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dt-pub-year=2024
dt-pub=202412
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kn-title=ナトリウムチャネル異常とてんかん
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kn-abstract=
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kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=大守（川﨑）伊織
kn-aut-sei=大守（川﨑）
kn-aut-mei=伊織
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affil-num=1
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kn-affil=岡山大学学術研究院教育学域
END

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no-issue=1
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dt-accepted=
dt-pub-year=2024
dt-pub=20240401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Progressive myoclonus epilepsy
kn-title=進行性ミオクローヌスてんかんについて
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KobayashiKatsuhiro
en-aut-sei=Kobayashi
en-aut-mei=Katsuhiro
kn-aut-name=小林勝弘
kn-aut-sei=小林
kn-aut-mei=勝弘
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Pediatrics (Child Neurology), Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　発達神経病態学
en-keyword=難治てんかん
kn-keyword=難治てんかん
en-keyword=ミオクローヌス
kn-keyword=ミオクローヌス
en-keyword=失調
kn-keyword=失調
en-keyword=知的退行
kn-keyword=知的退行
en-keyword=ポリグラフ
kn-keyword=ポリグラフ
END

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cd-journal=joma
no-vol=135
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no-issue=3
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dt-received=
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dt-accepted=
dt-pub-year=2023
dt-pub=20231201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Child neurology and childhood-onset intractable diseases
kn-title=小児神経学と小児期発症難病
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KobayashiKatsuhiro
en-aut-sei=Kobayashi
en-aut-mei=Katsuhiro
kn-aut-name=小林勝弘
kn-aut-sei=小林
kn-aut-mei=勝弘
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Pediatrics (Child Neurology), Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学学術研究院医歯薬学域　発達神経病態学
en-keyword=指定難病
kn-keyword=指定難病
en-keyword=小児慢性特定疾患
kn-keyword=小児慢性特定疾患
en-keyword=発達性てんかん性脳症
kn-keyword=発達性てんかん性脳症
en-keyword=先天性代謝異常症
kn-keyword=先天性代謝異常症
END

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kn-subject=
en-title=欠神発作を示す日本人てんかん患者のGABRA1遺伝子、GABRB2遺伝子およびGABRG2遺伝子解析
kn-title=Mutation screen of GABRA1, GABRB2 and GABRG2 genes in Japanese patients with absence seizures
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
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kn-copyright=

en-aut-name=ItoMinako
en-aut-sei=Ito
en-aut-mei=Minako
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kn-aut-mei=美奈子
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ORCID=

affil-num=1
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kn-affil=岡山大学
END

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kn-subject=
en-title=小児結節性硬化症患者におけるてんかんの臨床経過と頭皮上脳波で記録された高周波振動との長期的な関連
kn-title=Longitudinal correspondence of epilepsy and scalp EEG fast (40?200 Hz) oscillations in pediatric patients with tuberous sclerosis complex
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
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kn-copyright=

en-aut-name=TSUCHIYAHiroki
en-aut-sei=TSUCHIYA
en-aut-mei=Hiroki
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kn-aut-sei=土屋
kn-aut-mei=弘樹
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

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dt-pub-year=2022
dt-pub=20220325
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kn-subject=
en-title=
kn-title=高速液体クロマトグラフィーを用いた血中プロポフォール濃度の測定方法の確立と抗てんかん薬が全静脈麻酔からの覚醒に及ぼす影響について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=NakanouMai
en-aut-sei=Nakanou
en-aut-mei=Mai
kn-aut-name=中納麻衣
kn-aut-sei=中納
kn-aut-mei=麻衣
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

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cd-journal=joma
no-vol=
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dt-received=
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dt-accepted=
dt-pub-year=2020
dt-pub=20200325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Multi-drug therapy for epilepsy influenced on the anesthetic effect of propofol without affecting its pharmacokinetics
kn-title=抗てんかん薬の多剤併用はプロポフォールの麻酔効果に影響を与えるが、薬物動態には影響しない
en-subtitle=
kn-subtitle=
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kn-abstract=
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kn-copyright=

en-aut-name=KodamaMatsuri
en-aut-sei=Kodama
en-aut-mei=Matsuri
kn-aut-name=兒玉茉莉
kn-aut-sei=兒玉
kn-aut-mei=茉莉
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

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cd-journal=joma
no-vol=
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dt-received=
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dt-accepted=
dt-pub-year=2019
dt-pub=20190925
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=てんかんを持つ小児患者の福祉制度利用の現状と課題－大学病院小児神経科における実態調査－
en-subtitle=
kn-subtitle=
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kn-copyright=

en-aut-name=UmenoJunko
en-aut-sei=Umeno
en-aut-mei=Junko
kn-aut-name=梅野潤子
kn-aut-sei=梅野
kn-aut-mei=潤子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

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cd-journal=joma
no-vol=130
cd-vols=
no-issue=2
article-no=
start-page=85
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dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20180801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Drug interaction (42. Drug interaction of new-generation antiepileptic drugs)
kn-title=薬物相互作用（42―新規抗てんかん薬の薬物相互作用）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TatebeYasuhisa
en-aut-sei=Tatebe
en-aut-mei=Yasuhisa
kn-aut-name=建部泰尚
kn-aut-sei=建部
kn-aut-mei=泰尚
aut-affil-num=1
ORCID=

en-aut-name=EsumiSatoshi
en-aut-sei=Esumi
en-aut-mei=Satoshi
kn-aut-name=江角悟
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kn-aut-mei=悟
aut-affil-num=2
ORCID=

en-aut-name=KitamuraYoshihisa
en-aut-sei=Kitamura
en-aut-mei=Yoshihisa
kn-aut-name=北村佳久
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aut-affil-num=3
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
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kn-aut-sei=千堂
kn-aut-mei=年昭
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=岡山大学病院　薬剤部

affil-num=2
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=岡山大学病院　薬剤部

affil-num=3
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=岡山大学病院　薬剤部

affil-num=4
en-affil=Department of Pharmacy, Okayama University Hospital
kn-affil=岡山大学病院　薬剤部
END

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no-vol=
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dt-pub-year=2017
dt-pub=20170324
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en-subject=
kn-subject=
en-title=
kn-title=小児のてんかんと嚥下障害との関連について
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kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TamechikaYuko
en-aut-sei=Tamechika
en-aut-mei=Yuko
kn-aut-name=爲近ゆう子
kn-aut-sei=爲近
kn-aut-mei=ゆう子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学医歯薬学総合研究科
END

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no-vol=
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dt-pub-year=2017
dt-pub=20170324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=小児てんかん患者における10年間のfollow-up研究：てんかん診断の経時的変化
kn-title=A ten-year follow-up cohort study of childhood epilepsy: Changes in epilepsy diagnosis with age
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HanaokaYoshiyuki
en-aut-sei=Hanaoka
en-aut-mei=Yoshiyuki
kn-aut-name=花岡義行
kn-aut-sei=花岡
kn-aut-mei=義行
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
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dt-pub-year=2017
dt-pub=20170324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=小児期の特発性部分てんかんの脳波における高周波活動と棘波焦点の関係性の研究
kn-title=A study on spike focus dependence of high-frequency activity in idiopathic focal epilepsy in childhood
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=ShibataTakashi
en-aut-sei=Shibata
en-aut-mei=Takashi
kn-aut-name=柴田敬
kn-aut-sei=柴田
kn-aut-mei=敬
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
kn-affil=岡山大学大学院医歯薬学総合研究科
END

start-ver=1.4
cd-journal=joma
no-vol=128
cd-vols=
no-issue=3
article-no=
start-page=183
end-page=189
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2016
dt-pub=20161201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Electroencephalography：an old examination tool with a new meaning for childhood epilepsy
kn-title=脳波：小児てんかんにおける古くて新しい検査
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KobayashiKatsuhiro
en-aut-sei=Kobayashi
en-aut-mei=Katsuhiro
kn-aut-name=小林勝弘
kn-aut-sei=小林
kn-aut-mei=勝弘
aut-affil-num=1
ORCID=

affil-num=1
en-affil=Department of Child Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=岡山大学大学院医歯薬学総合研究科　発達神経病態学
en-keyword=頭皮脳波
kn-keyword=頭皮脳波
en-keyword=点頭てんかん
kn-keyword=点頭てんかん
en-keyword=てんかん外科
kn-keyword=てんかん外科
en-keyword=高周波振動
kn-keyword=高周波振動
en-keyword=時間・周波数分析
kn-keyword=時間・周波数分析
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=てんかん制御を可能とする代謝酵素の同定
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=SadaNagisa
en-aut-sei=Sada
en-aut-mei=Nagisa
kn-aut-name=佐田渚
kn-aut-sei=佐田
kn-aut-mei=渚
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
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dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2015
dt-pub=20150930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=West症候群における副腎皮質刺激ホルモン療法後のてんかん性スパズムの再発予測因子
kn-title=Predictive factors for relapse of epileptic spasms after adrenocorticotropic hormone therapy in West syndrome
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HayashiYumiko
en-aut-sei=Hayashi
en-aut-mei=Yumiko
kn-aut-name=林裕美子
kn-aut-sei=林
kn-aut-mei=裕美子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=2
article-no=
start-page=133
end-page=135
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Treatment for a non-compliant patient with cancer and epilepsy
kn-title=癌告知後の精神症状の治療に難渋したてんかん既往のある癌患者の１例
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=　A 58-year-old man with cervical esophageal cancer and a history of epilepsy was treated with chemoradiotherapy from May of 2013. When tube feeding was initiated due to aspiration pneumonitis, the patient showed a degree of irritability that affected routine staff work and treatment compliance. We attempted to perform supportive care for maladjustment by the notice, the fast, and the tube feeding, but there was no improvement. After we added carbamazepine, primidone, and propericiazine (which had been canceled at the initiation of the tube feeding) to the patient's intravenous phenytoin, the symptoms and treatment compliance improved significantly. We concluded that the causes of the patient's irritability were maladjustment and his epilepsy.
en-copyright=
kn-copyright=

en-aut-name=MinamiDaisuke
en-aut-sei=Minami
en-aut-mei=Daisuke
kn-aut-name=南大輔
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aut-affil-num=1
ORCID=

en-aut-name=IchiharaEiki
en-aut-sei=Ichihara
en-aut-mei=Eiki
kn-aut-name=市原英基
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kn-aut-mei=英基
aut-affil-num=2
ORCID=

en-aut-name=OkabeNobuyuki
en-aut-sei=Okabe
en-aut-mei=Nobuyuki
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kn-aut-mei=伸幸
aut-affil-num=3
ORCID=

en-aut-name=YokomichiNaosuke
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kn-aut-mei=直佑
aut-affil-num=4
ORCID=

en-aut-name=KougeNoriko
en-aut-sei=Kouge
en-aut-mei=Noriko
kn-aut-name=高下典子
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kn-aut-mei=典子
aut-affil-num=5
ORCID=

en-aut-name=KajizonoMakoto
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en-aut-mei=Makoto
kn-aut-name=鍛治園誠
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kn-aut-mei=誠
aut-affil-num=6
ORCID=

en-aut-name=AkimotoYutaka
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aut-affil-num=7
ORCID=

en-aut-name=HoriKeisuke
en-aut-sei=Hori
en-aut-mei=Keisuke
kn-aut-name=堀圭介
kn-aut-sei=堀
kn-aut-mei=圭介
aut-affil-num=8
ORCID=

en-aut-name=MatsubaraMinoru
en-aut-sei=Matsubara
en-aut-mei=Minoru
kn-aut-name=松原稔
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kn-aut-mei=稔
aut-affil-num=9
ORCID=

en-aut-name=NasuJunichiro
en-aut-sei=Nasu
en-aut-mei=Junichiro
kn-aut-name=那須淳一郎
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kn-aut-mei=淳一郎
aut-affil-num=10
ORCID=

