi: 10.1097/ALN.0b013e3181f697f5.
    1. Breshears JD, Roland JL, Sharma M, Gaona CM, Freudenburg ZV, Tempelhoff R, Avidan MS, Leuthardt EC. Stable and dynamic cortical electrophysiology of induction and emergence with propofol anesthesia. Proceedings of the National Academy of Sciences of USA. 2010;107:21170–21175. doi: 10.1073/pnas.1011949107.
    1. Brody BA, Kinney HC, Kloman AS, Gilles FH. Sequence of central nervous system myelination in human Infancy. I. an autopsy atudy of myelination. Journal of Neuropathology and Experimental Neurology. 1987;46:283–301. doi: 10.1097/00005072-198705000-00005.
    1. Brown EN, Lydic R, Schiff ND. General anesthesia, sleep, and coma. The New England Journal of Medicine. 2010;363:2638–2650. doi: 10.1056/NEJMra0808281.
    1. Brown EN, Purdon PL, Van Dort CJ. General anesthesia and altered states of arousal: a systems neuroscience analysis. Annual Review of Neuroscience. 2011;34:601–628. doi: 10.1146/annurev-neuro-060909-153200.
    1. Brown EN, Solt K, Purdon PL, Akeju O. Miller's anesthesia. 8th Edition. Volume 1. Cambridge: Elsevier Health Sciences; 2015. Monitoring brain state during general anesthesia and sedation; p. 50.
    1. Casali AG, Gosseries O, Rosanova M, Boly M, Sarasso S, Casali KR, Casarotto S, Bruno MA, Laureys S, Tononi G, Massimini M. A theoretically based index of consciousness independent of sensory processing and behavior. Science Translational Medicine. 2013;5:198ra105. doi: 10.1126/scitranslmed.3006294.
    1. Catts VS, Fung SJ, Long LE, Joshi D, Vercammen A, Allen KM, Fillman SG, Rothmond DA, Sinclair D, Tiwari Y, Tsai SY, Weickert TW, Shannon Weickert C. Rethinking schizophrenia in the context of normal neurodevelopment. Frontiers in Cellular Neuroscience. 2013;7:60. doi: 10.3389/fncel.2013.00060.
    1. Ching S, Brown EN. Modeling the dynamical effects of anesthesia on brain circuits. Current Opinion in Neurobiology. 2014;25:116–122. doi: 10.1016/j.conb.2013.12.011.
    1. Ching S, Cimenser A, Purdon PL, Brown EN, Kopell NJ. Thalamocortical model for a propofol-induced alpha-rhythm associated with loss of consciousness. Proceedings of the National Academy of Sciences of USA. 2010;107:22665–22670. doi: 10.1073/pnas.1017069108.
    1. Chugani HT, Phelps ME. Maturational changes in cerebral function in infants determined by 18FDG positron emission tomography. Science. 1986;231:840–843. doi: 10.1126/science.3945811.
    1. Chugani HT, Phelps ME, Mazziotta JC. Positron emission tomography study of human brain functional development. Annals of Neurology. 1987;22:487–497. doi: 10.1002/ana.410220408.
    1. Cimenser A, Purdon PL, Pierce ET, Walsh JL, Salazar-Gomez AF, Harrell PG, Tavares-Stoeckel C, Habeeb K, Brown EN. Tracking brain states under general anesthesia by using global coherence analysis. Proceedings of the National Academy of Sciences of USA. 2011;108:8832–8837. doi: 10.1073/pnas.1017041108.
    1. Constant I, Sabourdin N. The EEG signal: a window on the cortical brain activity. Paediatric Anaesthesia. 2012;22:539–552. doi: 10.1111/j.1460-9592.2012.03883.x.
    1. Davidson AJ. Monitoring the anaesthetic depth in children—an update. Current Opinion in Anaesthesiology. 2007;20:236–243. doi: 10.1097/ACO.0b013e3280c60c66.
    1. Davidson AJ, Sale SM, Wong C, McKeever S, Sheppard S, Chan Z, Williams C. The electroencephalograph during anesthesia and emergence in infants and children. Paediatric Anaesthesia. 2008;18:60–70. doi: 10.1111/j.1460-9592.2007.02359.x.
    1. Dehorter N, Vinay L, Hammond C, Ben-Ari Y. Timing of developmental sequences in different brain structures: physiological and pathological implications. The European Journal of Neuroscience. 2012;35:1846–1856. doi: 10.1111/j.1460-9568.2012.08152.x.
