Comparison of the qCON and qNOX indices for the assessment of unconsciousness level and noxious stimulation response during surgery

The objective of this work is to compare the performances of two electroencephalogram based indices for detecting loss of consciousness and loss of response to nociceptive stimulation. Specifically, their behaviour after drug induction and during recovery of consciousness was pointed out. Data was recorded from 140 patients scheduled for general anaesthesia with a combination of propofol and remifentanil. The qCON 2000 monitor (Quantium Medical, Barcelona, Spain) was used to calculate the qCON and qNOX. Loss of response to verbal command and loss of eye-lash reflex were assessed during the transition from awake to anesthetized, defining the state of loss of consciousness. Movement as a response to laryngeal mask (LMA) insertion was interpreted as the response to the nociceptive stimuli. The patients were classified as movers or non-movers. The values of qCON and qNOX were statistically compared. Their fall times and rise times defined at the start and at the end of the surgery were calculated and compared. The results showed that the qCON was able to predict loss of consciousness such as loss of verbal command and eyelash reflex better than qNOX, while the qNOX has a better predictive value for response to noxious stimulation such as LMA insertion. From the analysis of the fall and rise times, it was found that the qNOX fall time (median: 217 s) was significantly longer (p value <0.05) than the qCON fall time (median: 150 s). At the end of the surgery, the qNOX started to increase in median at 45 s before the first annotation related to response to stimuli or recovery of consciousness, while the qCON at 88 s after the first annotation related to response to stimuli or recovery of consciousness (p value <0.05). The indices qCON and qNOX showed different performances in the detection of loss of consciousness and loss of response to stimuli during induction and recovery of consciousness. Furthermore, the qCON showed faster decrease during induction. This behaviour is associated with the hypothesis that the loss of response to stimuli (analgesic effect) might be reached after the loss of consciousness (hypnotic effect). On the contrary, the qNOX showed a faster increase at the end of the surgery, associated with the hypothesis that a higher probability of response to stimuli might be reached before the recovery of consciousness.Postprint (author's final draft

A new dynamic property of human consciousness

As pointed out by William James, &#x22;the consciousness is a dynamic process, not a thing&#x22; , during which short term integration is succeeded by another differentiated neural state through the continual interplay between the environment, the body, and the brain itself. Thus, the dynamic structure underlying successive states of the brain is important for understanding human consciousness as a process. In order to investigate the dynamic property of human consciousness, we developed a new method to reconstruct a state space from electroencephalogram(EEG), in which a trajectory, reflecting states of consciousness, is constructed based on the global information integration of the brain. EEGs were obtained from 14 subjects received an intravenous bolus of propopol. Here we show that the degree of human consciousness is directly associated with the information integration capacity of gamma wave, which is significantly higher in the conscious state than in the unconscious state. And we found a new time evolutional property of human consciousness. The conscious state showed a lower dimensional dynamic process which changed to a random-like process after loss of consciousness. This characteristic dynamic property, appeared only in the gamma band, might be used as an indicator to distinguish the conscious and unconscious states and also considered as an important fact for the human consciousness model

Is Consciousness Computable? Quantifying Integrated Information Using Algorithmic Information Theory

In this article we review Tononi's (2008) theory of consciousness as integrated information. We argue that previous formalizations of integrated information (e.g. Griffith, 2014) depend on information loss. Since lossy integration would necessitate continuous damage to existing memories, we propose it is more natural to frame consciousness as a lossless integrative process and provide a formalization of this idea using algorithmic information theory. We prove that complete lossless integration requires noncomputable functions. This result implies that if unitary consciousness exists, it cannot be modelled computationally.Comment: Maguire, P., Moser, P., Maguire, R. & Griffith, V. (2014). Is consciousness computable? Quantifying integrated information using algorithmic information theory. In P. Bello, M. Guarini, M. McShane, & B. Scassellati (Eds.), Proceedings of the 36th Annual Conference of the Cognitive Science Society. Austin, TX: Cognitive Science Societ

Epilepsy – A Brief Overview

Epilepsy is a neurological condition in which an individual experiences chronic abnormal bursts of electrical discharge in the brain. These seizures can cause a variety symptoms depending on the areas of the brain affected. Symptoms can vary from mild to severe and can include complete or partial loss of consciousness, loss of speech, uncontrollable motor behavior, and/or unusual sensory experiences. From various studies worldwide6, approximately 0.5% of the population is reported to be affected by active epilepsy

