• Clinical and Experimental Pediatrics
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• v.50 no.11
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• pp.1097-1103
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• 2007

Purpose : Acute symptomatic seizure is defined as a temporary seizure together with acute systemic, metabolic, or toxic insult in association with an acute central nervous system insult. And unprovoked seizure is defined as seizure without provocating factors. We studied the risk factors of unprovoked seizures after acute symptomatic seizure in children. Methods : We retrospectively reviewed the records of one hundred and ten children with acute symptomatic seizures who were admitted to the pediatric department of Chungbuk National University Hospital between January, 1998 and December, 2003. We analyzed overall risk factors of unprovoked seizures after acute symptomatic seizures involving etiology, incidence, type of seizure, duration and neuroimaging. Results : We analyzed records of 110 children with acute symptomatic seizures aged from 1 month to 17 years. 24 children had unprovoked seizures (21.8%) after acute symptomatic seizures. Causes in order of frequency were encephalopathy, central nervous system infection, brain tumor, cerebrovascular disease. The risk of unprovoked seizure was significantly greater for those with status epilepticus (68.4%) than without status epilepticus, with partial seizure (64.7%) than generalized seizure. And the risk of unprovoked seizure was strongly associated with abnormal finding of electroencephalogram (79.1%) and neuroimaging (41.6%). Conclusion : In conclusion, the leading cause of subsequent unprovoked seizure in children with acute symptomatic seizure was encephalopathy and age specific incidence was high in the group aged 24-72 months. The risk for subsequent unprovoked seizure was greater for those with partial seizure, status epilepticus, abnormal finding of neuroimaging and electroencephalography.

• Journal of The Korean Society of Clinical Toxicology
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• v.7 no.2
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• pp.77-82
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• 2009

Purpose: In highly doses, endosulfan lowers the seizure threshold and elicits central nervous system stimulation, which can result in seizures, respiratory failure, and death. Management of seizure control is essential for survival and prognosis of intoxicated patients. This study assessed whether seizure time was an independent predictor mortality in patients with endosulfan poisoning. Methods: This retrospective study enrolled patients with endosulfan poisoning presenting to Masan Samsung Hospital and Gyeongsang National University Hospital from January 2003 to December 2008. The data were collected from clinical records and laboratory files. Using a multivariate logistic analysis, data on the total population was retrospectively analyzed for association with mortality. Results: Of the 24 patients with endosulfan poisoning, nineteen (79.1%) experienced seizure. The patients in the seizure group showed significantly lower Glasgow coma scale score, base excess, bicarbonate, and significant existence of mechanical ventilation, as compared to the non seizure group (n=5). Seizure, Glasgow coma scale score, systolic blood pressure, bicarbonate level, need for respiratory support, pulse rate, respiratory rate, pH, base excess, and seizure time were associated with mortality. The fatality rate of endosulfan poisoning was 54.1% with higher mortality among patients experiencing. Longer seizure time was associated with higher mortality. Conclusion: Seizure time can be a significant independent predictor of mortality in patients with acute endosulfan poisoning. Physicians should aggressively treat for seizure control in patients with acute endosulfan poisoning.

• Journal of The Korean Society of Clinical Toxicology
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• v.16 no.1
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• pp.49-56
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• 2018

Purpose: Glufosinate ammonium poisoning can cause seizures, even after a symptom-free period. This study was conducted to evaluate the relationship between serum neuron specific enolase (NSE) level and the occurrence of seizures in patients with acute glufosinate ammonium poisoning. Methods: For this retrospective observational study, data from patients diagnosed with acute glufosinate ammonium poisoning were collected between January 2016 and June 2016. Serum NSE was measured within 2 hours of arrival at the emergency department. The patients were divided into a seizure group and a non-seizure group. Results: The seizure group included eight of the 15 total patients (53.3%). The serum NSE level was significantly higher in the seizure group than in the non-seizure group ($32.4{\pm}11.9ng/mL$ vs. $19.5{\pm}5ng/mL$, p=0.019). The amount of glufosinate ingested and initial and peak serum ammonia levels were significantly higher in the seizure group than in the non-seizure group. There was no significant difference in the area under the curve of the serum NSE level or the initial and peak serum ammonia levels in terms of predicting the occurrence of seizures. Conclusion: In acute glufosinate poisoning, initial serum NSE levels may help in prediction of seizures.

