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Temporal lobe epilepsy in children: etiology in a cohort with new-onset seizures
László Sztriha1, Aithala K Gururaj, Abdulbari Bener
1Department of Pediatrics, Faculty of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates. sztriha@uaeu.ac.ae
Insights
This study investigated the causes of new-onset temporal lobe epilepsy (TLE) in children. Half of the cases were cryptogenic (no clear cause), while the other half involved developmental issues or prior medical events.
Area of Science:
- Pediatric Neurology
- Epileptology
Background:
- Temporal lobe epilepsy (TLE) is a common focal epilepsy.
- Understanding the etiology of new-onset TLE in children is crucial for prognosis.
Purpose of the Study:
- To characterize the incidence and etiology of new-onset temporal lobe epilepsy (TLE) in a community-based pediatric cohort.
- To identify potential prognostic factors based on TLE etiology in children.
Main Methods:
- A cohort of 30 children with new-onset TLE (diagnosed before age 14 between 1995-1999) was studied.
- Investigations included clinical assessment, electroencephalography (EEG), and magnetic resonance imaging (MRI).
- Etiologies were categorized based on established criteria.
Main Results:
- Children were grouped by etiology: Group 1 (26.7%) had malformations or tumors (developmental TLE).
- Group 2 (23.3%) had significant antecedents or hippocampal sclerosis (HS), including perinatal events, encephalitis, trauma, or febrile seizures.
- Group 3 (50%) had cryptogenic TLE with normal neuroimaging and no significant history.
Conclusions:
- Etiologic classification of pediatric TLE has prognostic implications.
- Children with TLE, significant antecedents, or HS face a higher risk of persistent seizures and psychological issues.
Purpose:
The aim of this study was to characterize the incidence and etiology of temporal lobe epilepsy (TLE) in a community-based cohort of children with new-onset disease.
Methods:
A community-based cohort of 30 children with TLE was studied. The patients had new-onset disease before age 14 years between 1995 and 1999. They underwent clinical, EEG, and magnetic resonance imaging investigations.
Results:
The patients could be divided in three main groups according to likely etiology, as suggested by Harvey et al. (Neurology 1997;49:960-8). Group 1 consisted of eight (26.7%) children with malformations or long-standing, nonprogressive tumors (developmental TLE). Arachnoid cysts were found in three, dual pathology [cortical dysplasia and hippocampal sclerosis (HS)] in one, and focal cortical dysplasia with glioproliferative changes in one patient. Dysembryoplastic neuroepithelial tumor was responsible for the epilepsy in one, and ganglioglioma, in two children. Group 2 consisted of seven (23.3%) children with a significant antecedent and/or HS. Five children had a significant illness or event before the onset of TLE, including perinatal hypoxic-ischemic encephalopathy in one, encephalitis in one, traumatic brain injury in two, and complex febrile seizures in one. HS was found in the patients with traumatic brain injury and complex febrile seizures in the history in addition to two children without known antecedents. Group 3 comprised 15 (50%) children with no abnormality on neuroimaging and no significant antecedents (cryptogenic TLE).
Conclusions:
Etiologic differences between children with new-onset TLE may have prognostic implications: children with TLE and significant antecedents/HS are expected to have the greatest risk of continued seizures and psychological problems.
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