Nonconvulsive Seizures Research Articles

Automatic detection of non-convulsive seizures: A reduced complexity approach

Detection of non-convulsive seizures (NCSz) is a challenging task because they lack convulsions, meaning no physical visible symptoms are there to detect the presence of a seizure activity. Hence their diagnosis is not easy, also continuous observation of full length EEG for the detection of non-convulsive seizures (NCSz) by an expert or a technician is a very exhaustive, time consuming job. A technique for the automatic detection of NCSz is proposed in this paper. The database used in this research was recorded at the All India Institute of Medical Sciences (AIIMS), New Delhi. 13 EEG recordings of 9 subjects consisting of a total 23 seizures of 29.42min duration were used for analysis. Normalized modified Wilson amplitude is used as a key feature to classify between normal and seizure activity. The main advantage of this study lies in the fact that no classifier is used here and hence algorithm is very simple and computationally fast. With the use of only one feature, all of the seizures under test were detected correctly, and hence the median sensitivity and specificity of 100% and 99.21% were achieved respectively.

Continuous electroencephalogram detection of non-convulsive seizures in the pediatric intensive care unit: review of the utility and impact on management and outcomes.

Non-convulsive seizures (NCS) are common among critically ill children with acute encephalopathy. Continuous electroencephalogram (CEEG) monitoring is an indispensable tool to detect NCS, which is essential to guiding management and assessing prognosis. Risk factors for NCS are highest in pediatric intensive care unit (PICU) patients with altered mental status (AMS) and a recently witnessed clinical seizure, acute changes on neuroimaging, and/or interictal abnormalities on CEEG. Screening for at least 24 hours in at risk pediatric populations is ideal, but around half of NCS may be detected within the first hour. Rapid treatment of prolonged seizures or status epilepticus is critical, as higher seizure burdens have been associated with poorer outcomes in critically ill children. This review integrates current information on critically ill children with AMS and the use of CEEGs, risk factors for NCS, duration of CEEG monitoring, and how the detection of NCS impacts management and outcomes.

Safety, Tolerability, and Pharmacokinetics of Fosphenytoin Loading in Patients With Subarachnoid Hemorrhage.

Fosphenytoin is frequently used for the rapid delivery of phenytoin in subarachnoid hemorrhage (SAH) patients. The present study was performed to investigate the safety, tolerability, and pharmacokinetic profiles of rapid intravenous loading of fosphenytoin in SAH patients. Fosphenytoin was administered intravenously as a single loading dose of 20 mg phenytoin-equivalent/kg at an infusion rate of 150 mg PE/min to 30 adult patients with SAH, who experienced seizures or had a clinical suspicion of nonconvulsive seizures. Serum concentrations of free phenytoin were determined, and adverse events were assessed at 0, 10, 20 minutes, and 24 hours after the infusion of fosphenytoin. Four patients experienced transient lowering of blood pressure, but other adverse events were not observed. All patients achieved the therapeutic level of free phenytoin (1-2 mg/L) at the end of infusion, but most patients (28/30) entered the markedly supratherapeutic range and the mean serum concentration was 17.7 ± 8.13 mg/L; higher serum concentration was maintained up to 20 minutes after infusion (mean concentration; 3.46 ± 3.75 mg/L). At 24 hours after loading, a majority of the patients (25/30) maintained their levels within the therapeutic range of free phenytoin. Rapid intravenous loading of fosphenytoin was well tolerated and effective in promptly achieving the therapeutic level of free phenytoin, but most patients experienced overshoot of free phenytoin at the end of infusion. Because increased serum concentrations may increase the risk of cardiovascular complications, additional studies are needed to determine the optimal dose and infusion rate of fosphenytoin in SAH patients.

