• Annals of Clinical Neurophysiology
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• v.4 no.2
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• pp.137-139
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• 2002

Background : Subtle status epilepticus (SE) is an end-stage of convulsive SE. This phenomenon might be a clinical expression of neuronal exhaustion caused by sustained electrical discharges. As subtle SE may show diverse clinical features, early detection depends on clinical suspicion. Case : A 68-year-old woman was presented with repetitive involuntary movement of right limbs after two generalized tonic-clonic seizures. She experienced right middle cerebral artery infarction 4 months ago, and after the event, left side hemiplegia sustained. These seizures were first-ever after the cerebral infarction. Orientation and verbal responses were fairly preserved but general cognitive function was minimally slowed. During the video-EEG monitoring, repetitive sharp waves were noted in the right hemisphere and these sharp waves occasionally spread to the contralateral side. Her right side involuntary movement was identifiable when the epileptic discharges were found on her right hemisphere. Conclusion : We suggested that this unexpected convulsive movement is a reflection of earlier exhaustion in the right hemisphere or deefferentation of right hemisphere because of preexisting neuronal damage.

• The Korean Journal of Physiology and Pharmacology
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• v.17 no.1
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• pp.15-21
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• 2013

Aspirin (acetylsalicylic acid) is one of the most widely used therapeutic agents based on its pharmacological actions, including anti-inflammatory, analgesic, anti-pyretic, and anti-thrombotic effects. In this study, we investigated the effects of aspirin on seizure susceptibility and hippocampal neuropathology following pilocarpine-induced status epilepticus (SE). SE was induced by pilocarpine hydrochloride (280 mg/kg, i.p.) administration in C57BL/6 mice (aged 8 weeks). Aspirin was administered daily (15 mg/kg or 150 mg/kg, i.p.) for 10 days starting 3 days before SE, continuing until 6 days after SE. After pilocarpine injection, SE onset time and mortality were recorded. Neuronal cell death was examined using cresyl violet and Fluoro-Jade staining, and glial responses were observed 7 days post SE using immunohistochemistry. In the aspirin-treated group, the onset time of SE was significantly shortened and mortality was markedly increased compared to the control group. However, in this study, aspirin treatment did not affect SE-induced neuronal cell death or astroglial and microglial responses in the hippocampus. In conclusion, these results suggest that the safety of aspirin should be reevaluated in some patients, especially with neurological disorders such as temporal lobe epilepsy.

• Journal of Life Science
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• v.30 no.6
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• pp.513-521
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• 2020

B-cell-specific Moloney murine leukemia virus integration site 1 (Bmi1) is a polycomb group protein and a core component of polycomb repressive complex 1. Initial research into Bmi1 has focused on its role in tumorigenesis, and it is generally accepted that it is important for the proliferation and survival of cancer cells. However, more recent studies have revealed that Bmi1 is downregulated in brains with neurodegenerative disease and that it regulates the function of mitochondria and reactive oxygen species levels. In this study, we tested the therapeutic potential of Bmi1 in pilocarpine-induced seizures in Bmi1-knockout mice. Bmi1 expression transiently increased in the hippocampal CA1 and CA3 and the dentate gyrus following pilocarpine-induced status epilepticus (SE). In terms of seizure behavior, SE induction was 43.14% and 53.57% for Bmi1^+/+ and Bmi1^+/- mice, respectively. However, there was no significant difference in mortality or hippocampal damage between the two groups. Two months after SE induction, the frequency of epileptic seizures in the Bmi1^+/- mice was 50% lower than in the control group, although the difference was not statistically significant. In addition, mossy fiber outgrowth in the Bmi1^+/- mice was significantly higher than in their wild-type littermates. Taken together, these data indicate that reduced Bmi1 activity increases pilocarpine-induced seizure probability and mossy fiber outgrowth.

• 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.

• Neonatal Medicine
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• v.16 no.1
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• pp.1-9
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• 2009

Seizures are the most common clinical manifestation of a neurologic insult during the neonatal period. Neonatal seizures continue to present a diagnostic and therapeutic challenge to pediatricians because the recognition and classification of neonatal seizures remains problematic, particularly when clinicians rely only on clinical criteria. Neonatal seizures can permanently disrupt neuronal development, induce synaptic reorganization, alter plasticity, and "prime" the brain to increased damage from seizures later in life. Since neonatal seizures, particularly status epilepticus, predict an increased risk for later epilepsy and other neurologic sequelae, accurate diagnoses are needed for aggressive antiepileptic drug use. The present review summarizes the pathophysiology, etiology, and diagnosis of neonatal seizures.