Usefulness of brain signals for the detection of loss of consciousness in anesthesia

Loss of consciousness (LOC) detection is essential for better anesthesia guidance. Clinical signs and brain monitoring are currently used in operating rooms to assess the state of consciousness. However, a patientindependent, accurate and reliable indicator of LOC is not currently available. We studied 69 patients undergoing general anesthesia, investigating a possible relationship between loss of consciousness and BIS and EMG signals registered during induction. Neither BIS and EMG values at LOC, nor their abrupt fall proved to be good indicators of loss of consciousness. Further work needs to be done in order to reliably detect loss of consciousness.info:eu-repo/semantics/publishedVersio

Etiology of phantom limb syndrome: Insights from a 3D default space consciousness model

In this article, we examine phantom limb syndrome to gain insights into how the brain functions as the mind and how consciousness arises. We further explore our previously proposed consciousness model in which consciousness and body schema arise when information from throughout the body is processed by corticothalamic feedback loops and integrated by the thalamus. The parietal lobe spatially maps visual and non-visual information and the thalamus integrates and recreates this processed sensory information within a three-dimensional space termed the ‘‘3D default space.’’ We propose that phantom limb syndrome and phantom limb pain arise when the afferent signaling from the amputated limb is lost but the neural circuits remain intact. In addition, integration of conflicting sensory information within the default 3D space and the loss of inhibitory afferent feedback to efferent motor activity from the amputated limb may underlie phantom limb pain

Loss of consciousness due to propofol

In this literary review, a possible mechanism used by propofol and the consequences of this mechanism are discussed. Propofol is able to bring about loss of consciousness by inhibiting the Ih current in hyperpolarization-activated cyclic nucleotide-gated type 2 (HCN2) channels. The inhibition leads to an increase in the hyperpolarization of the thalamocortical neurons, which results in temporally impaired delta oscillations (Ying et al., 2006). This leads to significant phase offsets which result in fragmentation and the isolation of neural networks. Propofol also leads to a breakdown in the basal ganglia-thalamo-cortical (BGTC) loop, which disrupts cortical and subcortical communication. This breakdown is a result of decreases seen in beta band coherence and the phase amplitude coupling (PAC) between subcortical and cortical regions of the loop. The reduction in coupling leads to interrupted communication which contributes to neural network fragmentation (Swann et al., 2016). Although fragmentation is seen, there are instances of increased global connectivity. The default mode network (DMN) increases its connections to structures outside its network during sedation. However, these connections are not representations of efficient global communication. Instead, they lead to a decrease local efficiency resulting in local network deterioration and an overall decrease in efficient global and local network interactions (Stamatakis et al., 2010). Certain characteristics of the transition from consciousness to loss of consciousness were identified. Delta oscillations are significantly more powerful during sedation, and the sharp increase that can be seen in their power is indicative of loss of consciousness (Lewis et al., 2012). Another indicator of loss of consciousness can be seen in frontal EEG channels by way of PAC analysis of alpha power and slow oscillations. Negative trough-max PAC exists at baseline, but switches to positive peak-max PAC during moderate sedation in those who are more sensitive to propofol. An increased propofol sensitivity can be detected at baseline and is represented by a weak alpha network that is not very small-worldly (Chennu et al., 2016). In summary, it is clear that the timing of our neural networks is crucial to consciousness and that it is through temporal modifications that propofol is able to induce its effects

Clinical Evaluation of Two Ke0 in the same Pharmacokinetic Propofol Model: Study on Loss and Recovery of Consciousness

SummaryBackground and objectiveThe constant equilibrium between the plasma and effect site (ke0) is used by pharmacokinetic models to calculate a drug concentration in its site of action (Ce). It would be interesting if Ce of propofol was similar at loss and recovery of consciousness. The objective of this study was to evaluate the clinical performance of two different ke0 (fast = 1.21 min-1, and slow = 0.26 min-1) in relation to Ce during loss and recovery of consciousness using Marsh pharmacokinetic model.MethodsTwenty healthy adult male volunteers participated in this study. In all volunteers propofol was administered as target-controlled infusion, Marsh pharmacokinetic model for fast ke0 and, at a different time, the same pharmacokinetic model with slow ke0 was used. Initially, propofol was infused with a serum target-controlled infusion of 3.0 μg.mL-1. Loss of consciousness and recovery of consciousness were based on response to verbal stimulus. Ce was recorded at the moment of loss and recovery of consciousness.ResultsOn loss and recovery of consciousness, the Ce for fast ke0 was different (3.64 ± 0.78 and 1.47 ± 0.29 μg.mL-1, respectively, p < 0.0001), while with slow ke0 the Ce was similar (2.20 ± 0.70 and 2.14 ± 0.43 μg.mL-1, respectively, p = 0.5425).ConclusionsClinically, the slow ke0 (0.26 min-1) incorporated in the Marsh pharmacokinetic model showed better performance than the fast ke0 (1.21 min-1), since the calculated concentration of propofol at the effect site on loss and recovery of consciousness was similar

