Epileptiform EEG Patterns Research Articles

Epileptiform patterns predicting unfavorable outcome in postanoxic patients: A matter of time?

ObjectiveHistorically, epileptiform malignant EEG patterns (EMPs) have been considered to anticipate an unfavorable outcome, but an increasing amount of evidence suggests that they are not always or invariably associated with poor prognosis. We evaluated the prognostic significance of an EMP onset in two different timeframes in comatose patients after cardiac arrest (CA): early-EMPs and late-EMPs, respectively. MethodsWe included all comatose post-CA survivors admitted to our intensive care unit (ICU) between 2016 and 2018 who underwent at least two 30-minute EEGs, collected at T0 (12–36 h after CA) and T1 (36–72 h after CA). All EEGs recordings were re-analyzed following the 2021 ACNS terminology by two senior EEG specialists, blinded to outcome. Malignant EEGs with abundant sporadic spikes/sharp waves, rhythmic and periodic patterns, or electrographic seizure/status epilepticus, were included in the EMP definition. The primary outcome was the cerebral performance category (CPC) score at 6 months, dichotomized as good (CPC 1–2) or poor (CPC 3–5) outcome. ResultsA total of 58 patients and 116 EEG recording were included in the study. Poor outcome was seen in 28 (48%) patients. In contrast to late-EMPs, early-EMPs were associated with a poor outcome (p = 0.037), persisting after multiple regression analysis. Moreover, a multivariate binomial model coupling the timing of EMP onset with other EEG predictors such as T1 reactivity and T1 normal voltage background can predict outcome in the presence of an otherwise non-specific malignant EEG pattern with quite high specificity (82%) and moderate sensitivity (77%). ConclusionsThe prognostic significance of EMPs seems strongly time-dependent and only their early-onset may be associated with an unfavorable outcome. The time of onset of EMP combined with other EEG features could aid in defining prognosis in patients with intermediate EEG patterns.

WS1.3. Normal EEG: Drowsiness and Sleep, and Normal Variants

The EEG in the normal awake child and adult is well known and needs to be known for proper reading and reporting and identifying an abnormal transient or pattern. The following are points of emphasis: Alpha rhythm seen after age of 5 years, Significant theta activity (4–7 Hz) is present in the EEG of children and adolescents. Delta activity in the awake tracing is rarely seen after the age of 5 years. Beta rhythm is seen anteriorly. All these will be discussed in details with traces. In the evaluation of abnormalities in the EEG, one needs to be constantly aware that there are many EEG transients that morphologically resemble epileptiform discharges and that need to be distinguished from diagnostically crucial epileptiform abnormalities to avoid overdiagnosis or misdiagnosis. These include: Artifacts: for example, electrode pop, muscle potentials, eye movements, electrocardiogram (EKG), chewing, electrical, etc. Normal components of ongoing background activity: for example, vertex sharp transients of sleep, f waves, slow wave sleep, POSTs, mu rhythm, lambda waves, drowsy activity during sleep in children that may often be associated with sharp components, etc. Epileptiform variants of dubious clinical significance: there are a large number of benign epileptiform variants that must be recognized, lest they be misinterpreted. Although morphologically similar, they are nonepileptogenic as they have no established relationship with the process responsible for generating epileptic seizures. Such sharp transients include 14 to 6 per second positive spikes, small sharp spikes or benign epileptiform transients of sleep, 6 Hz spike wave or phantom spike wave, wicket spikes, psychomotor variant pattern or rhythmic midtemporal discharges, breach rhythm, etc. Sleep not only activates diagnostically useful epileptiform EEG patterns, but also unmasks several types of nonepileptogenic sharp transients. It is necessary that anyone dedicating a career in epilepsy be well aware of these. Often reading EEG requires eyeballing and identifying patterns. The more the number of EEGs reviewed the more the possibility of not missing out normal patterns and rhythms. These will be demonstrated in various EEG epochs in the workshop.

Natural History Studies and Clinical Trial Readiness for Genetic Developmental and Epileptic Encephalopathies.

