Paroxysmal Abnormalities Research Articles

CDKL5-associated developmental and epileptic encephalopathy: A long-term, longitudinal electroclinical study of 22 cases

ObjectiveThe study was conducted to analyze the possible diagnostic value of the electroclinical semiology of the epileptic seizures. MethodsWe evaluated the medical records of 17 females and 5 males with CDKL5 deficiency disorder (CDD) considering the long-term evolution, including the polygraphic video-EEG recordings. ResultsWe recognized three disease phases. We found that the seizure semiology was already recognizable in the first phase of the syndrome. In the short-term evolution, all patients had focal motor and 12/21 hypermotor seizures. Both epileptic spasms and myoclonic seizures were already present in more than half of the cases in the first 2 months after onset. In the second phase, the intermediate period, the polymorphic pattern was maintained, but in eight patients the electroclinical pattern of epileptic encephalopathy with hypsarrhythmia appeared. In the long-term period, the seizure polymorphism continued but myoclonic and epileptic spasms diminished. Tonic seizures appeared in the last 2 phases. Progressively, with the aggravation of seizures and paroxysmal EEG abnormalities impairment of the neurocognitive status was observed. Severe behavioral disturbances were seen in eight and autistic-like features in 14. ConclusionCDD is a true developmental and epileptic encephalopathy with a specific etiology characterized by the early appearance of epileptic seizures that quickly become polymorphic and drug resistant in infants that are most often female and already have neurological impairment. Polygraphic video-EEG recordings are important to recognize ictal events of the association of hypermotor seizures, epileptic spasms in clusters, and massive myoclonic jerks, already present at onset.

Association between EEG Paroxysmal Abnormalities and Levels of Plasma Amino Acids and Urinary Organic Acids in Children with Autism Spectrum Disorder.

Abnormalities in the plasma amino acid and/or urinary organic acid profile have been reported in autism spectrum disorder (ASD). An imbalance between excitatory and inhibitory neuronal activity has been proposed as a mechanism to explain dysfunctional brain networks in ASD, as also suggested by the increased risk of epilepsy in this disorder. This study explored the possible association between presence of EEG paroxysmal abnormalities and the metabolic profile of plasma amino acids and urinary organic acids in children with ASD. In a sample of 55 children with ASD (81.8% male, mean age 53.67 months), EEGs were recorded, and 24 plasma amino acids and 56 urinary organic acids analyzed. EEG epileptiform discharges were found in 36 (65%) children. A LASSO regression, adjusted by age and sex, was applied to evaluate the association of plasma amino acids and urinary organic acids profiles with the presence of EEG epileptiform discharges. Plasma levels of threonine (THR) (coefficient = −0.02, p = 0.04) and urinary concentration of 3-Hydroxy-3-Methylglutaric acid (HMGA) (coefficient = 0.04, p = 0.02) were found to be associated with the presence of epileptiform discharges. These results suggest that altered redox mechanisms might be linked to epileptiform brain activity in ASD.

Effect of anti-attention-deficit hyperactivity disorder (ADHD) medication on clinical seizures and sleep EEG: A retrospective study of Japanese children with ADHD.

AimsPatients with attention‐deficit hyperactivity disorder (ADHD) often exhibit basic or paroxysmal wave abnormalities on electroencephalography (EEG). Methylphenidate (MPH), an anti‐ADHD stimulant, has been reported to lower the seizure threshold. However, there have been no reports comparing EEG changes before and after administration of the central nervous system (CNS) stimulant MPH, or atomoxetine (ATX) hydrochloride, a non‐CNS stimulant. In this study, we investigated changes in sleep EEG before and after the administration of ADHD treatment drugs.MethodWith the approval of the ethics committee, the medical records of 28 children with ADHD (23 men and 5 women) who gave consent were retrospectively investigated. The appearance of sudden abnormal waves during a 10‐minute sleep EEG recording was measured in 0.1‐second units, and the duration of these waves was calculated as the paroxysmal index (PI).ResultsParoxysmal index did not differ significantly between patients who received MPH and those who received ATX. In addition, there were no exacerbations of clinical seizures.ConclusionIt was concluded that ADHD medications do not have an adverse effect on epileptic seizures or abnormal sleep EEGs.