Association of Alcohol-Induced Loss of Consciousness and Overall Alcohol Consumption With Risk for Dementia

This cohort study examines the association of overall consumption of alcohol and resultant loss of consciousness with risk for dementia. Question Are alcohol-induced loss of consciousness and heavy weekly alcohol consumption associated with increased risk of future dementia? Findings In this multicohort study of 131x202f;415 adults, a 1.2-fold excess risk of dementia was associated with heavy vs moderate alcohol consumption. Those who reported having lost consciousness due to alcohol consumption, regardless of their overall weekly consumption, had a 2-fold increased risk of dementia compared with people who had not lost consciousness and were moderate drinkers. Meaning The findings of this study suggest that alcohol-induced loss of consciousness is a long-term risk factor for dementia among both heavy and moderate drinkers. Importance Evidence on alcohol consumption as a risk factor for dementia usually relates to overall consumption. The role of alcohol-induced loss of consciousness is uncertain. Objective To examine the risk of future dementia associated with overall alcohol consumption and alcohol-induced loss of consciousness in a population of current drinkers. Design, Setting, and Participants Seven cohort studies from the UK, France, Sweden, and Finland (IPD-Work consortium) including 131x202f;415 participants were examined. At baseline (1986-2012), participants were aged 18 to 77 years, reported alcohol consumption, and were free of diagnosed dementia. Dementia was examined during a mean follow-up of 14.4 years (range, 12.3-30.1). Data analysis was conducted from November 17, 2019, to May 23, 2020. Exposures Self-reported overall consumption and loss of consciousness due to alcohol consumption were assessed at baseline. Two thresholds were used to define heavy overall consumption: greater than 14 units (U) (UK definition) and greater than 21 U (US definition) per week. Main Outcomes and Measures Dementia and alcohol-related disorders to 2016 were ascertained from linked electronic health records. Results Of the 131x202f;415 participants (mean [SD] age, 43.0 [10.4] years; 80x202f;344 [61.1%] women), 1081 individuals (0.8%) developed dementia. After adjustment for potential confounders, the hazard ratio (HR) was 1.16 (95% CI, 0.98-1.37) for consuming greater than 14 vs 1 to 14 U of alcohol per week and 1.22 (95% CI, 1.01-1.48) for greater than 21 vs 1 to 21 U/wk. Of the 96x202f;591 participants with data on loss of consciousness, 10x202f;004 individuals (10.4%) reported having lost consciousness due to alcohol consumption in the past 12 months. The association between loss of consciousness and dementia was observed in men (HR, 2.86; 95% CI, 1.77-4.63) and women (HR, 2.09; 95% CI, 1.34-3.25) during the first 10 years of follow-up (HR, 2.72; 95% CI, 1.78-4.15), after excluding the first 10 years of follow-up (HR, 1.86; 95% CI, 1.16-2.99), and for early-onset (= 65 y: HR, 2.25; 95% CI, 1.38-3.66) dementia, Alzheimer disease (HR, 1.98; 95% CI, 1.28-3.07), and dementia with features of atherosclerotic cardiovascular disease (HR, 4.18; 95% CI, 1.86-9.37). The association with dementia was not explained by 14 other alcohol-related conditions. With moderate drinkers (1-14 U/wk) who had not lost consciousness as the reference group, the HR for dementia was twice as high in participants who reported having lost consciousness, whether their mean weekly consumption was moderate (HR, 2.19; 95% CI, 1.42-3.37) or heavy (HR, 2.36; 95% CI, 1.57-3.54). Conclusions and Relevance The findings of this study suggest that alcohol-induced loss of consciousness, irrespective of overall alcohol consumption, is associated with a subsequent increase in the risk of dementia.Peer reviewe