    1. Delorme A, Makeig S. EEGLAB: an open source toolbox for analysis of single-trial EEG dynamics including independent component analysis. Journal of Neuroscience Methods. 2004;134:9–21. doi: 10.1016/j.jneumeth.2003.10.009.
    1. Feshchenko VA, Veselis RA, Reinsel RA. Propofol-induced alpha rhythm. Neuropsychobiology. 2004;50:257–266. doi: 10.1159/000079981.
    1. Hayashi K, Shigemi K, Sawa T. Neonatal electroencephalography shows low sensitivity to anesthesia. Neuroscience Letters. 2012;517:87–91. doi: 10.1016/j.neulet.2012.04.028.
    1. Hensch T. Critical period regulation. Annual Review of Neuroscience. 2004;27:549–579. doi: 10.1146/annurev.neuro.27.070203.144327.
    1. Huttenlocher PR, de Courten C, Garey LJ, Van der Loos H. Synaptogenesis in human visual cortex—evidence for synapse elimination during normal development. Neuroscience Letters. 1982;33:247–252. doi: 10.1016/0304-394090379-2.
    1. Huttenlocher PR, Dabholkar AS. Regional differences in synaptogenesis in human cerebral cortex. The Journal of Comparative Neurology. 1997;387:167–178. doi: 10.1002/(SICI)1096-9861(19971020)387:2<167::AID-CNE1>;2-Z.
    1. Jevtovic-Todorovic V, Absalom AR, Blomgren K, Brambrink A, Crosby G, Culley DJ, Fiskum G, Giffard RG, Herold KF, Loepke AW, Ma D, Orser BA, Planel E, Slikker W, Jr, Soriano SG, Stratmann G, Vutskits L, Xie Z, Hemmings HC., Jr Anaesthetic neurotoxicity and neuroplasticity: an expert group report and statement based on the BJA Salzburg Seminar. British Journal of Anaesthesia. 2013;111:143–151. doi: 10.1093/bja/aet177.
    1. Johnson MH. Functional brain development in humans. Nature Reviews Neuroscience. 2001;2:475–483. doi: 10.1038/35081509.
    1. Kanold PO, Luhmann HJ. The subplate and early cortical circuits. Annual Review of Neuroscience. 2010;33:23–48. doi: 10.1146/annurev-neuro-060909-153244.
    1. Kinnala A, Suhonen-Polvi H, Aärimaa T, Kero P, Korvenranta H, Ruotsalainen U, Bergman J, Haaparanta M, Solin O, Nuutila P, Wegelius U. Cerebral metabolic rate for glucose during the first six months of life: An FDG positron emission tomography study. Archives of Disease in Childhood. Fetal and Neonatal Edition. 1996;74:F153–F157. doi: 10.1136/fn.74.3.F153.
    1. Kinney HC, Brody BA, Kloman AS, Gilles FH. Sequence of central nervous system myelination in human infancy. II. patterns of myelination in autopsied infants. Journal of Neuropathology and Experimental Neurology. 1988;47:217–234. doi: 10.1097/00005072-198805000-00003.
    1. Kirch C, Politis DN. Tft-bootstrap: resampling time series in the frequency domain to obtain replicates in the time domain. The Annals of Statistics. 2011;39:1427–1470. doi: 10.1214/10-AOS868.
    1. Kostović I, Judas M. The development of the subplate and thalamocortical connections in the human foetal brain. Acta Paediatrica. 2010;99:1119–1127. doi: 10.1111/j.1651-2227.2010.01811.x.
    1. Lee U, Ku S, Noh G, Baek S, Choi B, Mashour GA. Disruption of frontal-parietal communication by ketamine, propofol, and sevoflurane. Anesthesiology. 2013;118:1264–1275. doi: 10.1097/ALN.0b013e31829103f5.
    1. Lewis LD, Weiner VS, Mukamel EA, Donoghue JA, Eskandar EN, Madsen JR, Anderson WS, Hochberg LR, Cash SS, Brown EN, Purdon PL. Rapid fragmentation of neuronal networks at the onset of propofol-induced unconsciousness. Proceedings of the National Academy of Sciences of USA. 2012;109:E3377–E3386. doi: 10.1073/pnas.1210907109.
    1. Lin EP, Soriano SG, Loepke AW. Anesthetic neurotoxicity. Anesthesiology Clinics. 2014;32:133–155. doi: 10.1016/j.anclin.2013.10.003.
    1. Liu X, Lauer KK, Ward BD, Li SJ, Hudetz AG. Differential effects of deep sedation with propofol on the specific and nonspecific thalamocortical systems: a functional magnetic resonance imaging study. Anesthesiology. 2013;118:59–69. doi: 10.1097/ALN.0b013e318277a801.