Further delineation and long-term evolution of electroclinical phenotype in Mowat Wilson Syndrome. A longitudinal study in 40 individuals

BackgroundEpilepsy is a main feature of Mowat Wilson Syndrome (MWS), a congenital malformation syndrome caused by ZEB2 variants. The aim of this study was to investigate the long-term evolution of the electroclinical phenotype of MWS in a large population. MethodsForty-individuals with a genetically confirmed diagnosis were enrolled. Three age groups were identified (t1 = 0–4; t2 = 5–12; t3 = >13 years); clinical data and EEG records were collected, analyzed, and compared for age group. Video-EEG recorded seizures were reviewed. ResultsThirty-six of 40 individuals had epilepsy, of whom 35/35 aged >5 years. Almost all (35/36) presented focal seizures at onset (mean age at onset 3.4 ± 2.3 SD) that persisted, reduced in frequency, in 7/22 individuals after the age of 13. Absences occurred in 22/36 (mean age at onset 7.2 ± 0.9 SD); no one had absences before 6 and over 16 years old. Paroxysmal interictal abnormalities in sleep also followed an age-dependent evolution with a significant increase in frequency at school age (p = 0.002) and a reduction during adolescence (p = 0.008). Electrical Status Epilepticus during Sleep occurred in 14/36 (13/14 aged 5–13 years old at onset). Seven focal seizure ictal video-EEGs were collected: all were long-lasting and more visible clinical signs were often preceded by prolonged electrical and/or subtle (erratic head and eye orientation) seizures.Valproic acid was confirmed as the most widely used and effective drug, followed by levetiracetam. ConclusionsEpilepsy is a major sign of MWS with a characteristic, age-dependent, electroclinical pattern. Improvement with adolescence/adulthood is usually observed. Our data strengthen the hypothesis of a GABAergic transmission imbalance underlying ZEB2-related epilepsy.

Clinical Predictive Factors of Pathological EEG in Children with Febrile Seizures and Their Association with Subsequent Epileptic Seizures

AbstractThe objective of this study was to identify clinical parameters predicting either a pathological EEG or a subsequent epileptic seizure (SES), based on the relation between paroxysmal EEG abnormalities and clinical features in children who presented at least one febrile seizure (FS). We collected data of children who presented to our department during the period 2013 to 2018 for EEG recording as part of their febrile seizure assessment. Only children aged between 1 month to 5 years were included. Both the clinical and EEG data were retrospectively collected and statistically studied. We performed a detailed analysis of the EEG recordings. SES was identified for patients with sufficient follow-up. A total of 120 children were included in the study, of whom 48% had EEG abnormalities. Psychomotor retardation (p = 0.002), completion of an EEG within 7 days of the last FS (p = 0.046), and late age (> 3 years) of the first FS onset (p = 0.021) were significantly associated with a pathological EEG. In multivariate analysis, performing early EEG (< 7 days from the last FS) (odds ratio [OR]: 2.35; p = 0.043; confidence interval [CI]: 1.028–5.375) and psychomotor retardation (OR: 4.19; p = 0.008; CI: 1.46–12) were independent predictors of a pathological EEG. Of 120 patients, 45 had a follow-up. However, only 10 (22.22%) had SES. Children with SES tended more to have a psychomotor delay, compared with children without SES (50% vs. 14.28%, p = 0.029). Moreover, the percentage of initial abnormal EEG in patients with SES was significantly higher than those without SES (70% vs. 34.28%, p = 0.05). Even though some FS characteristics predict EEG abnormalities, they are not always associated with SES. We highlight the importance of performing an EEG in the group of children who had both FS and psychomotor retardation. This is most likely the group at the highest risk of developing epilepsy.