Ethosuximide Induces Hippocampal Neurogenesis and Reverses Cognitive Deficits in an Amyloid-β Toxin-induced Alzheimer Rat Model via the Phosphatidylinositol 3-Kinase (PI3K)/Akt/Wnt/β-Catenin Pathway

Neurogenesis involves generation of new neurons through finely tuned multistep processes, such as neural stem cell (NSC) proliferation, migration, differentiation, and integration into existing neuronal circuitry in the dentate gyrus of the hippocampus and subventricular zone. Adult hippocampal neurogenesis is involved in cognitive functions and altered in various neurodegenerative disorders, including Alzheimer disease (AD). Ethosuximide (ETH), an anticonvulsant drug is used for the treatment of epileptic seizures. However, the effects of ETH on adult hippocampal neurogenesis and the underlying cellular and molecular mechanism(s) are yet unexplored. Herein, we studied the effects of ETH on rat multipotent NSC proliferation and neuronal differentiation and adult hippocampal neurogenesis in an amyloid β (Aβ) toxin-induced rat model of AD-like phenotypes. ETH potently induced NSC proliferation and neuronal differentiation in the hippocampus-derived NSC in vitro. ETH enhanced NSC proliferation and neuronal differentiation and reduced Aβ toxin-mediated toxicity and neurodegeneration, leading to behavioral recovery in the rat AD model. ETH inhibited Aβ-mediated suppression of neurogenic and Akt/Wnt/β-catenin pathway gene expression in the hippocampus. ETH activated the PI3K·Akt and Wnt·β-catenin transduction pathways that are known to be involved in the regulation of neurogenesis. Inhibition of the PI3K·Akt and Wnt·β-catenin pathways effectively blocked the mitogenic and neurogenic effects of ETH. In silico molecular target prediction docking studies suggest that ETH interacts with Akt, Dkk-1, and GSK-3β. Our findings suggest that ETH stimulates NSC proliferation and differentiation in vitro and adult hippocampal neurogenesis via the PI3K·Akt and Wnt·β-catenin signaling.

308 EMF Utility of a Brief Training Module on Improving Emergency Physicians’ Ability to Identify Non-Convulsive Seizure on Emergent Electroencephalography Performed in Patients With Altered Mental Status

308 EMF Utility of a Brief Training Module on Improving Emergency Physicians’ Ability to Identify Non-Convulsive Seizure on Emergent Electroencephalography Performed in Patients With Altered Mental Status

Posttraumatic seizures and epilepsy in adult rats after controlled cortical impact

Posttraumatic epilepsy (PTE) has been modeled with different techniques of experimental traumatic brain injury (TBI) using mice and rats at various ages. We hypothesized that the technique of controlled cortical impact (CCI) could be used to establish a model of PTE in young adult rats. A total of 156 male Sprague-Dawley rats of 2–3 months of age (128 CCI-injured and 28 controls) was used for monitoring and/or anatomical studies. Provoked class 3–5 seizures were recorded by video monitoring in 7/57 (12.3%) animals in the week immediately following CCI of the right parietal cortex; none of the 7 animals demonstrated subsequent spontaneous convulsive seizures. Monitoring with video and/or video-EEG was performed on 128 animals at various time points 8–619 days beyond one week following CCI during which 26 (20.3%) demonstrated nonconvulsive or convulsive epileptic seizures. Nonconvulsive epileptic seizures of >10s were demonstrated in 7/40 (17.5%) animals implanted with 2 or 3 depth electrodes and usually characterized by an initial change in behavior (head raising or animal alerting) followed by motor arrest during an ictal discharge that consisted of high-amplitude spikes or spike-waves with frequencies ranging between 1 and 2Hz. Class 3–5 epileptic seizures were recorded by video monitoring in 17/88 (19%) and by video-EEG in 2/40 (5%) CCI-injured animals. Ninety of 156 (58%) animals (79 CCI-injured, 13 controls) underwent transcardial perfusion for gross and microscopic studies. CCI caused severe brain tissue loss and cavitation of the ipsilateral cerebral hemisphere associated with cell loss in the hippocampal CA1 and CA3 regions, hilus, and dentate granule cells, and thalamus. All Timm-stained CCI-injured brains demonstrated ipsilateral hippocampal mossy fiber sprouting in the inner molecular layer. These results indicate that the CCI model of TBI in adult rats can be used to study the structure–function relationships that underlie epileptogenesis and PTE.

