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• Comatose critically-ill children are at risk for seizures, often being electrographic-only, without accompanying clinical signs. • EEG features of the first 5 minutes of critical care EEG recordings differed among children who went on to develop acute seizures. • If validated in other cohorts, EEG features may be an effective seizure risk stratification tool for critically-ill children. We aimed to test the hypothesis that computational features of the first several minutes of EEG recording can be used to estimate the risk for development of acute seizures in comatose critically-ill children. In a prospective cohort of 118 comatose children, we computed features of the first five minutes of artifact-free EEG recording (spectral power, inter-regional synchronization and cross-frequency coupling) and tested if these features could help identify the 25 children who went on to develop acute symptomatic seizures during the subsequent 48 hours of cEEG monitoring. Children who developed acute seizures demonstrated higher average spectral power, particularly in the theta frequency range, and distinct patterns of inter-regional connectivity, characterized by greater connectivity at delta and theta frequencies, but weaker connectivity at beta and low gamma frequencies. Subgroup analyses among the 97 children with the same baseline EEG background pattern (generalized slowing) yielded qualitatively and quantitatively similar results. These computational features could be applied to baseline EEG recordings to identify critically-ill children at high risk for acute symptomatic seizures. If confirmed in independent prospective cohorts, these features would merit incorporation into a decision support system in order to optimize diagnostic and therapeutic management of seizures among comatose children. [ABSTRACT FROM AUTHOR]

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 1 Hz for 1 min 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. [ABSTRACT FROM AUTHOR]

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]

Abstract: Some forms of electrographic seizures are generated at the level of the cortical network. Neocortical kindling exhibits a resistance to produce generalized convulsive seizures, and therefore, it was rather difficult to use it to study the cortical epileptogenesis. Here, using supra-threshold cortical kindling, we report electrophysiological patterns of field-potential synchronization and intracellular activities in chronically implanted non-anesthetized cats, during different states of vigilance, and during acute seizures elicited by prolonged (20–60 s) electrical stimulation. Acute seizures were easily elicited during transition from slow-wave sleep (SWS) to waking state. The seizures were mainly clonic accompanied with tonic components followed by prolonged postictal depression. Delayed rhythmic outlasting activities (OA) at ~1.5 Hz, first time reported here, followed the postictal depression, and lasted up to 2 h. These activities were clear during waking state, slightly reduced during SWS and completely absent during rapid-eye movement sleep. They started focally and following daily stimulations generalized over the entire cortical surface. Extra- and intracellular neuronal recordings during OA displayed spike-doublets, built on the summation of successive excitatory postsynaptic potentials and fast-prepotentials, entailing an increased dendritic excitation. Our results suggest that such rhythmic long-lasting oscillatory activity outlasting seizures are the key factor of epileptogenesis, leading to epilepsy. [Copyright &y& Elsevier]

To study the possible mechanism(s) underlying unresponsiveness following neocortical seizures, we recorded excitatory postsynaptic potentials (EPSPs) of cortical neurons evoked by ipsilateral cortical stimulation before and after spontaneous or elicited seizures. Regular-spiking neurons (n = 32) were intracellularly recorded in association area five of cats under ketamine–xylazine or barbiturate anesthesia. Compared with control responses, cortically evoked EPSPs were characterized by decreased amplitude after electrographic seizures. Synaptic responses and intrinsic properties were measured by applying extracellular electrical stimuli followed by intracellular hyperpolarizing current pulses. The input resistance decreased during seizures but quickly recovered to control level after the paroxysms, whereas the amplitude of evoked EPSPs remained lower following seizures, generally for 2–12 min, suggesting that the decreased EPSPs were not due to an alteration of intrinsic response. Data demonstrate a long-lasting decreased synaptic responsiveness following generalized spike-wave seizures slowly recovering in time. [ABSTRACT FROM AUTHOR]

