• Clinical and Experimental Pediatrics
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• v.51 no.8
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• pp.861-867
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• 2008

Purpose : We carried out this study to determine if there is any difference in the occurrence rate of the epileptiform discharge between awake EEG and sleep EEG and if there are any factors influencing on the occurrence rate of EEG. Methods : This study included 178 epileptic children who had visited neurology clinic of the department of pediatrics, Pusan National University Hospital from July 2005 to July 2006. The medical and EEG records of these children who had had both awake EEG and sleep EEG were reviewed. We analysed the occurrence rate of the epileptiform discharge between awake EEG and sleep EEG. We investigated the related clinical factors which included sex, seizure types, underlying causes, age at first seizure, antiepileptic drug (AED) medication, age at recording, and background activity. Results : Among 178 epileptic children, 91 patients (51.1%) showed epileptiform discharge in awake or sleep states, 10 patients (11.0%) abnormal only in awake, 40 patients (44.0%) abnormal only in sleep, 41 patients (45.0%) abnormal in both awake EEG and sleep EEG. The occurrence rate of sleep EEG was 81 of 178 patients (45.5%) which was more than that of the awake EEG (28.7%) (P<0.001). The occurrence rate of sleep EEG is more than that of the awake EEG regardless of sex and underlying causes. But there is no significant difference from awake EEG and sleep EEG in finding the epileptiform discharge in the patient with generalized seizure, younger than 5 years old at first seizure, younger than 10 years old at recording, no antiepileptic medication, and abnormal background activity. Conclusion : The sleep EEG is thought to be more helpful in the diagnosis of childhood epilepsy.

• Clinical and Experimental Pediatrics
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• v.53 no.4
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• pp.560-564
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• 2010

Purpose : Electroencephalography (EEG) findings can play a critical role in a variety of decisions, including initiation and withdrawal of antiepileptic drugs (AEDs) therapy. Interictal epileptiform discharges (IEDs) are predictor of recurrent seizures. We investigated IEDs in EEG after AED therapy and related factors in epileptic children. Methods : The subjects were 257 children [151 males and 106 females; age, 6.79 (3.40) years; duration of therapy, 2.48 (1.85) years] diagnosed with epilepsy at the Department of Pediatrics, Pusan National University Hospital between January 2001 and December 2007, who received AEDs for more than 6 months. EEG was performed at the intervals of 6-12 months. We divided patients into 4 groups according to IED detection before and after AEDs treatment. Related clinical factors, including gender, age at the start of treatment, seizure type, cause of seizure, AED frequency, seizure control, duration of AED therapy, and background activity were investigated in the 4 groups. Results : Generalized epilepsy was relatively frequen in patients who did not show IEDs in last follow-up EEG. There were no clinically significant differences according to gender, age at the start of treatment, cause of seizure, AED frequency, seizure control, duration of AED medication, and background activity in the 4 groups ($P$>0.05). Conclusion : IEDs changed after AED treatment in one-third of the patients. Generalized epilepsy is positive factor for negative IEDs in last follow-up EEG.

• Journal of Life Science
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• v.15 no.3 s.70
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• pp.505-512
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• 2005

Excitotoxicity and epileptogenesis have often been associated with glutamate receptor activation. Accumulating evidences indicates that topiramate (TPM), an antiepileptic drug with multiple mechanisms of action has neuroprotective activity. We explored the neuroprotective effect of TPM on the status epilepticus (SE)-induced hippocampal neuronal death. After development of SE by kainite injection (15 mg/Kg), rats were treated with TPM (10mg/kg) for 1 week. The neuronal death was detected by Apop tag in situ detection kit, and the expression levels of glutamate receptors were semi-quantitatively analyzed by immunoblot. Kainate-induced SE caused a significant neuronal death and cell loss in CAI and CA3 regions of hippocampus at 1 week. However, treatment of TPM for 1 week after SE markedly reduced hippocampal neuronal death. The expression of N-methyl-D-aspartate (NMDA) receptor subunit 1, was increased by SE, but was not affected by 1 week treatment of TPM. The expressions of NMDA receptor subunit 2a and 2b were not changed by either SE or TPM. As for ${\alpha}-amino-3-hydroxy-5-methyl-4-isoxazole-propionate$ (AMPA) glutamate receptors (GluR), kainate-induced SE markedly up-regulated GluR1 expression but down-regulated GluR2 expression, leading to increased formation of $Ca^{2+}$ permeable GluR2- lacking AMPA receptors. TPM administration for 1 week attenuated SE-induced expression of both the up-regulation of GluR1 and down-regulation of GluR2, reversing the ratio of GluR1/GluR2 to the control value. In conclusion, TPM protects neuronal cell death against glutamate induced excitotoxicity in kainate-induced SE model, supporting the potential of TPM as a neuroprotective agent.