Generalized periodic discharges and ‘triphasic waves’: A blinded evaluation of inter-rater agreement and clinical significance

ObjectivesGeneralized periodic discharges (GPDs) are associated with nonconvulsive seizures. Triphasic waves (TWs), a subtype of GPDs, have been described in relation to metabolic encephalopathy and not felt to be associated with seizures. We sought to establish the consistency of use of this descriptive term and its association with seizures. Methods11 experts in continuous EEG monitoring scored 20 cEEG samples containing GPDs using Standardized Critical Care EEG Terminology. In the absence of patient information, the inter-rater agreement (IRA) for EEG descriptors including TWs was assessed along with raters’ clinical EEG interpretation and compared with actual patient information. ResultsThe IRA for ‘generalized’ and ‘periodic’ was near-perfect (kappa=0.81), but fair for ‘triphasic’ (kappa=0.33). Patients with TWs were as likely to develop seizures as those without (25% vs 26%, N.S.) and surprisingly, patients with TWs were less likely to have toxic-metabolic encephalopathy than those without TWs (55% vs 79%, p<0.01). ConclusionsWhile IRA for the terms “generalized” and “periodic” is high, it is only fair for TWs. EEG interpreted as TWs presents similar risk for seizures as GPDs without triphasic appearance. GPDs are commonly associated with metabolic encephalopathy, but ‘triphasic’ appearance is not predictive. SignificanceConventional association of ‘triphasic waves’ with specific clinical conditions may lead to inaccurate EEG interpretation.

Importance of EEG in intensive care unit

Electroencephalography (EEG) is very important, noninvasive, bedside diagnostic procedure, for relatively quick differentiating the etiology and therapeutically efficacy in critically ill patients, with variety of cerebral injures and altered states of consciousness. It is essential to differentiate artifact from pathophysiologic EEG changes that would suggest encephalopathy, epileptiform activity or seizures. There are particular patterns typical of deepening encephalopathy, as well as, coma patterns, that have diagnostic and prognostic significance. Epileptiform patterns, including periodic lateralized epileptiform discharges, bilateral independent periodic lateralized epileptiform discharges and generalized periodic epileptiform discharges, present particular challenges, as there is a gray-zone between interictal patterns and the evolving patterns of nonconvulsive seizures. EEG is the only procedure for diagnosing nonconvulsive status epilepticus, showing generalized slow waves for idiopathic generalized epilepsy or regional spikes or sharp waves in focal epilepsy. Furthermore, it is the most frequently used test worldwide for confirmation of brain death. Together with polysomnography, EEG is used for showing cyclic variations and pathological changes during sleep and their relation to eye movements, body motility and dreaming. Accurate use of EEG in the intensive care unit requires optimal EEG technical expertise in performing the study, as well as, appropriate interpretation by a trained electrophysiologist.

Incidence of recurrent seizures following hospital discharge in patients with LPDs (PLEDs) and nonconvulsive seizures recorded on continuous EEG in the critical care setting.