en-aut-name=TanimotoMitsune
en-aut-sei=Tanimoto
en-aut-mei=Mitsune
kn-aut-name=谷本光音
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kn-aut-mei=光音
aut-affil-num=11
ORCID=

en-aut-name=KiuraKatsuyuki
en-aut-sei=Kiura
en-aut-mei=Katsuyuki
kn-aut-name=木浦勝行
kn-aut-sei=木浦
kn-aut-mei=勝行
aut-affil-num=12
ORCID=

en-aut-name=MatsuokaJunzi
en-aut-sei=Matsuoka
en-aut-mei=Junzi
kn-aut-name=松岡順治
kn-aut-sei=松岡
kn-aut-mei=順治
aut-affil-num=13
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　緩和支持医療科

affil-num=2
en-affil=
kn-affil=岡山大学病院　血液・腫瘍・呼吸器内科

affil-num=3
en-affil=
kn-affil=岡山大学病院　精神科神経科

affil-num=4
en-affil=
kn-affil=岡山大学病院　緩和支持医療科

affil-num=5
en-affil=
kn-affil=岡山大学病院　看護部

affil-num=6
en-affil=
kn-affil=岡山大学病院　薬剤部

affil-num=7
en-affil=
kn-affil=岡山大学病院　消化器内科

affil-num=8
en-affil=
kn-affil=岡山大学病院　消化器内科

affil-num=9
en-affil=
kn-affil=岡山大学病院　消化器内科

affil-num=10
en-affil=
kn-affil=岡山大学病院　消化器内科

affil-num=11
en-affil=
kn-affil=岡山大学病院　血液・腫瘍・呼吸器内科

affil-num=12
en-affil=
kn-affil=岡山大学病院　血液・腫瘍・呼吸器内科

affil-num=13
en-affil=
kn-affil=岡山大学病院　緩和支持医療科
en-keyword=てんかん（epilepsy）
kn-keyword=てんかん（epilepsy）
en-keyword=易怒性（irritability）
kn-keyword=易怒性（irritability）
en-keyword=適応障害（maladjustment）
kn-keyword=適応障害（maladjustment）
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Scn1a遺伝子変異ラットを用いた抗てんかん薬の熱性けいれん抑制効果
kn-title=Therapy for hyperthermia-induced seizures in Scn1a mutant rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HayashiKeiichiro
en-aut-sei=Hayashi
en-aut-mei=Keiichiro
kn-aut-name=林桂一郎
kn-aut-sei=林
kn-aut-mei=桂一郎
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=126
cd-vols=
no-issue=1
article-no=
start-page=55
end-page=58
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2014
dt-pub=20140401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Clinical guideline for epilepsy
kn-title=てんかん治療ガイドラインについて
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MorimotoNobutoshi
en-aut-sei=Morimoto
en-aut-mei=Nobutoshi
kn-aut-name=森本展年
kn-aut-sei=森本
kn-aut-mei=展年
aut-affil-num=1
ORCID=

en-aut-name=AbeKoji
en-aut-sei=Abe
en-aut-mei=Koji
kn-aut-name=阿部康二
kn-aut-sei=阿部
kn-aut-mei=康二
aut-affil-num=2
ORCID=

affil-num=1
en-affil=
kn-affil=香川県立中央病院　神経内科

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　脳神経内科学
END

start-ver=1.4
cd-journal=joma
no-vol=11
cd-vols=
no-issue=2
article-no=
start-page=163
end-page=173
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=199306
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=小児期における遅発性てんかんの臨床的脳波学的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=大日方修
kn-aut-sei=大日方
kn-aut-mei=修
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=124
cd-vols=
no-issue=2
article-no=
start-page=115
end-page=117
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Therapy for hyperthermia-induced seizures in Scn1a mutant rats
kn-title=Scn1a遺伝子変異ラットを用いた抗てんかん薬の熱性けいれん抑制効果
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HayashiKeiichiro
en-aut-sei=Hayashi
en-aut-mei=Keiichiro
kn-aut-name=林桂一郎
kn-aut-sei=林
kn-aut-mei=桂一郎
aut-affil-num=1
ORCID=

en-aut-name=OhmoriIori
en-aut-sei=Ohmori
en-aut-mei=Iori
kn-aut-name=大守伊織
kn-aut-sei=大守
kn-aut-mei=伊織
aut-affil-num=2
ORCID=

en-aut-name=MatsuiHideki
en-aut-sei=Matsui
en-aut-mei=Hideki
kn-aut-name=松井秀樹
kn-aut-sei=松井
kn-aut-mei=秀樹
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学
en-keyword=febrile seizures
kn-keyword=febrile seizures
en-keyword=animal model
kn-keyword=animal model
en-keyword=Scn1a gene
kn-keyword=Scn1a gene
en-keyword=generalized epilepsy with febrile seizures plus
kn-keyword=generalized epilepsy with febrile seizures plus
en-keyword=severe myoclonic epilepsy of infancy
kn-keyword=severe myoclonic epilepsy of infancy
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2012
dt-pub=20120323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=障害者歯科治療時の全身麻酔において抗てんかん薬の服用が静脈内投与したミダゾラムの薬物動態に及ぼす影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=HayashiTomoko
en-aut-sei=Hayashi
en-aut-mei=Tomoko
kn-aut-name=林知子
kn-aut-sei=林
kn-aut-mei=知子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=123
cd-vols=
no-issue=2
article-no=
start-page=91
end-page=95
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110801
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A long-term follow-up study of Dravet syndrome up to adulthood
kn-title=成人期に達したDravet症候群の長期経過に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=AkiyamaMari
en-aut-sei=Akiyama
en-aut-mei=Mari
kn-aut-name=秋山麻里
kn-aut-sei=秋山
kn-aut-mei=麻里
aut-affil-num=1
ORCID=

en-aut-name=KobayashiKatsuhiro
en-aut-sei=Kobayashi
en-aut-mei=Katsuhiro
kn-aut-name=小林勝弘
kn-aut-sei=小林
kn-aut-mei=勝弘
aut-affil-num=2
ORCID=

en-aut-name=YoshinagaHarumi
en-aut-sei=Yoshinaga
en-aut-mei=Harumi
kn-aut-name=吉永治美
kn-aut-sei=吉永
kn-aut-mei=治美
aut-affil-num=3
ORCID=

en-aut-name=OhtsukaYoko
en-aut-sei=Ohtsuka
en-aut-mei=Yoko
kn-aut-name=大塚頌子
kn-aut-sei=大塚
kn-aut-mei=頌子
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　発達神経病態学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　発達神経病態学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　発達神経病態学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　発達神経病態学
en-keyword=Dravet症候群
kn-keyword=Dravet症候群
en-keyword=乳児重症ミオクロニーてんかん
kn-keyword=乳児重症ミオクロニーてんかん
en-keyword=予後
kn-keyword=予後
en-keyword=けいれん性てんかん重積状態
kn-keyword=けいれん性てんかん重積状態
END

start-ver=1.4
cd-journal=joma
no-vol=123
cd-vols=
no-issue=1
article-no=
start-page=59
end-page=62
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Drug interaction (20. combination with enteral nutrition formulas)
kn-title=薬物相互作用（20―経腸栄養剤の薬物相互作用）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=TairaKentaro
en-aut-sei=Taira
en-aut-mei=Kentaro
kn-aut-name=平健太郎
kn-aut-sei=平
kn-aut-mei=健太郎
aut-affil-num=1
ORCID=

en-aut-name=MatsunagaHisashi
en-aut-sei=Matsunaga
en-aut-mei=Hisashi
kn-aut-name=松永尚
kn-aut-sei=松永
kn-aut-mei=尚
aut-affil-num=2
ORCID=

en-aut-name=SendoToshiaki
en-aut-sei=Sendo
en-aut-mei=Toshiaki
kn-aut-name=千堂年昭
kn-aut-sei=千堂
kn-aut-mei=年昭
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学病院　薬剤部

affil-num=2
en-affil=
kn-affil=岡山大学病院　薬剤部

affil-num=3
en-affil=
kn-affil=岡山大学病院　薬剤部
END

start-ver=1.4
cd-journal=joma
no-vol=102
cd-vols=
no-issue=3-4
article-no=
start-page=453
end-page=463
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1990
dt-pub=199004
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Acetylcholine turnover on the experimental epileptic focus of the rat cerebral cortex
kn-title=鉄イオン脳内注入による実験的てんかん原性焦点組織におけるacetylcholine代謝の研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The effect of iron ion injection on acetylcholine (ACh) turnover was studied in the cerebral cortex of male Sprague-Dawley rats. Rats were divided into 3 groups: rats of the Fe-group were injected with 500 nmol of Fe(3+) in the left sensorimotor cortex, rats of the HCl-group were injected with HCl-acidified saline (pH 1.8) in the left sensorimotor cortex, and a shamoperated group acted as a control (Sham-group).
On both sides of the cortex, the choline acetyltransferase (CAT) activity of the HCI- and Fe-groups decreased 30 min after, increased 6h after, and then decreased 24h after the injection compared with the activity of the Sham-group. A no time was there any difference between the CAT activities of the HCl- and Fe-groups. On both sides of the cortex, the ACh content of the HCl- and Fe-groups decreased transiently 24h after injection, but there was no difference in ACh content between the two groups. In the left cortex of the Fe- and HCl-groups, acetylcholinesterase (AChE) activity, which showed no difference between the two groups, decreased 30 min after injection.
These findings suggested that cortical neurons especially AChergic neurons might be irritated by a transient increase in intracranial pressure due to brain edema induced by the injection of acid into the cortex, as no specific effct of Fe(3+)-injection was observed in this study.
en-copyright=
kn-copyright=

en-aut-name=KawakamiYunosuke
en-aut-sei=Kawakami
en-aut-mei=Yunosuke
kn-aut-name=河上雄之介
kn-aut-sei=河上
kn-aut-mei=雄之介
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=acetylcholine turnover
kn-keyword=acetylcholine turnover
en-keyword=head injury
kn-keyword=head injury
en-keyword=choline acetyltransferase
kn-keyword=choline acetyltransferase
en-keyword=cholinesterase
kn-keyword=cholinesterase
en-keyword=brain edema
kn-keyword=brain edema
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=ラットの外側膝状体キンドリングにより生ずる光誘発電位の変化および抗てんかん薬の効果に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=IshikawaTakashi
en-aut-sei=Ishikawa
en-aut-mei=Takashi
kn-aut-name=石川崇
kn-aut-sei=石川
kn-aut-mei=崇
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=エリスロポエチンの抗てんかん作用：ニューロペプチドYの活性化と海馬歯状回における異常な神経新生の抑制と関連して
kn-title=Erythropoietin exerts anti-epileptic effects with the suppression of aberrant new cell formation in the dentate gyrus and upregulation of neuropeptide Y in seizure model of rats
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KondoAkihiko
en-aut-sei=Kondo
en-aut-mei=Akihiko
kn-aut-name=近藤聡彦
kn-aut-sei=近藤
kn-aut-mei=聡彦
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=6
cd-vols=
no-issue=
article-no=
start-page=18
end-page=23
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1988
dt-pub=198804
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=てんかんモデルマウス（E1, CBA, AKR, A/St, IDT, ICRマウス）
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KatayamaYasuto
en-aut-sei=Katayama
en-aut-mei=Yasuto
kn-aut-name=片山泰人
kn-aut-sei=片山
kn-aut-mei=泰人
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=10-12
article-no=
start-page=785
end-page=789
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1961
dt-pub=19611230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Metabolism of γ-Aminobutyric Acid Part 3. Transamilase Activity in Epileptic Brain
kn-title=γ-アミノ酪酸の代謝に関する研究 第3編 てんかん脳のtransaminase活性について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A genuine epileptic and experimental animals such as L. C. L. A. rabbit, ep-mouse and vitamin B(6) deficient mouse were utilized for this study to measure the transamilase activity. 1) The focus in the epileptic brain manifested the decrease of the transamilase activity compared with the non-focus and also the non epileptic. 2) There was, however, no significant difference between the transamilase activities of the epileptic non-focus and of the non-epileptic. 3) In both cases of L. C. L. A. rabbit and ep-mouse, no difference could be found in the activity in contrast to the control groups. 4) The transamilase activity of the VB(6) deficient mouse brain was seemed to be considerably decreased in contrast to the control.
en-copyright=
kn-copyright=

