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Examines what happens to the unconscious mind while under the effects of anesthesia, tracing the author's own experiences with surgery and the personal accounts of others who have experienced trauma, hallucinations, and submerged memories while under its influence.

Despite the absence of responsiveness during anesthesia, conscious experience may persist. However, reliable, easily acquirable and interpretable neurophysiological markers of the presence of consciousness in unresponsive states are still missing. A promising marker is based on the decay-rate of the power spectral density (PSD) of the resting EEG. We acquired resting electroencephalogram (EEG) in three groups of healthy participants (n = 5 each), before and during anesthesia induced by either xenon, propofol or ketamine. Dosage of each anesthetic agent was tailored to yield unresponsiveness (Ramsay score = 6). Delayed subjective reports assessed whether conscious experience was present (‘Conscious report’) or absent/inaccessible to recall (‘No Report’). We estimated the decay of the PSD of the resting EEG—after removing oscillatory peaks—via the spectral exponent β, for a broad band (1–40 Hz) and narrower sub-bands (1–20 Hz, 20–40 Hz). Within-subject anesthetic changes in β were assessed. Furthermore, based on β, ‘Conscious report’ states were discriminated against ‘no report’ states. Finally, we evaluated the correlation of the resting spectral exponent with a recently proposed index of consciousness, the Perturbational Complexity Index (PCI), derived from a previous TMS-EEG study. The spectral exponent of the resting EEG discriminated states in which consciousness was present (wakefulness, ketamine) from states where consciousness was reduced or abolished (xenon, propofol). Loss of consciousness substantially decreased the (negative) broad-band spectral exponent in each subject undergoing xenon or propofol anesthesia—indexing an overall steeper PSD decay. Conversely, ketamine displayed an overall PSD decay similar to that of wakefulness—consistent with the preservation of consciousness—yet it showed a flattening of the decay in the high-frequencies (20–40 Hz)—consistent with its specific mechanism of action. The spectral exponent was highly correlated to PCI, corroborating its interpretation as a marker of the presence of consciousness. A steeper PSD of the resting EEG reliably indexed unconsciousness in anesthesia, beyond sheer unresponsiveness. •Unconsciousness does not imply unresponsiveness.•Consciousness is abolished during xenon and propofol, yet preserved during ketamine.•EEG Spectral exponent indexes the 1/f-like decay of non-oscillatory PSD background.•Xenon and propofol steepen broad-band decay; ketamine flattens high-frequency decay.•Spectral exponent separates un/consciousness in anesthesia-induced unresponsiveness.

This study of targeted temperature interventions in 295 children who were comatose after cardiac arrest showed no significant difference between the hypothermia group (33.0°C) and the normothermia group (36.8°C) with respect to 1-year survival with a good functional outcome. Out-of-hospital cardiac arrest in children often results in death or in poor long-term functional outcome in survivors. 1 – 3 In 2002, two trials involving adults showed that therapeutic hypothermia improved neurologic outcomes in comatose survivors after out-of-hospital cardiac arrest with ventricular fibrillation or ventricular tachycardia. 4 , 5 International guidelines recommend therapeutic hypothermia for adults with out-of-hospital cardiac arrest who have similar characteristics. 6 , 7 Recently, another trial involving adults after out-of-hospital cardiac arrest showed that therapeutic hypothermia with the use of a target temperature of 33°C, as compared with actively maintained therapeutic normothermia (36°C), did not improve outcomes. 8 The fundamental difference between this . . .

Unconsciousness is a fundamental component of general anesthesia (GA), but anesthesiologists have no reliable ways to be certain that a patient is unconscious. To develop EEG signatures that track loss and recovery of consciousness under GA, we recorded high-density EEGs in humans during gradual induction of and emergence from unconsciousness with propofol. The subjects executed an auditory task at 4-s intervals consisting of interleaved verbal and click stimuli to identify loss and recovery of consciousness. During induction, subjects lost responsiveness to the less salient clicks before losing responsiveness to the more salient verbal stimuli; during emergence they recovered responsiveness to the verbal stimuli before recovering responsiveness to the clicks. The median frequency and bandwidth of the frontal EEG power tracked the probability of response to the verbal stimuli during the transitions in consciousness. Loss of consciousness was marked simultaneously by an increase in low-frequency EEG power (<1 Hz), the loss of spatially coherent occipital alpha oscillations (8–12 Hz), and the appearance of spatially coherent frontal alpha oscillations. These dynamics reversed with recovery of consciousness. The low-frequency phase modulated alpha amplitude in two distinct patterns. During profound unconsciousness, alpha amplitudes were maximal at low-frequency peaks, whereas during the transition into and out of unconsciousness, alpha amplitudes were maximal at low-frequency nadirs. This latter phase–amplitude relationship predicted recovery of consciousness. Our results provide insights into the mechanisms of propofol-induced unconsciousness, establish EEG signatures of this brain state that track transitions in consciousness precisely, and suggest strategies for monitoring the brain activity of patients receiving GA.

