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Clinical and Electrophysiologic Characteristics of Malformation of Cortical Development with Childhood Epilepsy.

Jeong Soo LEE ; Jung Chae PARK ; Heung Dong KIM

Journal of Korean Epilepsy Society.2001;5(1):10-17.

PURPOSE: To evaluate the clinical and electrophysiological characteristics of malformation of cortical development (MCD) with epilepsy. METHOD: We studied clinical and electroencephalographic (EEG) features of 54 childhood epilepsy patients with MCD diagnosed by magnetic resonance imaging (MRI) and pathologic examinations. RESULTS: 1) Bilateral diffuse MCD's were in 5 patients, bilateral focal MCD's were in 8, unilateral diffuse MCD's in 7, and unilateral focal MCD's were noted in 34 patients. 2) Partial seizures were manifested in 35 patients, and 4 of them evolve to infantile spasm (IS), isolated IS was noted in 15 cases, and generalized seizures were noticed in 2 cases 3) Asymmetric EEG backgraound slowing was noted in 30 patients, and 29 patients (96.7%) had MCD's in abnormal side of brain. 4) Polymorphic slowing was noted in 36 patients, and 28 cases (77.8%) had MCD's in those area. 5) Sensitivity of partial epileptiform discharges (ED's) for MCD was 79.6%, but specificity was 68.5%. 6) Localized paroxysmal fast activity was noted in 16 cases (29.6%), and specificity for MCD was 90.7%. 7) Spindle shaped fast activity was noted in 8 patients (14.8%), and its specificity was 100%. 8) Thirty-one cases (57.4%) were intractable to antiepileptic drugs (AED's). Seventeen cases of them were treated by ketogenic diet, and 12 patients (66.7%) were completely controlled. Among 12 cases of surgical resection, 11 patients (91.7%) became seizure free for 6 months to 2 years. 9) In pathologically confirmed cases, EEG sensitivity for MCD lesion was 100%, but sensitivity of MRI was 69.2%. CONCLUSION: EEG is most sensitive diagnostic tool for MCD in childhood epilepsy. and many of intractable epilepsy could be controlled by ketogenic diet and surgery.
Anticonvulsants ; Brain ; Electroencephalography ; Epilepsy* ; Humans ; Infant ; Infant, Newborn ; Ketogenic Diet ; Magnetic Resonance Imaging ; Seizures ; Sensitivity and Specificity ; Spasms, Infantile

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Neuronal Cell Death in the Contralateral Hippocampus after Unilateral Hippocampal Kainic Acid-induced Seizure in Rats.

Soung Kyeong PARK ; Dong Weon YANG ; Sang Bong LEE ; Seong Min PARK ; Jae Young CHOI ; Yeong In KIM

Journal of Korean Epilepsy Society.2001;5(1):3-9.

BACKGROUND: The recurrent temporal lobe epilepsy induces contralateral cell damage and secondary epileptogenesis in the contralateral hippocampus of rats. This phenomenon is fairly constant and has been used as a model of human temporal lobe epilepsy. It is necessary to understand this patho-mechanism in order to prevent this cell damage. METHODS: We have investigated the patho-mechanism of secondary epileptogenesis by using the rat model injected with kainic acid (KA) into the unilateral hippocampus. KA model shows initial complex partial seizures originating from the limbic structures and following convulsive status epilepticus. Immunohistochemical staining for c-fos expression, TUNEL stain for apoptosis, and hematoxylin-eosin (H-E) stain for morphologic changes were used. RESULTS: In the injected hippocampus, transient activation of c-fos was expressed in the dentate gyrus and CA3 hippocampal area, which were shaded out within 24 hours after the onset of limbic seizure. The stained cell with normal appearance was not observed in the H-E stain after 72 hours due to diffuse cell death. In the contralateral hippocampus, transient expression of c-fos was observed in the dentate gyrus, hilus, CA3, and CA1 area. But the expression of c-fos in the CA3 and CA1 area was sustained to 24 hours. Cell loss was mild in the CA3 and hilus, and mild cell degeneration and shrinkage were observed in the CA1 area. Apoptotic body was expressed in the CA1 area at 72 hours after the onset of seizure. CONCLUSION: These results mean that the area of prolonged expression of c-fos is vulnerable to apoptosis. Also it suggests that the patho-mechanism of ipsilateral hippocampus is an acute cytotoxic edema, whereas the contralateral damage is an apoptosis.
Animals ; Apoptosis ; Cell Death* ; Dentate Gyrus ; Edema ; Epilepsy, Temporal Lobe ; Hippocampus* ; Humans ; In Situ Nick-End Labeling ; Kainic Acid ; Models, Animal ; Neurons* ; Rats* ; Seizures* ; Status Epilepticus

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Pharmacogenetics and Antiepileptic Drugs.

Myeong Kyu KIM

Journal of Korean Epilepsy Society.2003;7(2):96-100.

Anticonvulsants* ; Pharmacogenetics*

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Genetics of Epilepsy.

Ki Joong KIM

Journal of Korean Epilepsy Society.2003;7(2):91-95.