en-aut-name=UnoKazuaki
en-aut-sei=Uno
en-aut-mei=Kazuaki
kn-aut-name=宇野和昌
kn-aut-sei=宇野
kn-aut-mei=和昌
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第1（陣内）外科教室
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=10-12
article-no=
start-page=777
end-page=784
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1961
dt-pub=19611230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Metabolism of γ-Aminobutyric Acid Part 2. Metabolism of (14)C-γ-Aminobutyric Acid in an Epileptic Brain Slice
kn-title=γ-アミノ酪酸の代謝に関する研究 第2編 てんかん脳切片による(14)C-γ-Aminobutyric aicdの代謝について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Studies were carried out to clearfy GABA metabolism in the brains of an epileptic, the latent cerebral local anaphylactic (L. C. L. A.) rabbit and ep-mouse administered with (14)C-GABA. 1) Incubated with a brain slice, radioactivity of (14)C-GABA was slightly detected in glutamic acid, aspartic acid and glutamine in the incubation medium. 2) In this case, most of the radioactive carbon of GABA was converted into (14)CO(2). 3) The epileptic brain appeared to decreased in the (14)CO(2)-activity, compared with the non-epileptic. In case of the epileptic brain, the activity in the focus was lower than the one in the non-focus. 4) The study with L. C. L. A. rabbit and ep-mouse could not manifest any difference in GAGA metabolism in contrast to the normal control groups.
en-copyright=
kn-copyright=

en-aut-name=UnoKazuaki
en-aut-sei=Uno
en-aut-mei=Kazuaki
kn-aut-name=宇野和昌
kn-aut-sei=宇野
kn-aut-mei=和昌
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第1（陣内）外科教室
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1-3
article-no=
start-page=153
end-page=157
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1961
dt-pub=19610330
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Biochemical Studies on Vitamin B(6) Deficient Mouse Brain in Experimental Epilepsy Part 2. A study on free amino acids in the B(6) deficient mouse brain
kn-title=実験的てんかん症としてのビタミンB(6)欠乏マウス脳の生化学的研究 第2編 ビタミンB(6)欠乏マウス脳の遊離アミノ酸について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Using mice with chronic B(6) deficiency induced by B(6) deficient diet and other group of mice with acute B(6) deficiency induced by the intravenous injection of desoxypyridoxine, the author carried out quantitative analysis of free amino acids in the cerebral cortex of these animals, and obtained the following results. 1. In both groups with acute and chronic B(6) deficiency glutamic acid is markedly iucreased, but no significant change can be recognized in the quantity of γ-aminobutyric acid (GABA). 2. An increase of glycerophoethanolamine and phosphoethanolamine can be recognized in the group with B(6) deficiency. 3. In the group given the intravenous injection of desoxypyridoxine there can be observed an increase in alanine, glycine and valine. 4. Cystathionine is increased in the group with B(6) deficiency. 5. In comparing the results of assay of free amino acids in the B(6) deficient mouse brain with those of idiopathic human epileptic brain, there seems to be no direct connection between human idiopathic epilepsy and B(6) deficiency.
en-copyright=
kn-copyright=

en-aut-name=MatanoSakae
en-aut-sei=Matano
en-aut-mei=Sakae
kn-aut-name=俣野栄
kn-aut-sei=俣野
kn-aut-mei=栄
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第1（陣内）外科教室
END

start-ver=1.4
cd-journal=joma
no-vol=73
cd-vols=
no-issue=1-3
article-no=
start-page=145
end-page=151
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1961
dt-pub=19610330
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Biochemical Studies on Vitamin B(6) Deficient Mouse Brain in Experimental Epilepsy Part 1. The cholinesterase activity, and the contents of Na, K, and water in vitamin B(6) deficient mouse cerebrum
kn-title=実験的てんかん症としてのビタミンB(6)欠乏マウス脳の生化学的研究 第1編 ビタミンB(6)欠乏マウス大脳のCholinesterase活性値，Na，K含有量および含水量について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=With young mice fed on B(6) deficient synthetic food for 30 days the author observed general conditions of these animals and also carried out biochemical studies on their cerebral cortex. Some of them were subjected to intravenous injection of desoxypyridoxine, known to possess competitive action against B(6), and changes in their cerebrum were investigated. The follwing are the results of the present study. 1. In the mice fed on B(6) deficient food the gain in the body weight is inhibited when compared with the control group kept on normal diet. More than one month later these B(6) deficient animals show the falling off of hairs and reddening around their mouth and the coarsening of body hairs. 2. In the mice fed on B(6) deficient food a definite decrease in cholinesterase activity (ChE) can be observed in their cerebral cortex when compared with the control group. In those with experimental epilepsy elicited by the intravenous injection of desoxypyridoxine, a marked diminution of ChE can be recognized. 3. While there can be seen no significant difference in the contents of Na and K in the cerebral cortex of the mice fed on B(6) deficient food when compared with those of the control an increase of Na and a decrease of K can be recognized in those animals with epilepsy induced by the intravenous injection of desoxypyirdoxine. 4. In the micc fed on B(6) deficient food there can also observed an increase in free water of the cerebral cortex.
en-copyright=
kn-copyright=

en-aut-name=MatanoSakae
en-aut-sei=Matano
en-aut-mei=Sakae
kn-aut-name=俣野栄
kn-aut-sei=俣野
kn-aut-mei=栄
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第1（陣内）外科教室
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=7-9
article-no=
start-page=675
end-page=693
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1963
dt-pub=19630930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Localization Study of Epileptogenic Focus by Means of Intracarotid Sodium Amobarbital Injection Part 111 Differentiation of Primary and Secondary Bilaterally Synchronous Spike and Wave Complex
kn-title=アモバルビタールソーダ頸動脈注射によるてんかん焦点局在診断に関する研究 第3編 1次的及び2次的両側同期性棘徐波複合の鑑別に関する臨床的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Intracarotid injection of 50 to 100 mg of 5 to 10 % sodium amobarbital was given to 30 cases of epileptics, and change of the abnormal EEG was followed. 1) Unilateral focal cortical epileptogenic spikes were abolished by the ipsilateral administration, but not by the contralateral. 2) Amongst the cases of bilaterally synchronous spike and wave complex, two types of marked responses were obtained at the administration. One group manifested an abolishment of the complex from all leads of both hemispheres by administration on one side, but a transient inhibition of the spike component from the ipsilateral hemisphere by administration on the other side. This appears to indicate the complex originates from unilateral cortical focus which is located at the first side. This group may correspond with the secondary bilateral synchrony. 3) Another group manifested a transient inhibition of the spike component from ipsilateral hemisphere without abolishment of the complex at either side of administration. This may correspond with the primary bilateral synchrony, the so-called "ceutrencephalic origin". 4) No activation of characteristic abnormal activities in epileptics was found at the intracarotid injection of sodium amobarbital.
en-copyright=
kn-copyright=

en-aut-name=YagiTakashi
en-aut-sei=Yagi
en-aut-mei=Takashi
kn-aut-name=八木健
kn-aut-sei=八木
kn-aut-mei=健
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第1外科教室
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=7-9
article-no=
start-page=665
end-page=673
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1963
dt-pub=19630930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Localization Study of Epileptogenic Focus by Means of Intracarotid Sodium Amobarbital Injection Part 11 Intracarotid Sodium Amobarbital Injection Effect on Human EEG
kn-title=アモバルビタールソーダ頸動脈注射によるてんかん焦点局在診断に関する研究 第2編 アモバルビタールソーダ頸動脈注射の脳波基礎律動に及ぼす影響に関する臨床的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=An attempt was made to analyze the changes of EEG secondary to the intracarotid injection of 50 to 100 mg of sodium amobarbital: 33 trials on 20 patients. 1) There appeared to be a marked change in all cases; limited or dominant ipsilaterally to the side of administration. 2) The latter was found in 22 out of 33 trials, and noted at the records of the frontal leads. 3) The change was composed of high amplitude and low frequency or of low amplitude and high frequency or of the mixed of both, occurring at 3 to 6 seconds after the onset of the injection and gradually disappearing to regain the normal state within 30 minutes. 4) These changes, especially the high amplitude and slow waves immediately after the injection at the same side were markedly noticed when the injection was in large dosage and in high speed. 5) There was no difference in such changes given arise by either side of administration in the same patient. 6) It is to be noted that there were no hazardous complications at the intracarotid injection of 10 % sodium amobarbital under sufficient attention.
en-copyright=
kn-copyright=

en-aut-name=YagiTakeshi
en-aut-sei=Yagi
en-aut-mei=Takeshi
kn-aut-name=八木健
kn-aut-sei=八木
kn-aut-mei=健
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第1外科教室
END

start-ver=1.4
cd-journal=joma
no-vol=75
cd-vols=
no-issue=7-9
article-no=
start-page=649
end-page=663
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1963
dt-pub=19630930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Localization Study of Epileptogenic Focus by Means of Intracarotid Sodium Amobarbital Injection Part 1 Intracarotid Sodium Amobarbital Injection Effect on Experimentally Produced Focal Epileptogenic Discharge of Cat
kn-title=アモバルビタールソーダ頸動脈注射によるてんかん焦点局在診断に関する研究 第1編 実験的てんかん焦点に対するアモバルビタールソーダ頸動脈注射の影響に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Twenty adult cats were utilized for this study under unanesthetized condition. Penicillin was locally given in various parts of cortex and subcortical nucleus or thalamus to elicit epileptogenic discharges and sodium amobarbital was intracarotidly injected to give arise transient functional depression of hemisphere. EEG was followed up in the course of this experiment. 1) Local application of penicillin into cortex or subcortical nucleus or thalamus considerably elicited epileptogenic discharges. 2) In case of focal cortical epileptogenic discharge, the first spike appearing at the neighbouring area of the focus was followed to be associated with the synchronous spike discharge at the opposite side and then the focal seizure discharge was built. The discharge was occaionally interrupted by the interictal state, building, in some of the cases, the final stage of generalized seizure discharge. 3) So was noted in its appearance and process in case of focal subcortical epileptogenic discharge. But there was a more tendency of transmission of its activity to the opposite side in comparison with the cortical epileptogenic discharge. 4) The epileptogenic discharge originated from unilateral cortical focus was abolished or inhibited by means of ipsilateral intracarotid injection of 5 to 10 mg sodium amobarbital, but was not affected by the contralateral administration. However, either side of the injection could not inhibit the discharge activity after it became a focal seigure discharge. 5) Subcortically elicited epileptogenic discharge, in contrast, could not be interfered by either side of the intracarotid administration. 6) In cases of both focal cortical and subcortical discharge, intracarotid injection of sodium amobarbital manifested a tendency of flattening and slowing of back ground activity at the injected side, but not at the opposide side. 7) The intracarotid administration could not activate the epileptogenic discharges either from cortex and subcortex.
en-copyright=
kn-copyright=

en-aut-name=YagiTakeshi
en-aut-sei=Yagi
en-aut-mei=Takeshi
kn-aut-name=八木健
kn-aut-sei=八木
kn-aut-mei=健
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第1外科教室
END