We studied the mechanisms underlying CO(2)-dependent DC potential shifts, using epicranial, epidural, epicortical, intraventricular, and intraparenchymal (intraneuronal, intraglial, and field) recordings in ketamine-xylazine-anesthetized cats. DC shifts were elicited by changes in artificial ventilation, causing end-tidal CO(2) variations within a 2-5% range. Hypercapnia was consistently associated with negative scalp DC shifts (average shift -284.4 microV/CO(2)%, range -216 to -324 microV/CO(2)%), whereas hypocapnia induced positive scalp DC shifts (average shift 307.8 microV/CO(2)%, range 234 to 342 microV/CO(2)%) in all electrodes referenced versus the nasium bone. The former condition markedly increased intracranial pressure (ICP), whereas the latter only slightly reduced ICP. Breakdown of the blood-brain barrier (BBB) resulted in a positive DC shift and drastically reduced subsequent DC responses to hypo-/hypercapnia. Thiopental and isoflurane also elicited a dose-dependent positive DC shift and, at higher doses, hypo-/hypercapnia responses displayed reverted polarity. As to the possible implication of neurons in the production of DC shifts, no polarity reversal was recorded between scalp, various intracortical layers, and deep brain structures. Moreover, the membrane potential of neurons and glia did not show either significant or systematic variations in association with the scalp-recorded CO(2)-dependent DC shifts. Pathological activities of neurons during spike-wave seizures produced DC shifts of significantly smaller amplitude than those generated by hyper-/hypocapnia. DC shifts were still elicited when neuronal circuits were silent during anesthesia-induced burst-suppression patterns. We suggest that potentials generated by the BBB are the major source of epicortical/cranial DC shifts recorded under conditions affecting brain pH and/or cerebral blood flow. [ABSTRACT FROM AUTHOR]

Anti–glutamic acid decarboxylase directed antibodies are a rare cause of autoimmune limbic encephalitis that is relatively resistant to immunotherapy. Here we report a 15-year-old boy with nonparaneoplastic, anti–glutamic acid decarboxylase limbic encephalitis presenting with subacute headache, memory disturbance, psychiatric symptoms, and seizures. At onset, his memory disturbance manifested as transient global amnesia-like episodes. Clinical remission was achieved with rituximab, intravenous immunoglobulin, and corticosteroids. [ABSTRACT FROM PUBLISHER]

Background: The identification of a biomarker for sudden unexpected death in epilepsy (SUDEP) has the potential to save lives. Generalized convulsive seizures and postictal generalized suppression on electroencephalography (EEG) most often precede sudden unexpected death in epilepsy (SUDEP) and are potential biomarkers. We identify the EEG and seizure characteristics associated with postictal generalized EEG suppression in children with epilepsy.Methods: Video EEGs were reviewed for seizure type, duration and semiology, and electrographic features. To identify predictors of postictal generalized EEG suppression, we identified 40 children with generalized convulsive seizures from a group of 399 patients who experienced an electroclinical seizure during video-EEG. Seventy-seven generalized convulsive seizures with and without postictal generalized EEG suppression were anayzed.Results: Age of seizure onset was older in 19 children with postictal generalized EEG suppression (mean 6.8 years old, 95% CI [4.7-8.9]) than in 21 without postictal generalized EEG suppression (3.0 years old, [1.1-4.1], P = 0.041). Postictal generalized EEG suppression occurred significantly more often from sleep than awake (point of estimate 16.67; 95% CI [0.97-32.36], P < 0.038). Shorter duration of the clonic phase (-0.76; [-1.338, -0.133], P = 0.018) was significantly associated with postictal generalized EEG suppression. Ictal symmetric tonic extension posturing significantly increased the odds of postictal generalized EEG suppression (42.94; [18.77, 67.12], P = 0.001). All 15 generalized convulsive seizures with a terminal burst-suppression pattern were followed by postictal generalized EEG suppression in contrast to 19 of 62 generalized convulsive seizures without burst-suppression (15.32, P < 0.001).Conclusions: Ictal decerebrate-like symmetric tonic extension posturing with shorter clonic phase and a terminal burst-suppression pattern identify malignant generalized convulsive seizures, associated with postictal generalized EEG suppression and a potentially increased risk of sudden unexpected death in epilepsy. [ABSTRACT FROM AUTHOR]

