Typical Childhood Absence Epilepsy Research Articles

The interictal activities load and cognitive performance of children with typical absence epilepsy

BackgroundThe description of childhood absence epilepsy (CAE) a benign self-limited generalized epilepsy has become a matter of debate. The objectives of this work were to evaluate the existence of psychiatric and cognitive impairments among patients with typical CAE and to correlate their possible relation to seizure frequency, duration of epilepsy, IISL, and valproate therapy.MethodsThe study was conducted on 19 typical CAE patients receiving valproate therapy, 11 newly diagnosed CAE patients not receiving AEDs, and 30 healthy control subjects (HCS). Participants were subjected to medical history taking, EEG monitoring, child behavior checklist (CBCL), Stanford Binet Intelligence Scale 5th edition, and computerized psychometric tests that assess cognitive domains and executive functions.ResultsThe study revealed a high rate of cognitive and psychiatric dysfunctions in CAE patients. 53.3% of patients had psychiatric problems versus 16.6% in HCS. Attention deficit hyperactive disorder (ADHD) (26.6%), anxiety (16.6%), and depression (6.6%) were the most common psychiatric disorders in the patient group. Withdrawn/depressed symptoms, thought problems, social problems, and attention problems in CAE patients were significantly increased compared to HCS. At the same time, CAE patients perform worse in cognitive scales than HCS with comparable intelligent quotient (IQ) scores.ConclusionCognitive and psychiatric impairments in typical CAE patients appear multifactorial in origin with epilepsy-related factors including the duration of epilepsy and interictal spike load (IISL).

De novo SCN1A, SCN8A, and CLCN2 mutations in childhood absence epilepsy

This study aimed to identify monogenic mutations from Chinese patients with childhood absence epilepsy (CAE) and summarize their characteristics. A total of 100 patients with CAE were recruited in Peking University First Hospital from 2005 to 2016 and underwent telephone and outpatient follow-up review. We used targeted disease-specific gene capture sequencing (involving 300 genes) to identify pathogenic variations for these patients. We identified three de novo epilepsy-related gene mutations, including missense mutations of SCN1A (c. 5399 T > A; p. Val1800Asp), SCN8A (c. 2371 G > T; p. Val791Phe), and CLCN2 (c. 481 G > A; p. Gly161Ser), from three patients, separately. All recruited patients presented typical CAE features and good prognosis. To date, CAE has been considered a complex disease caused by multiple susceptibility genes. In this study, we observed that 3% of typical CAE patients had a de novo mutation of a known monogenic epilepsy-related gene. Our study suggests that a significant proportion of typical CAE cases may be monogenic forms of epilepsy. For genetic generalized epilepsies, such as CAE, further studies are needed to clarify the contributions of de novo or inherited rare monogenic coding, noncoding and copy number variants.

Prevalence of idiopathic epilepsy among school children in Gharbia Governorate, Egypt

BackgroundEpilepsy is one of the most common neurological disorders among children. Data about its prevalence in Egypt is limited. Our aim was to study the prevalence of idiopathic epilepsy among school children in Gharbia governorate, Egypt. Subjects and MethodsA Cross-sectional school-based survey study was conducted; a validated screening questionnaire was distributed among urban and rural primary and preparatory school children. Students with suspected epilepsy were subjected to clinical evaluation, Electroencephalogram (EEG), and neuroimaging. Results9545 students completed the questionnaire, of whom 69 children proved to have idiopathic epilepsy. The lifetime prevalence of idiopathic epilepsy among school students aged 6–14 years was 7.2/1000. Higher prevalence was reported in males (7.7/1000) and in children from urban areas (8.25/1000). Generalized seizures were observed in 56.5% of the children with epilepsy, whereas focal seizures were present in 43.5%. Thirty-four (49.27%) children were diagnosed with specific childhood epileptic syndrome: 25 children had benign childhood epilepsy with centrotemporal spikes and nine children had typical childhood absence epilepsy. Treatment gap is around 12.5% in the studied children. Family history of epilepsy and parental consanguinity were evident in 73.9% and 21.7% of the epileptic children, respectively. The odds ratio for idiopathic epilepsy in children with family history of epilepsy was 23.9. ConclusionThe prevalence of idiopathic epilepsy among school students aged 6–14 years in Gharbia Governorate was 7.2/1000. The reported prevalence is similar to the prevalence of epilepsy in other Arab countries, but lower than the prevalence in Upper Egypt and in most developing countries.