start-ver=1.4
cd-journal=joma
no-vol=72
cd-vols=
no-issue=2
article-no=
start-page=515
end-page=520
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1960
dt-pub=19600130
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Transaminase of Brain (Ⅱ) Effects of Psychotropic and Neurotropic Drugs on the Transaminase Activities
kn-title=脳のトランスアミナーゼ 第2編 各種向精神・神経薬のダイコクネズミ脳組織トランスアミナーゼ活性に及ぼす影響
en-subtitle=
kn-subtitle=
en-abstract=Effects of 18 psychotropic and 3 neurotropic drugs were measured by the author on the glutamic-aspartic transaminase (GAT) activities in the rat brain homogenates. 1. Chlorpromazine, chlopromazine sulfoxide, acetylpromazine, levomepromazine, mepazine and perphenazine inhibited GAT, while prochlorperazine showed no effect. Both of diethazine and promethazine did not effect on GAT. 2. Pipradrol and dimethylaminoethanol activated GAT, while methylphenidate showed no effect. 3. Azacyclonol, amobarbital, phenobarbital, methyprylon, glutethimide and primidone were inhibitory in acion on GAT. 4. LSD-25 inhibited to GAT and bemegride did not effect on. 5. In the effect on GAT, similarities of imipramine to the phenothiazine derived depressants, or differences of diethazine and promethazine from other phenothiazine derivatives seemed to be causad due to the resemble or different distance between two nitrogen atoms.
kn-abstract=ダイコクネズミ脳homogenateを用い，グルタミン酸-アスパラギン酸トランスアミナーゼ（GAT）活性に及ぼす18種の向精神薬，および3種の向神経薬の影響を測定した. 1. フエノチアジン系向精神薬は， Prochlorperazineを除く他の6種はいずれもGAT阻害を示し，阻害作用はChlorpromazineに最も強かつた. Chlorpromazine S-oxideはChlorpromazineに比してGAT阻害作用は著しく弱い. 2種のフエノチアジン系向神経薬はGAT活性に影響をみなかつた. 2. AzacyclonolはGAT阻害を示し， LSD-25は高濃度で阻害を示したが低濃度では影響を与えなかつた. 3. 中枢刺戟剤4種のうち， PipradrolとDMAEは促進， Methylphenidateは影響なく， Tofranilは阻害を示した. 4. バルビツール酸系睡眠剤AmobarbitalとPhenobarbital，非バルビツール酸系睡眠剤MethyprylonとGlutethimideは，すべて阻害を示した.しかるにバルビツール酸拮抗剤BemegrideはGATに無影響であつた.抗てんかん剤Primidoneは阻害を示した. 5. 実験に用いた中枢抑制剤13種のうち12種が阻害を示した. 6. GATに及ぼす作用において， ImipramineとChlorpromazineの類似， DiethazineやPromethazineとChlorpromazineとの差異を，化学構造における2個のN原子間の距離の一致と相異に対応すると考えた.
en-copyright=
kn-copyright=

en-aut-name=OnoMasaya
en-aut-sei=Ono
en-aut-mei=Masaya
kn-aut-name=小野昌也
kn-aut-sei=小野
kn-aut-mei=昌也
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=8-9
article-no=
start-page=629
end-page=634
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1962
dt-pub=19620930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on Glutamic Decarboxylase in the Brain Ⅱ. Glutamic Decarboxyase Activity of Epileptogenic Cerebral Cortex
kn-title=脳のglutamic decarboxylaseに関する研究 第2編 てんかん脳のglutamic decarboxylase活性について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The activity of glutamic decarboxylase was measured with the use of cerebral cortices in human idiopathic epilpsy and in experimental epilespy of ep (epileptogenic) mice, of rabbits with local anaphylaxis of the brain and of vitamin B(6) deficiency mice and the folowing results were obtained. 1. While there can be recognized no significant defference in the activity of glutamic decarboxylase in non-focal cerebral cortex of human idiopathic epilepsy from that in the control (non-epileptic brain), the glutamic decarboxylase activity in the focal cortex of the human idiopathic epilepsy is markedly lower than that in the non-focal area. 2. The activity of glutamic decarboxylase in the cerebral cortex of adult ep mice is considerably decreased, but in the immature ep-mice that had not yet experienced convulsion its activity is rather accelerated. 3. The glutamic decarboxylase activity in the cerebral cortex of the rabbit with a local anaphylaxis is not significantly different from that in the normal control rabbit. 4. The activity of glutamic decarboxyase in the brain of vitamin B(6) deficient mice is markedly lower than that in the normal mice brain.
en-copyright=
kn-copyright=

en-aut-name=KondoOsamu
en-aut-sei=Kondo
en-aut-mei=Osamu
kn-aut-name=近藤整
kn-aut-sei=近藤
kn-aut-mei=整
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第1（陣内）外科教室
END

start-ver=1.4
cd-journal=joma
no-vol=74
cd-vols=
no-issue=4-7
article-no=
start-page=439
end-page=461
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1962
dt-pub=19620730
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Experimental Studies on Insulin-Hypoglycemia ......With a Special Reference to Electrophysiological Changes of Central Nervous System......
kn-title=インシュリン低血糖状態に関する実験的研究―主として中枢神経系の電気生理学的変化について―
en-subtitle=
kn-subtitle=
en-abstract=With the use of unrestrained and unanesthetized cats implanted with electrodes the author observed normal EEG as well as that of the cats under insulin-hypoglycemia. In addition, observations were carried on the influences of some drugs and electrical stimulation on hypoglycemic EEG. The results are as follows. 1. The low voltage fast waves observable in awaking state change to characteristic sleep spindle of abort 12 c/s as the cat falls into sleeping state, and in deeper sleeping state high voltage slow waves appear in the cortex and various nuclei of subcortex. 2. Hypoglycemic state was classified into lethargic, preconvulsive, convulsive and comatose stages on the basis of characteristic behavior, blood-sugar level and EEG. In the lethargic stage, normal EEG from awaking to deep sleeping state appeared in all leads. In the preconvulsive stage, disturbances of sympathetic nervous system and large slow wave burst were characteristic. In the convulsive stage, spikes and sharp waves were predominant, and furthermore, myoclonic jerk in all muscles and occasionally general convulsion broke out suddenly. In the comatose stage, cats were completely relaxed and 1 cycle/sec or less large slow waves appeared on EEG. In this instance when hypoglycemia was in progress, voltage diminished lower and lower. 3. Arousal effect of excitatory agents and amino acids on insulinhypoglycemia in comparison with that of glucose a) General convulsion Only when general convulsion was induced by electrical stimulation, metrazol and megimide, there could be observed hyperglycemia, awaking patterns on EEG and behavioral wakefulness. In comparison with glucose, however, arousal effect was transient and uncertain. b) Amino acids Sodium glutamate next to glucose had hyperglycemic and arousal action on hypoglycemic cats, but its action was not so fast and long as glucose. The greater the dosage of sodium glutamate administered, the more certain was the effect. Fast administration of large dose, however, is dangerous because it is apt to induce general convulsion. GABA (gamma-amino butyric acid) showed transient hyperglycemic action and arousal patterns on EEG, but no essential change took place in behavior. Although GABOB (gamma-amino beta-hydroxybutyric acid) was administered in the convulsive stage, no definite action was seen. 4. Administration of inhibitory agents to insulin-hypoglycemia a) Nembutal Nembutal administered intravenously in the convulsive stage caused spikes and sharp waves on EEG to disappear and then elicited spindle burst. While myoclonic seizures and convulsions were being suppressed, hypoglycemia continued to progress. In the comatose stage Nembutal was non-effective. b) Chlorpromazine (Cp) Although not so effective as Nembutal, an optimal dose of Cp allows hypoglycemia to proceed gradually. Precaution is necessary with this drug because, when a large dose of Cp is injected rapidly into vein in the convulsive state, it is apt to induce convulsion and then the animal cannot be aroused even by administration of glucose.
kn-abstract=植え込み電極を施しに慢性猫を用いて,正常脳波,インシュリン低血糖状態およびそれに対する中枢神経刺戟, 2, 3のアミノ酸と中枢神経抑制物質の影響を観察した.その結果は次の如くである. 1) 覚醒時に認められる低振巾速波は,猫が眠りに傾くと特徴的な12c/s前後のsleep spindleに変り,更に深睡眠では皮質および皮質下諸核に高電位徐波が出現する. 2) インシュリン低血糖状態は一般状態,血糖値,脳波を基準として,嗜眠期,痙攣前期,痙攣期,昏睡期とに分け得た.嗜眠期には正常猫で認められた深睡眠に至るまでのあらゆる脳波が認められた.痙攣前期は自律神経系の嵐と大徐波のburstを特徴とし,痙攣期は棘・鋭波を盛んに認め,ミオクロヌス攣縮・全身痙攣が起る.昏睡期にはあらゆる刺戟に応ぜず,脳波では1c/s以下の大徐波を認め,更に低血糖状態を続けると電位を減ずる. 3) インシュリン昏睡に対する中枢神経賦活剤およびアミノ酸の覚醒効果を葡萄糖を基準として検討すると, i) 中枢神経刺戟 電気刺戟,メトラゾール,メジマイドを用いたが,全身てんかん様痙攣発作を起した時のみ血糖上昇と脳波および一般状態の覚醒を認めた.葡萄糖に較べその効果は一過性不確実であつた. ii) アミノ酸 グルタミン酸ソーダは葡萄糖に次いで血糖上昇作用と覚醒作用を持ち,脳波を完全に覚醒パターンに置換しうるが,糖ほど迅速,且持続時間が長くない.この効果はグルタミン酸の投与が多いほど確実であるが,あまり大量を急速に投与すると危険である(全身痙攣を誘発). GABAにも一過性の血糖上昇作用と脳波上の覚醒効果を認めたが,一般状態には変化がない. GABOBを痙攣期に用いたが,確かな抑制作用は認められなかつた. 4) 更にインシュリン低血糖状態に神経抑制物質を加重して検討すると, i) Nembutal
痙攣期にNembutalを静注すると,脳波上の棘波・鋭波を消失せしめ,特有な紡錘形の高振巾速波群を生ぜしめ,攣縮及び痙攣を完全に抑制したまま低血糖を進行させる.
深昏睡期にはNembutalの影響はない. ii) Chlorpromazine 痙攣前期以後に適当量のCpを適用すると, Nembutalほどではないが,低血糖を静かに進行せしめる.大量のCpを急激に痙攣期の猫に静注すると,痙攣を誘発し易く,その後に糖水を補給しても覚醒しにくい事があるので注意を要する.
en-copyright=
kn-copyright=

en-aut-name=ShohmoriToshikiyo
en-aut-sei=Shohmori
en-aut-mei=Toshikiyo
kn-aut-name=庄盛敏廉
kn-aut-sei=庄盛
kn-aut-mei=敏廉
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経科
END

start-ver=1.4
cd-journal=joma
no-vol=76
cd-vols=
no-issue=1-3
article-no=
start-page=41
end-page=46
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1964
dt-pub=19640330
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A case report of Epilepsia partialis continua
kn-title=持続性部分性てんかんの一症例
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=We reported a case of epilepsia partialis continua. Movements consist of almost continuous rhythmic jerking which is limited to the right lower limb. Angioma arteriovenosum was seen in the left parietal region on the angiogram of left carotid artery. The clonic jerk of this case was much improved on the anticonvulsants.
en-copyright=
kn-copyright=

en-aut-name=HiramatsuTadashi
en-aut-sei=Hiramatsu
en-aut-mei=Tadashi
kn-aut-name=平松直
kn-aut-sei=平松
kn-aut-mei=直
aut-affil-num=1
ORCID=

en-aut-name=YokoyamaShigeo
en-aut-sei=Yokoyama
en-aut-mei=Shigeo
kn-aut-name=横山茂生
kn-aut-sei=横山
kn-aut-mei=茂生
aut-affil-num=2
ORCID=