Continuous EEG (cEEG) has helped to identify nonconvulsive seizures (NCS) and nonconvulsive status epilepticus (NCSE) along with lateralized periodic patterns (LPDs or PLEDs) in ICU patients with much higher frequency than previously appreciated, but understanding their implications may be more complex. The aim of this study was to investigate the incidence of recurrent seizures after hospital discharge and their associated factors in patients with PLEDs and NCS in the critical care setting. After IRB approval, we used our EEG reporting database to find 200 consecutive patients who had PLEDs and/or NCSs on cEEG. Patients with less than 3 months of follow-up were excluded. Remaining patients were divided into three groups: PLEDs+Seizure (NCS/NCSE), PLEDs only, and Seizures (NCS/NCSE) only. Medical records were reviewed to gather demographical and clinical details. Univariate data analysis was done using JMP 9.0 (Marlow, Buckinghamshire, UK). There were 51 patients in 'PLEDs+Seizure' group, 45 in 'PLEDs only' group, and 22 in 'Seizure only' group. Ischemic stroke, hemorrhage, and tumors were the top three etiologies. Nearly 47% of our study population had postdischarge seizures during a mean follow-up period of 11.9 (+/-6) months. We found that 24.4% of patients in the PLEDs only group had seizures after discharge, which increased to 60.7% if they had seizures as well during their ICU stay. Slightly more than 52% of patients had a postdischarge EEG, of which, 59% was in the form of inpatient cEEG during a rehospitalization, accounting for 30.5% of the total study population. It was an indicator of high readmission rates in this population. Almost every other patient with PLEDs and/or NCS on cEEG had seizures after ICU discharge. A quarter of patients on cEEG in the ICU with PLEDs alone had seizures after discharge, and after excluding prior epilepsy, 17% of patients with PLEDs had seizures on follow-up. This was dramatically increased with the recording of PLEDs with NCS, with 60% of patients having seizures after discharge from the ICU and 48% of patients after excluding prior epilepsy. Patients with NCS on cEEG alone had 63% chance of seizure recurrence that dropped to 38% with exclusion of prior epilepsy. Future studies are needed to define the postdischarge outcomes including seizure recurrence in this patient population. This article is part of a Special Issue entitled "Status Epilepticus".

Immediate Epileptogenesis after Kainate-Induced Status Epilepticus in C57BL/6J Mice: Evidence from Long Term Continuous Video-EEG Telemetry.

The C57BL/6J mouse as a model of seizure/epilepsy is challenging due to high mortality and huge variability in response to kainate. We have recently demonstrated that repeated administration of a low dose of kainate by intraperitoneal route can induce severe status epilepticus (SE) with 94% survival rate. In the present study, based on continuous video-EEG recording for 4-18 weeks from epidurally implanted electrodes on the cortex, we demonstrate that this method also induces immediate epileptogenesis (<1-5 days post-SE). This finding was based on identification of two types of spontaneous recurrent seizures; behavioral convulsive seizures (CS) and electrographic nonconvulsive seizures (NCS). The identification of the spontaneous CS, stage 3-5 types, was based on the behaviors (video) that were associated with the EEG characteristics (stage 3-5 epileptiform spikes), the power spectrum, and the activity counts. The electrographic NCS identification was based on the stage 1-2 epileptiform spike clusters on the EEG and their associated power spectrum. Severe SE induced immediate epileptogenesis in all the mice. The maximum numbers of spontaneous CS were observed during the first 4-6 weeks of the SE and they decreased thereafter. Mild SE also induced immediate epileptogenesis in some mice but the CS were less frequent. In both the severe and the mild SE groups, the spontaneous electrographic NCS persisted throughout the 18 weeks observation period, and therefore this could serve as a chronic model for complex seizures. However, unlike rat kainate models, the C57BL/6J mouse kainate model is a unique regressive CS model of epilepsy. Further studies are required to understand the mechanism of recovery from spontaneous CS in this model, which could reveal novel therapeutic targets for epilepsy.

Lacosamide in status epilepticus: Update on the TRENdS study.

Many patients with critical illness have been noted to have nonconvulsive seizures (NCSs) and nonconvulsive status epilepticus (NCSE). How aggressively these seizures should be treated is unclear. Many investigators feel that the morbidity of NCSs and NCSE is different from that of generalized convulsive status epilepticus (GCSE), so treatment should be less urgent. Consequently, many nonsedating AEDs have been used to treat NCSs and NCSE in patients with critical illness. Randomized, controlled trials demonstrating the efficacy of AEDs in NCSs and NCSE are lacking. The Treatment of Recurrent Electrographic Nonconvulsive Seizures (TRENdS) study compared lacosamide to fosphenytoin in the treatment of NCSs. An update of the study is presented. This article is part of a Special Issue entitled "Status Epilepticus".