EEG Patterns in Patients with Prader-Willi Syndrome.

Prader–Willi syndrome (PWS) is a rare disease determined by the loss of the paternal copy of the 15q11-q13 region, and it is characterized by hypotonia, hyperphagia, obesity, short stature, hypogonadism, craniofacial dysmorphisms, and cognitive and behavioral disturbances. The aims of this retrospective study were to analyze interictal EEG findings in a group of PWS patients and to correlate them with genetic, clinical, and neuroimaging data. The demographic, clinical, genetic, EEG, and neuroimaging data of seventy-four patients were collected. Associations among the presence of paroxysmal EEG abnormalities, genotype, and clinical and neuroimaging features were investigated. Four patients (5.4%) presented drug-sensitive epilepsy. Interictal paroxysmal EEG abnormalities—focal or multifocal—were present in 25.7% of the cases, and the normalization of the EEG occurred in about 25% of the cases. In 63.2% of the cases, the paroxysmal abnormalities were bilaterally localized over the middle–posterior regions. Brain magnetic resonance imaging (MRI) was performed on 39 patients (abnormal in 59%). No relevant associations were found between paroxysmal EEG abnormalities and all of the other variables considered. Interictal paroxysmal EEG abnormalities—in particular, with a bilateral middle–posterior localization—could represent an important neurological feature of PWS that is not associated with genotype, cognitive or behavioral endophenotypes, MRI anomalies, or prognosis.

Language regression as a manifestation of epilepsy

Introduction: Childhood epileptic encephalopathies are age-dependent brain disorders in which ictal and interictal epileptogenic activity is the apparent cause of progressive cognitive and neuro-psychological impairment. Case report: A previously healthy four-year-old boy presented to the Emergency Department with a history of receptive and expressive language regression with four days of evolution, associated with seizure onset. Clinical features and electroencephalographic findings led to diagnosis of Landau-Kleffner syndrome. The boy was treated with valproate, clobazam, and prednisolone, with language improvement. Discussion/Conclusion: Landau-Kleffner syndrome is a rare epileptic encephalopathy with pathognomonic sudden aphasia, epilepsy, and paroxysmal electroencephalographic abnormalities. The condition should be suspected in children with normal development who show a deterioration of established language skills. Early diagnosis and treatment are important to improve outcome.

Shared genetic basis between genetic generalized epilepsy and background electroencephalographic oscillations.

ObjectiveParoxysmal epileptiform abnormalities on electroencephalography (EEG) are the hallmark of epilepsies, but it is uncertain to what extent epilepsy and background EEG oscillations share neurobiological underpinnings. Here, we aimed to assess the genetic correlation between epilepsy and background EEG oscillations.MethodsConfounding factors, including the heterogeneous etiology of epilepsies and medication effects, hamper studies on background brain activity in people with epilepsy. To overcome this limitation, we compared genetic data from a genome‐wide association study (GWAS) on epilepsy (n = 12 803 people with epilepsy and 24 218 controls) with that from a GWAS on background EEG (n = 8425 subjects without epilepsy), in which background EEG oscillation power was quantified in four different frequency bands: alpha, beta, delta, and theta. We replicated our findings in an independent epilepsy replication dataset (n = 4851 people with epilepsy and 20 428 controls). To assess the genetic overlap between these phenotypes, we performed genetic correlation analyses using linkage disequilibrium score regression, polygenic risk scores, and Mendelian randomization analyses.ResultsOur analyses show strong genetic correlations of genetic generalized epilepsy (GGE) with background EEG oscillations, primarily in the beta frequency band. Furthermore, we show that subjects with higher beta and theta polygenic risk scores have a significantly higher risk of having generalized epilepsy. Mendelian randomization analyses suggest a causal effect of GGE genetic liability on beta oscillations.SignificanceOur results point to shared biological mechanisms underlying background EEG oscillations and the susceptibility for GGE, opening avenues to investigate the clinical utility of background EEG oscillations in the diagnostic workup of epilepsy.

