Our finding also enforced the current genotype-phenotype relationship theory about EAS. The neuropsychological deterioration in children with EAS might not only be completely affected by electric discharge severity but also genetic etiology. The hub protein in PPI network is GluN2A, which might affect language function via foxp2-srpx2/uPAR signal network.Ĭonclusion: Our data suggested that when children suspected with benign epilepsy of children with centrotemporal spikes (BECTs) have early-onset age, changed seizure semiology, and deterioration of behavior/cognition/motor function, neurologists should be alert of the appearance of ESES. EAS-related genes were enriched in the biological process of chemical synaptic transmission and vocalization (FDR, <0.01). Of these mutations, 9 (31.0%) are situated in amino (N)-terminal domain, 6 (20.7%) in linger-binding domain S1, and 10 (34.5%) in linger-binding domain S2. By literature reviewing, 18 GRIN2A missense mutations and 11 GRIN2A truncating mutations which lead to N-methyl- D-aspartate receptors' loss of function has been reported. Two pathogenic de novo GRIN2A null variants were identified in patients with ABPE who had less severe ID, despite the electrical status epilepticus during slow-wave sleep (ESES). The baseline severity of the spike-wave index (SWI) was not significantly correlated with intellectual disability (ID) level. Results: The mean age at seizure onset was 55.4 ± 27.0 months. In addition, we reviewed all the published literatures reporting EAS patients with pathogenic variants until June 2019 and conducted Gene Ontology (GO) analysis, as well as protein-protein interaction (PPI) network. Whole-exome sequencing was performed in six patients, and epileptic panel was carried out in two. Methods: A retrospective study was conducted on the participants diagnosed with Landau-Kleffner syndrome (LKS), epileptic encephalopathy with continuous spike-and-wave during sleep (CSWS), and atypical benign partial epilepsy (ABPE) at the Children's Hospital of Chongqing Medical University from January 2013 to June 2019. Objective: This study aims to analyze the electroclinical characteristics and gene test results of children on the severe end of the epilepsy aphasia spectrum (EAS) and also the correlation of EAS-related GRIN2A genes to explore the genotype-phenotype relationships, as well as potential pathogenic mechanism of EAS.
3National Clinical Research Center for Child Health and Disorders, Chongqing, China.2Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China.1Department of Neurology, Children's Hospital of Chongqing Medical University, Chongqing, China.The Natus ® NeuroWorks ® Platform enables seamless HL7 integration with facility medical records. Patient and study management with reliable and flexible study acquisition and review features are the foundations of a cyber secure solution that simplifies EEG diagnostics.Xiao Li 1,2,3,4,5, Ling-Ling Xie 1,2,3,4,5, Wei Han 1,2,3,4,5, Si-Qi Hong 1,2,3,4,5, Jian-Nan Ma 1,2,3,4,5, Juan Wang 1,2,3,4,5 and Li Jiang 1,2,3,4,5 * Providing the high quality signals and ease of use, the EEG32U amplifier is designed to meet all EEG needs. The EEG32U amplifier can be used for clinical EEG studies in an outpatient or in-patient setting, long-term EEG monitoring and ECOG or other operating room procedures.
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