Evaluation of deep gray matter volume, cortical thickness and white matter integrity in patients with typical absence epilepsy: a study using voxelwise-based techniques.

The objective of this study was to evaluate the cortical thickness and the volume of deep gray matter structures, measured from 3D T1-weighted gradient echo imaging, and white matter integrity, by diffusion tensor imaging (DTI) in patients with typical absence epilepsy (AE). Patients (n=19) with typical childhood AE and juvenile AE, currently taking antiepileptic medication, were compared with control subjects (n=19), matched for gender and age. 3D T1 magnetization-prepared rapid gradient echo-weighted imaging and DTI along 30 noncolinear directions were performed using a 1.5-T MR scanner. FreeSurfer was used to perform cortical volumetric reconstruction and segmentation of deep gray matter structures. For tract-based spatial statistics analysis of DTI, a white matter skeleton was created, along with a permutation-based inference with 5000 permutations. A threshold of p<0.05 was used to identify abnormalities in fractional anisotropy (FA). The mean, radial, and axial diffusivities were also projected onto the mean FA skeleton. Patients with AE presented decreased FA and increased mean diffusivity and radial diffusivity values in the genu and the body of the corpus callosum and right anterior corona radiata, as well as decreased axial diffusivity in the left posterior thalamic radiation, inferior cerebellar peduncle, right cerebral peduncle, and right corticospinal tract. However, there were no significant differences in cortical thickness or deep gray matter structure volumes between patients with AE and controls. Abnormalities found in white matter integrity may help to better understand the pathophysiology of AE and optimize diagnosis and treatment strategies.

Therapeutic Outcomes and Prognostic Factors in Childhood Absence Epilepsy.

Background and PurposeChildhood absence epilepsy (CAE) is one of the most common types of pediatric epilepsy. It is generally treated with ethosuximide (ESM), valproic acid (VPA), or lamotrigine (LTG), but the efficacy and adverse effects of these drugs remain controversial. This study compared initial therapy treatment outcomes, including VPA-LTG combination, and assessed clinical factors that may predict treatment response and prognosis.MethodsSixty-seven patients with typical CAE were retrospectively enrolled at the Korea University Medical Center. We reviewed patients' clinical characteristics, including age of seizure onset, seizure-free interval, duration of seizure-free period, freedom from treatment failure, breakthrough seizures frequency, and electroencephalogram (EEG) findings.ResultsThe age at seizure onset was 7.9±2.7 years (mean±SD), and follow-up duration was 4.4±3.7 years. Initially, 22 children were treated with ESM (32.8%), 23 with VPA (34.3%), 14 with LTG (20.9%), and 8 with VPA-LTG combination (11.9%). After 48 months of therapy, the rate of freedom from treatment failure was significantly higher for the VPA-LTG combination therapy than in the three monotherapy groups (p=0.012). The treatment dose administrated in the VPA-LTG combination group was less than that in the VPA and LTG monotherapy groups. The shorter interval to loss of 3-Hz spike-and-wave complexes and the presence of occipital intermittent rhythmic delta activity on EEG were significant factors predicting good treatment response.ConclusionsThis study showed that low-dose VPA-LTG combination therapy has a good efficacy and fewer side effects than other treatments, and it should thus be considered as a firstline therapy in absence epilepsy.

Assessment of Control in Typical Childhood Absence Epilepsy

We report relevant results of a survey that was aimed at understanding current practice variations in the assessment of control of typical childhood absence epilepsy.

