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

Cautious reporting choices can artificially enhance how well analyses of brain activity reflect conscious and unconscious experiences, making distinguishing between the two more challenging.

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.

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.

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.

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.

Brain-wide activation patterns reveal the distinct and shared neurophysiological impacts of ketamine and isoflurane, highlighting key nuclei involved in the modulation of general anesthesia.

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.