The developmental and epileptic encephalopathies (DEEs) are the most severe group of epilepsies. They usually begin in infancy or childhood with drug-resistant seizures, epileptiform EEG patterns, developmental slowing or regression, and cognitive impairment. DEEs have a high mortality and profound morbidity; comorbidities are common including autism spectrum disorders. With advances in genetic sequencing, over 400 genes have been implicated in DEEs, with a genetic cause now identified in over 50% patients. Each genetic DEE typically has a broad genotypic-phenotypic spectrum, based on the underlying pathophysiology. There is a pressing need to improve health outcomes by developing novel targeted therapies for specific genetic DEE phenotypes that not only improve seizure control, but also developmental outcomes and comorbidities. Clinical trial readiness relies firstly on a deep understanding of phenotype-genotype correlation and evolution of a condition over time, in order to select appropriate patients for clinical trials. Understanding the natural history of the disorder informs assessment of treatment efficacy in terms of both clinical outcome and biomarker utility. Natural history studies (NHS) provide a high quality, integrated, comprehensive approach to understanding a complex disease and underpin clinical trial design for novel therapies. NHS are pre-planned observational studies designed to track the course of a disease and identify demographic, genetic, environmental, and other variables, including biomarkers, that correlate with the disease's evolution and outcomes. Due to the rarity of individual genetic DEEs, appropriately funded high-quality DEE NHS will be required, with sustainable frameworks and equitable access to affected individuals globally.

A characteristic occipital epileptiform EEG pattern in ADCK3-related mitochondrial disease.

ADCK3-related disease is a mitochondrial disorder associated with an abnormality of coenzyme Q10 metabolism. Ataxia and epilepsy are common, and the phenotype overlaps with other mitochondrial encephalopathies, particularly POLG-related disease. CoQ10 supplementation may be beneficial. We have noted a remarkable epileptiform pattern in ADCK3-related encephalopathy, and since EEG studies in this rare condition are limited, we wished to assess the evolution of EEG characteristics in patients with this disorder. All EEG recordings of the four known patients from Mid-Norway were systematically reviewed. EEG graphoelements were classified according to the standardized computer-based organized reporting of EEG (SCORE) and international glossary terms. The evolution of EEG features was assessed. A total of 96 recordings spanning over 15-32 years were available, with a mean of 24 per patient (range: 17-28). Altogether, 50 digital recordings were reviewed, including four long-term and 46 selected paper segments. In three patients, EEG showed prominent bilateral asynchronous and synchronous epileptiform discharges in occipital and posterior-temporal regions. This intense activity included multiple epileptiform graphoelements, which occurred continuously, nearly continuously or in prolonged runs. The findings remained stable over many years. Although the number of patients is small, we suggest that interictal EEG findings of continuous/nearly continuous bi-occipital spike-waves may serve as a biomarker for this potentially treatable condition. This peculiar EEG pattern might help to differentiate ADCK3-related disease from the more common POLG-related disease, which is usually characterized by lateralized or focal slowing with more sporadic epileptiform elements of similar topography.

The clinical significance of small sharp spikes: A retrospective study of 909 patients in epilepsy monitoring unit

ObjectivesTo determine the incidence and clinical significance of small sharp spikes (SSS) in the patient population of the adult Epilepsy Monitoring Unit (EMU). MethodsThis is a retrospective study of EEG data and medical records from consecutive patients who underwent video-EEG recording in the adult EMU from March 2013 to February 2019. SSS, interictal epileptiform discharges (IEDs), and ictal patterns were identified. ResultsOf the 909 patients reviewed, SSS were observed in110 (12.1 %) patients. Epilepsy was present in 101 of the 110 (91.8 %) patients with SSS and in 441 of the 799 (55.2 %) patients without SSS. The incidence of epilepsy was significantly higher in patients with SSS than in those without SSS (OR = 9.1, 95 % CI: 4.5–18.3, P < 0.01). The sensitivity of SSS for epilepsy was 18.6 % and the specificity was 97.5 %. The incidence of SSS was strongly correlated with the frequency of IEDs (OR 1.89; 95 %CI: 1.60–2.24, P < 0.01). When both present, SSS and IEDs were co-lateralized in the same hemisphere. ConclusionsThere is a statistically significant association between SSS and focal epilepsy. SSS have similar clinical implications to IEDs in the lateralization and localization of temporal lobe seizures. SSS can be an epileptiform EEG pattern for temporal lobe epilepsy.

How soon should urgent EEG be performed following a first epileptic seizure?