Ethosuximide-Induced Conversion of Typical Childhood Absence to Rolandic Spikes

Coexistence of 2 idiopathic epilepsy syndromes (ie, childhood absence and Rolandic epilepsy), as evidenced by electroencephalographic (EEG) findings with or without clinical features of the 2 conditions, is uncommon and remains controversial. Few case reports support this coexistence either as a continuum or drug-induced conversion, whereas a large sample case review did not find such co-occurrence. The authors report a case of conversion of typical absence to Rolandic spikes after treatment with ethosuximide. An 11-year-old girl was diagnosed with typical childhood absence epilepsy at the age of 6 years with classic clinical and EEG features. She became seizure-free on ethosuximide but her follow-up EEGs consistently recorded right centrotemporal and centroparietal spikes without associated clinical seizures. This case may suggest simultaneous presence of these 2 common childhood idiopathic epilepsies either as a continuum or a drug-induced conversion.

Focal and generalized EEG paroxysms in childhood absence epilepsy: Topographic associations and distinctive behaviors during the first cycle of non‐REM sleep

To better understand the nature of the focal spike-wave discharges (FSWDs) and focally led generalized spike-wave discharges (GSWDs) in typical childhood absence epilepsy (CAE) and by implication their nosologic and taxonomic significance. Twenty-four abnormal video-electroencephalography (EEG) studies from 13 consecutive children with CAE and good response to appropriate antiepileptic drugs (AEDs) were analyzed. We studied the association between the topography of absence onset and the ictal automatisms, and the topographic correlation between FSWDs and GSWDs and their respective behavior during hyperventilation and the different states of phasic and nonphasic non-rapid eye movement (NREM) sleep. GSWDs were considered as of "focal" onset if a lead-in could be visibly recognized at a paper speed of 60 mm/s, and were classified by their topography. (1) Multifocal absences occurred in 10 children; anterior onset was noted in 81 absences (73.6%) from 12 children and posterior in 18 (16.4%) from 7 children; there was no association between topography of absence onset and ictal automatisms; (2) FSWDs occurred in 85% of children and were multifocal in 73% of them; 85% of FSWDs were anterior and 14% posterior; (3) there was good topographic association between FSWDs and the leading spike of GSWDs of "focal" onset in all children with FSWDs; (4) both FSWDs and GSWDs increased during hyperventilation; (5) FSWDs occurred mainly during noncyclical NREM sleep and during periods of reduced vigilance of cyclical NREM sleep, whereas GSWDs occurred during the periods of enhanced vigilance of NREM sleep; GSWDs occurred significantly more frequently than FSWDs at the transition from reduced to enhanced vigilance of NREM sleep. Our findings suggest that in CAE focal EEG paroxysms reflect a system of multifocal nonlocalizing electrically unstable cortical areas that under the facilitatory influence of exogenous or endogenous factors like sleep instability can foster a corticothalamic response of sufficient strength to generate 3-Hz GSWDs that are conditionally sustainable and potentially ictal. FSWDs can be viewed as incomplete forms of the GSWDs; together they define the EEG identity of idiopathic "generalized" epileptogenesis.

Early-onset versus typical childhood absence epilepsy; clinical and electrographic characteristics

PurposeChildhood absence epilepsy (CAE) is characterized by absence attacks with stereotyped electrographic discharges. Epidemiologic data concerning early-onset CAE is scarce. We tried to specifically analyze the early-onset CAE and compare it with typical CAE. MethodsIn this retrospective study, all patients with a clinical diagnosis of CAE were recruited in the outpatient epilepsy clinic at Shiraz University of Medical Sciences from 2008 to 2011. We considered the age of onset at four years or earlier as early-onset and above four years as typical CAE. Age, gender, age at seizure onset, seizure type(s), epilepsy risk factors, and EEG findings of all patients were registered routinely. Statistical analyses were performed using Chi square and Fisher's Exact tests. ResultsForty-six patients were diagnosed as having CAE. Sixteen patients (35%) had early-onset and 30 (65%) patients had typical CAE. Sex ratio (female to male) in early-onset was 7:9 and in typical CAE was 19:11 (P=0.2). Generalized tonic-clonic and myoclonic seizures were reported in both early-onset and typical CAE. The differences were not statistically significant. Epilepsy risk factors were similarly reported in both conditions. The EEG findings were similar in both groups. ConclusionWe did not observe any significant differences between early-onset and typical childhood absence epilepsies with respect to the demographic, clinical and electroencephalographic characteristics.

