The Neuroscientist
January 4, 2005
Olaf Blanke, Shahar Arzy
468 citations
Out-of-body experiences (OBEs), where one's perspective and sense of self seem to leave the body, challenge the everyday assumption that the self resides inside the body. Evidence from neurology, cognitive neuroscience, and neuroimaging indicates that OBEs arise from a failure to integrate multisensory information about one's own body at the temporo-parietal junction (TPJ). This multisensory disintegration disrupts self-processing, producing illusory reduplication, self-location, perspective, and agency that together constitute the OBE.
The Neuroscientist
September 1, 2017
Selen Atasoy, Gustavo Deco, Morten L. Kringelbach et al.
131 citations
Spontaneous brain activity exhibits coherent oscillations across a wide range of frequencies, with temporal patterns highly correlated across distributed cortical areas, forming resting state networks. This work introduces harmonic brain modes as fundamental building blocks of complex spatiotemporal neural activity, defined as harmonic modes of structural connectivity (connectome harmonics) that yield fully synchronous activity patterns with different frequency oscillations constrained by brain structure. This framework links space and time in brain dynamics. The authors show how harmonic brain modes explain neurophysiological, temporal, and network-level changes across mental states (wakefulness, sleep, anesthesia, psychedelic). Spatial and temporal characteristics emerge from the interplay between excitation and inhibition, fitting changes associated with different mental states, offering tools for understanding brain dynamics in various states of consciousness.
The Neuroscientist
December 26, 2025
Kallol Bera, Loren L. Looger, Alex Proekt et al.
5 citations
Ketamine, an anesthetic that produces dissociative anesthesia—characterized by perceptual detachment, analgesia, and altered consciousness—also acts as a rapid antidepressant at low doses and serves as a tool to study consciousness and neuropsychiatric disorders. Its effects stem from actions on cortical circuits: blocking NMDA receptors and HCN1 channels, disinhibiting pyramidal neurons, and altering thalamocortical connectivity. The review synthesizes findings from pharmacology, cell-specific imaging, and systems neuroscience to explain how ketamine alters cortical dynamics to drive dissociation. It also explores the possibility that ketamine enters intracellular compartments, modulating neuronal excitability, signaling, and epigenetic state after a single dose. Understanding these processes may inform new treatments for treatment-resistant depression and the study of consciousness.