Early-onset absence epilepsy: Clinical and electroencephalographic features in three children

Fernández‐Torre, José L.; Herranz, J L; Martínez-Martínez, Marián; Maestro, Iratxe; Arteaga, Rosa; Barrasa, J

doi:10.1016/j.braindev.2005.10.009

Cited by 15 publications

(29 citation statements)

References 7 publications

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“…We studied the topography of the FSWDs and the focal lead‐in of the GSWDs in CAE, focusing on attributes that could provide important clues about the nature of these focalities, and therefore their possible clinical and taxonomic significance. To avoid blurring our findings by focal EEG changes that could reflect acquired (for example age‐related vascular) structural irritative lesions, we studied children with typical CAE (ILAE, 1989); children with other absence syndromes of either mixed or uncertain etiology, such as epilepsy with myoclonic absences (Bureau & Tassinari, 2005) or absences with onset before the age of 3 years (Fernandez‐Torre et al., 2006), or of presumed idiopathic nature but of uncertain prognosis, such as eyelid myoclonia with absences (Caraballo et al., 2009) were excluded. In this way, any insight on EEG focalities in CAE, the purest form of idiopathic childhood absence IGE, could pertain to other forms of idiopathic absence epilepsy of childhood, adolescence, and adulthood.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2012

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SUMMARYPurpose: 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. Methods: 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. Key Findings: (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. Significance: 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.

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Section: Discussionmentioning

confidence: 99%

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

et al. 2012

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“…Onset is commonly between 12 and 36 months (5,6,9–16), but in a few infants, it starts earlier (7–9,11). Both sexes appear equally affected (5,7,8,11–16).…”

Section: Demographic and Electroclinical Datamentioning

confidence: 99%

“…Although lowest age at onset compatible with CAE is uncertain, children with TAS starting from a few months to 4 years of age have been reported in literature (4–16). Some authors believe that TAS in this age group may be merely a common denominator of various IGEs (4,17).…”

Section: Introductionmentioning

confidence: 99%

“…Some authors believe that TAS in this age group may be merely a common denominator of various IGEs (4,17). Nevertheless, there are reports supporting the existence of a distinct early childhood epileptic syndrome primarily characterized by TAS, normal early psychomotor development, good antiepileptic drug (AED) seizure control and normal cognitive outcome (5–16).…”

Section: Introductionmentioning

confidence: 99%

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Early‐onset pure absence epilepsy: a distinct epileptic syndrome

Verrotti¹,

Agostinelli²,

Olivieri³

et al. 2011

Acta Paediatrica

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“…VPA monotherapy should represent the first-line treatment because it controls absences in the majority of cases [60,69]. Ethosuximide (ESM) had been previously used in some patients with a good seizure control [70].…”

Section: Introductionmentioning

confidence: 99%

"Electro-clinical syndromes" with onset in paediatric age: the highlights of the clinical-EEG, genetic and therapeutic advances

et al. 2011

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The genetic causes underlying epilepsy remain largely unknown, and the impact of available genetic data on the nosology of epilepsy is still limited. Thus, at present, classification of epileptic disorders should be mainly based on electroclinical features. Electro-clinical syndrome is a term used to identify a group of clinical entities showing a cluster of electro-clinical characteristics, with signs and symptoms that together define a distinctive, recognizable, clinical disorder. These often become the focus of treatment trials as well as of genetic, neuropsychological, and neuroimaging investigations. They are distinctive disorders identifiable on the basis of a typical age onset, specific EEG characteristics, seizure types, and often other features which, when taken together, permit a specific diagnosis which, in turn, often has implications for treatment, management, and prognosis. Each electro-clinical syndrome can be classified according to age at onset, cognitive and developmental antecedents and consequences, motor and sensory examinations, EEG features, provoking or triggering factors, and patterns of seizure occurrence with respect to sleep. Therefore, according to the age at onset, here we review the more frequently observed paediatric electro-clinical syndrome from their clinical-EEG, genetic and therapeutic point of views.

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Early-onset absence epilepsy: Clinical and electroencephalographic features in three children

Cited by 15 publications

References 7 publications

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

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

Early‐onset pure absence epilepsy: a distinct epileptic syndrome

"Electro-clinical syndromes" with onset in paediatric age: the highlights of the clinical-EEG, genetic and therapeutic advances

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