Early‐onset childhood absence epilepsy: is it a distinct entity?

Childhood absence epilepsy (CAE) typically starts between four and seven years of age. Onset before three years is rare and has not been previously reported from North America. We retrospectively reviewed the electroencephalography laboratory database and paediatric neurology clinic records (from January 2000 to June 2009) at our institution in order to identify patients with absence seizures beginning before age three. Information was collected for age, gender, neurodevelopment, antiepileptic drugs (AEDs) used, seizure control, follow-up, and side effects. Of 12 patients identified, mean age at onset was 20.5 months (range: 11 months to two years; follow-up: six months to 11 years). Seven of 12 patients had normal neurodevelopment and five had speech delay. Four patients were seizure-free without AEDs, three were seizure-free with a single AED, and five still had seizures with multiple AEDs. Three patients had recurrences after medication withdrawal. Other previously published series have identified better seizure control than that reported here, however, 16% of the 130 patients so far documented are reported to have poorly controlled epilepsy, indicating that early-onset CAE is not a homogeneous condition. The debate as to whether early-onset CAE is a distinct epilepsy syndrome therefore continues. We believe that early-onset CAE may be a distinct epilepsy syndrome, with some features that overlap with those of typical CAE, as well as unique distinguishing features. Large prospective multicentric studies would be necessary to definitely resolve this matter.

Genetics of the epilepsies: Channelopathies and beyond

Genetics of the epilepsies: Channelopathies and beyond

Atypical childhood absence epilepsy with preceding or simultaneous generalized tonic clonic seizures

Objective Although the current diagnostic criteria for childhood absence epilepsy (CAE) do not specifically exclude children with generalized tonic clonic seizures (GTCSs) occurring before or early in the course of the active absence seizures, some workers have suggested that they should be interpreted as doing so. The aim of this study was to compare the clinical features between children with typical CAE and those with atypical CAE with preceding or simultaneous episodes of GTCS (atypical CAE-GTCS). Methods A total of 11 patients with atypical CAE-GTCS and 30 with typical CAE were identified by using the current CAE criteria. Their clinical data, including age, sex, family history of epilepsy, personal history of febrile convulsions, onset ages of absences and GTCS, treatment, and outcome were statistically analyzed. Results The two groups had the same mean onset age of absences (6 years), and their seizure outcome was comparably favorable in terms of both absences and GTCS. There was no significant difference in other clinical data except for the onset age of GTCS between the groups. Conclusion These findings show the similarity in the main clinical features between the groups, suggesting that some patients with atypical CAE-GTCS may have a variant form of CAE with early onset of GTCS.