PurposePatients with a first unprovoked epileptic seizure are often seen in emergency services. Electroencephalography (EEG) is indicated for diagnosing epilepsy, but the optimal time to perform this test has not been defined. This study aimed to determine the time interval following a seizure within which EEG has the greatest diagnostic yield. MethodsWe conducted a retrospective study of all adult patients with a first unprovoked seizure who had undergone emergency EEG (July 2014–December 2019). Data collection included demographics, seizure type, time interval to EEG study, EEG pattern identified, and the prescription after emergency assessment. An optimal cut-off point for time to EEG was obtained, and an adjusted regression model was performed to establish associations with the presence of epileptiform abnormalities. ResultsA total of 170 patients were included (mean age: 50.7 years, 40.6% women). Epileptiform discharges were identified in 34.1% of recordings, nonepileptiform abnormalities in 46.5%, and normal findings in 19.4%. A lower latency from seizure to EEG was associated with a higher probability of finding epileptiform discharges (median: 12.7 in the epileptiform EEGs vs. 20 h in the nonepileptiform EEGs, p < 0.001). The time interval associated with the highest probability of detecting an epileptiform EEG pattern was within the first 16 h after seizure onset: 52.1% of recordings performed before the 16-h cut-off showed these abnormal patterns compared with 20.2% performed after (p < 0.001). These findings were not related to the presence of an epileptogenic lesion in neuroimaging or to other clinical variables. The finding of epileptiform abnormalities was followed by a greater prescription of antiseizure drugs (96.4% vs. 66% in nonepileptiform patterns, p < 0.001). ConclusionThe diagnostic yield of EEG following a first unprovoked epileptic seizure is highest when this test is performed within the first 16 h after onset of the event.

Assessment of the Validity of the 2HELPS2B Score for Inpatient Seizure Risk Prediction

Seizure risk stratification is needed to boost inpatient seizure detection and to improve continuous electroencephalogram (cEEG) cost-effectiveness. 2HELPS2B can address this need but requires validation. To use an independent cohort to validate the 2HELPS2B score and develop a practical guide for its use. This multicenter retrospective medical record review analyzed clinical and EEG data from patients 18 years or older with a clinical indication for cEEG and an EEG duration of 12 hours or longer who were receiving consecutive cEEG at 6 centers from January 2012 to January 2019. 2HELPS2B was evaluated with the validation cohort using the mean calibration error (CAL), a measure of the difference between prediction and actual results. A Kaplan-Meier survival analysis was used to determine the duration of EEG monitoring to achieve a seizure risk of less than 5% based on the 2HELPS2B score calculated on first- hour (screening) EEG. Participants undergoing elective epilepsy monitoring and those who had experienced cardiac arrest were excluded. No participants who met the inclusion criteria were excluded. The main outcome was a CAL error of less than 5% in the validation cohort. The study included 2111 participants (median age, 51 years; 1113 men [52.7%]; median EEG duration, 48 hours) and the primary outcome was met with a validation cohort CAL error of 4.0% compared with a CAL of 2.7% in the foundational cohort (P = .13). For the 2HELPS2B score calculated on only the first hour of EEG in those without seizures during that hour, the CAL error remained at less than 5.0% at 4.2% and allowed for stratifying patients into low- (2HELPS2B = 0; <5% risk of seizures), medium- (2HELPS2B = 1; 12% risk of seizures), and high-risk (2HELPS2B, ≥2; risk of seizures, >25%) groups. Each of the categories had an associated minimum recommended duration of EEG monitoring to achieve at least a less than 5% risk of seizures, a 2HELPS2B score of 0 at 1-hour screening EEG, a 2HELPS2B score of 1 at 12 hours, and a 2HELPS2B score of 2 or greater at 24 hours. In this study, 2HELPS2B was validated as a clinical tool to aid in seizure detection, clinical communication, and cEEG use in hospitalized patients. In patients without prior clinical seizures, a screening 1-hour EEG that showed no epileptiform findings was an adequate screen. In patients with any highly epileptiform EEG patterns during the first hour of EEG (ie, a 2HELPS2B score of ≥2), at least 24 hours of recording is recommended.