Tachycardia dependent early repolarisation pattern in subarachnoid haemorrhage related takotsubo syndrome.

We present a case of a patient who suffered subarachnoid haemorrhage (SAH), complicated by takotsubo syndrome, paroxysmal atrial fibrillation and ECG repolarisation abnormality, compatible with Brugada phenocopy. The early repolarisation morphology showed a paradox association with the cardiac cycle length; a relationship not yet documented in SAH. Our observation also sheds light on the genesis of the “spiked helmet” ECG sign.

S17-3 Association between ADHD/ASD and paroxysmal EEG abnormality

S17-3 Association between ADHD/ASD and paroxysmal EEG abnormality

Bone marrow failure

Bone marrow failure Abstract. Bone marrow failure involves a heterogeneous spectrum of rare benign hematological disorders caused by an impaired bone marrow function. Bone marrow failure can be acquired (acquired aplastic anemia) or congenital (inherited bone marrow failures). The disease is clinically characterized by cytopenias of one or more blood cell line (anemia, neutropenia and / or thrombocytopenia), possibly combined with signs of hemolysis and thrombophilia in paroxysmal nocturnal hemoglobinuria or morphological abnormalities in inherited forms. Due to significant advances in molecular genetic diagnostics, a comprehensive differentiation of an acquired or congenital form is central, since the cause of disease significantly affects the choice of therapy. Standard therapy has changed little in past decades (immunosuppression and / or allogeneic stem cell transplantation), however thrombopoietin receptor agonists just recently showed an improvement of all three blood cell lines in acquired aplastic anemia and are likely to be included in the future treatment algorithms. This article gives an overview of the disease, diagnosis and therapy of this heterogeneous disease group.

NMDA-receptor antibodies alter cortical microcircuit dynamics

NMDA-receptor antibodies (NMDAR-Abs) cause an autoimmune encephalitis with a diverse range of EEG abnormalities. NMDAR-Abs are believed to disrupt receptor function, but how blocking this excitatory synaptic receptor can lead to paroxysmal EEG abnormalities-or even seizures-is poorly understood. Here we show that NMDAR-Abs change intrinsic cortical connections and neuronal population dynamics to alter the spectral composition of spontaneous EEG activity and predispose brain dynamics to paroxysmal abnormalities. Based on local field potential recordings in a mouse model, we first validate a dynamic causal model of NMDAR-Ab effects on cortical microcircuitry. Using this model, we then identify the key synaptic parameters that best explain EEG paroxysms in pediatric patients with NMDAR-Ab encephalitis. Finally, we use the mouse model to show that NMDAR-Ab-related changes render microcircuitry critically susceptible to overt EEG paroxysms when these key parameters are changed, even though the same parameter fluctuations are tolerated in the in silico model of the control condition. These findings offer mechanistic insights into circuit-level dysfunction induced by NMDAR-Ab.

Quantitative EEG Tomography of Early Childhood Malnutrition.