Simultaneous EEG, fMRI, and behavior in typical childhood absence seizures

Absence seizures cause transient impairment of consciousness. Typical absence seizures occur in children, and are accompanied by 3-4-Hz spike-wave discharges (SWDs) on electroencephalography (EEG). Prior EEG-functional magnetic resonance imaging (fMRI) studies of SWDs have shown a network of cortical and subcortical changes during these electrical events. However, fMRI during typical childhood absence seizures with confirmed impaired consciousness has not been previously investigated. We performed EEG-fMRI with simultaneous behavioral testing in 37 children with typical childhood absence epilepsy (CAE). Attentional vigilance was evaluated by a continuous performance task (CPT), and simpler motor performance was evaluated by a repetitive tapping task (RTT). SWD episodes were obtained during fMRI scanning from 9 patients among the 37 studied. fMRI signal increases during SWDs were observed in the thalamus, frontal cortex, primary visual, auditory, somatosensory, and motor cortex, and fMRI decreases were seen in the lateral and medial parietal cortex, cingulate gyrus, and basal ganglia. Omission error rate (missed targets) with SWDs during fMRI was 81% on CPT and 39% on RTT. For those seizure epochs during which CPT performance was impaired, fMRI changes were seen in cortical and subcortical structures typically involved in SWDs, whereas minimal changes were observed for the few epochs during which performance was spared. These findings suggest that typical absence seizures involve a network of cortical-subcortical areas necessary for normal attention and primary information processing. Identification of this network may improve understanding of cognitive impairments in CAE, and may help guide development of new therapies for this disorder.

Familial form of typical childhood absence epilepsy in a consanguineous context

Causative genes for childhood absence epilepsy (CAE) are unknown partly because families are small or phenotypically heterogeneous. In five consanguineous Tunisian families with at least two sibs with CAE, 14 patients fulfilled the diagnostic criteria for CAE (Epilepsia 1989; 30:389-399). Linkage analyses or direct sequencing excluded CACNG2, CACNA1A, CACNB4, and CACNA2D2, orthologs of genes responsible for autosomal recessive (AR) absence seizures in mice. These families will help identify (a) gene(s) responsible for CAE.

Spatiotemporal imaging of &amp;lsquo;generalized' seizure activity using MEG

Event Abstract Back to Event Spatiotemporal imaging of ‘generalized' seizure activity using MEG Pauly Ossenblok1*, Bert Kornips1, Hans Carpay2, Paul Boon1 and Gilles Van Luijtelaar3 1 Epilepsy Centre Kempenhaeghe, Netherlands 2 Tergooi Hospitals , Netherlands 3 Donders Center for Cognition, Netherlands Studies in the WAG/Rij rat [1] challenge the theory of primary generalized absence epilepsy by showing a crucial role for the cortex in generating the spike-and-wave discharges (SWDs). Association analysis of MEG signals recorded for children with absence epilepsy also demonstrated a focal onset region, followed by a recurrent pattern of regional activity during the spikes alternated by generalized activity during the slow-wave of the SWDs [2]. More recent findings of our study raised the question whether clinically distinct types of absence epilepsy differ by origin, while sharing a common corticothalamic network during the evolvement of the SWDs. The population studied (n=20; 6 – 14 years of age) ranges from patients with typical childhood absence epilepsy, who can be treated quite successfully with anti-epileptics, to more complex atypical forms and children who had absences and complex partial clinical features. For each of the seizures of these children the non-linear association analysis was performed, yielding both the dynamics of the SWDs and the regional distribution of the spikes, while the cortical origin of the SWDs was studied using advanced source analysis. The association analysis results of the SWDs indicated the involvement of mesiofrontal cortex and the bilateral frontal and temporoparietal regions during the spikes of the SWDs for each of the patients studied. However, the initial onset of the SWDs of the patients differing with regard to their clinical features may reflect either left or right frontal or temporoparietal regional activity or in case of complex partial semiology regional onset activity e.g. at the temporal lobe, a result which was in concordance with the dipole scan (MUSIC). If cortical structures activated before generalization can be identified for distinct subpopulations of absence epilepsy patients, this will change not only the concept of epilepsy, but also will improve the differential diagnosis of childhood absence epilepsy and may open new ways for treatment.