P10-T Correlation of various EEG patterns with multimodal prognostic factors in patients with post-anoxic coma

Bilateral absence of N20, elevated NSE levels and anoxic brain injury signs in neuroimaging, are noted as predictors of poor outcome in comatose patients after cardiac arrest (CA). We evaluated the association of various EEG patterns with these prognostic factors in comatose patients post AC. In our study, 166 patients with cardiac arrest in coma were stratified according to 4 independent EEG patterns: benign, RSE, generalized periodic discharges [GPDs], malignant non-epileptiform. NSE level > 68 ng/mL, bilateral absence of median nerve SEP and moderate to severe anoxic brain injury on neuroimaging, were considered indicators of poor prognosis. Of 166 patients that were included, a benign EEG pattern was recorded in 76 patients (45.8%); RSE occurred in 36 patients, a periodic pattern (GPDs) was seen in 13 patients (7.8%); and a malignant non epileptiform EEG pattern was recorded in 41 patients (24.7%). The four EEG patterns were highly associated with different prognostic indicators. Patients with benign EEG pattern and RSE showed lower NSE levels and were less likely to show bilateral absence N20 responses and severe anoxic brain injury on neuroimaging. On the other side, patients with GPDs and malignant pattern were associated more frequently with bilateral absence of N20 responses, higher NSE levels and severe anoxic brain injury on neuroimaging. These data show that the a benign EEG pattern and RSE without periodisms, may be a predictor of a good outcome and a more aggressive treatment may be indicated in this patients, given the possibility of a better prognosis.

P16-T Early signs of transformation of neocortical activity to epileptiform patterns in experimental model of epilepsy

This study was aimed at receiving information concerning organization of the cortical cellular activity in relation to the epileptiform EEG patterns, using ionic model of experimental formation of epileptic focus. This investigation was supported by the KBN grant, Nr4-T11E-006-22. Evaluation of the relationship between EEG patterns and cellular activity was attempted in the region of parietal association cortex (middle suprasylvian gyrus) in the group of five adult cats. Multiunit cellular activity was recorded with sampling frequency 4 kHz, using permanently implanted multicontact concentric electrode: 16 contacts, each about 40 micrometers of diameter and the distance between contacts of 200 micrometers. The electrode was implanted in the vicinity of cannula enabling subdural transfer of artificial cerebrospinal fluid with increased concentration of potassium ions. The recording and perfusion was performed in quiet, awake animal without necessity of using any pharmacological treatment. Early signs of transformation of neocortical activity to epileptiform patterns show considerable degree of independence of the patterns of cellular activity with respect to EEG. The incident of increased intensity and generalization of cellular activity creates the development of variable, irregular superficial electric fields within wide frequency range. This early stage of transformation of cortical activity to epileptiform patterns ends with the appearance of definite patterns of cellular activity, predominantly in internal cortical cell layers with corresponding EEG slow waves and/or spikes. The results suggest the possibility of existence of transient “paroxysmal” cellular activities without coexistence of standard epileptiform patterns in EEG records.

Epileptiform EEG patterns during different techniques of induction of general anaesthesia with sevoflurane and propofol: a randomised trial

The aim of the study was to assess the influence of volatile induction of general anaesthesia with sevoflurane using two different techniques and intravenous anaesthesia with propofol on the possible presence of epileptiform electroencephalograph patterns during the induction of general anaesthesia. Sixty patients (age 18-70 years) were recruited. Exclusion criteria included history of epilepsy, neurological or neurosurgical diseases, pre-existing EPs in initial EEG recordings, medication interfering with EEG patterns. Patients were randomly allocated into three different groups: A (sevoflurane, increasing concentrations technique); B (sevoflurane, vital capacity technique); C (intravenous propofol). The clinical and instrumental monitoring included arterial blood pressure, heart rate, standard electrocardiography II, arterial oxygen saturation, facial electromyography, fraction of inspired sevoflurane, fraction of expired sevoflurane, minimal alveolar concentration of sevoflurane, and BIS. Neurophysiological analysis of EEGs showed different EPs: polyspikes (PS), rhythmic polyspikes (PSR), and periodic epileptiform discharges (PED). EPs (p < 0.05) were observed in Group A (56%) and Group B (37%), but not in Group C. One patient in group B presented with clinical seizures. No significant differences in the vital parameters and anaesthesia parameters between groups was observed, regardless of the presence of EPs, which were associated with both low and more likely high (falsely indicating awakening from anaesthesia) BIS scores. Our study shows that the BIS score variations do not detect epileptiform activity, which was associated with both low and high scores. The sevoflurane concentration reached either sedative or toxic concentrations.

Acute Non-Convulsive Status Epilepticus after Experimental Traumatic Brain Injury in Rats.