• Journal of The Korean Society of Clinical Toxicology
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• v.13 no.2
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• pp.71-77
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• 2015

Purpose: Acute endosulfan poisoning is rare but causes significant morbidity and mortality. The aim of our study is to describe complications and features of seizure and determine factors associated with mortality in acute endosulfan poisoning. Methods: Twenty-eight adult patients with acute endosulfan poisoning admitted to our emergency department during a 15-year period were studied retrospectively. The clinical features of seizure, use of antiepileptic drugs during seizure, and hospital courses were evaluated. Clinical factors between survived group and non-survived group were compared for identification of factors associated with mortality. Results: Of the 28 patients with endosulfan poisoning, 4 patients (14.3%) died and 15 (53.6%) patients developed generalized tonic-clonic seizure. Thirteen patients (46.4%) and 5 patients (17.9%) progressed to status epilepticus (SE) and refractory status epilepticus (RSE), respectively. SE and RSE were associated with mortality. Almost all significant complications including shock, acute renal failure, hepatic toxicity, rhabdomyolysis, and cardiac injury developed in SE and RSE patients. Conclusion: SE and RSE were important contributors to death in endosulfan poisoning. Emergency physicians treating endosulfan poisoning should make an effort not to progress seizure following endosulfan poisoning to SE and RSE using a rapid and aggressive antiepileptic drug.

• Investigative Magnetic Resonance Imaging
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• v.17 no.4
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• pp.312-315
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• 2013

When cerebral cortical hyperintensities on diffusion-weighted image are seen in patients with suspected acute stroke accompanying seizure, it is necessary to differentiate whether they are caused by infarction or seizure-related change. We report a case of seizure-related cortical hypertensities in a patient with suspected acute infarction. With perfusion MR imaging, we could differentiate from acute infarction.

• Archives of Pharmacal Research
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• v.2 no.2
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• pp.121-125
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• 1979

Piperine showed a central nervous system depressant activity which was characterized by the antagonistic effect against chemoshock seizure as well as potent muscular incoordination in mice.

• Journal of The Korean Society of Clinical Toxicology
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• v.1 no.1
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• pp.47-50
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• 2003

Endosulfan, one of organochlorine insecticides, is $\gamma$-aminobutyric acid (GABA) antagonist. In sufficient dose, this pesticide lower the seizure threshold and produce CNS stimulation, with resultant seizures, respiratory failure, and death. In patients with endosulfan intoxication, the first manifestation of toxicity is largely a generalized seizure without prodromal signs or symptoms. So the management of airway and seizure control are essential for survival and prognosis of intoxicated patients. We report two cases of acute endosulfan poisoning who manifest 'status epilepticus' similarly, but have different prognosis.

• International Journal of Oral Biology
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• v.31 no.2
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• pp.33-43
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• 2006