Prominent theories of consciousness emphasise different aspects of neurobiology, such as the integration and diversity of information processing within the brain. Here, we combine graph theory and dynamic functional connectivity to compare resting-state functional MRI data from awake volunteers, propofol-anaesthetised volunteers, and patients with disorders of consciousness, in order to identify consciousness-specific patterns of brain function. We demonstrate that cortical networks are especially affected by loss of consciousness during temporal states of high integration, exhibiting reduced functional diversity and compromised informational capacity, whereas thalamo-cortical functional disconnections emerge during states of higher segregation. Spatially, posterior regions of the brain’s default mode network exhibit reductions in both functional diversity and integration with the rest of the brain during unconsciousness. These results show that human consciousness relies on spatio-temporal interactions between brain integration and functional diversity, whose breakdown may represent a generalisable biomarker of loss of consciousness, with potential relevance for clinical practice. How do diversity (entropy) and integration of activity across brain regions interact to support consciousness? Here the authors show that anaesthetised individuals and patients with disorders of consciousness exhibit overlapping reductions in both diversity and integration in the brain’s default mode network.

General anesthesia (GA) is a reversible drug-induced state of altered arousal required for more than 60,000 surgical procedures each day in the United States alone. Sedation and unconsciousness under GA are associated with stereotyped electrophysiological oscillations that are thought to reflect profound disruptions of activity in neuronal circuits that mediate awareness and cognition. Computational models make specific predictions about the role of the cortex and thalamus in these oscillations. In this paper, we provide in vivo evidence in rats that alpha oscillations (10–15 Hz) induced by the commonly used anesthetic drug propofol are synchronized between the thalamus and the medial prefrontal cortex. We also show that at deep levels of unconsciousness where movement ceases, coherent thalamocortical delta oscillations (1–5 Hz) develop, distinct from concurrent slow oscillations (0.1–1 Hz). The structure of these oscillations in both cortex and thalamus closely parallel those observed in the human electroencephalogram during propofol-induced unconsciousness. During emergence from GA, this synchronized activity dissipates in a sequence different from that observed during loss of consciousness. A possible explanation is that recovery from anesthesia-induced unconsciousness follows a “boot-up” sequence actively driven by ascending arousal centers. The involvement of medial prefrontal cortex suggests that when these oscillations (alpha, delta, slow) are observed in humans, self-awareness and internal consciousness would be impaired if not abolished. These studies advance our understanding of anesthesia-induced unconsciousness and altered arousal and further establish principled neurophysiological markers of these states.

During anesthetic-induced unconsciousness (AIU), the brain undergoes a dramatic change in its capacity to exchange information between regions. However, the spatial distribution of information exchange loss/gain across the entire brain remains elusive. In the present study, we acquired and analyzed resting-state functional magnetic resonance imaging (rsfMRI) data in rats during wakefulness and graded levels of consciousness induced by incrementally increasing the concentration of isoflurane. We found that, regardless of spatial scale, the functional connectivity (FC) change (i.e., ∆FC) was proportionally dependent on the FC strength at the awake state across all connections. This dependency became stronger at higher doses of isoflurane. In addition, the relative FC change at each anesthetized condition (i.e., ∆FC normalized to the corresponding FC strength at the awake state) was exclusively negative across the whole brain, indicating a global loss of meaningful information exchange between brain regions during AIU. To further support this notion, we showed that during unconsciousness, the entropy of rsfMRI signal increased to a value comparable to random noise while the mutual information decreased appreciably. Importantly, consistent results were obtained when unconsciousness was induced by dexmedetomidine, an anesthetic agent with a distinct molecular action than isoflurane. This result indicates that the observed global reduction in information exchange may be agent invariant. Taken together, these findings provide compelling neuroimaging evidence suggesting that the brain undergoes a widespread disruption in the exchange of meaningful information during AIU and that this phenomenon may represent a common system-level neural mechanism of AIU.

