Anesthetic-induced Loss Of Consciousness Research Articles

Developing new neurophysiological signatures of general anesthesia induced loss of consciousness

General anesthesia is currently defined in the context of its use in clinical care [1]. The mechanism by which anesthetic drugs induce general anesthesia is not well understood. There is therefore a need to incorporate neurophysiological characterizations into the definition and understanding of anesthesia. Distinct patterns in the electroencephalogram have been associated with anesthesia-induced loss of consciousness [2-4] and are used as part of protocols to monitor integrity of brain function [5]. However, the transition to unconsciousness during a gradual induction of general anesthesia has not been studied systematically.

Baseline brain energy supports the state of consciousness

An individual, human or animal, is defined to be in a conscious state empirically by the behavioral ability to respond meaningfully to stimuli, whereas the loss of consciousness is defined by unresponsiveness. PET measurements of glucose or oxygen consumption show a widespread approximately 45% reduction in cerebral energy consumption with anesthesia-induced loss of consciousness. Because baseline brain energy consumption has been shown by (13)C magnetic resonance spectroscopy to be almost exclusively dedicated to neuronal signaling, we propose that the high level of brain energy is a necessary property of the conscious state. Two additional neuronal properties of the conscious state change with anesthesia. The delocalized fMRI activity patterns in rat brain during sensory stimulation at a higher energy state (close to the awake) collapse to a contralateral somatosensory response at lower energy state (deep anesthesia). Firing rates of an ensemble of neurons in the rat somatosensory cortex shift from the gamma-band range (20-40 Hz) at higher energy state to <10 Hz at lower energy state. With the conscious state defined by the individual's behavior and maintained by high cerebral energy, measurable properties of that state are the widespread fMRI patterns and high frequency neuronal activity, both of which support the extensive interregional communication characteristic of consciousness. This usage of high brain energies when the person is in the "state" of consciousness differs from most studies, which attend the smaller energy increments observed during the stimulations that form the "contents" of that state.

Neurophysiologic mechanism of anesthesia-induced loss of consciousness

Recent studies demonstrate that anesthesia-induced loss of consciousness is a cascade process occurring in hierarchical sequences, including brainstem depression-reduced the influences of the ascending reticular activating system on thalamus and cortex,depression of mesolimbic-dorsolateral prefrontal cortex interactions and thalamic-thalamocortical reverberations, interruption of prefrontal-parietal transactions critical for perception, inhibition of prefrontal cortex, etc. Among them thalamus plays a central role. Anesthesia-induced loss of consciousness can be accomplished by inhibiting any taches of the cascade and the corresponding couples and integration. Key words: anesthesia; loss of consciousness; neurophysiology

Halothane augments event-related γ oscillations in rat visual cortex

Cortical γ oscillations have been associated with neural processes supporting cognition and the state of consciousness but the effect of general anesthesia on γ oscillations is controversial. Here we studied the concentration-dependent effect of halothane on γ (20–60 Hz) power of event-related potentials (ERP) in rat primary visual cortex. ERP to light flashes repeated at 5-s intervals was recorded with chronically implanted, bipolar, intracortical electrodes at selected steady-state halothane concentrations between 0 and 2%. γ-Band power was calculated for 0–1000, 0–300 and 300–1000 ms poststimulus periods and corresponding prestimulus (PS) periods. Multitaper power spectral analysis was used to estimate γ power from both single-trial and average ERP in order to differentiate between phase-locked (evoked) and non-phase-locked (induced) γ activities. Significant PS γ power was present at all halothane concentrations. Flash elicited an increase in γ power that lasted up to 1 s poststimulus at all halothane concentrations. Halothane at intermediate concentrations (0.5–1.2%) augmented both PS and ERP γ power two to four times relative to the waking baseline. γ Power was not different between waking and deeply anesthetized (2%) levels. γ Power reached maximum, as predicted by a Gaussian fit of power-concentration data, at halothane concentration (0.86%) similar to the concentration (0.73%) that abolished the righting reflex, a behavioral index of loss of consciousness. Evoked, i.e. stimulus-locked, γ power was present during the first 300 ms poststimulus but not later, and was approximately 50% of single-trial ERP γ power. Single-trial γ power was present also at 300–1000 ms poststimulus, reflecting ERP not phase-locked to the stimulus. In summary, these observations suggest that (1) γ activity is present in states ranging from waking to deep halothane anesthesia, (2) halothane does not prevent the transfer of visual input to striate cortex even at surgical plane of anesthesia, and (3) anesthetic-induced loss of consciousness, as reflected by the loss of righting reflex, is not correlated with a reduction in γ power. Variance with other studies may be due to an underestimation of γ power by ERP signal averaging as compared with single-trial analysis.