The goal of this study is to identify the quantitative electroencephalographic (qEEG) signature of early childhood malnutrition [protein-energy malnutrition (PEM)]. To this end, archival digital EEG recordings of 108 participants in the Barbados Nutrition Study (BNS) were recovered and cleaned of artifacts (46 children who suffered an episode of PEM limited to the first year of life) and 62 healthy controls). The participants of the still ongoing BNS were initially enrolled in 1973, and EEGs for both groups were recorded in 1977–1978 (at 5–11 years). Scalp and source EEG Z-spectra (to correct for age effects) were obtained by comparison with the normative Cuban Human Brain Mapping database. Differences between both groups in the z spectra (for all electrode locations and frequency bins) were assessed by t-tests with thresholds corrected for multiple comparisons by permutation tests. Four clusters of differences were found: (a) increased theta activity (3.91–5.86 Hz) in electrodes T4, O2, Pz and in the sources of the supplementary motor area (SMA); b) decreased alpha1 (8.59–8.98 Hz) in Fronto-central electrodes and sources of widespread bilateral prefrontal are; (c) increased alpha2 (11.33–12.50 Hz) in Temporo-parietal electrodes as well as in sources in Central-parietal areas of the right hemisphere; and (d) increased beta (13.67–18.36 Hz), in T4, T5 and P4 electrodes and decreased in the sources of bilateral occipital-temporal areas. Multivariate Item Response Theory of EEGs scored visually by experts revealed a neurophysiological latent variable which indicated excessive paroxysmal and focal abnormality activity in the PEM group. A robust biomarker construction procedure based on elastic-net regressions and 1000-cross-validations was used to: (i) select stable variables and (ii) calculate the area under ROC curves (AUC). Thus, qEEG differentiate between the two nutrition groups (PEM vs Control) performing as well as visual inspection of the EEG scored by experts (AUC = 0.83). Since PEM is a global public health problem with lifelong neurodevelopmental consequences, our finding of consistent differences between PEM and controls, both in qualitative and quantitative EEG analysis, suggest that this technology may be a source of scalable and affordable biomarkers for assessing the long-term brain impact of early PEM.

F168. An EEG fingerprint of early protein-energy malnutrition

Early childhood Protein Energy Malnutrition (PEM) is an increasing worldwide phenomenon with lifelong neurodevelopmental consequences. There is thus a need for inexpensive imaging technologies to objectively identify and follow up the neural impact of malnutrition—Electroencephalography being an obvious choice. But EEG studies of PEM are scarce, performed on subjects with multiple stressors, only in the acute phase. A unique opportunity to improve these enquiries is the still ongoing Barbados Nutrition Study (BNS) which enrolled (1967–72) children with PEM during their first year of life. Under the direction of Frank Ramsey and E. Roy John, 248 digital EEG recordings were obtained (children 5–11 years) at the time that the Brain Research Lab and the Cuban Neuroscience Centre were developing quantitative EEG (qEEG; John et al., 1977). Recently, a large subsample of these digital EEGs was recovered. A unique opportunity to identify a qEEG fingerprint of early PEM has thus arisen, and which we here report. The final sample comprised 46 PEM and 62 control recordings (1 min resting state, eyes-closed,19 electrodes 10/20 system, sampling 100 Hz). Qualitative EEG was evaluated using a Likert-type scale. Multivariate Item Response Theory identified a neurophysiological state (NS) as a single latent variable explaining 0.88 of sample variance. qEEG evaluation at the electrodes (topography) consisted in calculating the log-power spectrum both at the scalp electrodes and sources and computing the z transform with regard to the Cuban normative database. Quantitative tomographic EEG (qEEGt) was carried out with CNEURO’s VARETA source analysis procedure based upon an MNI probabilistic template—necessary since MRIs where not available at that time. Multivariate permutation tests (N = 1000) were applied to t-tests in order to assess differences between groups. Qualitative analysis revealed highly significant changes in the latent variable (NS) with the PEM group showing excessive slow-wave, paroxysmal and focal abnormality activity, with a statistically significant effect for groups (p < 0.00001). qEEG (topographic) revealed (PEM) an increment of slow activities (<5 Hz) in centro-parietal electrodes and a decrease of alpha in fronto-central electrodes around 8.98 Hz as well as a significant increase of fast activity >15.2 Hz. qEEGT analysis: the PEM group, showed a significant increment in source power at lower frequencies (<5 Hz) and a decrease of power in alpha (8.9 Hz) in frontal region. The consistent differences in qEEG and qEEGt values between PEM and controls suggest they may be affordable biomarkers for the long-term actual brain impact of early childhood PEM. Excess slow-waves activity and decreased alpha activity in PEM children, may be a qEEG fingerprint of early PEM predicting which is correlated with many types of neuropathology, learning and performance difficulties.

