1. Human neural correlates of sevoflurane-induced unconsciousness
B.J.A. Palanca, M.S. Avidan, G.A. Mashour 
British Journal of Anaesthesia 
Volume 119, Issue 4, Pages (October 2017)
DOI: /bja/aex244
Copyright © 2017 The Author(s) Terms and Conditions

2. Fig 1
Frontal electroencephalographic patterns during sevoflurane general anaesthesia. (A and B) Simultaneous frontal EEG traces acquired from a single patient during 1 MAC sevoflurane general anesthesia. (A) Red dashed vertical lines highlight the interhemispheric phase alignment of oscillatory activity in the alpha frequency band (8–13 Hz) of these two signals, despite a fluctuating baseline. (B) In contrast, the slow oscillations in the delta frequency band (0.5–4 Hz) appear to be out of phase for the two hemispheres (peaks indicated by white arrows). EEG acquired using bipolar montages F7-Fp1 (EEG1) or F8-Fp2 (EEG2) are displayed at 25 mm/sec (A) or 50 mm/sec (B). (C) Population average power spectrogram of EEG acquired during sevoflurane general anaesthesia shows consistent power over time in the alpha, theta (4-8 Hz), and delta frequency bands. (D) Population average power coherogram of EEG recorded during sevoflurane general anaesthesia illustrates greater consistency within the alpha band compared with theta and delta bands. (E) Single patient frontal EEG power spectrogram during the transition from wakefulness, through sedation, sevoflurane-induced unconsciousness, and recovery. Beta band (13–30 Hz) power emerges after drug initiation (first white vertical dashed lines) and during sedation (red arrowhead). With loss of responsiveness (Blue arrow), beta power persists without any emergence in alpha power. EEG were acquired using F7 and a Hjorth reference. These figures were modified from Akeju and colleagues (C-D) and Kaskinoro and colleagues (E). Reproduced with permissions, Wolters Kluwer Health, Inc. and John Wiley and Sons.
British Journal of Anaesthesia  , DOI: ( /bja/aex244)
Copyright © 2017 The Author(s) Terms and Conditions

3. Fig 2
Sevoflurane-induced unconsciousness and altered cross-frequency and cross-regional coupling. (A) Significant parietal cross-frequency phase-amplitude coupling (Modulation Index) is reduced after induction of unresponsiveness with sevoflurane (transition from the period of sedation, S to unconsciousness, U). The phase of slow delta (0.1–1 Hz) modulates the amplitude of alpha (8–13 Hz) in parietal EEG during wakefulness (W), sedation and recovery (R). This relationship is observed in parietal EEG during unconsciousness or in frontal EEG during any epoch. (B) Alpha (8–13 Hz) phase lag between frontal and posterior cortical regions is present at baseline and reversibly attenuated during sevoflurane unconsciousness. Frontal-parietal (F-P), frontal-temporal (F-T), and frontal-occipital (F-O) phase lag index is a measure of the timing phase difference in EEG signals of corresponding cortical lobes. (C) Directed connectivity between frontal and parietal regions is disrupted, following loss of consciousness (LOC) induced by sevoflurane. Normalized symbolic transfer entropy, a surrogate measure of information flow, is preferentially altered for feedback and not feedforward interactions. These figures were modified from Blain-Moraes and colleagues (A-B) and Lee et al., (C). Reproduced with permissions, Wolters Kluwer Health, Inc.
British Journal of Anaesthesia  , DOI: ( /bja/aex244)
Copyright © 2017 The Author(s) Terms and Conditions

4. Fig 3
Distributed alterations in cerebral blood flow and functional connectivity are localized to cortical and thalamic regions during sevoflurane-induced unconsciousness. (A) Upper panel: Cortical and subcortical regions demonstrate correlated changes in cerebral blood flow (CBF) and Bispectral index (BIS) values during positron emission tomography (PET) across the range of 0, 2, 3, and 4% sevoflurane. Superior, lateral, and medial surface registrations show localization mainly to posterior medial and lateral parietal regions. Lower panel: Similarly, another processed EEG measure, spectral entropy, covaries with CBF to lateral parietal and midline frontal regions during sevoflurane general anesthesia. (B) Resting-state functional connectivity magnetic resonance images showing sevoflurane-induced weakening of correlated activity following loss of response to noxious stimulation. At 1.2% sevoflurane, correlations are weaker between medial prefrontal cortex and a midline posterior parietal cortical region of the default mode network (DMN, Upper panel, left), known as the posterior cingulate cortex. Correlations among frontal and posterior regions of the ventral attention network (VAN, Upper panel, right) are also disrupted. Altered thalamocortical connectivity during inhalation of 1.2% sevoflurane is also observed (Thalamus, Lower panel). (C) Reduced thalamocortical resting-state functional connectivity at 2%, 3%, or burst suppression during sevoflurane general anaesthesia. Dark voxels represent weakening of connectivity relative to baseline wakefulness. While mainly frontoparietal (DMN) connectivity is attenuated at 2% sevoflurane, diffuse changes are observed at higher doses. These figures were modified from Kaisti and colleagues (A, Upper panel), Maksimow et al., (A, Lower panel), Palanca and colleagues (B, Upper and lower panels), Ranft and colleagues (C, Upper and lower panels). Reproduced with permission, Wolters Kluwer Health, Inc. and John Wiley and Sons.
British Journal of Anaesthesia  , DOI: ( /bja/aex244)
Copyright © 2017 The Author(s) Terms and Conditions