Which EEG patterns in coma are nonconvulsive status epilepticus?

Nonconvulsive status epilepticus (NCSE) is common in patients with coma with a prevalence between 5% and 48%. Patients in deep coma may exhibit epileptiform EEG patterns, such as generalized periodic spikes, and there is an ongoing debate about the relationship of these patterns and NCSE. The purposes of this review are (i) to discuss the various EEG patterns found in coma, its fluctuations, and transitions and (ii) to propose modified criteria for NCSE in coma. Classical coma patterns such as diffuse polymorphic delta activity, spindle coma, alpha/theta coma, low output voltage, or burst suppression do not reflect NCSE. Any ictal patterns with a typical spatiotemporal evolution or epileptiform discharges faster than 2.5 Hz in a comatose patient reflect nonconvulsive seizures or NCSE and should be treated. Generalized periodic diacharges or lateralized periodic discharges (GPDs/LPDs) with a frequency of less than 2.5 Hz or rhythmic discharges (RDs) faster than 0.5 Hz are the borderland of NCSE in coma. In these cases, at least one of the additional criteria is needed to diagnose NCSE (a) subtle clinical ictal phenomena, (b) typical spatiotemporal evolution, or (c) response to antiepileptic drug treatment. There is currently no consensus about how long these patterns must be present to qualify for NCSE, and the distinction from nonconvulsive seizures in patients with critical illness or in comatose patients seems arbitrary. The Salzburg Consensus Criteria for NCSE [1] have been modified according to the Standardized Terminology of the American Clinical Neurophysiology Society [2] and validated in three different cohorts, with a sensitivity of 97.2%, a specificity of 95.9%, and a diagnostic accuracy of 96.3% in patients with clinical signs of NCSE. Their diagnostic utility in different cohorts with patients in deep coma has to be studied in the future. This article is part of a Special Issue entitled "Status Epilepticus".

Status epilepticus epidemiology—tracking a moving target

A surprisingly high rate of nonconvulsive seizures and status epilepticus is found during continuous EEG monitoring in critically ill patients. A recent analysis of data regarding hospitalization and mortality in patients with status epilepticus emphasizes the relevance not only of how status epilepticus is defined, but also of how it is detected.

Progressive, Seizure-Like, Spike-Wave Discharges Are Common in Both Injured and Uninjured Sprague-Dawley Rats: Implications for the Fluid Percussion Injury Model of Post-Traumatic Epilepsy.

Variable-duration oscillations and repetitive, high-voltage spikes have been recorded in the electrocorticogram (ECoG) of rats weeks and months after fluid percussion injury (FPI), a model of traumatic brain injury. These ECoG events, which have many similarities to spike-wave-discharges (SWDs) and absence seizures, have been proposed to represent nonconvulsive seizures characteristic of post-traumatic epilepsy (PTE). The present study quantified features of SWD episodes in rats at different time points after moderate to severe FPI, and compared them with age-matched control rats. Control and FPI-injured rats at 1 year of age displayed large-amplitude and frequent SWD events at frontal and parietal recording sites. At 3-6 months, SWDs were shorter in duration and less frequent; extremely brief SWDs (i.e., "larval") were detected as early as 1 month. The onset of the SWDs was nearly always synchronous across electrodes and of larger amplitude in frontal regions. A sensory stimulus, such as a click, immediately and consistently stopped the occurrence of the SWDs. SWDs were consistently accompanied by behavioral arrest. All features of SWDs in control and experimental (FPI) rats were indistinguishable. None of the FPI-treated rats developed nonconvulsive or convulsive seizures that could be distinguished electrographically or behaviorally from SWDs. Because SWDs have features similar to genetic absence seizures, these results challenge the hypothesis that SWDs after FPI reflect PTE.

Prediction of rhythmic and periodic EEG patterns and seizures on continuous EEG with early epileptiform discharges.