The forsaking of the clinical EEG by psychiatry: how justified?

Despite decades of publications attesting to the role of the clinical EEG in diagnosing and managing psychiatric disorders, the procedure remains highly underutilized in the practice of psychiatry. The visually inspected EEG (vEEG) can detect various forms of abnormalities, each with its own clinical significance. Abnormalities can be paroxysmal (i.e., suggestive of an epileptic-like process) or stationary. The most important unanswered question remains the value of detecting epileptiform activity in a nonepileptic psychiatric patient in predicting favorable responses to anticonvulsant treatment. Despite the many shortcomings of vEEG, the available evidence suggests that in the presence of paroxysmal activity in a nonepileptic psychiatric patient a trial of a psychotropic anticonvulsant may be warranted if standard treatment has failed. More research on the contribution of paroxysmal EEG abnormalities to the problem of episodic psychiatric symptoms (e.g., panic attacks, dissociative episodes, repeated violence) is sorely needed. It is postulated that at least some of these conditions may represent an epilepsy spectrum disorder. Similarly, the significance of the presence of a slow-wave activity (whether focal or generalized) also deserves further well-designed research to ascertain the exact clinical significance. Nonetheless, the available data suggest that further medical workup is necessary to ascertain the nature and degree of the pathology when present.

EEG abnormalities and severity of symptoms in non-epileptic autistic children

Background It has been recently shown that electroencephalogram (EEG) paroxysmal abnormalities are frequently recorded in patients with autism despite the absence of seizures. Objective On the basis of the increasing evidence of EEG abnormalities in autism, the aim of this study was to detect the EEG abnormalities in relation to the degree of severity of autism. Patients and methods EEG was measured in 40 autistic children aged 2–12 years, in comparison with 40 typically developing matched children. The severity of autism was assessed using the Childhood Autism Rating Scale. Results We found that 50% of the autistic children had abnormal EEG findings. There was a statistically significant relation between the EEG abnormalities and the severity of autism. Moreover, there was a statistically significant relation between the site of the wave abnormalities and the severity of autism. Conclusion Our study suggests that the use of neurological investigative techniques such as EEG be considered routinely during the evaluation of autistic children.

Long-term follow-up of cognitive functions in patients with continuous spike-waves during sleep (CSWS).

Continuous spike-waves during sleep (CSWS) are associated with several cognitive, neurological, and psychiatric disorders, which sometimes persist after CSWS disappearance. The purpose of this retrospective study was to investigate the correlation between general (clinical and instrumental) and neuropsychological findings in CSWS, to identify variables that predispose patients to a poorer long-term neuropsychological outcome. Patients with spikes and waves during sleep with a frequency ≥25/min (spikes and waves frequency index - SWFI) were enrolled. There were patients presenting abnormal EEG activity corresponding to the classic CSWS and patients with paroxysmal abnormalities during sleep <85% with SWFI ≥25/min that was defined as excessive spike-waves during sleep (ESWS). Clinical and instrumental features and neuropsychological findings during and after the spike and wave active phase period were considered. A statistical analysis was performed utilizing the Spearman correlation test and multivariate analysis. The study included 61 patients; the mean follow-up (i.e., the period between SWFI ≥25 first recording and last observation) was 7years and 4months. The SWFI correlated inversely with full and performance IQ during CSWS/ESWS. Longer-lasting SWFI ≥25 was related to worse results in verbal IQ and performance IQ after CSWS/ESWS disappearance. Other variables may influence the neuropsychological outcome, like age at SWFI ≥25 first recording, perinatal distress, pathologic neurologic examination, and antiepileptic drug resistance. This confirms that CSWS/ESWS are a complex pathology and that many variables contribute to its outcome. The SWFI value above all during CSWS/ESWS and long-lasting SWFI ≥25 after CSWS/ESWS disappearance are the most significant indexes that appear mostly to determine cognitive evolution. This finding underscores the importance of EEG recordings during sleep in children with a developmental disorder, even if seizures are not reported, as well as the importance of using therapy with an early efficacy.

