Mechanisms of Anesthetic Emergence: Evidence for Active Reanimation

Abstract

Historically, emergence from anesthesia was believed to progress only through the passive elimination of pharmacologic agents from the brain. However, recent studies indicate that anesthetic emergence may not simply be a process mirroring the induction of anesthesia. Several substances reduce the duration of anesthesia but not its induction time. Their action is not the result of a passive process, because they actively affect the kinetics of neurotransmitters or the endogenous sleep circuit to shorten anesthesia. The latest notable substance among this group of agents is methylphenidate, an inhibitor of dopamine and norepinephrine transporters. Studies on emergence from anesthesia aim not only to stimulate scientific interest but also to improve the clinical course following general anesthesia, when patients sometimes experience life-threatening complications such as myocardial infarction, bronchial asthma, and cerebral hemorrhage. This review discusses recent advances in this field, focusing mainly on the role of neurotransmitters and neuromodulators in anesthetic emergence.

Understanding the Effects of General Anesthetics on Cortical Network Activity Using Ex Vivo Preparations

“…This distinction is not only of theoretical interest but is vital for understanding clinically relevant behavioral phenomena associated with anesthesia. For example, even though emergence from anesthesia may not be a simple passive reversal of the induction process 56 , knowing the relative influence of dwindling anesthetic concentrations on the spiking activity at cortical vs subcortical sites is pivotal for understanding the nature of these transitions. If the subcortex is more sensitive than the cortex, emergence from anesthesia may be dominated by lingering anesthetic effects on subcortical structures (breathing, detection of sensory stimuli).…”

Emergence from general anesthesia and the sleep-manifold

“…Characterization of the changes that occur during emergence has attracted attention both from researchers searching for the neural correlates of consciousness (Mashour and Alkire, 2013 ) and from more clinically oriented studies, whose focus is on the quality of recovery of patients following surgery (e.g., Law et al, 2011 ). Much of this interest has come from the realization that the induction process (the entrance to the anesthetized state) and emergence process (the exit from the anesthetized state) are not simply the mirror image of each other, but rather that emergence is an active process characterized by a distinct neurobiology (Kelz et al, 2008 ; Lee et al, 2011 ; Kushikata and Hirota, 2014 ). For example, the time required for the return to consciousness shows a much greater variability than the time required for the loss of consciousness.…”

Mechanisms underlying brain monitoring during anesthesia: limitations, possible improvements, and perspectives

“…Although EEG patterns proceed in approximately the reverse order, from several different maintenance period phases, it is possible to observe a progressive decrease in alpha power and increased peak alpha frequency before the return of responsiveness. However, emergence is an active process with a distinct neurobiology [ 16 ]. Moreover, as recently shown by Hight et al [ 17 ] the classic EEG pattern of emergence is not the only pattern of emergence from deep anesthesia.…”