en-aut-name=IkedaHisao
en-aut-sei=Ikeda
en-aut-mei=Hisao
kn-aut-name=池田久男
kn-aut-sei=池田
kn-aut-mei=久男
aut-affil-num=3
ORCID=

en-aut-name=YamamotoMasatomo
en-aut-sei=Yamamoto
en-aut-mei=Masatomo
kn-aut-name=山本昌知
kn-aut-sei=山本
kn-aut-mei=昌知
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室

affil-num=2
en-affil=
kn-affil=岡山大学医学部神経精神医学教室

affil-num=3
en-affil=
kn-affil=岡山大学医学部神経精神医学教室

affil-num=4
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
END

start-ver=1.4
cd-journal=joma
no-vol=81
cd-vols=
no-issue=1-2
article-no=
start-page=71
end-page=83
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1969
dt-pub=19690228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A case of atypical psychosis characterized by periodic stupor, with marked epileptic factors
kn-title=著明なてんかん性要因を示し，挿間性昏迷状態をくりかえした非定型精神病の1例
en-subtitle=
kn-subtitle=
en-abstract=A 16-year old girl. It is said that there was a psychotic case in the relatives on the paternal side of the patient. Her hereditary history remains obscure, but her own history is uneventful. A review was made of this case who had episodes of stuporous state six times, and episodes of delutional-hallucinatory state twice since the age of 13. Clinical and EEG observations were carried out from Nov. 1965 to Aug. 1966, and from March 1967 to July 1967 when she was admitted to our clinic. The results are breifly summarized as follows. The stuporous state which presented mutism and akinesia as the principal symptom was difficult to differentiate from the stupor observable in schizophrenia, and it developed in a day or two at the onset, which lasted for about two weeks and then was alleviated. During this period of episodes she showed no noteworthy symptom of disturbed consciousness and she could recall what had happened to her precisely. Her EEG revealed that paroxysmal abnormal waves characterized by spike wave were inhibited during the stuporous state, but in the stage of remission paroxysmal abnormal waves appeared spontaneously and were activated easily by hyperventilation. This stuporous state could be alleviated transiently by the administration of amytal sodium, and also with a large dose of valium it was improved. On the contrary, anti-epileptic agents had no effect at all on the stuporous state. From the characteristic features of the psychotic state, this case could be construed as a type of atypical psychosis, but paroxysmal abnomality on EEG was similar to that of epilepsy, and so this was the case that had clearly shown to stand on the boundary line between atypical psychosis and epilepsy. Therefore, it seemed that epileptic factors of atypical psychosis should be dicided only after long, continuous observations of the case. Some discussion was made on physiological mechanism inducing a stuporous state. Namely, the mechanism that induced a stuporous state seemed to have a close relation to the excitation of system which tried to inhibit the abnormal EEG, and this system was provably the reticular formation system of the midbrain.
kn-abstract=症例は13才女子.患者の7親等にあたる父系に精神病者があつたというが遺伝歴の詳細は不明.既往歴に特記すべきものはない.本症例に招来した前後7回の昏迷状態と,その他幻覚妄想の表面化した,昏迷状態と異なる状態像をあわせ観察し,発病より入院に至る経過,及び前後2回の入院の経過を詳述した.昏迷状態はつよい無動無言を主兆とする分裂病性昏迷と区別のつかないもので,始まりは急で1日を境にして訪れ,2週間前後続き寛解をみる.この間認むべき意識障害はなく,患者は些細な出来事迄すべてを想起できる.前後18回の脳波による継時的観察を行なつた結果,昏迷状態下では,棘波を中心とする発作性異常波は抑制され,寛解期にはこれが出現しやすい傾向を認めた.昏迷状態はAmytal sodiumで,一時的ではあるが劇的に改善され, Valiumの大量内服でも臨床像を改善できた.しかし抗てんかん剤は,むしろ昏迷状態には奏効しなかつた.本症は精神病像からは非定型精神病群の1型としてみられるが,発作波の消長からは,てんかんにみられる所見と同一の傾向を有し,両者を結ぶ1点を鮮やかに示した1例であつた.非定型精神病のてんかん性要因はかかる症例の継時的観察から決定されるべきものであると考えた.その他昏迷状態の出現と,発作波の消長に関し,若干の生理学的推論を試み,考察を加えた.
en-copyright=
kn-copyright=

en-aut-name=HosokawaK.
en-aut-sei=Hosokawa
en-aut-mei=K.
kn-aut-name=細川清
kn-aut-sei=細川
kn-aut-mei=清
aut-affil-num=1
ORCID=

en-aut-name=NishimuraS.
en-aut-sei=Nishimura
en-aut-mei=S.
kn-aut-name=西村幸子
kn-aut-sei=西村
kn-aut-mei=幸子
aut-affil-num=2
ORCID=

en-aut-name=IkedaH.
en-aut-sei=Ikeda
en-aut-mei=H.
kn-aut-name=池田久男
kn-aut-sei=池田
kn-aut-mei=久男
aut-affil-num=3
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学神経精神医学教室

affil-num=2
en-affil=
kn-affil=岡山大学神経精神医学教室

affil-num=3
en-affil=
kn-affil=岡山大学神経精神医学教室
END

start-ver=1.4
cd-journal=joma
no-vol=90
cd-vols=
no-issue=9-10
article-no=
start-page=1105
end-page=1109
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1978
dt-pub=19781030
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Two cases of Aleviatin (Diphenylhydantoin) intoxication
kn-title=抗てんかん剤（アレビアチン）による平衡障害の2症例
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Aleviatin (Diphenylhydantoin) is well known as an excellent antiepileptic drug, especially against grand-mal convulsion. Side reaction of this drug, however, was various and the reports concerning side reaction were many. The authors have reported two patients of Aleviatin intoxication with the complaint of postural disturbance. Some discussions and comments were made on the cases and literatures. Summarizing the symptoms of these side reactions, 1. acute intoxication a. skin manifestations: rash like scarlet fever or urticaria, exfoliative dermatitis, systemic lupus erythematoid eruption, Stevens-Johnson syndrome b. neurological signs: postural disturbance, ataxia, tremor, dysarthria, diplopia, nystagmus, tinnitus, hearing impairment, choreoathetoid movement c. psychological signs: nervousness, excitement, disorientation, insomnia, pseudodementia d. blood manifestation: leucopenia, anemia, leukemoid change e. digestive disorders: thirst, nausea, vomiting, constipation 2. chronic intoxication a. gum hypertrophy b. hypertrichosis c. hyperglycemia
en-copyright=
kn-copyright=

en-aut-name=ShibataShiro
en-aut-sei=Shibata
en-aut-mei=Shiro
kn-aut-name=柴田四郎
kn-aut-sei=柴田
kn-aut-mei=四郎
aut-affil-num=1
ORCID=

en-aut-name=TakedaTsuneo
en-aut-sei=Takeda
en-aut-mei=Tsuneo
kn-aut-name=武田恒雄
kn-aut-sei=武田
kn-aut-mei=恒雄
aut-affil-num=2
ORCID=

en-aut-name=KajiharaMasayuki
en-aut-sei=Kajihara
en-aut-mei=Masayuki
kn-aut-name=梶原正行
kn-aut-sei=梶原
kn-aut-mei=正行
aut-affil-num=3
ORCID=

en-aut-name=SaitoRyusuke
en-aut-sei=Saito
en-aut-mei=Ryusuke
kn-aut-name=斉藤龍介
kn-aut-sei=斉藤
kn-aut-mei=龍介
aut-affil-num=4
ORCID=

en-aut-name=EndoYoichi
en-aut-sei=Endo
en-aut-mei=Yoichi
kn-aut-name=遠藤洋一
kn-aut-sei=遠藤
kn-aut-mei=洋一
aut-affil-num=5
ORCID=

en-aut-name=OguraYoshio
en-aut-sei=Ogura
en-aut-mei=Yoshio
kn-aut-name=小倉義郎
kn-aut-sei=小倉
kn-aut-mei=義郎
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部耳鼻咽喉科

affil-num=2
en-affil=
kn-affil=岡山大学医学部耳鼻咽喉科

affil-num=3
en-affil=
kn-affil=岡山大学医学部耳鼻咽喉科

affil-num=4
en-affil=
kn-affil=岡山大学医学部耳鼻咽喉科

affil-num=5
en-affil=
kn-affil=岡山大学医学部耳鼻咽喉科

affil-num=6
en-affil=
kn-affil=岡山大学医学部耳鼻咽喉科
END

start-ver=1.4
cd-journal=joma
no-vol=87
cd-vols=
no-issue=5-6
article-no=
start-page=463
end-page=480
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1975
dt-pub=19750630
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Experimental and clinical studies on the catecholamine metabolism 2. Experimental and clinical studies on the catecholamine metabolism in epilepsy.
kn-title=カテコールアミン代謝に関する基礎的ならびに臨床的研究 第Ⅱ編 てんかんのカテコールアミン代謝に関する基礎的ならびに臨床的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Catecholamine and its metabolites level in cerebrospinal fluid (CSF), serum and urine of the 62 patients with epilepsy (38 males and 24 females, 12 cases of Lennox's syndrome, 48 cases of centrencephalic epilepsy, one case of focal cortical epilepsy and one case of temporal lobe epilepsy) were determined by gas chromatographic method (using an Electron Capture Detector) and fluorometric method. Studies on the epilepsy was performed with a special reference to catecholamine metabolism. As the results, 1) 3, 4-dihydroxyphenylalanine (DOPA) and dopamine in CSF of the epileptics were significantly lower than in the control group. 2) Homovanillic acid (HVA: end-product of dopamine) in CSF of the epileptics was also significantly lower than in the control group. 3) In epileptics tyramine, octopamine and synephrine were detected in CSF. 4) It is speculated in epileptics that the suppression of the pathway from tyrosine to dopamine may act to enhance the side pathway from tyrosine to tyramine followed by octopamine, synephrine and epinephrine. 5) Serum DOPA levels of epileptics being treated with anticonvulsants were abnormal in about half of the cases. 6) Serum MAO activity of epileptics was significantly lower than in the control group. 7) HVA in urine of epileptics tended to increase, but its level was changeable. Based on these clinical studies of epileptics, a penicillin focus was made on the cortex of cats. And effects of the catecholamines to penicillin focus were electroencephalographically examined. 8) Penicillin spikes were strongly inhibited by topical application of dopamine. 9) When octopamine was injected into cisterna magna after the appearance of penicillin spikes, spike frequency increased and abnormal spike discharges were observed.
en-copyright=
kn-copyright=

en-aut-name=KishikawaHidemi
en-aut-sei=Kishikawa
en-aut-mei=Hidemi
kn-aut-name=岸川秀実
kn-aut-sei=岸川
kn-aut-mei=秀実
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設病態生化学部門
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20090930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=小児てんかん患者におけるバルプロ酸血中遊離型濃度の変動解析とこれに基づく至適投与設計法の開発
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=UeshimaSatoshi
en-aut-sei=Ueshima
en-aut-mei=Satoshi
kn-aut-name=上島智
kn-aut-sei=上島
kn-aut-mei=智
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=121
cd-vols=
no-issue=3
article-no=
start-page=149
end-page=156
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2009
dt-pub=20091201
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=A CACNB4 mutation showing altered Ca(v)2.1 function in a patient with Dravet syndrome
kn-title=Dravet 症候群患者に認められたカルシウムチャネル　機能異常を引き起こす CACNB4 遺伝子変異
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OhmoriIori
en-aut-sei=Ohmori
en-aut-mei=Iori
kn-aut-name=大守伊織
kn-aut-sei=大守
kn-aut-mei=伊織
aut-affil-num=1
ORCID=

en-aut-name=OuchidaMamoru
en-aut-sei=Ouchida
en-aut-mei=Mamoru
kn-aut-name=大内田守
kn-aut-sei=大内田
kn-aut-mei=守
aut-affil-num=2
ORCID=