Continuous EEG (cEEG) is necessary to document nonconvulsive seizures (NCS), nonconvulsive status epilepticus (NCSE), as well as rhythmic and periodic EEG patterns of 'ictal-interictal uncertainty' (RPPIIU) including periodic discharges, rhythmic delta activity, and spike-and-wave complexes in neurological intensive care patients. However, cEEG is associated with significant recording and analysis efforts. Therefore, predictors from short-term routine EEG with a reasonably high yield are urgently needed in order to select patients for evaluation with cEEG. The aim of this study was to assess the prognostic significance of early epileptiform discharges (i.e., within the first 30 min of EEG recording) on the following: (1) incidence of ictal EEG patterns and RPPIIU on subsequent cEEG, (2) occurrence of acute convulsive seizures during the ICU stay, and (3) functional outcome after 6 months of follow-up. We conducted a separate analysis of the first 30 min and the remaining segments of prospective cEEG recordings according to the ACNS Standardized Critical Care EEG Terminology as well as NCS criteria and review of clinical data of 32 neurological critical care patients. In 17 patients with epileptiform discharges within the first 30 min of EEG (group 1), electrographic seizures were observed in 23.5% (n = 4), rhythmic or periodic EEG patterns of 'ictal-interictal uncertainty' in 64.7% (n = 11), and neither electrographic seizures nor RPPIIU in 11.8% (n = 2). In 15 patients with no epileptiform discharges in the first 30 min of EEG (group 2), no electrographic seizures were recorded on subsequent cEEG, RPPIIU were seen in 26.7% (n = 4), and neither electrographic seizures nor RPPIIU in 73.3% (n = 11). The incidence of EEG patterns on cEEG was significantly different between the two groups (p = 0.008). Patients with early epileptiform discharges developed acute seizures more frequently than patients without early epileptiform discharges (p = 0.009). Finally, functional outcome six months after discharge was significantly worse in patients with early epileptiform discharges (p=0.01). Epileptiform discharges within the first 30 min of EEG recording are predictive for the occurrence of ictal EEG patterns and for RPPIIU on subsequent cEEG, for acute convulsive seizures during the ICU stay, and for a worse functional outcome after 6 months of follow-up. This article is part of a Special Issue entitled Status Epilepticus.

Adding Insult to Injury: Nonconvulsive Seizures in Abusive Head Trauma.

The primary objectives of this study were to determine the prevalence of nonconvulsive seizures and nonconvulsive status epilepticus in patients with abusive head trauma who underwent electroencephalography (EEG) monitoring and to describe predictive factors for this population. Children with a diagnosis of abusive head trauma were studied retrospectively to determine the rate of EEG monitoring, the rate of nonconvulsive seizures and nonconvulsive status epilepticus, and the associated neuroimaging findings. Over 11 years, 73 of 199 (36.8%) children with abusive head trauma had electroencephalography monitoring performed. Of these, 20 (27.4%) had nonconvulsive seizures and 3 (4.1%) had nonconvulsive status epilepticus. The presence of subarachnoid hemorrhage and cortical T2 / fluid-attenuated inversion recovery signal abnormalities were both significantly associated with the presence of nonconvulsive seizures / nonconvulsive status epilepticus. Nonconvulsive seizures are relatively common in abusive head trauma and may go unrecognized. Specific neuroimaging characteristics increase the likelihood of nonconvulsive seizures on EEG.

Subconvulsive dose of kainic acid transiently increases the locomotor activity of adult Wistar rats.

Kainic acid (KA) is a potent neurotoxic substance valuable in research of temporal lobe epilepsy. We tested how subconvulsive dose of KA influences spontaneous behavior of adult Wistar rats. Animals were treated with 5 mg/kg of KA and tested in Laboras open field test for one hour in order to evaluate various behavioral parameters. Week after the KA treatment animals were tested again in Laboras open field test. Finally, rat's brains were sliced and stained with Fluoro-Jade B to detect possible neuronal degeneration. Treatment with KA increased the time spent by locomotion (p<0.01), exploratory rearing (p<0.05) and animals traveled longer distance (p<0.01). These parameters tended to increase thirty minutes after KA administration. Week after the treatment we did not found differences in any measured behavioral parameter. Histology in terms of Fluoro-Jade B staining did not reveal any obvious neuronal damage in hippocampus. These results demonstrate that subconvulsive KA dose changes the behavioral parameters only transiently. Clarification of timing of the KA induced changes may contribute to understand mutual relationship between non-convulsive seizures and behavioral/cognitive consequences.

