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21. Resective Epilepsy Surgery after Corpus Callosotomy in Children with Lennox-Gastaut Syndrome.

Author

Park, Soyoung, Kwon, Hye Eun, Koo, Chung Mo, Hur, Yun Jung, Kang, Hoon-Chul, Lee, Joon Soo, and Kim, Heung Dong

Subjects
LENNOX-Gastaut syndrome, EPILEPSY surgery, TREATMENT effectiveness, ANTICONVULSANTS, COGNITIVE ability
Abstract

Purpose: This study examined the characteristics and outcomes of resective epilepsy surgery following corpus callosotomy (CC) in children with Lennox-Gastaut syndrome (LGS). Methods: We retrospectively analyzed 17 children with LGS who underwent resective surgery (RS) after CC over a span of 10 years, with a minimum of 2 years of follow-up, at a single tertiary epilepsy center in Korea. Results: Of the 17 patients, 13 (73.5%) demonstrated favorable surgical outcomes (Engel class I or II) at 1 year after RS, and eight (47.1%) were ultimately free of seizures 2 years after surgery. A significantly larger decrease in the number of anti-seizure medications taken from before to 2 years after the final surgical procedure was observed in the group that became seizure-free than in the group with persistent seizures (P=0.062). Furthermore, a significantly greater decline in daily adaptive function was found in the persistent seizure group (P=0.059). The baseline characteristics, results of presurgical evaluation, and treatment-related factors assessed prior to surgery showed no significant differences between the seizure-free group and the group with persistent seizures. Conclusion: In conclusion, RS may be a viable option for patients with LGS who exhibit lateralization and/or localization on presurgical evaluation after CC, as the procedure may reveal a concealed primary focus. The proactive implementation of two-stage epilepsy surgery could provide significant seizure reduction and preservation of cognitive function in carefully selected patients with LGS. [ABSTRACT FROM AUTHOR]

Published
2024
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36. Efficacy and Safety of Lamotrigine Adjunctive Therapy in Lennox-Gastaut Syndrome.

Author

Shin, Hui Jin, Ko, Ara, Kim, Se Hee, Lee, Joon Soo, Kim, Heung Dong, and Kang, Hoon-Chul

Subjects
LAMOTRIGINE, LENNOX-Gastaut syndrome, SEIZURES (Medicine), ANTICONVULSANTS, MYOCLONUS
Abstract

Purpose: Lamotrigine (LTG) is often used as adjunctive therapy in Lennox-Gastaut syndrome (LGS); however, it may worsen myoclonic and atypical absence seizures in LGS patients. This study reviewed the overall efficacy and safety of LTG in children with LGS. Methods: This retrospective study included 38 patients (aged <18 years) with LGS who underwent LTG adjunctive therapy between October 2020 and March 2022 at Severance Children's Hospital. The primary outcome was the change in seizure frequency at 3, 6, and 12 months after starting LTG treatment. A favorable treatment response was defined as a ≥50% reduction in seizure frequency. Results: The main seizure semiology at the start of treatment was tonic-clonic in 15 (39.5%) patients, spasm in 14 (36.8%), atonic in five (13.2%), myoclonic in three (7.9%), and absence in one (2.6%). The median number of anti-seizure medications (ASMs) was 3.95 (interquartile range, 3 to 4.75). The most common concomitant ASMs were valproate (35/38, 92.1%), levetiracetam (23/38, 60.5%), and topiramate (20/38, 52.6%). After 3 months, seizure frequency was reduced by >50% in 47.4% of patients (18/38). After 6 months, 20 patients (20/36, 55.6%) showed a favorable response. After 12 months, five patients (5/11, 45.5%) responded to treatment. Three patients showed myoclonic seizures at the start of treatment and >50% amelioration in seizure frequency at the 3- and 6-month follow-up visits. Conclusion: This study reaffirms the efficacy and safety of LTG in children with LGS. Therefore, LTG is strongly recommended as an adjunctive therapy for children with LGS. [ABSTRACT FROM AUTHOR]

Published
2023
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38. Clinical analysis of catastrophic epilepsy in infancy and early childhood: Results of the Far-East Asia Catastrophic Epilepsy (FACE) study group

Author

Oguni, Hirokazu, Otsuki, Taisuke, Kobayashi, Katsuhiro, Inoue, Yushi, Watanabe, Eiji, Sugai, Kenji, Takahashi, Akio, Hirose, Shinichi, Kameyama, Shigeki, Yamamoto, Hitoshi, Hamano, Shinichiro, Baba, Koichi, Baba, Hiroshi, Hong, Seung-Chyul, Kim, Heung-Dong, Kang, Hoon-Chul, Luan, Guoming, and Wong, Tai-Tong

Published
2013
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43. Brain somatic mutations in MTOR cause focal cortical dysplasia type II leading to intractable epilepsy

Author

Lim, Jae Seok, Kim, Woo-il, Kang, Hoon-Chul, Kim, Se Hoon, Park, Ah Hyung, Park, Eun Kyung, Cho, Young-Wook, Kim, Sangwoo, Kim, Ho Min, Kim, Jeong A., Kim, Junho, Rhee, Hwanseok, Kang, Seok-Gu, Kim, Heung Dong, Kim, Daesoo, Kim, Dong- Seok, and Lee, Jeong Ho

Subjects
Brain research, Seizures (Medicine) -- Genetic aspects, Dysplasia -- Genetic aspects, Somatic motor system -- Research, Epilepsy -- Genetic aspects, Biological sciences, Health
Abstract

Focal cortical dysplasia type II (FCDII) is a sporadic developmental malformation of the cerebral cortex characterized by dysmorphic neurons, dyslamination and medically refractory epilepsy (1,2). It has been hypothesized that FCD is caused by somatic mutations in affected regions (3,4). Here, we used deep whole-exome sequencing (read depth, 412-668x) validated by site-specific amplicon sequencing (100-347,499x) in paired brain-blood DNA from four subjects with FCDII and uncovered a de novo brain somatic mutation, mechanistic target of rapamycin (MTOR) c.7280T>C (p.Leu2427Pro) in two subjects. Deep sequencing of the MTOR gene in an additional 73 subjects with FCDII using hybrid capture and PCR amplicon sequencing identified eight different somatic missense mutations found in multiple brain tissue samples of ten subjects. The identified mutations accounted for 15.6% of all subjects with FCDII studied (12 of 77). The identified mutations induced the hyperactivation of mTOR kinase. Focal cortical expression of mutant MTOR by in utero electroporation in mice was sufficient to disrupt neuronal migration and cause spontaneous seizures and cytomegalic neurons. Inhibition of mTOR with rapamycin suppressed cytomegalic neurons and epileptic seizures. This study provides, to our knowledge, the first evidence that brain somatic activating mutations in MTOR cause FCD and identifies mTOR as a treatment target for intractable epilepsy in FCD., FCD is an important cause of epilepsy that is difficult to control with available anti-epileptic drugs, and this condition accounts for up to 50% of children undergoing epilepsy surgery (1,5). [...]

Published
2015

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