Severe traumatic brain injury (TBI) induces seizures or status epilepticus (SE) in 20-30% of patients during the acute phase. We hypothesized that severe TBI induced with lateral fluid-percussion injury (FPI) triggers post-impact SE. Adult Sprague-Dawley male rats were anesthetized with isoflurane and randomized into the sham-operated experimental control or lateral FPI-induced severe TBI groups. Electrodes were implanted right after impact or sham-operation, then video-electroencephalogram (EEG) monitoring was started. In addition, video-EEG was recorded from naïve rats. During the first 72 h post-TBI, injured rats had seizures that were intermingled with other epileptiform EEG patterns typical to non-convulsive SE, including occipital intermittent rhythmic delta activity, lateralized or generalized periodic discharges, spike-and-wave complexes, poly-spikes, poly-spike-and-wave complexes, generalized continuous spiking, burst suppression, or suppression. Almost all (98%) of the electrographic seizures were recorded during 0-72 h post-TBI (23.2 ± 17.4 seizures/rat). Mean latency from the impact to the first electrographic seizure was 18.4 ± 15.1 h. Mean seizure duration was 86 ± 57 sec. Analysis of high-resolution videos indicated that only 41% of electrographic seizures associated with behavioral abnormalities, which were typically subtle (Racine scale 1-2). Fifty-nine percent of electrographic seizures did not show any behavioral manifestations. In most of the rats, epileptiform EEG patterns began to decay spontaneously on Days 5-6 after TBI. Interestingly, also a few sham-operated and naïve rats had post-operation seizures, which were not associated with EEG background patterns typical to non-convulsive SE seen in TBI rats. To summarize, our data show that lateral FPI-induced TBI results in non-convulsive SE with subtle behavioral manifestations; this explains why it has remained undiagnosed until now. The lateral FPI model provides a novel platform for assessing the mechanisms of acute symptomatic non-convulsive SE and for testing treatments to prevent post-injury SE in a clinically relevant context.

Evaluating the impact of fast-fMRI on dynamic functional connectivity in an event-based paradigm.

The human brain is known to contain several functional networks that interact dynamically. Therefore, it is desirable to analyze the temporal features of these networks by dynamic functional connectivity (dFC). A sliding window approach was used in an event-related fMRI (visual stimulation using checkerboards) to assess the impact of repetition time (TR) and window size on the temporal features of BOLD dFC. In addition, we also examined the spatial distribution of dFC and tested the feasibility of this approach for the analysis of interictal epileptiforme discharges. 15 healthy controls (visual stimulation paradigm) and three patients with epilepsy (EEG-fMRI) were measured with EPI-fMRI. We calculated the functional connectivity degree (FCD) by determining the total number of connections of a given voxel above a predefined threshold based on Pearson correlation. FCD could capture hemodynamic changes relative to stimulus onset in controls. A significant effect of TR and window size was observed on FCD estimates. At a conventional TR of 2.6 s, FCD values were marginal compared to FCD values using sub-seconds TRs achievable with multiband (MB) fMRI. Concerning window sizes, a specific maximum of FCD values (inverted u-shape behavior) was found for each TR, indicating a limit to the possible gain in FCD for increasing window size. In patients, a dynamic FCD change was found relative to the onset of epileptiform EEG patterns, which was compatible with their clinical semiology. Our findings indicate that dynamic FCD transients are better detectable with sub-second TR than conventional TR. This approach was capable of capturing neuronal connectivity across various regions of the brain, indicating a potential to study the temporal characteristics of interictal epileptiform discharges and seizures in epilepsy patients or other brain diseases with brief events.

Epileptiform and periodic EEG activities induced by rapid sevoflurane anaesthesia induction

ObjectivesThe aim of the study was to compare the EEG findings and haemodynamic parameters of adult male patients while undergoing mask induction with sevoflurane anaesthesia with either controlled hyperventilation (CH) or spontaneous breathing (SB). MethodsTwenty male patients, aged 23–52 (mean 42) years were anaesthetized randomly with either spontaneous breathing or mild controlled hyperventilation via mask. EEG was recorded using a full 10–20 electrode set. ResultsAnaesthesia induction with high inhaled concentrations of sevoflurane produced several epileptiform and periodic EEG patterns. CH doubled the amount of these EEG patterns compared to SB. Higher heart rate was recorded in the CH group. ConclusionsWe describe a high incidence of paroxysmal EEG activity: epileptiform and generalized periodic discharges (GPDs) during rapid sevoflurane in nitrous oxide-oxygen mask induction in hyperventilated male patients. However these activities have no effect to the heart rate or the mean arterial pressure. SignificanceThe monitoring of GPDs and burst suppression patterns during rapid anaesthesia induction with sevoflurane provides possibility to study the effects of volatile anaesthetics in the healthy brain. In order to analyse the different sources of EEG patterns a wide-band multichannel EEG recording is necessary.