Objective To evaluate whether structural and microstructural brain abnormalities in neonates with congenital heart disease (CHD) correlate with neuronal network dysfunction measured by analysis of EEG connectivity. Methods We studied a prospective cohort of 20 neonates with CHD who underwent continuous EEG monitoring before surgery to assess functional brain maturation and network connectivity, structural magnetic resonance imaging ( MRI) to determine the presence of brain injury and structural brain development, and diffusion tensor MRI to assess brain microstructural development. Results Neonates with MRI brain injury and delayed structural and microstructural brain development demonstrated significantly stronger high-frequency (beta and gamma frequency band) connectivity. Furthermore, neonates with delayed microstructural brain development demonstrated significantly weaker low-frequency (delta, theta, alpha frequency band) connectivity. Neonates with brain injury also displayed delayed functional maturation of EEG background activity, characterized by greater background discontinuity. Interpretation These data provide new evidence that early structural and microstructural developmental brain abnormalities can have immediate functional consequences that manifest as characteristic alterations of neuronal network connectivity. Such early perturbations of developing neuronal networks, if sustained, may be responsible for the persistent neurocognitive impairment prevalent in adolescent survivors of CHD. These foundational insights into the complex interplay between evolving brain structure and function may have relevance for a wide spectrum of neurological disorders manifesting early developmental brain injury. [ABSTRACT FROM AUTHOR]

Objective A post-spike slow wave (PSS) as part of a spike and slow wave is presumably related to inhibition of epileptic activity. In this study, we evaluated dynamic changes of PSS power toward seizure onset in patients with focal cortical dysplasia (FCD) type II. Methods We collected data from 10 pediatric patients with FCD type II, who underwent invasive monitoring with subdural grids. The PSS were averaged based on spike-triggering in 30 s epochs during both interictal and preictal periods. We quantitatively measured and compared PSS power and distribution between interictal and preictal periods, both within and outside the seizure onset zone (SOZ). Results PSS power was significantly higher in all areas during preictal period compared with interictal period. During preictal period, PSS power within SOZ was significantly higher than outside SOZ. From interictal to preictal period, the number of electrodes with high power PSS significantly increased within SOZ and decreased outside SOZ. Conclusions Toward seizure onset, PSS power increased in all areas, predominantly within SOZ, and became confined into SOZ in a subset of FCD type II patients. Significance Preictal PSS power increase and confinement into SOZ accompany transition to seizures. [ABSTRACT FROM AUTHOR]

Objective We analyzed the spatial distribution and concordance of fast (>10 Hz) and slow (<5 Hz) 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. [ABSTRACT FROM AUTHOR]

Acute cerebral cortical trauma often leads to paroxysmal activities that terminate in a few hours, but several months later, patients can develop epilepsy. The process occurring between the initial acute triggered seizures and the onset of spontaneous unprovoked seizures is termed epileptogenesis. Here the authors summarize recent morphological, electrophysiological, and computational studies demonstrating that partial cortical isolation increases the number and duration of silent states in the cortical network, boosting neuronal connectivity and network excitability. These changes develop progressively, and after several weeks their synergetic action leads to epilepsy. [ABSTRACT FROM AUTHOR]

Global cerebral ischemia induces, within seconds, suppression of spontaneous electrocortical activity, partly due to alterations in synaptic transmission. In vitro studies have found that repeated brief hypoxic episodes prolong the persistence of synaptic transmission due to weakened adenosine release. The aim of this study was to investigate in vivo whether the time to ischemic electrocortical suppression ( TES) could be altered during energy stress conditions such as rapid repeated global cerebral ischemia and kainate-induced seizures. Experiments were carried out in adult rats under chloral hydrate anaesthesia. Repeated episodes of 1 min of ischemia were induced by transiently clamping the carotid arteries in a ‘four-vessel occlusion’ model. We devised an automatic method of TES estimation based on the decay of the root mean square of two-channel electrocorticographic recordings. To distinguish the alterations in spontaneous electrocortical activity we compared TES with the ischemic suppression of visual evoked potentials (VEP). During the first ischemic episode, TES was ∼ 15 s and remained unchanged when five ischemic episodes were separated by 10-min reperfusion intervals. When ischemia was repeated after 2 min of reperfusion TES progressively increased, reaching a plateau value of ∼ 24 s. A similar plateau was reached during kainate-induced seizures. The TES plateau occurred prior to ischemic suppression of VEP. Our data suggest that, under conditions of acute metabolic stress in vivo, the ischemic suppression of spontaneous electrocortical activity may be delayed up to a plateau value. These findings are consistent with the hypothesis of a depletable adenosine pool; however, the restoration of synaptic transmission may be faster in vivo than in vitro. [ABSTRACT FROM AUTHOR]