    1. Lo SS, Sobol JB, Mallavaram N, Carson M, Chang C, Grieve PG, Emerson RG, Stark RI, Sun LS. Anesthetic-specific electroencephalographic patterns during emergence from sevoflurane and isoflurane in infants and children. Paediatric Anaesthesia. 2009;19:1157–1165. doi: 10.1111/j.1460-9592.2009.03128.x.
    1. Martuzzi R, Ramani R, Qiu M, Shen X, Papademetris X, Constable RT. A whole-brain voxel based measure of Intrinsic connectivity contrast reveals local changes in tissue connectivity with anesthetic without a priori assumptions on thresholds or regions of interest. Neuroimage. 2011;58:1044–1050. doi: 10.1016/j.neuroimage.2011.06.075.
    1. McCann ME, Soriano SG. General anesthetics in pediatric anesthesia: influences on the developing brain. Current Drug Targets. 2012;13:944–951. doi: 10.2174/138945012800675768.
    1. McKeever S, Johnston L, Davidson AJ. An observational study exploring amplitude-integrated electroencephalogram and spectral edge frequency during paediatric anaesthesia. Anaesthesia and Intensive Care. 2012;40:275–284.
    1. Mhuircheartaigh RN, Rosenorn-Lanng D, Wise R, Jbabdi S, Rogers R, Tracey I. Cortical and subcortical connectivity changes during decreasing levels of consciousness in humans: a functional magnetic resonance imaging study using propofol. The Journal of Neuroscience. 2010;30:9095–9102. doi: 10.1523/JNEUROSCI.5516-09.2010.
    1. Murphy M, Bruno MA, Riedner BA, Boveroux P, Noirhomme Q, Landsness EC, Brichant JF, Phillips C, Massimini M, Laureys S, Tononi G, Boly M. Propofol anesthesia and sleep: a high-density EEG study. Sleep. 2011;34:283–291A.
    1. Ní Mhuircheartaigh R, Warnaby C, Rogers R, Jbabdi S, Tracey I. Slow-wave activity saturation and thalamocortical isolation during propofol anesthesia in humans. Science Translational Medicine. 2013;5:208ra148. doi: 10.1126/scitranslmed.3006007.
    1. Purdon PL, Pierce ET, Mukamel EA, Prerau MJ, Walsh JL, Wong KF, Salazar-Gomez AF, Harrell PG, Sampson AL, Cimenser A, Ching S, Kopell NJ, Tavares-Stoeckel C, Habeeb K, Merhar R, Brown EN. Electroencephalogram signatures of loss and recovery of consciousness from propofol. Proceedings of the National Academy of Sciences of USA. 2013;110:E1142–E1151. doi: 10.1073/pnas.1221180110.
    1. Rabbitts JA, Groenewald CB, Moriarty JP, Flick R. Epidemiology of ambulatory anesthesia for children in the United States: 2006 and 1996. Anesthesia and Analgesia. 2010;111:1011–1015. doi: 10.1213/ANE.0b013e3181ee8479.
    1. Semple BD, Blomgren K, Gimlin K, Ferriero DM, Noble-Haeusslein LJ. Brain development in rodents and humans: identifying benchmarks of maturation and vulnerability to injury across species. Progress in Neurobiology. 2013;106–107:1–16. doi: 10.1016/j.pneurobio.2013.04.001.
    1. Sury MR, Worley A, Boyd SG. Age-related changes in EEG power spectra in infants during sevoflurane wash-out. British Journal of Anaesthesia. 2014;112:686–694. doi: 10.1093/bja/aet409.
    1. Tau GZ, Peterson BS. Normal development of brain circuits. Neuropsychopharmacology. 2010;35:147–168. doi: 10.1038/npp.2009.115.
    1. Vijayan S, Ching S, Purdon PL, Brown EN, Kopell NJ. Thalamocortical mechanisms for the anteriorization of Α rhythms during propofol-induced unconsciousness. The Journal of Neuroscience. 2013;33:11070–11075. doi: 10.1523/JNEUROSCI.5670-12.2013.
    1. Vizuete JA, Pillay S, Ropella KM, Hudetz AG. Graded defragmentation of cortical neuronal firing during recovery of consciousness in rats. Neuroscience. 2014;275:340–351. doi: 10.1016/j.neuroscience.2014.06.018.

Source: PubMed

Sponsorer og samarbejdspartnere

Medicinske tilstande

Narkotikainterventioner

3
Abonner