Loss of consciousness due to propofol

Abstract

In this literary review, a possible mechanism used by propofol and the consequences of this mechanism are discussed. Propofol is able to bring about loss of consciousness by inhibiting the Ih current in hyperpolarization-activated cyclic nucleotide-gated type 2 (HCN2) channels. The inhibition leads to an increase in the hyperpolarization of the thalamocortical neurons, which results in temporally impaired delta oscillations (Ying et al., 2006). This leads to significant phase offsets which result in fragmentation and the isolation of neural networks. Propofol also leads to a breakdown in the basal ganglia-thalamo-cortical (BGTC) loop, which disrupts cortical and subcortical communication. This breakdown is a result of decreases seen in beta band coherence and the phase amplitude coupling (PAC) between subcortical and cortical regions of the loop. The reduction in coupling leads to interrupted communication which contributes to neural network fragmentation (Swann et al., 2016). Although fragmentation is seen, there are instances of increased global connectivity. The default mode network (DMN) increases its connections to structures outside its network during sedation. However, these connections are not representations of efficient global communication. Instead, they lead to a decrease local efficiency resulting in local network deterioration and an overall decrease in efficient global and local network interactions (Stamatakis et al., 2010). Certain characteristics of the transition from consciousness to loss of consciousness were identified. Delta oscillations are significantly more powerful during sedation, and the sharp increase that can be seen in their power is indicative of loss of consciousness (Lewis et al., 2012). Another indicator of loss of consciousness can be seen in frontal EEG channels by way of PAC analysis of alpha power and slow oscillations. Negative trough-max PAC exists at baseline, but switches to positive peak-max PAC during moderate sedation in those who are more sensitive to propofol. An increased propofol sensitivity can be detected at baseline and is represented by a weak alpha network that is not very small-worldly (Chennu et al., 2016). In summary, it is clear that the timing of our neural networks is crucial to consciousness and that it is through temporal modifications that propofol is able to induce its effects