en-aut-name=MimakiNobuyoshi
en-aut-sei=Mimaki
en-aut-mei=Nobuyoshi
kn-aut-name=御牧信義
kn-aut-sei=御牧
kn-aut-mei=信義
aut-affil-num=3
ORCID=

en-aut-name=NishikiTeiichi
en-aut-sei=Nishiki
en-aut-mei=Teiichi
kn-aut-name=西木禎一
kn-aut-sei=西木
kn-aut-mei=禎一
aut-affil-num=4
ORCID=

en-aut-name=TomizawaKazuhito
en-aut-sei=Tomizawa
en-aut-mei=Kazuhito
kn-aut-name=富澤一仁
kn-aut-sei=富澤
kn-aut-mei=一仁
aut-affil-num=5
ORCID=

en-aut-name=MatsuiHideki
en-aut-sei=Matsui
en-aut-mei=Hideki
kn-aut-name=松井秀樹
kn-aut-sei=松井
kn-aut-mei=秀樹
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　分子遺伝学

affil-num=3
en-affil=
kn-affil=倉敷成人病センター　小児科

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学

affil-num=6
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学
en-keyword=てんかん
kn-keyword=てんかん
en-keyword=Dravet 症候群
kn-keyword=Dravet 症候群
en-keyword=CACNB4遺伝子
kn-keyword=CACNB4遺伝子
en-keyword=SCN1A 遺伝子
kn-keyword=SCN1A 遺伝子
END

start-ver=1.4
cd-journal=joma
no-vol=91
cd-vols=
no-issue=11-12
article-no=
start-page=1649
end-page=1664
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1979
dt-pub=19791230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The therapeutic prognosis of patients with epilepsy during long-term follow-up
kn-title=てんかんの治療予後
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The purpose of this study was to investigate the therapeutic prognosis of adult patients with epilepsy during long-term follow-up. The subjects of the present study were 286 epileptic patients seen by the author at the Department of Neuro-Psychiatry, Okayama University Hospital and Tsuyama Sekizen Hospital. All patients had been on therapy for more than five years. The age, onset of seizure and period of treatment of these patients were in order 35.1±11.5 y.o. (mean±SD), 15.9±10.2 y.o. (mean±SD), and 12.4±4.9 years (mean±SD). As classified by the criteria of the International League Against Epilepsy, the present study consisted of cases with; Partial Seizures 167 (58.4%) Primary Ceneralized Seizures 115 (40.2%) Secondary Generalized Seizures 4 (1.4%) The clinical course over the past three years was used as the period to determine the therapeutic prognosis. To describe the therapeutic prognosis, four categories were created taking types and frequency of seizures into consideration; i.e., "seizure-free", "mild", "moderate", and "severe". Results were: 1) "Seizure-free" 99 (34.6%), "mild" 91 (31.8%), "moderate" 54 (18.9%), and "severe" 42(14.7%). 2) In 187 patients, seizures were not abolished. In 89 cases (47.6%) change of seizure type occurred under treatment. The facts elucidated were; a) Partial seizures were resistent even to continued therapeutic efforts. b) Tonic-clonic general convulsions in primary generalized seizures and partial seizure with secondarily generalized responded well to therapy, disappearing promptly and permanently. c) "Abortive-minor seizure" occurred under treatment. d) The change from primary generalized seizures to partial seizures was seen in several cases. 3) Multidimensional comparisons regarding factors which may influence therapeutic prognosis were conducted. In "seizure-free" and "severe" cases, factors which showed statistically significant differences were as follows; In "seizure-free" cases, the first of each following pair showed the better prognosis; a) Seizure types: Primary generalized seizures and partial seizures. b) Etiology: "hereditary" and "residual". c) Etiology: "cryptogenic" and "residual". d) Duration prior to therapy: "within 3 years" and "over 3 years". In "severe" cases, the first of each following pair showed the poorer prognosis; a) Seizure types: partial seizures and primary generalized seizures. b) Etiology: "residual" and "cryptogenic". c) Sexual differences: women and men. 4) Psychiatric problems were observed in 143 cases (50.0%). These patients had a poor prognosis. Patients with partial seizures had more psychiatric problems than patients with primary generalized seizures.
en-copyright=
kn-copyright=

en-aut-name=KugohToshiaki
en-aut-sei=Kugoh
en-aut-mei=Toshiaki
kn-aut-name=久郷敏明
kn-aut-sei=久郷
kn-aut-mei=敏明
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=Epilepsy
kn-keyword=Epilepsy
en-keyword=Prognosis
kn-keyword=Prognosis
en-keyword=Change of seizure types
kn-keyword=Change of seizure types
en-keyword=International
kn-keyword=International
en-keyword=Classification
kn-keyword=Classification
END

start-ver=1.4
cd-journal=joma
no-vol=93
cd-vols=
no-issue=11-12
article-no=
start-page=1137
end-page=1150
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1981
dt-pub=19811230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=CBA mouse convulsion and brain monoamine
kn-title=CBAマウスの痙攣と脳内モノアミンに関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Convulsions were induced in 80% of CBA mice by throwing stimulation six from eight weeks after birth, and continued for more than one year. The procedure for causing a CBA mouse convulsion was as follows: the mouse was rolled over suddenly by throwing stimulation and set in tonic flexion. After a few seconds of clonic convulsion, tonic extension followed, and opisthotonus was observed in this stage. After a convulsion, the mouse rose, seemed stunned for a few seconds, then recovered to a normal state. This convulsive process took about 10-15 seconds for the whole procedure. Urinary incontinence was observed. Bilateral sporadic spikes of about 100-150μV were induced in the resting stage of stimulated CBA mice, but the EEG was not abnormal in normal untreated mice. Dopamine (DA) in the cortex and brainstem of the CBA mouse at the pre-convulsive stage was significantly decreased compared with the resting stage, and these changes recovered during the convulsion stage. DA in the cerebellum was also significantly decreased one hour after convulsion. Norepinephrine (NE) of CBA cortex was significantly decreased before, during, and one hour after, a convulsion, compared with the resting stage. 5-Hydroxytryptamine (5-HT) in the CBA brainstem was significantly decreased compared with the resting stage, and this change recovered to the normal level one hour after a convulsion. DA and 5 HT of the cortex of CBA mice, which convulsions had induced for more than one year, were significantly decreased compared with untreated CBA mice of the same age. There was no difference in the monoamines of CBA mouse brain between females and males.
en-copyright=
kn-copyright=

en-aut-name=TsuoMichio
en-aut-sei=Tsuo
en-aut-mei=Michio
kn-aut-name=津尾道雄
kn-aut-sei=津尾
kn-aut-mei=道雄
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=CBAマウス (CBA mouse)
kn-keyword=CBAマウス (CBA mouse)
en-keyword=痙攣 (convulsion)
kn-keyword=痙攣 (convulsion)
en-keyword=てんかん様スパイク (epileptic discharges)
kn-keyword=てんかん様スパイク (epileptic discharges)
en-keyword=脳内モノアミン (brain monoamine)
kn-keyword=脳内モノアミン (brain monoamine)
END

start-ver=1.4
cd-journal=joma
no-vol=93
cd-vols=
no-issue=11-12
article-no=
start-page=1105
end-page=1119
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1981
dt-pub=19811230
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=α-Guanidinoglutaric acid and other guanidino compounds in a cobalt epileptogenic focus of cat cerebral cortex
kn-title=コバルトてんかん源性焦点組織のα-guanidinoglutaric acid及びその他のguanidino化合物に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=An epileptogenic cortical focus was induced by the topical application of cobalt powder to the sensori-motor cortex, then guanidino compounds in the cobalt focus were analysed by HPLC. An extraordinally high peak was observed in the epileptogenic focus 24 hours after the cobalt application. α-Guanidinoglutaric acid (GGA), which is synthesized from glutamic acid and S-methylisothiourea sulfate, was confirmed by GC/MS as a dimethylpyrimidyl derivative of GGA. An unknown substance was isolated from the cobalt focus and identified as GGA by the same GC/MS technique as in the case of an authentic sample. GGA was present in the normal cat cortex in amounts of 1n mol/g. GGA increased after cobalt application, and reached a maximum after 24 hours. The abnormal GGA recovered to the normal level about 40days after the application by which time the cobalt focus had disappeared. Other guanidino compounds, that is taurocyamine, guanidinosuccinic acid, guanidinoacetic acid, β-guanidinopropionic acid, creatinine, γ-guanidinobutyric acid, arginine, and methylguanidine, except for guanidine tended to decrease in the cobalt focus. Taurocyamine and α-guanidinobutyric acid were still decreased 40 days after the cobalt application. Spike and wave complex was induced after topical application of 0.2M GGA to the sensori-motor cortex, and a burst continued for one hour.
en-copyright=
kn-copyright=

en-aut-name=AkagiMasayuki
en-aut-sei=Akagi
en-aut-mei=Masayuki
kn-aut-name=赤木正幸
kn-aut-sei=赤木
kn-aut-mei=正幸
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=コバルト焦点 (cobalt focus)
kn-keyword=コバルト焦点 (cobalt focus)
en-keyword=α-guanidinoglutaric acid
kn-keyword=α-guanidinoglutaric acid
en-keyword=guanidino化合物 (guanidino compounds)
kn-keyword=guanidino化合物 (guanidino compounds)
en-keyword=EEG
kn-keyword=EEG
en-keyword=発作機序 (seizure mechanism)
kn-keyword=発作機序 (seizure mechanism)
END

start-ver=1.4
cd-journal=joma
no-vol=94
cd-vols=
no-issue=1-2
article-no=
start-page=87
end-page=102
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1982
dt-pub=19820228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The nucleus accumbens septi and the limbic seizure: Studied by kindling preparation.
kn-title=側坐核と辺縁系発作―燃え上がり現象を用いた研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=An antagonistic relationship between epilepsy and psychosis has been claimed. On the other hand, abnormality of the N. accumbens is thought to be involved in schizophrenia and temporal lobe epilepsy. In order to examine the role of the N. accumbens in limbic seizure and psychosis, the following were studied: 1. Amygdaloid kindling and the functional change of the N. accumbens, 2. Accumbens kindling, 3. Functional change of limbic nuclei following the accumbens kindling, and 4. The effects of lesioning of the N. accumbens on the amygdaloid kindling. The results were as follows: 1. The amygdaloid kindling induced epileptic focus and positive transfer into the N. accumbens. 2. The kindling phenomenon was confirmed positive by repeated stimulation of the N. accumbens. Clinicoelectrographic seizure development during the N. accumbens kindling resembled that of amygdaloid kindling. The mean minimum intensities to induce afterdischarge and kindling rate were 620μA and 23days, respectively. 3. Positive transfer was found in the N. amygdala and hippocampus following the accumbens kindling. 4. Lesioning of the N. accumbens had no effect on amygdaloid seizure development, but lowered the threshold intensity to induce amygdaloid afterdischarge after kindling. It was concluded that the N. accumbens and the N. amygdala formed epileptic hyperexcitability reciprocally and that the N. accumbens had an inhibitory effect on the limbic seizure, but no effect on the developed amygdaloid kindling.
en-copyright=
kn-copyright=

en-aut-name=YamashitaMotoshi
en-aut-sei=Yamashita
en-aut-mei=Motoshi
kn-aut-name=山下元司
kn-aut-sei=山下
kn-aut-mei=元司
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=側坐核
kn-keyword=側坐核
en-keyword=燃え上がり現象
kn-keyword=燃え上がり現象
en-keyword=辺縁系発作
kn-keyword=辺縁系発作
en-keyword=中脳辺縁ドパミン系
kn-keyword=中脳辺縁ドパミン系
en-keyword=側頭葉てんかん
kn-keyword=側頭葉てんかん
END

