How the cortico-thalamic feedback affects the EEG power spectrum over frontal and occipital regions during propofol-induced sedation

Abstract

Increasing concentrations of the anaesthetic agent propofol initially induces sedation before achieving full general anaesthesia. During this state of anaesthesia, the observed specific changes in electroencephalographic (EEG) rhythms comprise increased activity in the δ- (0.5-4 Hz) and α- (8-13 Hz) frequency bands over the frontal region, but increased δ- and decreased α-activity over the occipital region. It is known that the cortex, the thalamus, and the thalamo-cortical feedback loop contribute to some degree to the propofol-induced changes in the EEG power spectrum. However the precise role of each structure to the dynamics of the EEG is unknown. In this paper we apply a thalamo-cortical neuronal population model to reproduce the power spectrum changes in EEG during propofol-induced anaesthesia sedation. The model reproduces the power spectrum features observed experimentally both in frontal and occipital electrodes. Moreover, a detailed analysis of the model indicates the importance of multiple resting states in brain activity. The work suggests that the α-activity originates from the cortico-thalamic relay interaction, whereas the emergence of δ-activity results from the full cortico-reticular-relay-cortical feedback loop with a prominent enforced thalamic reticular-relay interaction. This model suggests an important role for synaptic GABAergic receptors at relay neurons and, more generally, for the thalamus in the generation of both the δ- and the α- EEG patterns that are seen during propofol anaesthesia sedation.

Lack of Responsiveness during the Onset and Offset of Sevoflurane Anesthesia Is Associated with Decreased Awake-Alpha Oscillation Power

“…Studies of anesthesia-induced neural oscillations provide a framework that currently guide investigations of the neural circuit mechanisms of anesthesia-induced altered arousal states (McCarthy et al, 2008; Ching et al, 2010; Murphy et al, 2011; Supp et al, 2011; Boly et al, 2012; Vijayan and Kopell, 2012; Lee et al, 2013; Ní Mhuircheartaigh et al, 2013; Purdon et al, 2013; Vijayan et al, 2013; Hashemi et al, 2015). These studies suggest that by disrupting the oscillatory dynamics that are associated with arousal states, anesthesia-induced oscillations are a putative mechanism through which anesthetic drugs produce altered states of arousal (McCarthy et al, 2008; Ching et al, 2010; Murphy et al, 2011; Boly et al, 2012; Vijayan and Kopell, 2012; Lee et al, 2013; Ní Mhuircheartaigh et al, 2013; Purdon et al, 2013; Vijayan et al, 2013; Hashemi et al, 2015). Further, each anesthetic drug class has been shown to produce distinct neural oscillations that can be related to the drug’s mechanism of action (Purdon et al, 2015).…”

“…Extensive work has been done to relate the neural oscillations induced by propofol (2,6-di-isopropylphenol), an intravenous anesthetic that primarily potentiates γ-Aminobutyric acid A (GABA A ) receptors, to its neural circuit mechanisms (Ching et al, 2010; Murphy et al, 2011; Supp et al, 2011; Boly et al, 2012; Lewis et al, 2012; Purdon et al, 2013; Vijayan et al, 2013; Hashemi et al, 2015). Beta (13–33 Hz) oscillations are associated with propofol sedation (Purdon et al, 2013, 2015), while large amplitude slow-delta (0.1–4 Hz) and coherent frontal alpha (8–12 Hz) are associated with propofol GA (Murphy et al, 2011; Lewis et al, 2012; Ní Mhuircheartaigh et al, 2013; Purdon et al, 2013; Akeju et al, 2014a,b; Hashemi et al, 2015).…”

“…Beta (13–33 Hz) oscillations are associated with propofol sedation (Purdon et al, 2013, 2015), while large amplitude slow-delta (0.1–4 Hz) and coherent frontal alpha (8–12 Hz) are associated with propofol GA (Murphy et al, 2011; Lewis et al, 2012; Ní Mhuircheartaigh et al, 2013; Purdon et al, 2013; Akeju et al, 2014a,b; Hashemi et al, 2015). Propofol beta oscillations likely result from a modest increase in GABA A decay-time and conductance, which causes low threshold spiking (LTS) interneuron antisynchrony that patterns pyramidal cell spiking into a beta rhythm (McCarthy et al, 2008).…”

“…Additional increases in GABA A decay-time and conductance results in cortical alpha oscillatory dynamics and enhanced rebound spiking of thalamic relay cells, which strengthen the intrinsic alpha oscillatory dynamics of the thalamus (Ching et al, 2010; Vijayan and Kopell, 2012; Vijayan et al, 2013). The net result is reciprocal thalamic-cortical alpha oscillation coupling (Ching et al, 2010; Vijayan and Kopell, 2012; Vijayan et al, 2013; Hashemi et al, 2015). Slow oscillations may result from decreased excitatory cortical inputs from brainstem arousal nuclei, and from simultaneous drug action in the thalamus and cortex (Brown et al, 2010; Hashemi et al, 2015).…”

“…The net result is reciprocal thalamic-cortical alpha oscillation coupling (Ching et al, 2010; Vijayan and Kopell, 2012; Vijayan et al, 2013; Hashemi et al, 2015). Slow oscillations may result from decreased excitatory cortical inputs from brainstem arousal nuclei, and from simultaneous drug action in the thalamus and cortex (Brown et al, 2010; Hashemi et al, 2015). …”