• Clinical and Experimental Emergency Medicine
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• v.5 no.4
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• pp.286-287
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• 2018

• Pediatric Infection and Vaccine
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• v.18 no.1
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• pp.97-102
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• 2011

The Multidrug-resistant Acinetobactor baumanii (MDRAB) is an opportunistic pathogen. Patients with long periods of hospital stay and/or under intensive care unit (ICU) receiving invasive management are more susceptible to this pathogen. In this report, four children with MDRAB infection are reviewed and described their clinical characteristics. There had been concurrent outbreaks of MDRAB infection in adult patients in the ICU at this period of time. The first child had received a craniotomy and epidural hematoma evacuation. The second child was admitted for status epilepticus with hydrocephalus. The third child had pneumonia with status epilepticus with hydrocephalus. The fourth child had poor activity due to hypoxic ischemic encephalopathy and convulsive disorder. Except the fourth child, all had not been exposed to carbapenem prior to infection of MDRAB. That imply the cause of MDRAB infections may be associated with invasive management and prolonged hospitalization together with the previous exposure to carbapenem in our cases. We would like to emphasize the importance and minimizing the spread of hospital infection in patients under prolonged intensive care management regardless of the use of carbapenem.

• 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.

• BMB Reports
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• v.53 no.4
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• pp.234-239
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• 2020

Epilepsy is a chronic neurological disease characterized by spontaneous recurrent seizures and caused by various factors and mechanisms. Malfunction of the olfactory bulb is frequently observed in patients with epilepsy. However, the morphological changes in the olfactory bulb during epilepsy-induced neuropathology have not been elucidated. Therefore, in the present study, we investigated the expression of parvalbumin (PV), one of the calcium-binding proteins, and morphological changes in the rat main olfactory bulb (MOB) following pilo-carpine-induced status epilepticus (SE). Pilocarpine-induced SE resulted in neuronal degeneration in the external plexiform layer (EPL) and glomerular layer (GL) of the MOB. PV immunoreactivity was observed in the neuronal somas and processes in the EPL and GL of the control group. However, six hours after pilocarpine administration, PV expression was remarkably decreased in the neuronal processes compared to the somas and the average number of PV-positive interneurons was significantly decreased. Three months after pilocarpine treatment, the number of PV-positive interneurons was also significantly decreased compared to the 6 hour group in both layers. In addition, the number of NeuN-positive neurons was also significantly decreased in the EPL and GL following pilocarpine treatment. In double immunofluorescence staining for PV and MAP2, the immunoreactivity for MAP2 around the PV-positive neurons was significantly decreased three months after pilocarpine treatment. Therefore, the present findings suggest that decreases in PV-positive GABAergic interneurons and dendritic density in the MOB induced impaired calcium buffering and reciprocal synaptic transmission. Thus, these alterations may be considered key factors aggravating olfactory function in patients with epilepsy.

• Clinical and Experimental Pediatrics
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• v.49 no.6
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• pp.659-664
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• 2006

Purpose : To evaluate the morbidity and mortality of children with status epilepticus(SE) as an initial seizure and to compare these according to age groups. Methods : The 78 cases(38 cases <2 years and 38 cases ${\geq}2$ years) with SE as an initial seizure admitted to the Chonnam national university hospital from Jan. 2000 to Jan. 2004 were reviewed. Developmental profiles, laboratory findings, etiologies and seizure types of SE and outcomes were compared in between two age groups, under and over 2 years. Results : SE occurred predominantly in less than 5 years old. Febrile causes were the most common, which is significantly more in those under 2 years than over 2 years(P<0.05). whereas idiopathic and acute symptomatic causes were more common in those over 2 years(P<0.05). Generalized tonic-clonic seizures was the most common type. The mortality rate was 6.4 percent(5 cases : 1 case <2 years and 4 cases ${\geq}2$ years). The estimated occurrence of epilepsy after SE was 24.4 percent(19 cases : 8 cases <2 years and 11 cases ${\geq}2$ years). The neurologic sequelae after SE in cases that had developed normally before SE(62 cases : 32 cases <2 years and 30 cases ${\geq}2$ years) were observed in 20 cases(32.3 percent), and were more frequent over 2 years(21.9 percent vs. 43.3 percent, P<0.05). Conclusion : In this study death was less common and the neurologic sequelaes of SE as an initial seizure were less severe in children under 2 years of age. The reason seemed to be the difference in the etiology of SE with age.