Dysplasia-associated seizure disorders are markedly resistant to pharmacological intervention. Relatively little research has been conducted studying the effects of antiepileptic drugs(AEDs)on seizure activity in a rat model of dysplasia. We have used rats exposed to methylazoxymethanol acetate(MAM) in utero, an animal model featuring nodular heterotopia, to investigate the effects of AEDs in the dysplastic brain. Pilocarpine was used to induce acute seizure in MAM-exposed and age-matched vehicle-injected control animals. Field potential recordings were used to monitor amplitude and numbers of population spikes, and paired pulse inhibition in response to stimulation of commissural pathway. Two commonly used AEDs were tested: diazepam 5, 2.5 mg/kg; phenytoin 40, 60 mg/kg. Diazepam(DZP) and phenytoin(PHT) reduced the amplitude of population spike in control and MAM-exposed rats. However, the amplitude of population spike was nearly eliminated in control rats as compared to the MAM-exposed rats. Pharmaco-resistance was tested by measuring seizure latencies in awake rats after pilocarpine administration(320 mg/kg, i.p.) with and without pretreatment with AEDs. Pre-treatment with PHT 60 mg prolonged seizure latency in control rats, but not in MAM-exposed animals. The main findings of this study are that acute seizures initiated in MAM-exposed rats are relatively resistant to standard AEDs assessed in vivo. These data suggest that animal model with cortical dysplasia can be used to screen the effects of potential AEDs.

• Clinical and Experimental Pediatrics
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• v.59 no.1
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• pp.35-39
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• 2016

Purpose: This study compared the efficacy and tolerability of intravenous (i.v.) phenobarbital (PHB) and i.v. levetiracetam (LEV) in children with status epilepticus (SE) or acute repetitive seizure (ARS). Methods: The medical records of children (age range, 1 month to 15 years) treated with i.v. PHB or LEV for SE or ARS at our single tertiary center were retrospectively reviewed. Seizure termination was defined as seizure cessation within 30 minutes of infusion completion and no recurrence within 24 hours. Information on the demographic variables, electroencephalography and magnetic resonance imaging findings, previous antiepileptic medications, and adverse events after drug infusion was obtained. Results: The records of 88 patients with SE or ARS (median age, 18 months; 50 treated with PHB and 38 with LEV) were reviewed. The median initial dose of i.v. PHB was 20 mg/kg (range, 10-20 mg/kg) and that of i.v. LEV was 30 mg/kg (range, 20-30 mg/kg). Seizure termination occurred in 57.9% of patients treated with i.v. LEV (22 of 38) and 74.0% treated with i.v. PHB (37 of 50) (P=0.111). The factor associated with seizure termination was the type of event (SE vs. ARS) in each group. Adverse effects were reported in 13.2% of patients treated with i.v. LEV (5 of 38; n=4, aggressive behavior and n=1, vomiting), and 28.0% of patients treated with i.v. PHB (14 of 50). Conclusion: Intravenous LEV was efficacious and safe in children with ARS or SE. Further evaluation is needed to determine the most effective and best-tolerated loading dose of i.v. LEV.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.5
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• pp.235-242
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• 2006

Cortical malformation-associated epileptic seizures are resistant to conventional anticonvulsant drugs. Relatively little research has been conducted on the effects of antiepileptic drugs (AEDs) on seizure activity in a rat model of dysplasia. We have used rats exposed to methylazoxymethanol acetate (MAM) in utero, an animal model featuring nodular heterotopia, to investigate the effects of ethosuximide (ETX) in the dysplastic brain. Pilocarpine was used to induce acute seizure in MAM-exposed and age-matched vehicle-injected control animals. Field potential recordings were used to monitor the amplitude and number of population spikes, and paired pulse inhibition in response to stimulation of the commissural pathway. Pharmaco-resistance was tested by measuring seizure latencies after pilocarpine administration (320 mg/kg, Lp.) with and without pre-treatment with ETX. Pre-treatment with 300 mg of ETX significantly prolonged the latency to the status epilepticus (SE) in both control and MAM-treated groups. Pre-treatment with ETX 100mg and ETX 200 mg had little effect in MAMexposed rats. However, ETX 200 mg prolonged the latency to the SE in control groups. Spontaneous field potential and secondary after-discharges were higher for MAM-treated rat in comparison with control rats injects with ETX. The main findings of this study are that acute seizures initiated in MAM-exposed rats are relatively resistant to standard ETX assessed in vivo. These data suggest that ETX do not prolong seizure latencies in MAM-rats exposed to pilocarpine.