start-ver=1.4
cd-journal=joma
no-vol=95
cd-vols=
no-issue=3-4
article-no=
start-page=271
end-page=282
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1983
dt-pub=19830430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Brain active oxygen, free radicals, lipid peroxide and the redox state of glutathione in the Fe(3+) induced epileptic focus of the rat
kn-title=鉄イオンてんかん源性焦点組織のフリーラジカル反応と発作発現機構に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Epileptic discharges were induced 15 minutes after 0.1M FeCl(3) was injected into the rat sensory motor cortex and continued for 6 months after the injection. In order to study the Fe(3+) induced seizure mechanism, Fe(3+) bound methemoglobin, free radicals, active oxygen, malondialdehyde and reduced and oxidized glutathione were measured in the foci of rats after the FeCl(3) injection. It was found that Fe(3+) induced a significant increase in Fe(3+) bound methemoglobin, active oxygen and malondialdehyde and accelerated the glutathione redox reaction 5 minutes after the injection. Fe(3+) was thought to induce lipid peroxidation by free radical reaction and thus produce the peileptic focus.
en-copyright=
kn-copyright=

en-aut-name=KhochiHiroyoshi
en-aut-sei=Khochi
en-aut-mei=Hiroyoshi
kn-aut-name=高知宏喜
kn-aut-sei=高知
kn-aut-mei=宏喜
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=鉄イオンてんかん
kn-keyword=鉄イオンてんかん
en-keyword=フリーラジカル
kn-keyword=フリーラジカル
en-keyword=活性酸素
kn-keyword=活性酸素
en-keyword=過酸化脂質
kn-keyword=過酸化脂質
en-keyword=グルタチオン
kn-keyword=グルタチオン
END

start-ver=1.4
cd-journal=joma
no-vol=96
cd-vols=
no-issue=3-4
article-no=
start-page=313
end-page=325
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1984
dt-pub=19840430
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Analysis of guanidino compounds in human cerebrospinal fluid. -Guanidinoethanesulfonic acid is observed in some epileptics-
kn-title=ヒト髄液中のグアニジノ化合物に関する研究 ―特にてんかん患者について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Guanidino compounds in cerebrospinal fluid (CSF) of nonneurological and epileptic patients were investigated. After separating using high performance liquid chromatography, and reacting with phenanthrenequinone, the compounds were analyzed fluorometrically. Arginine (Arg), creatinine (CRN) and homoarginine (HArg) were found in all subjects. Trace amounts of guanidinosuccinic acid (GSA) and guanidinoacetic acid (GAA) were detected in some subjects regardless of disease state. Positive correlations were noted in females between Arg and CRN levels and age. Serum Arg and HArg levels were related to in urine concentrations, but there was no association between CSF guanidino compound levels and serum levels. Guanidinoethanesulfonic acid (GES) was detected in the CSF of some epileptic patients. This was confirmed by high voltage paper electrophoresis. This finding suggests that GES may relate to epileptic seizure mechanism.
en-copyright=
kn-copyright=

en-aut-name=FujimotoNoboru
en-aut-sei=Fujimoto
en-aut-mei=Noboru
kn-aut-name=藤本昇
kn-aut-sei=藤本
kn-aut-mei=昇
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=グアニジノ化合物
kn-keyword=グアニジノ化合物
en-keyword=髄液
kn-keyword=髄液
en-keyword=てんかん
kn-keyword=てんかん
en-keyword=グアニジノエタンスルホン酸
kn-keyword=グアニジノエタンスルホン酸
END

start-ver=1.4
cd-journal=joma
no-vol=97
cd-vols=
no-issue=9-10
article-no=
start-page=855
end-page=870
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1985
dt-pub=19851030
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The effects of bilateral ventral hippocampal lesions on amygdaloid kindling in cats
kn-title=両側腹側海馬破壊による扁桃核キンドリングへの影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The clinical relevance of Ammon's horn sclerosis in epilepsy has not been fully ellucidated. This study was designed to examine the effects of bilateral ventral hippocampal lesions (Ammon's horn + dentate gyrus) on the minimal electroconvulsive threshold (ECT) intensity, kindling rates and transference phenomenon in cats kindled from the amygdala (AM). Ten adult cats were used. In the first experiment, lesions were made electrolytically in the bilateral hippocampi after completion of the primary site (PS) kindling from the left AM. Subsequently, the right AM (secondary site: SS) was kindled. In the second experiment, the hippocampal lesion was made prior to the PS-kindling which was followed by the SS-kindling. In the first experiment, the ECT intensity was unchanged by the hippocampal lesions after PS-kindling. The seizure pattern and EEG pattern in the generalized convultion were changed to show an asymmetrical, asynchronous pattern by the lesions. Facilitation of SS-kindling following the PS-kindling (positive transfer) was diminished by the lesions. In the second experiment, the formation of hippocampal lesions prior to the kindling retarded the PS kindling rates slightly. The seizure pattern and EEG pattern of the generalized convulsion was asymmetrical and asynchronous. In addition, positive transfer from PS to SS was blocked by the lesions. These results indicate that the ventral hippocampal formation and hippocampal commissure may be critical brain sites for the establishment of the transference phenomenon that reflects secondary epileptogenic changes in the brain.
en-copyright=
kn-copyright=

en-aut-name=NakatsuTakeshi
en-aut-sei=Nakatsu
en-aut-mei=Takeshi
kn-aut-name=中津武志
kn-aut-sei=中津
kn-aut-mei=武志
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=扁桃核キンドリング
kn-keyword=扁桃核キンドリング
en-keyword=腹側海馬破壊
kn-keyword=腹側海馬破壊
en-keyword=転移現象
kn-keyword=転移現象
en-keyword=二次てんかん原性
kn-keyword=二次てんかん原性
END

start-ver=1.4
cd-journal=joma
no-vol=97
cd-vols=
no-issue=1-2
article-no=
start-page=149
end-page=160
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1985
dt-pub=19850225
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Electroencephalographic studies of iron-induced focal epilepsy
kn-title=鉄塩誘導焦点性てんかんの脳波学的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Electrocorticograms (ECoGs) and somatosensory evoked potentials (SEPs) were recorded, and convulsion thresholds were determined in rats in which FeCl(2) solution was injected into the unilateral sensorimotor cortex. Isolated spikes appeared immediately after the injection of FeCl(2) solution in ECoGs of the cortex near the injection site and the contralateral homotopic cortex. The injection of FeCl(2) solution produced different electrocorticographic features in which the frequency of isolated spikes was dominant on the side ipsilateral or contralateral to the injection site or nearly equal on the two sides. The spike frequency increased up to 30 to 50 days after the injection, and then was almost constant in most of the rats up to 90 days after the injection. In rats showing nearly equal spike activity on the two sides, there was a tendency for the spike frequency to decrease gradually after 30 to 50 days. Most of the spike and slow wave complexes appeared bilaterally one month or more after the injection in rats in which the isolated spike activity was dominant on the side ipsilateral to the injection site or nearly equal on the two sides. The proportion of rats showing spike and slow wave complexes increased steeply until three months after the injection, and reached 36% of all the FeCl(2) solution-injected rats six months after the injection. In ECoGs of these rats, isolated spikes were also detected. In rats showing dominant spike activity on either side of the cortex, most of spikes appeared unilaterally, while in rats showing nearly equal spike activity on the two sides and those showing spike and slow wave complexes, the frequency of almost synchronous spikes on both sides was higher than that of unilateral spikes. In rats showing dominant spike activity on the side contralateral to the injection site, SEPs recorded at the cortex near the injection site were devoid of the initial positive deflection and were monophasic. They were biphasic in other FeCl(2) solution-injected rats. In rats showing only isolated spikes, abnormal behavior was seldom observed, and convulsion thresholds were lowered. In most of the rats showing spike and slow wave complexes, head nodding was observed. The induction and development of epileptic focus by FeCl(2) solution are discussed.
en-copyright=
kn-copyright=

en-aut-name=NishidaNobuyoshi
en-aut-sei=Nishida
en-aut-mei=Nobuyoshi
kn-aut-name=西田宜可
kn-aut-sei=西田
kn-aut-mei=宜可
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一生理学教室
en-keyword=鉄塩誘導てんかん
kn-keyword=鉄塩誘導てんかん
en-keyword=ラット大脳皮質
kn-keyword=ラット大脳皮質
en-keyword=脳波
kn-keyword=脳波
en-keyword=体性感覚誘発電位
kn-keyword=体性感覚誘発電位
en-keyword=けいれん
kn-keyword=けいれん
en-keyword=閾値
kn-keyword=閾値
END

start-ver=1.4
cd-journal=joma
no-vol=97
cd-vols=
no-issue=1-2
article-no=
start-page=127
end-page=147
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1985
dt-pub=19850225
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Studies on the cyclic AMP-generating system of cerebral cortex with iron-induced epileptic focus
kn-title=鉄塩誘導てんかん性大脳皮質のサイクリックAMP合成系に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The cyclic AMP contents of cortical slices after incubation with or without agents such as norepinephrine were determined in four areas of rat cerebral cortex in which FeCl(2) solution was injected into the unilateral sensorimotor cortex to induce an epileptic focus. Norepinephrine, isoproterenol and phenylephrine elevated the cyclic AMP levels of cortical slices 4- to 7-fold, 2- to 4-fold and 1.5- to 3-fold, respectively. The elicitation of cyclic AMP accumulation by norepinephrine was inhibited by 30 to 60% with phentolamine and 65 to 80% with propranolol. 8-Phenyltheophylline almost completely inhibited the elicitation of cyclic AMP accumulation by a norepinephrine-propranolol combination but not by a norepinephrine-phentolamine combination. In anterior cortical areas of rats in which the appearance of isolated spikes in electrocorticograms was dominant either ipsilaterally or contralaterally to the injection site 8 to 10 days after the injection of FeCl(2) solution, the elevated levels of cyclic AMP elicited by norepinephrine, isoproterenol and a norepinephrine-phentolamine combination were higher on the side of dominant spike activity than on the other. In anterior cortical areas of rats showing dominant spike activity on either side of the cortex 31 to 60 days after the injection, the elevated levels of cyclic AMP elicited by norepinephrine and phenylephrine were lower on the dominant side than on the other. In anterior cortical areas of rats showing nearly equal spike activity on the two sides 31 to 60 days after the injection, the elevated levels of cyclic AMP elicited by norepinephrine, isoproterenol and a norepinephrine-phentolamine combination were higher on the side ipsilateral to the injection site than on the other. In these rats, a similar regional difference in the norepinephrine-elicited accumulation of cyclic AMP was detected 19 to 21 days after the injection. In anterior and posterior cortical areas of rats in which the appearance of spike and slow wave complexes as well as isolated spikes were detected 31 to 60 days after the injection, the elevated levels of cyclic AMP elicited by norepinephrine, isoproterenol, phenylephrine and combinations of norepinephrine and phentolamine or propranolol were higher on the side ipsilateral to the injection site than on the other. The tendency for the norepinephrine-elicited accumulation of cyclic AMP to be related to the epileptic discharge patterns in rats 61 to 90 days after the injection was similar to that in rats 31 to 60 days after the injection. The regional differences in cyclic AMP contents of incubated cortical slices are discussed with regard to the neurochemical process of iron-induced epilepsy.
en-copyright=
kn-copyright=

en-aut-name=YasuharaHiromichi
en-aut-sei=Yasuhara
en-aut-mei=Hiromichi
kn-aut-name=安原弘通
kn-aut-sei=安原
kn-aut-mei=弘通
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一生理学教室
en-keyword=サイクリックAMP
kn-keyword=サイクリックAMP
en-keyword=ノルエピネフリン
kn-keyword=ノルエピネフリン
en-keyword=ラット大脳皮質
kn-keyword=ラット大脳皮質
en-keyword=切片
kn-keyword=切片
en-keyword=鉄塩誘導てんかん
kn-keyword=鉄塩誘導てんかん
END