Seizure type and interictal epileptiform EEG patterns in Nigerians

Seizure type and interictal epileptiform EEG patterns in Nigerians

A definition and classification of status epilepticus--Report of the ILAE Task Force on Classification of Status Epilepticus.

The Commission on Classification and Terminology and the Commission on Epidemiology of the International League Against Epilepsy (ILAE) have charged a Task Force to revise concepts, definition, and classification of status epilepticus (SE). The proposed new definition of SE is as follows: Status epilepticus is a condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms, which lead to abnormally, prolonged seizures (after time point t1 ). It is a condition, which can have long-term consequences (after time point t2 ), including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures. This definition is conceptual, with two operational dimensions: the first is the length of the seizure and the time point (t1 ) beyond which the seizure should be regarded as "continuous seizure activity." The second time point (t2 ) is the time of ongoing seizure activity after which there is a risk of long-term consequences. In the case of convulsive (tonic-clonic) SE, both time points (t1 at 5min and t2 at 30min) are based on animal experiments and clinical research. This evidence is incomplete, and there is furthermore considerable variation, so these time points should be considered as the best estimates currently available. Data are not yet available for other forms of SE, but as knowledge and understanding increase, time points can be defined for specific forms of SE based on scientific evidence and incorporated into the definition, without changing the underlying concepts. A new diagnostic classification system of SE is proposed, which will provide a framework for clinical diagnosis, investigation, and therapeutic approaches for each patient. There are four axes: (1) semiology; (2) etiology; (3) electroencephalography (EEG) correlates; and (4) age. Axis 1 (semiology) lists different forms of SE divided into those with prominent motor systems, those without prominent motor systems, and currently indeterminate conditions (such as acute confusional states with epileptiform EEG patterns). Axis 2 (etiology) is divided into subcategories of known and unknown causes. Axis 3 (EEG correlates) adopts the latest recommendations by consensus panels to use the following descriptors for the EEG: name of pattern, morphology, location, time-related features, modulation, and effect of intervention. Finally, axis 4 divides age groups into neonatal, infancy, childhood, adolescent and adulthood, and elderly.

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".

Influence of the Sevoflurane Concentration on the Occurrence of Epileptiform EEG Patterns

Objectives and AimThis study was performed to analyse the effects of different sevoflurane concentrations on the incidence of epileptiform EEG activity during induction of anaesthesia in children in the clinical routine.BackgroundIt was suggested in the literature to use sevoflurane concentrations lower than 8% to avoid epileptiform activity during induction of anaesthesia in children.Methods100 children (age: 4.6±3.0 years, ASA I–III, premedication with midazolam) were anaesthetized with 8% sevoflurane for 3 min or 6% sevoflurane for 5 min in 100% O2 via face mask followed by 4% sevoflurane until propofol and remifentanil were given for intubation. EEGs were recorded continuously and were analysed visually with regard to epileptiform EEG patterns.ResultsFrom start of sevoflurane until propofol/remifentanil administration, 38 patients (76%) with 8% sevoflurane had epileptiform EEG patterns compared to 26 patients (52%) with 6% (p = 0.0106). Epileptiform potentials tended to appear later in the course of the induction with 6% than with 8%. Up to an endtidal concentration of 6% sevoflurane, the number of children with epileptiform potentials was similar in both groups (p = 0.3708). The cumulative number of children with epileptiform activity increased with increasing endtidal sevoflurane concentrations. The time from start of sevoflurane until loss of consciousness was similar in patients with 8% and 6% sevoflurane (42.2±17.5 s vs. 44.9 s ±14.0 s; p = 0.4073). An EEG stage of deep anaesthesia with continuous delta waves <2.0 Hz appeared significantly earlier in the 8% than in the 6% group (64.0±22.2 s vs. 77.9±20.0 s, p = 0.0022).ConclusionThe own analysis and data from the literature show that lower endtidal concentrations of sevoflurane and shorter administration times can be used to reduce epileptiform activity during induction of sevoflurane anaesthesia in children.

