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.

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.

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.

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

Human fMRI experiments reveal differences in the propagation of spontaneous brain activity during sleep versus wakefulness.

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.

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.

While minimizing the report-related motor confounding, event-related potential (ERP), high-frequency power, and functional connectivity of the local field potential (LFP) activity in human prefrontal cortex were enhanced under the emergence of visual awareness.

The strength of frequency-tagged neural activity during perceptual filling anti-correlates with the contents of consciousness, yet positively correlates with a neural measure of attention, dissociating these often confounded brain processes.