The neurophysiological mechanisms by which anesthetic drugs cause loss of consciousness are poorly understood. Anesthetic actions at the molecular, cellular, and systems levels have been studied in detail at steady states of deep general anesthesia. However, little is known about how anesthetics alter neural activity during the transition into unconsciousness. We recorded simultaneous multiscale neural activity from human cortex, including ensembles of single neurons, local field potentials, and intracranial electrocorticograms, during induction of general anesthesia. We analyzed local and global neuronal network changes that occurred simultaneously with loss of consciousness. We show that propofol-induced unconsciousness occurs within seconds of the abrupt onset of a slow (<1 Hz) oscillation in the local field potential. This oscillation marks a state in which cortical neurons maintain local patterns of network activity, but this activity is fragmented across both time and space. Local (<4 mm) neuronal populations maintain the millisecond-scale connectivity patterns observed in the awake state, and spike rates fluctuate and can reach baseline levels. However, neuronal spiking occurs only within a limited slow oscillation-phase window and is silent otherwise, fragmenting the time course of neural activity. Unexpectedly, we found that these slow oscillations occur asynchronously across cortex, disrupting functional connectivity between cortical areas. We conclude that the onset of slow oscillations is a neural correlate of propofol-induced loss of consciousness, marking a shift to cortical dynamics in which local neuronal networks remain intact but become functionally isolated in time and space.

The intravenous injection of the anaesthetic propofol is clinical routine to induce loss of responsiveness (LOR). However, there are only a few studies investigating the influence of the injection rate on the frontal electroencephalogram (EEG) during LOR. Therefore, we focused on changes of the frontal EEG especially during this period. We included 18 patients which were randomly assigned to a slow or fast induction group and recorded the frontal EEG. Based on this data, we calculated the power spectral density, the band powers and band ratios. To analyse the behaviour of processed EEG parameters we calculated the beta ratio, the spectral entropy, and the spectral edge frequency. Due to the prolonged induction period in the slow injection group we were able to distinguish loss of responsiveness to verbal command (LOvR) from loss of responsiveness to painful stimulus (LOpR) whereas in the fast induction group we could not. At LOpR, we observed a higher relative alpha and beta power in the slow induction group while the relative power in the delta range was lower than in the fast induction group. When concentrating on the slow induction group the increase in relative alpha power pre-LOpR and even before LOvR indicated that frontal EEG patterns, which have been suggested as an indicator of unconsciousness, can develop before LOR. Further, LOvR was best reflected by an increase of the alpha to delta ratio, and LOpR was indicated by a decrease of the beta to alpha ratio. These findings highlight the different spectral properties of the EEG at various levels of responsiveness and underline the influence of the propofol injection rate on the frontal EEG during induction of general anesthesia.

By employing transcranial magnetic stimulation (TMS) in combination with high-density electroencephalography (EEG), we recently reported that cortical effective connectivity is disrupted during early non-rapid eye movement (NREM) sleep. This is a time when subjects, if awakened, may report little or no conscious content. We hypothesized that a similar breakdown of cortical effective connectivity may underlie loss of consciousness (LOC) induced by pharmacologic agents. Here, we tested this hypothesis by comparing EEG responses to TMS during wakefulness and LOC induced by the benzodiazepine midazolam. Unlike spontaneous sleep states, a subject's level of vigilance can be monitored repeatedly during pharmacological LOC. We found that, unlike during wakefulness, wherein TMS triggered responses in multiple cortical areas lasting for >300 ms, during midazolam-induced LOC, TMS-evoked activity was local and of shorter duration. Furthermore, a measure of the propagation of evoked cortical currents (significant current scattering, SCS) could reliably discriminate between consciousness and LOC. These results resemble those observed in early NREM sleep and suggest that a breakdown of cortical effective connectivity may be a common feature of conditions characterized by LOC. Moreover, these results suggest that it might be possible to use TMS-EEG to assess consciousness during anesthesia and in pathological conditions, such as coma, vegetative state, and minimally conscious state.