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Objective: Burst-suppression is an electroencephalographic pattern observed during coma. In individuals without known brain pathologies undergoing deep general anesthesia, somatosensory stimulation transiently increases the occurrence of bursts. We investigated the reactivity of burst-suppression in children with acquired brain injury., Methods: Intensive care unit electroencephalographic monitoring recordings containing burst-suppression were obtained from 5 comatose children with acquired brain injury of various etiologies. Intermittent photic stimulation was performed at 1Hz for 1min to assess reactivity. We quantified reactivity by measuring the change in the burst ratio (fraction of time in burst) following photic stimulation., Results: Photic stimulation evoked bursts in all patients, resulting in a transient increase in the burst ratio, while the mean heart rate remained unchanged. The regression slope of the change in burst ratio, referred to as the standardized burst ratio reactivity, correlated with subjects' Glasgow Coma Scale scores., Conclusions: Reactivity of the burst-suppression pattern to photic stimulation occurs across diverse coma etiologies. Standardized burst ratio reactivity appears to reflect coma severity., Significance: Measurement of burst ratio reactivity could represent a simple method to monitor coma severity in critically ill children., (Copyright © 2016 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)

Objective: We analyzed the spatial distribution and concordance of fast (>10Hz) and slow (<5Hz) electroencephalogram (EEG) components of ictal activities and interictal epileptiform discharges (IIED) recorded by intracranial video EEG (IVEEG) in children with epileptic spasms (ES)., Methods: We studied eight children with ES, who underwent IVEEG before resective surgery for epilepsy. We quantified the root-mean-square (RMS) amplitude of the fast and slow components of ictal activities during ES and IIED. We compared the concordance between the spatial distributions of the fast and slow components of ES and IIED., Results: There was a larger concordance between the spatial distributions of the fast and slow components in IIED than in ES (p=0.0206 and 0.0401)., Conclusions: The spatial concordance between the fast and slow EEG components was significantly different between ES and IIED., Significance: The mechanisms underlying the generation of slow EEG components may differ between ES and IIED. The slow EEG components of ES might indicate an extensive epileptic network involving remote symptomatic zones for ES in either the cortical or subcortical areas. The high spatial concordance between the fast and slow components of IIED suggests the involvement of a local inhibitory process within the epileptic cortex., (Copyright © 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)

We investigated the dependency of electrical seizures produced by cortical undercut upon behavioral states of vigilance in chronically implanted cats. Experiments were performed 1-12 weeks after white matter transection. Multisite field potentials and intracellular activity were recorded from suprasylvian and marginal gyri. Paroxysmal activity developed within days and consisted of spike-wave complexes at 3-4 Hz occurring during the waking state (correlated with eye movements), being enhanced during slow-wave sleep (SWS) and blocked during rapid eye movement (REM) sleep. Prolonged hyperpolarizing events were seen not only during SWS (which is the case in normal animals) but also during both waking and REM, thus resulting in bimodal distribution of the membrane potential in all 3 natural states of vigilance. The increased synchrony of field potential activity expressed by shorter time of propagation over the cortical surface and the tendency toward generalization are ascribed to changes in intrinsic neuronal properties and potential disinhibition following cortical undercut.

This study aims at understanding complex interactions between cortical neurons, glia and blood supply developing during the transition from slow-wave sleep to wakefulness. In spite of essential advances from in vitro and culture preparations, the basic mechanisms of glial interactions with their cellular and ionic environment had remained uninvestigated in vivo. Here we approach this issue by performing simultaneous intracellular recordings of cortical neurons and glia, together with measurements of cerebral blood flow (CBF), extracellular K+ concentrations and local field potentials in both anesthetized (ketamine-xylazine) and naturally behaving cats. Under anesthesia, cortical activation was elicited with electric stimulation of cholinergic nuclei (pedunculopontine tegmental in the brainstem and/or nucleus basalis in the basal forebrain). Iontophoretic application of acetylcholine on the recorded cells was also used. In the vast majority of cases (> 80%) glial cells were hyperpolarized during electric stimulation or spontaneous activation. This result was also obtained in all cases where iontophoresis was used or when glutamatergic kainate/quisqualate receptors were blocked with 6-cyano-7-nitroquinoxaline-2,3-dione. The glial hyperpolarization was associated with steady neuronal depolarization, increased CBF, lower extracellular K+ concentration, increased membrane resistance, decreased membrane capacitance and persistent positive DC field potentials. In some cases of cortical activation (< 20%), glial cells displayed sustained depolarizing potentials, in parallel with neuronal depolarization, decreased CBF and more negative DC field potentials. The above-mentioned effects of cholinergic activation were blocked by the muscarinic antagonist scopolamine. We propose that the glial response to cholinergic activation results from the balance between the direct hyperpolarizing action of acetylcholine and the depolarizing modulation of glutamate from the neighboring neurons, in addition to the modulation of the interglial communication pathway and/or the ionic traffic across blood vessels.

Cortical injury may lead to clinical seizures. We investigated the changing patterns of the sleeplike slow oscillation and its tendency to develop into paroxysmal activity consisting of spike-wave (SW) complexes at 2-4 Hz after partial deafferentation of the suprasylvian gyrus. Experiments were carried out in anesthetized cats, at different time intervals (wk 1 to wk 5, W1-W5) after cortical undercut. Multisite field potentials and single or dual intracellular recordings from the whole extent of the deafferented gyrus were used. The field components of the slow oscillation increased in amplitudes and were transformed into paroxysmal patterns, expressed by increased firing rates and tendency to neuronal bursting. The incidence of SW seizures was higher with transition from semiacute (W1) to chronic (W2-W5) stages after cortical undercut. The propagation delay of low-frequency activities decreased from W1 to W5, during both the slow oscillation and seizures. The initiation of seizures took place in territories contiguous to the relatively intact cortex (area 5 in the anterior part of the gyrus), as shown by cross-correlations of field potentials from different sites and simultaneous intracellular recordings from the anterior and posterior parts of the gyrus. The increased amplitudes of both slow oscillation and SW seizures, and their enhanced synchrony expressed by shorter time of propagation, are ascribed to increased neuronal and network excitability after cortical undercut.

Abstract: Kindling is an essential operating paradigm of the nervous system extensively used both as a model of epileptogenesis and neuroplasticity. In a parallel study conducted on chronically implanted non-anesthetized kindled cats, we report the occurrence of long-lasting slow oscillatory patterns (1.5–2 Hz) called outlasting activities (OA) following the acute seizures (AS) induced by cortical stimulation. Here, we asked if OA observed in the neocortex of kindled animals are generated exclusively by the cortical networks or if they also rely on the burst firing of thalamic neurons. We analyzed the electrophysiological patterns of synchronization of cortical EEG (areas 4, 5, 7, 21, 17, 18, 22) and thalamic field (EThG) (ventral posterior lateral nucleus—VPL), and the influence of modulatory systems originating in the pedunculo-pontine tegmentum (PPT) and locus coeruleus (LC) on the discharge pattern of thalamic neurons during OA. Synchrony analysis of field recordings showed that during AS cortical paroxysmal activities preceded thalamic ones, while during OA this sequential order was reversed. During OA thalamic neurons regularly discharged bursts with the frequency of OA. Electrical stimulation of either PPT or LC during OA decreased both the probability of bursts in thalamocortical neurons and the amplitude of OA. Yet, neither of them was able to block completely the expression of OA. Following PPT/LC stimulation the burst firing of thalamocortical neurons was replaced by tonic firing. We conclude that the thalamus is involved in the mechanism of generation of OA but that it does not play an exclusive role. [Copyright &y& Elsevier]