Electroencephalography and Dementia: A Literature Review and Future Perspectives

While many studies have investigated electroencephalographic (EEG) features of dementia, few have analysed the relationship between EEG and cerebrospinal fluid biomarkers in cognitive impairment. Seizures are frequently observed at the end stage of Alzheimer disease, and experimental animal studies support the view that epileptiform activity may contribute to the cognitive decline. In this paper, after reviewing literature findings concerning the role of EEG in dementia, we show the preliminary results of our study aimed to correlate the presence of epileptiform EEG patterns with cerebrospinal fluid biomarkers in order to better define the prognosis of dementia. Our study shows a clear relationship between phospho-tau protein levels and epileptiform EEG pattern. This finding seems to suggest in humans the observation made in animal models that not only β-amyloid protein, but also tau and phospho-tau proteins, are involved in the aberrant regulation of neural transmission possibly contributing to EEG deterioration, cognitive decline and worse prognosis. On the basis of the relationship between phospho-tau protein, cognitive decline and epileptogenicity we suspect that high liquoral phospho-tau levels and epileptiform EEG pattern may provide an early identification of patients with dementia and/or represent an aggressive phenotype of dementia. We propose that qualitative EEG analysis integrated with cerebrospinal biomarkers may be extensively used to better define dementia.

Nonconvulsive status epilepticus and coma

Nonconvulsive status epilepticus (NCSE) in a comatose patient cannot be diagnosed without electroencephalography (EEG). In many advanced coma stages, the EEG exhibits continuous or periodic EEG abnormalities, but their causal role in coma remains unclear in many cases. To date there is no consensus on whether to treat NCSE in a comatose patient in order to improve the outcome or to retract from treatment, as these EEG patterns might reflect the end stages of a dying brain. On the basis of EEG, NCSE in comatose patients may be classified as generalized or lateralized. This review aims to summarize the ongoing debate of NCSE and coma and to critically reassess the available literature on coma with epileptiform EEG pattern and its prognostic and therapeutic implications. The authors suggest distinguishing NCSE proper and comatose NCSE, which includes coma with continuous lateralized discharges or generalized epileptiform discharges (coma-LED, coma-GED). Although NCSE proper is accompanied by clinical symptoms suggestive of status epilepticus and mild impairment of consciousness, such as in absence status or complex focal status epilepticus, coma-LED and coma-GED represent deep coma of various etiology without any clinical motor signs of status epilepticus but with characteristic epileptiform EEG pattern. Hence coma-LED and coma-GED can be diagnosed with EEG only. Subtle or stuporous status epilepticus and epilepsia partialis continua-like symptoms in severe acute central nervous system (CNS) disorders represent the borderland in this biologic continuum between NCSE proper and comatose NCSE (coma-LED/GED). This pragmatic differentiation could act as a starting point to solve terminologic and factual confusion.

Broad Sharp Waves—An Underrecognized EEG Pattern in Patients with Epileptic Seizures

: Broad sharp waves (BSWs) are a rarely recognized EEG pattern, defined as focal or lateralized high voltage, biphasic, sharply contoured 0.5 to 1/sec waves distinguished from background activities by exceeding their voltage for at least two times. The aim of the study was to determine EEG criteria, frequency, and clinical significance of BSWs. During a 2-year period, we prospectively gathered EEG records exhibiting BSWs in a large EEG laboratory of a university hospital. Clinical variables and the relationship to epileptic seizures were analyzed. Forty-eight (0.6% of 7569) patients exhibited BSWs. In 38 (79%) patients, they were localized over the frontal region. In 31 (65%) patients, no spikes or sharp waves have been recorded. Thirty-four (71%) patients underwent previous neurosurgical interventions. All but one patient suffered one or more epileptic seizures corresponding to a positive predictive value of BSWs for seizures of 98%. A symptomatic etiology of the seizures, i.e., head trauma, brain tumor, aneurysm clipping after subarachnoid hemorrhage, and stroke could be established in all but two patients. In four patients, seizures have been classified as acute symptomatic, in 43 (86%) patients remote symptomatic epilepsy was diagnosed, and in 38 (79%) patients of frontal lobe origin. Broad sharp waves can be considered as an epileptiform EEG pattern on its own. Furthermore, BSWs are an indicator for acute and/or remote cerebral lesions.