Epilepsy* ; Genetics*

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Alterations of Neuropeptides and Neutrotrophic Factors in Kindled Seizures.

Su Yong EUN

Journal of Korean Epilepsy Society.2000;4(2):147-149.

No abstract available.
Neuropeptides* ; Seizures*

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Developmental Aspects of Epileptogenesis.

Soo Chul PARK

Journal of Korean Epilepsy Society.2000;4(2):142-146.

No abstract available.

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Morphological Alterations of Hippocampus in Temporal Lobe Epilepsy: Cell Loss, Synaptic Reorganization, Cell Birth.

Jang Sung KIM

Journal of Korean Epilepsy Society.2000;4(2):129-141.

No abstract available.
Epilepsy, Temporal Lobe* ; Hippocampus* ; Parturition* ; Temporal Lobe*

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Rational Combination of Antiepileptic Drugs: How?.

Kyoung HEO

Journal of Korean Epilepsy Society.2000;4(2):124-128.

No abstract available.
Anticonvulsants*

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Drug Interactions of Antiepileptic Drugs.

Jae Gook SHIN

Journal of Korean Epilepsy Society.2000;4(2):119-123.

No abstract available.
Anticonvulsants* ; Drug Interactions*

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Mechanisms of Antiepileptic Drugs.

Jae Moon KIM

Journal of Korean Epilepsy Society.2000;4(2):108-118.

Established antiepileptic drugs (AEDs) decrease membrane excitability by interacting with neurotransmitter receptors or ion channels. AEDs developed prior to 1980 appear to act on sodium channels, gamma-amino butyric acid type A (GABA(A)) receptors or calcium channels. Benzodiazepines and barbiturates enhance GABA(A) receptormediated inhibition. Barbiturates increase the duration of chloride channel opening and at higher doses, they block voltage-dependent calcium channels presynaptically, decreasing excitatory amino acid (EAAs) transmission. Benzodiazepines also interact with the GABA(A) receptor complex and increase the frequency of chloride channel opening. Phenytoin, carbamazepine and possibly sodium valproate decrease high frequency repetitive firing of action potentials by enhancing sodium channel inactivation. At higher doses, PHT may block sodium channels presynaptically and decrease EAAs release. In addition to the action on sodium channel, CBZ interacts with adenosine receptor and decrease C-AMP, and block reuptake of norepinephrine. VPA shows diverse mechanisms including sodium channel blocking. It increases synaptosomal GABA by increasing production and decreasing break-down and interacts with T-type calcium channels preventing thalamocortical interaction necessary for absence. Ethosuximide and sodium valproate reduce a low threshold (T-type) calcium channel current. The mechanisms of action of newly developed AEDs are not fully established. Felbamate is broad-spectrum, and probably has multiple actions on sodium channels, interaction with GABA(A) receptors, and interaction with NM.D.A receptors. Gabapentin binds to a high affinity site on neuronal membranes in a restricted regional distribution of the CNS. This binding site may be related to a possible active transport process of gabapentin into neurons. However this has not proven and the mechanism of action of gabapentin remains uncertain. It is structurally related to GABA and its action of antiepileptic activity is suspected due to change of neuronal amino acids (interfere glutamate synthesis, block GABA uptake, and enhance GABA release). Lamotrigine, initially developed as an antifolate drug, decreases sustained high frequency repetitive firing of voltage-dependent sodium action potentials that may result in a preferential decreased release of presynaptic glutamate. It may also interact with GABA receptors but its primary antiepileptic action is on the sodium channel similar to the PHT and CBZ. Because of such a diverse mechanism of action, LTG is one of the wide spectrum AEDs. Oxcarbazepine's mechanism of action is not known ; however, its similarity in structure and clinical efficacy to that of carbamazepine suggests that its mechanism of action may involve inhibition of sustained high frequency repetitive firing of voltage-dependent sodium action potentials. Vigabatrin is a "designer" drug as is developed rationally, and it reversibly inhibits GABA transaminase, the enzyme that degrades GABA, thereby producing greater available pools of presynaptic GABA for release in central synapses. Increased activity of GABA at postsynaptic receptors may underlie the clinical efficacy of VGB. Tiagabine is a potent blocker of GABA re-uptake by glia and neuron.
4-Aminobutyrate Transaminase ; Action Potentials ; Amino Acids ; Anticonvulsants* ; Barbiturates ; Benzodiazepines ; Binding Sites ; Biological Transport, Active ; Butyric Acid ; Calcium Channels ; Calcium Channels, T-Type ; Carbamazepine ; Chloride Channels ; Ethosuximide ; Excitatory Amino Acids ; Fires ; gamma-Aminobutyric Acid ; Glutamic Acid ; Ion Channels ; Membranes ; Neuroglia ; Neurons ; Neurotransmitter Agents ; Norepinephrine ; Phenytoin ; Receptors, GABA ; Receptors, GABA-A ; Receptors, Neurotransmitter ; Receptors, Purinergic P1 ; Sodium ; Sodium Channels ; Synapses ; Valproic Acid ; Vigabatrin

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