Recovery of consciousness and cognition after general anesthesia in humans

Abstract

Understanding how the brain recovers from unconsciousness can inform neurobiological theories of consciousness and guide clinical investigation. To address this question, we conducted a multicenter study of 60 healthy humans, half of whom received general anesthesia for three hours and half of whom served as awake controls. We administered a battery of neurocognitive tests and recorded electroencephalography to assess cortical dynamics. We hypothesized that recovery of consciousness and cognition is an extended process, with differential recovery of cognitive functions that would commence with return of responsiveness and end with return of executive function, mediated by prefrontal cortex. We found that, just prior to the recovery of consciousness, frontal-parietal dynamics returned to baseline. Consistent with our hypothesis, cognitive reconstitution after anesthesia evolved over time. Contrary to our hypothesis, executive function returned first. Early engagement of prefrontal cortex in recovery of consciousness and cognition is consistent with global neuronal workspace theory.

Inactivation of Prefrontal Cortex Delays Emergence From Sevoflurane Anesthesia

“…By contrast, our loss-of-function design enables causal inference regarding the role of prefrontal and posterior parietal cortices in anesthetic state transitions. Furthermore, the current data align with a multicenter study of healthy human volunteers finding that recovery of prefrontal electroencephalographic dynamics, which occur on a finer temporal scale than positron emission tomography, preceded return of consciousness and appeared more active than posterior cortex (Mashour et al, 2021). These data support the possibility of the translational relevance of our findings in rodents, but further investigation is clearly warranted.…”

The Effect of General Anesthesia vs. Regional Anesthesia on Postoperative Delirium—A Systematic Review and Meta-Analysis

“…However, the specific mechanism of action of general anesthetics is still elusive. According to animal and clinical studies, GA-related varieties of consciousness and cognition are reversible and transient ( 46 , 47 ). But some studies exhibited that GA or general anesthetics could produce neural toxicities, and be associated with short- or long-term cognitive dysfunction, and the extent of cognitive defect was proportional to the duration of anesthesia ( 48 , 49 ).…”

Changes of oscillatory and aperiodic neuronal activity in working memory following anaesthesia: a prospective observational study

“…[15][16][17][18] To date it remains unclear how fast this inhibition dissipates after drug administration is discontinued. While the healthy young brain is resilient to electrophysiological disturbances by anaesthesia 40 , elderly patients are more sensitive to anaesthetics and therefore more likely to enter burst suppression 4 -a pattern of brain activity induced by a maximum of inhibition where bursts of activity are followed by periods of neuronal silence. 41 Time spent in that (too) deep plane of anaesthesia is an independent risk factor for developing POD.…”

“…c, Association of EEG oscillatory power differences between memory sessions in frequency bands of interest (Δ Se2-Se1, n = 26) and NP z-score of CVLT total recall. d, Association of EEG oscillatory power differences between memory sessions in frequency bands of interest (Δ Se2-Se1, n = 26) and EEG spectral slope(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40) difference between memory sessions in cluster channels (Δ Se2-Se1 spectral slope cluster-permutation test: p = 0.073, Fig.5). e, Association of EEG oscillatory power differences between memory sessions in frequency bands of interest (Δ Se2-Se1, n = 26) and NP z-score of CVLT learning slope (Fig.5).…”