Burst-Suppression EEG Reactivity to Photic Stimulation-A Translational Biomarker in Hypoxic-Ischemic Brain Injury.

The reactivity of an electroencephalogram (EEG) to external stimuli is impaired in comatose patients showing burst-suppression (BS) patterns following hypoxic-ischemic brain injury (HIBI). We explored the reactivity of BS induced by isoflurane in rat models of HIBI and controls using intermittent photic stimulation (IPS) delivered to one eye. The relative time spent in suppression referred to as the suppression ratio (SR) was measured on the contralateral fronto-occipital cortical EEG channel.

Optogenetic Determination of Dynamic and Cell-Type-Specific Inhibitory Reversal Potentials.

The reversal potential refers to the membrane potential at which the net current flow through a channel reverses direction. The reversal potential is determined by transmembrane ion gradients and, in turn, determines how the channel's activity will affect the membrane potential. Traditional investigation into the reversal potential of inhibitory ligand-gated ion channels (E) has relied upon the activation of endogenous receptors, such as the GABA-A receptor (GABAR).

A genetically targeted ion sensor reveals distinct seizure-related chloride and pH dynamics in GABAergic interneuron populations.

Intracellular chloride and pH play fundamental roles in determining a neuron's synaptic inhibition and excitability. Yet it has been difficult to measure changes in these ions during periods of heightened network activity, such as occur in epilepsy. Here we develop a version of the fluorescent reporter, ClopHensorN, to enable simultaneous quantification of chloride and pH in genetically defined neurons during epileptiform activity.

Indirect Effects of Halorhodopsin Activation: Potassium Redistribution, Nonspecific Inhibition, and Spreading Depolarization.

The movement of ions in and out of neurons can exert significant effects on neighboring cells. Here we report several experimentally important consequences of activation of the optogenetic chloride pump, halorhodopsin. We recorded extracellular K concentration ([K]) in neocortical brain slices prepared from young adult mice (both sexes) which express halorhodopsin in pyramidal cells.

Burn mass casualty incidents in Europe: A European response plan within the European Union Civil Protection Mechanism.

Background: Burn care is centralized in highly specialized burn centers in Europe. These centers are of limited capacity and may be overwhelmed by a sudden surge in case of a burn mass casualty incident. Prior incidents in Europe and abroad have sustained high standards of care through well-orchestrated responses to share the burden of care in several burn centers.

Disrupting Epileptiform Activity by Preventing Parvalbumin Interneuron Depolarization Block.

Inhibitory synaptic mechanisms oppose epileptic network activity in the brain. The breakdown in this inhibitory restraint and propagation of seizure activity has been linked to the overwhelming of feedforward inhibition, which is provided in large part by parvalbumin-expressing (PV) interneurons in the cortex. The underlying cellular processes therefore represent potential targets for understanding and preventing the propagation of seizure activity.

A simplified fluid resuscitation formula for burns in mass casualty scenarios: Analysis of the consensus recommendation from the WHO Emergency Medical Teams Technical Working Group on Burns.

Background: Burn fluid resuscitation guidelines have not specifically addressed mass casualty with resource limited situations, except for oral rehydration for burns below 40% total body surface area (TBSA). The World Health Organization Technical Working Group on Burns (TWGB) recommends an initial fluid rate of 100 mL/kg/24 h, either orally or intravenously, beyond 20% TBSA burned. We aimed to compare this formula with current guidelines.

Excitatory GABAergic signalling is associated with benzodiazepine resistance in status epilepticus.

Status epilepticus is defined as a state of unrelenting seizure activity. Generalized convulsive status epilepticus is associated with a rapidly rising mortality rate, and thus constitutes a medical emergency. Benzodiazepines, which act as positive modulators of chloride (Cl-) permeable GABAA receptors, are indicated as first-line treatment, but this is ineffective in many cases.

Chemogenetic Recruitment of Specific Interneurons Suppresses Seizure Activity.

Current anti-epileptic medications that boost synaptic inhibition are effective in reducing several types of epileptic seizure activity. Nevertheless, these drugs can generate significant side-effects and even paradoxical responses due to the broad nature of their action. Recently developed chemogenetic techniques provide the opportunity to pharmacologically recruit endogenous inhibitory mechanisms in a selective and circuit-specific manner.

Burst-Suppression Ratio on Electrocorticography Depends on Interelectrode Distance.

Introduction: With deepening of anesthesia-induced comatose states, the EEG becomes fragmented by increasing periods of suppression. When measured from conventional EEG recordings, the binary burst-suppression signal (BS) appears similar across the scalp. As such, the BS ratio (BSR), quantifying the fraction of time spent in suppression, is clinically considered a global index of brain function in sedation monitoring.

Intraoperative somatosensory evoked potential monitoring decreases EEG burst suppression ratio during deep general anesthesia.

Purpose: The burst suppression (BS) EEG patterns induced by general anesthesia can react to somatosensory stimuli. We investigated this reactivity by studying the effect of peripheral nerve stimulation used for routine intraoperative spinal cord monitoring by somatosensory evoked potentials on BS patterns.

Methods: The relative time spent in suppression expressed as BS ratio (BSR) and mean burst duration were measured before (BSR(Pre)), during (BSR(Stim)), and after (BSR(Post)) a 60-second repetitive electrical ulnar nerve stimulation in nine patients under total intravenous general anesthesia with propofol.