Baseline EEG pattern on continuous ICU EEG monitoring and incidence of seizures.

To identify the probability of detecting nonconvulsive seizures based on the initial pattern seen in the first 30 minutes of continuous EEG (cEEG) monitoring. Continuous EEG monitoring reports from 243 adult patients were reviewed, assessing the baseline cEEG monitoring pattern and the presence of seizures during the entire monitoring period. The baseline EEG patterns were classified into nine categories: seizures, lateralized periodic discharges, generalized periodic discharges, focal epileptiform discharges, burst suppression, asymmetric background, generalized slowing, generalized periodic discharges with triphasic morphology, and normal. Overall, 51 patients (21%) had nonconvulsive seizures at any time during cEEG monitoring. Notably, 112 patients had generalized slowing as the initial EEG pattern, and none of these patients were noted to have seizures. Seizure rates among the types of baseline EEG findings were as follows: lateralized periodic discharges (56%, n = 9), burst suppression (50%, n = 10), generalized periodic discharges (50%, n = 2), normal (33%, n = 3), focal epileptiform discharges (31%, n = 35), and asymmetric background (11%, n = 46). Patients with only generalized slowing seen on the baseline EEG recording are unlikely to develop seizures on subsequent cEEG monitoring. Depending on the clinical circumstance, the standard duration of cEEG recording (24-48 hours) may be unnecessary in patients with generalized slowing as their only cEEG abnormality.

Consensus statement on continuous EEG in critically ill adults and children, part I: indications.

Critical Care Continuous EEG (CCEEG) is a common procedure to monitor brain function in patients with altered mental status in intensive care units. There is significant variability in patient populations undergoing CCEEG and in technical specifications for CCEEG performance. The Critical Care Continuous EEG Task Force of the American Clinical Neurophysiology Society developed expert consensus recommendations on the use of CCEEG in critically ill adults and children. The consensus panel recommends CCEEG for diagnosis of nonconvulsive seizures, nonconvulsive status epilepticus, and other paroxysmal events, and for assessment of the efficacy of therapy for seizures and status epilepticus. The consensus panel suggests CCEEG for identification of ischemia in patients at high risk for cerebral ischemia; for assessment of level of consciousness in patients receiving intravenous sedation or pharmacologically induced coma; and for prognostication in patients after cardiac arrest. For each indication, the consensus panel describes the patient populations for which CCEEG is indicated, evidence supporting use of CCEEG, utility of video and quantitative EEG trends, suggested timing and duration of CCEEG, and suggested frequency of review and interpretation. CCEEG has an important role in detection of secondary injuries such as seizures and ischemia in critically ill adults and children with altered mental status.

Non-convulsive seizures in children with infection-related altered mental status.

In the intensive care unit, the use of continuous electroencephalography (cEEG) in children with altered mental status often results in the detection of non-convulsive seizures (NCS). Children with influenza can occasionally display altered mental status, but the prevalence of NCS in children with influenza with altered mental status is yet to be determined. This study determined the prevalence of NCS in pediatric patients with altered mental status associated with influenza A(H1N1)pdm09 infection. We retrospectively reviewed admissions to the pediatric intensive care unit between September 2009 and February 2010 and confirmed the presence of NCS on cEEG in children with influenza A(H1N1)pdm09 and with altered mental status. Of the 15 patients (aged 41-159 months old), NCS was identified on cEEG in five children (33%). Approximately one-third of the children infected with influenza A(H1N1)pdm09 with altered mental status had NCS. Further research is needed to determine if the detection and management of NCS improve outcome in these children.