Burst suppression-MAC and burst suppression-CP50 as measures of cerebral effects of anaesthetics

Pilge, Stefanie; Jordan, Denis; Kreuzer, Matthias; Kochs, Eberhard; Schneider, Gerhard

doi:10.1093/bja/aeu016

Cited by 54 publications

(32 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This contrasts with data from neonatal rodent studies, which suggest that isoflurane and sevoflurane increase neuronal cortical activity leading to seizure like EEG patterns [11, 69]. In both our piglet and previous macaque studies [1–3] there is considerably less cell death than that seen in rodents following a similar exposure to isoflurane, which may be partly explained by the absence of seizure activity.…”

Section: Discussioncontrasting

confidence: 99%

Isoflurane Exposure Induces Cell Death, Microglial Activation and Modifies the Expression of Genes Supporting Neurodevelopment and Cognitive Function in the Male Newborn Piglet Brain

et al. 2016

View full text Add to dashboard Cite

Exposure of the brain to general anesthesia during early infancy may adversely affect its neural and cognitive development. The mechanisms mediating this are complex, incompletely understood and may be sexually dimorphic, but include developmentally inappropriate apoptosis, inflammation and a disruption to cognitively salient gene expression. We investigated the effects of a 6h isoflurane exposure on cell death, microglial activation and gene expression in the male neonatal piglet brain. Piglets (n = 6) were randomised to: (i) naive controls or (ii) 6h isoflurane. Cell death (TUNEL and caspase-3) and microglial activation were recorded in 7 brain regions. Changes in gene expression (microarray and qPCR) were assessed in the cingulate cortex. Electroencephalography (EEG) was recorded throughout. Isoflurane anesthesia induced significant increases in cell death in the cingulate and insular cortices, caudate nucleus, thalamus, putamen, internal capsule, periventricular white matter and hippocampus. Dying cells included both neurons and oligodendrocytes. Significantly, microglial activation was observed in the insula, pyriform, hippocampus, internal capsule, caudate and thalamus. Isoflurane induced significant disruption to the expression of 79 gene transcripts, of these 26 are important for the control of transcription and 23 are important for the mediation of neural plasticity, memory formation and recall. Our observations confirm that isoflurane increases apoptosis and inflammatory responses in the neonatal piglet brain but also suggests novel additional mechanisms by which isoflurane may induce adverse neural and cognitive development by disrupting the expression of genes mediating activity dependent development of neural circuits, the predictive adaptive responses of the brain, memory formation and recall.

show abstract

Section: Discussioncontrasting

confidence: 99%

Isoflurane Exposure Induces Cell Death, Microglial Activation and Modifies the Expression of Genes Supporting Neurodevelopment and Cognitive Function in the Male Newborn Piglet Brain

et al. 2016

View full text Add to dashboard Cite

show abstract

“…In humans, low doses of sevoflurane increase beta/low gamma power in the frontal EEG (Gugino et al, 2001; Brown et al, 2010), and higher doses increase slow-delta and alpha power (Akeju et al, 2014; Purdon et al, 2015) and induce burst suppression (Pilge et al, 2014). Loss of consciousness in humans under sevoflurane and propofol anesthesia is associated with an increase in slow-delta power in the frontal EEG (Gugino et al, 2001; Purdon et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane Induces Coherent Slow-Delta Oscillations in Rats

Guidera

Taylor

Lee

et al. 2017

Front. Neural Circuits

View full text Add to dashboard Cite

Although general anesthetics are routinely administered to surgical patients to induce loss of consciousness, the mechanisms underlying anesthetic-induced unconsciousness are not fully understood. In rats, we characterized changes in the extradural EEG and intracranial local field potentials (LFPs) within the prefrontal cortex (PFC), parietal cortex (PC), and central thalamus (CT) in response to progressively higher doses of the inhaled anesthetic sevoflurane. During induction with a low dose of sevoflurane, beta/low gamma (12–40 Hz) power increased in the frontal EEG and PFC, PC and CT LFPs, and PFC–CT and PFC–PFC LFP beta/low gamma coherence increased. Loss of movement (LOM) coincided with an abrupt decrease in beta/low gamma PFC–CT LFP coherence. Following LOM, cortically coherent slow-delta (0.1–4 Hz) oscillations were observed in the frontal EEG and PFC, PC and CT LFPs. At higher doses of sevoflurane sufficient to induce loss of the righting reflex, coherent slow-delta oscillations were dominant in the frontal EEG and PFC, PC and CT LFPs. Dynamics similar to those observed during induction were observed as animals emerged from sevoflurane anesthesia. We conclude that the rat is a useful animal model for sevoflurane-induced EEG oscillations in humans, and that coherent slow-delta oscillations are a correlate of sevoflurane-induced behavioral arrest and loss of righting in rats.

show abstract

“…On this basis a variety of efforts have been made to estimate the concentration dependent emergence of burst suppression during anesthesia. It has been found that during sole agent isoflurane anesthesia, the burst suppression pattern can emerge at end-tidal concentrations as low as 1.2% (Hoffman and Edelman, 1995; Pilge et al, 2014), i.e., aqueous concentrations of ≃ 0.25 mM at 37°C. However when arterial blood concentrations of isoflurane have been measured the onset of burst suppression has been reported for levels as low as 34.9 μg/ml or ≃ 0.19 mM (Loomis et al, 1986) – close to the value at which we observed the onset of burst suppression in our model.…”

Section: Discussionmentioning

confidence: 99%

Emergence of spatially heterogeneous burst suppression in a neural field model of electrocortical activity

Bojak

Stoyanov

Liley

2015

Front. Syst. Neurosci.

View full text Add to dashboard Cite

Burst suppression in the electroencephalogram (EEG) is a well-described phenomenon that occurs during deep anesthesia, as well as in a variety of congenital and acquired brain insults. Classically it is thought of as spatially synchronous, quasi-periodic bursts of high amplitude EEG separated by low amplitude activity. However, its characterization as a “global brain state” has been challenged by recent results obtained with intracranial electrocortigraphy. Not only does it appear that burst suppression activity is highly asynchronous across cortex, but also that it may occur in isolated regions of circumscribed spatial extent. Here we outline a realistic neural field model for burst suppression by adding a slow process of synaptic resource depletion and recovery, which is able to reproduce qualitatively the empirically observed features during general anesthesia at the whole cortex level. Simulations reveal heterogeneous bursting over the model cortex and complex spatiotemporal dynamics during simulated anesthetic action, and provide forward predictions of neuroimaging signals for subsequent empirical comparisons and more detailed characterization. Because burst suppression corresponds to a dynamical end-point of brain activity, theoretically accounting for its spatiotemporal emergence will vitally contribute to efforts aimed at clarifying whether a common physiological trajectory is induced by the actions of general anesthetic agents. We have taken a first step in this direction by showing that a neural field model can qualitatively match recent experimental data that indicate spatial differentiation of burst suppression activity across cortex.

show abstract

Burst suppression-MAC and burst suppression-CP50 as measures of cerebral effects of anaesthetics

Cited by 54 publications

References 51 publications

Isoflurane Exposure Induces Cell Death, Microglial Activation and Modifies the Expression of Genes Supporting Neurodevelopment and Cognitive Function in the Male Newborn Piglet Brain

Isoflurane Exposure Induces Cell Death, Microglial Activation and Modifies the Expression of Genes Supporting Neurodevelopment and Cognitive Function in the Male Newborn Piglet Brain

Sevoflurane Induces Coherent Slow-Delta Oscillations in Rats

Emergence of spatially heterogeneous burst suppression in a neural field model of electrocortical activity

Contact Info

Product

Resources

About