How the brain recovers from anesthetic-induced unconsciousness is poorly understood. Elucidating the neural mechanisms of recovery of consciousness is an essential step for understanding neurocognitive problems after anesthesia and surgery.
We studied neuronal dynamics during return of consciousness (ROC) and through performance recovery by directly recording intracortical local field potentials in the somatosensory and premotor network in two macaque monkeys. The animals were trained for a behavioral task to indicate alertness. We studied 3 anesthetics with a distinct receptor mechanism: propofol, ketamine, and dexmedetomidine (a2-adrenergic agonist).
The ROC after propofol coincided with an abrupt return of the beta oscillations and a decline of the slow-delta oscillations that were dominant during unconsciousness, though pharmacokinetic modeling assured a gradual change of the brain propofol concentration. Dexmedetomidine also showed an abrupt but unique oscillatory change at ROC followed by prolonged fluctuating dynamics. Awakening by a2 adrenergic antagonist completely eliminated this intermediate state and immediately restored awake brain dynamics. ROC following ketamine was observed during a more gradual oscillatory change.
The brain dynamics during recovery are unique to each anesthetic, but are often abrupt at ROC, suggesting that abrupt state transitions are a fundamental manner of how the brain functions.