Cognitive Consequences in Children with Epilepsy

Some epilepsy is, in general, often associated with cognitive problems that can also affect a patient’s adjustments. Epileptic seizures result from an excessive, synchronous discharge of cerebral neurons. Interictal paroxysmal electroencephalogram (EEG) abnormalities are regarded as a correlate of persistent pathological neuronal discharges. Thus, correlation between cognitive deterioration and seizure severities/EEG paroxysmal abnormalities should be investigated. We have previously measured frontal/prefrontal lobe volumes using three-dimensional (3D)-magnetic resonance imaging (MRI) in children with benign childhood epilepsy with centrotemporal spikes, epilepsy with continuous spike-waves during slow sleep, frontal lobe epilepsy, and Panayiotopoulos syndrome, and confirmed that longer active seizure period as frequent spike-waves coupled with the occurrence of frequent seizures and presence of status epilepticus may be associated with prefrontal lobe growth disturbance, which relates to cognitive impairments. These findings suggest that seizure severities such as repeated seizures and presence of status epilepticus, and the subclinical paroxysmal EEG abnormalities may induce prefrontal lobe growth disturbance, which leads to intellectual impairments. Achieving better seizure control and remission for paroxysmal EEG abnormalities is a key to improve quality of life (QOL) in children with epilepsy. From the perspective of decreased cognitive problems and improving QOL, management may be required to remit seizures and paroxysmal EEG abnormalities as soon as possible to achieve optimal prognosis in epilepsy.

Automatic interpretation of the adult waking EEG

Automatic interpretation of EEG has been faced with significant difficulties because of continuous fluctuation of the background activity, occurrence of paroxysmal activities, contamination with artifacts, and use of different electrode montages. Therefore, the previous attempts of automatic EEG interpretation have focused on a certain feature of EEG such as the background activity and paroxysmal abnormalities. The primary purpose of this study is to establish a computer-assisted, off-line system for automatic comprehensive interpretation of EEG, which takes into account all features of the adult waking EEG and provides the results in a written form. First, we extracted features of EEGer’s visual inspection to quantitatively score the background activity, and the parameters for each frequency band were selected. Automatic detection of artifacts and spikes and automatic judgment of vigilance and attention level of subjects were incorporated into the system. The results of this system were shown to be in good conformity with the results of visual inspection of the same records by EEGers in healthy subjects as well as in patients with brain disorders including epilepsy. This system can be used as a supplementary tool for EEGer’s visual inspection, and its modified form can be applied for training EEGers and EEG technicians.

Perceived Stigma in Children with Epilepsy

Children with epilepsy are more likely to have poorer quality of life (QOL) than the general population. Stigma is a global phenomenon associated with several chronic diseases with great negative impact on patients and their families and deleterious consequences in their QOL. People with epilepsy report that stigma is one of the greatest challenges that they face. Adolescents can be mentally and emotionally fragile, therefore, epilepsy can stigmatize children and impair their independence, social abilities, peer relations, self-esteem, mood, and cognition during this turbulent stage of life. To develop and implement interventions to improve the psychosocial health of individuals with epilepsy, it is important for researchers and clinicians to understand the effects of the stigma accompanying epilepsy. Our previous study using Child Stigma Scale showed that children with frequent seizures perceived themselves as significantly more stigmatized compared to seizure-free children (p < 0.01). These findings suggest that a relationship may be seen between current seizure frequency and perceived stigma. On the other hand, the responses of children with epilepsy on the Child Stigma Scale were different depending on the localization of EEG paroxysmal abnormality (PA). The scores of all questions were significantly higher in the frontal group than those with PA in other regions (p < 0.01). Frontal EEG PA may function as a mediator of emotional responses such as stigma. Organizing children and adolescents support groups and effective educational intervention programs for children with and without epilepsy should be given priority in reduced stigma of children with epilepsy.