The ketogenic diet has no effect on the expression of spike‐and‐wave discharges and nutrient transporters in genetic absence epilepsy rats from Strasbourg

The genetic absence epilepsy rat from Strasbourg is considered an isomorphic, predictive, and homologous model of typical childhood absence epilepsy. It is characterized by the expression of spike-and-wave discharges (SWDs) in the thalamus and cortex. The ketogenic diet (KD) is successfully used in humans and animals with various types of seizures, but was not effective in children with intractable atypical absence epilepsy. Here, we studied its potential impact on the occurrence of SWDs in genetic absence epilepsy rat from Strasbourg. Rats were fed the KD for 3 weeks during which they were regularly subjected to the electroencephalographic recording of SWDs. The KD did not influence the number and duration of SWDs despite a 15-22% decrease in plasma glucose levels and a large increase in beta-hydroxybutyrate levels. Likewise, the KD did not affect the level of expression of the blood-brain barrier glucose transporter GLUT1 or of the monocarboxylate transporters, MCT1 and MCT2. This report extends the observation in humans that the KD does not appear to show effectiveness in intractable atypical absence epilepsy to this model of typical childhood absence epilepsy which responds to specific antiepileptic drugs.

Paroxysmal eyelid movements: A confusing feature of generalized photosensitive epilepsy

Eyelid flutter is sometimes part of typical childhood absence epilepsy. In this study, the authors describe persistent, frequent, nonepileptic paroxysmal eyelid movements in 19 children and adults (17 females and 2 males) with well-controlled generalized epilepsy. The patients were identified from five epilepsy centers. All had generalized photosensitive epilepsy requiring antiepileptic drugs. In two children, paroxysmal eyelid movements began 2 to 4 years before their epilepsy was noted; in the remainder, it was noted when epilepsy was first diagnosed. Age at last follow-up was 8 to 38 years (average 21 years) with average follow-up of 9 years. All patients showed photosensitive generalized spike-wave discharges on EEG. Paroxysmal eyelid movements were a source of diagnostic confusion, but direct examination and video during EEG recording distinguished the attacks from absence seizures. In all cases, the epilepsy was well controlled with antiepileptic drugs, but the paroxysmal eyelid movements did not resolve with age. In 12 cases, there was a family history of the eyelid disorder without epilepsy. The authors suggest an association between paroxysmal eyelid movements and photosensitive generalized epilepsy.—Valerie Biousse

Childhood absence epilepsy and febrile seizures: a family with a GABA(A) receptor mutation.

Although several genes for idiopathic epilepsies from families with simple Mendelian inheritance have been found, genes for the common idiopathic generalized epilepsies, where inheritance is complex, presently are elusive. We studied a large family with epilepsy where the two main phenotypes were childhood absence epilepsy (CAE) and febrile seizures (FS), which offered a special opportunity to identify epilepsy genes. A total of 35 family members had seizures over four generations. The phenotypes comprised typical CAE (eight individuals); FS alone (15), febrile seizures plus (FS(+)) (three); myoclonic astatic epilepsy (two); generalized epilepsy with tonic-clonic seizures alone (one); partial epilepsy (one); and unclassified epilepsy despite evaluation (two). In three remaining individuals, no information was available. FS were inherited in an autosomal dominant fashion with 75% penetrance. The inheritance of CAE in this family was not simple Mendelian, but suggestive of complex inheritance with the involvement of at least two genes. A GABA(A) receptor gamma2 subunit gene mutation on chromosome 5 segregated with FS, FS(+) and CAE, and also occurred in individuals with the other phenotypes. The clinical and molecular data suggest that the GABA(A) receptor subunit mutation alone can account for the FS phenotype. An interaction of this gene with another gene or genes is required for the CAE phenotype in this family. Linkage analysis for a putative second gene contributing to the CAE phenotype suggested possible loci on chromosomes 10, 13, 14 and 15. Examination of these loci in other absence pedigrees is warranted.

Constrictive pericarditis and hepatic encephalopathy

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Long-term prognosis of typical childhood absence epilepsy

Reply from the Authors: Classifying all absence epilepsy in children into various subtypes can be a difficult task; however, we did not freely categorize patients as having childhood absence epilepsy (CAE). For our study,1 we used the definition of CAE given by Loiseau5 and the definition of juvenile absence epilepsy(JAE) given by Wolf.6 All patients in our study presented with both the clinical (multiple absence seizures per day) and EEG picture of CAE (3 cycle per second spike and wave discharge). …