Instant performance recovery is possible following general anesthesia-induced unconsciousness using antagonist, and the brain dynamics return abruptly to the awake state without intermediate recovery states.

Patterns of communication between the thalamus and the cortex are correlated with anesthesia-induced loss of consciousness and recovery.

Loss of nonstationary connectivity in a subcortical fronto-temporoparietal network distinguishes patients with minimal conscious state and unresponsive wakefulness state, strongly supporting the mesocircuit hypothesis.

The neural basis of consciousness is confounded by the mismatch between what participants report about their experience versus what they actually experience.

Anaesthesia and disorders of consciousness both reduce the capacity of the human brain to integrate information, specifically targeting interactions within a shared circuit of regions in the brain’s default network.

Understanding how general anesthesia changes neural dynamics in the cortex and thalamus can lead to its safer use and shed light on the nature of consciousness.

Cognitive reconstitution after pharmacologic unconsciousness is an extended process, executive function is more robust than expected, and the healthy human brain is resilient to the effects of deep general anesthesia.

The results of central nervous regulation in mice provide a new neural circuit and receptor regulatory mechanisms for the recovery of consciousness after midazolam administration.

Behavioral, pharmacological, optogenetic, electrophysiological and computational analyses suggest that the anterior dorsal striatum is a causal node in the network responsible for evidence accumulation.

The therapeutic effects of the sleeping pill zolpidem in patients with disorders of consciousness may be due to recruitment of brain cells idling in abnormally low-frequency brain waves.