start-ver=1.4
cd-journal=joma
no-vol=99
cd-vols=
no-issue=7-8
article-no=
start-page=787
end-page=806
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1987
dt-pub=19870830
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Guanidino compounds in iron-induced epileptogenic foci of rats
kn-title=鉄塩誘導てんかん原性焦点組織におけるグアニジノ化合物の変動に関する研究 ― 特にラジカル反応によるグアニジノ化合物の生成について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Changes in the levels of guanidino compounds in the cortex, hippocampus, striatum, hypothalamus, midbrain, pons and medulla oblongata and cerebellum were analyzed by high performance liquid chromatography after an injection of ferric chloride into the sensory motor cortex of SD rats. Levels of guanidinoacetic acid (GAA) and methylguanidine (MG) changed greatly 15 and 30 min after the injection, but recovered to normal levels 24 to 48 hours after the injection. GAA and MG increased two or three times the normal level 2 months after the injection, at which time iron-induced epileptogenic foci were formed. Levels of other guanidino compounds, i.e., N-acetylarginine, guanidinoacetic acid, arginine (Arg), homoarginine and creatinine (CRN) also changed, though the extent of the changes was not as marked as with GAA and MG. Rapidly increased generation of hydroxyl radical and peroxide intermediate radical(s) was observed by electron spin resonance analysis after addition of ferric chloride and hydrogen peroxide to rat brain homogenate. Levels of MG and GAA also increased. A significant relationship between the generation of hydroxyl radical and the formation of MG was recognized. The formation of MG in the system was dependent on the concentration of CRN but independent of the concentration of Arg and GAA. These results suggest that MG formed from CRN may act on neurones after iron injection into the rat brain, thus forming epileptogenic feci.
en-copyright=
kn-copyright=

en-aut-name=FukushimaMasato
en-aut-sei=Fukushima
en-aut-mei=Masato
kn-aut-name=福島正登
kn-aut-sei=福島
kn-aut-mei=正登
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部脳代謝研究施設機能生化学部門
en-keyword=鉄塩誘導てんかん原性焦点
kn-keyword=鉄塩誘導てんかん原性焦点
en-keyword=グアニジノ化合物
kn-keyword=グアニジノ化合物
en-keyword=ラット
kn-keyword=ラット
en-keyword=ラジカル反応
kn-keyword=ラジカル反応
en-keyword=メチルグアニジン
kn-keyword=メチルグアニジン
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=1
article-no=
start-page=31
end-page=35
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1997
dt-pub=19970910
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Correlative study of hippocampal atrophy assessed by MRI and clinical features in temporal lobe epilepsy.
kn-title=側頭葉てんかんの海馬萎縮と臨床像の検討 ―MRIを用いた海馬萎縮の簡易評価―
en-subtitle=
kn-subtitle=
en-abstract=We studied hippocampal atrophy in 39 patients with temporal lobe epilepsy using MRI. The ratio (a) of the width of the hippocampus on the atrophic side to that on the contralateral side was measured in coronal sections of the short SE in MRI. According to this ratio, the patients were divided into three groups : 11 with hippocampal atrophy (a<0.8), 13 with borderline atrophy (0.8≦a≦0.9), and 15 with no hippocampal atrophy (a≧0.8). In the patients of the group with hippocampal atrophy, the clinical history of epilepsy tended to be long, and the site of hippocampal atrophy was consistent with that of interictal spike foci on the electroencephalogram in 9 out of 11 patients. However, there was no difference between the three groups, with regard to age at onset, age when MRI was conducted, frequency of seizures, generalized seizures, the types and doses of antiepileptic drugs used, history of neonatal asphyxia, intelligence and epilpetic psychosis. These results suggest that hippocampal atrophy in temporal lobe epilepsy may be related to repetition of
epileptic dischargges in a localized part of the brain.
kn-abstract=側頭葉てんかん患者39例の海馬萎縮をMRIを用いて評価し,臨床像との関連を検討した｡MRIの冠状断short SE像で海馬の幅を計測し,萎縮側海馬の村側海馬に対する比(a)を求め,海馬萎縮(+)群;a<0.8,11例,境界群;0.8≦a<0.9,13例,海馬萎縮(-)群;a≧0.9,15例の3群に分けた｡海馬萎縮(+)群で罹病期間が長い傾向があった｡また,発作間歇期脳波の焦点側は海馬委縮(+)群の11例中9例で萎縮側と一致した。しかし,発病年齢,MRI撮影時年齢,発作頻度,全般化発作の有無,抗てんかん薬総服用量,知能障害,精神症状,生下時仮死の有無については3群間で差が認められなかった｡この結果から,側頭葉てんかんにおける海馬萎縮は,生下時や全身けいれん発作時の低酸素状態によるものではなく,脳局所の反復するてんかん性発射と関連する可能性が示唆され,海馬萎縮の機序を考えるうえで興味深く思われた。
en-copyright=
kn-copyright=

en-aut-name=SatoKeiko
en-aut-sei=Sato
en-aut-mei=Keiko
kn-aut-name=佐藤圭子
kn-aut-sei=佐藤
kn-aut-mei=圭子
aut-affil-num=1
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=岡本基
kn-aut-sei=岡本
kn-aut-mei=基
aut-affil-num=2
ORCID=

en-aut-name=JojaIkuo
en-aut-sei=Joja
en-aut-mei=Ikuo
kn-aut-name=上着郁夫
kn-aut-sei=上着
kn-aut-mei=郁夫
aut-affil-num=3
ORCID=

en-aut-name=NakatsuTakeshi
en-aut-sei=Nakatsu
en-aut-mei=Takeshi
kn-aut-name=中津武志
kn-aut-sei=中津
kn-aut-mei=武志
aut-affil-num=4
ORCID=

en-aut-name=MorimotoKiyoshi
en-aut-sei=Morimoto
en-aut-mei=Kiyoshi
kn-aut-name=森本清
kn-aut-sei=森本
kn-aut-mei=清
aut-affil-num=5
ORCID=

en-aut-name=HayabaraToshiyuki
en-aut-sei=Hayabara
en-aut-mei=Toshiyuki
kn-aut-name=早原敏之
kn-aut-sei=早原
kn-aut-mei=敏之
aut-affil-num=6
ORCID=

en-aut-name=KurodaShigetoshi
en-aut-sei=Kuroda
en-aut-mei=Shigetoshi
kn-aut-name=黒田重利
kn-aut-sei=黒田
kn-aut-mei=重利
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=国立療養所南岡山病院神経内科･臨床研究部

affil-num=2
en-affil=
kn-affil=岡山大学医療技術短期大学部衛生技術学科

affil-num=3
en-affil=
kn-affil=岡山大学医学部放射線医学教室

affil-num=4
en-affil=
kn-affil=岡山市立市民病院神経内科

affil-num=5
en-affil=
kn-affil=香川医科大学神経精神医学教室

affil-num=6
en-affil=
kn-affil=国立療養所南岡山病院神経内科･臨床研究部

affil-num=7
en-affil=
kn-affil=岡山大学医学部神経精神医学教室
en-keyword=側頭葉てんかん (temporal lobe epilepsy)
kn-keyword=側頭葉てんかん (temporal lobe epilepsy)
en-keyword=海馬委縮 (hippocampal atrophy)
kn-keyword=海馬委縮 (hippocampal atrophy)
en-keyword=罹病期間 (clinical history)
kn-keyword=罹病期間 (clinical history)
en-keyword=MRI
kn-keyword=MRI
en-keyword=発作間歇期脳波 (interictal EEG foci)
kn-keyword=発作間歇期脳波 (interictal EEG foci)
END

start-ver=1.4
cd-journal=joma
no-vol=103
cd-vols=
no-issue=7-8
article-no=
start-page=951
end-page=962
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1991
dt-pub=199108
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The cyclic AMP-generating system of cobalt-induced epileptic cerebral cortex
kn-title=コバルト誘導てんかん性大脳皮質のサイクリック AMP 合成系に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A cobalt chloride solution was injected into the unilateral sensorimotor cortex of rats to induce epileptic activity. The cyclic AMP contents of slices incubated with or without adenosine and 2-chloroadenosine were determined in four cortical areas after electroencephalography and behavioral examination in cobalt-injected rats. Electrographic spike activity appeared immediately after injection of cobalt. In the majority of cobalt-injected rats, the spike activity was dominant in the primary epileptic region of the cortex. The spike frequency reached a maximum level two to three weeks after the injection and declined thereafter. The electrographic activity was followed by abnormal behavior. Adenosine and 2-chloroadenosine elevated the cyclic AMP levels in the cortical slices 6-to 10-fold and 10-to 16-fold, respectively. The elicitation of cyclic AMP accumulation was strongly inhibited by the adenosine antagonist 8-phenyltheophylline. The cyclic AMP accumulation elicited by adenosine or 2-chloroadenosine was increased in the primary cortical area of cobalt-induced epilepsy, but in the other cortical areas there was no deviation in cyclic AMP accumulation. The increase in cyclic AMP accumulation was observed regardless of the presence or absence of the adenosine uptake inhibitor dipyridamole, phosphodiesterase inhibitor Ro 20-1724, and adenosine deaminase. The increased accumulation of cyclic AMP in the primary epileptic cortex was detected as early as 8 days after the injection. The cyclic AMP accumulation slightly increased thereafter. It reached a plateau 17 to 19 days after the injection and then turned to the control levels, in harmony with the electrographic and behavioral profiles. These findings suggest that alterations in adenosine-sensitive generation of cyclic AMP in the primary epileptic region of the cortex are part of the neurochemical process of cobalt-induced epilepsy.
en-copyright=
kn-copyright=

en-aut-name=AsakiHideki
en-aut-sei=Asaki
en-aut-mei=Hideki
kn-aut-name=浅木秀樹
kn-aut-sei=浅木
kn-aut-mei=秀樹
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部第一生理学教室
en-keyword=サイクリック AMP
kn-keyword=サイクリック AMP
en-keyword=アデノシン
kn-keyword=アデノシン
en-keyword=2 - クロロアデノシン
kn-keyword=2 - クロロアデノシン
en-keyword=コバルト誘導てんかん
kn-keyword=コバルト誘導てんかん
en-keyword=ラット大脳皮質
kn-keyword=ラット大脳皮質
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=小児てんかん患者における複雑部分発作重積状態
kn-title=Complex partial status epilepticus in children with epilepsy
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KikumotoKenichi
en-aut-sei=Kikumoto
en-aut-mei=Kenichi
kn-aut-name=菊本健一
kn-aut-sei=菊本
kn-aut-mei=健一
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=104
cd-vols=
no-issue=11-12
article-no=
start-page=1023
end-page=1032
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=199212
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effects of ferric citrate or hyperoxygenation on guanidino compounds in mouse organs
kn-title=クエン酸鉄投与及び純酸素負荷マウスのグアニジノ化合物の変動に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The guanidino compounds in various mouse organs after i.p. administration of ferric citrate(Fe) and after inhalation of pure oxygen(O(2)) were studied. Guanidinoacetic acid and N-acetylarginine levels were markedly higher in the kidney, and they decreased after administration of Fe or inhalation of O(2). Creatinine decreased in the liver after administration of Fe, and it decreased in the liver and muscle after inhalation of O(2). γ-Guanidinobutyric acid level was significantly higher in the normal liver, but decreased after administration of Fe or inhalation of O(2). Arginine(Arg) increased in the kidney and muscle after administration of Fe, while it decreased in the liver. Arg decreased in the kidney and the muscle after inhalation of O(2). Methylguanidine(MG) increased in the brain after administration of Fe or inhalation of O(2). However, MG decreased in the liver after administration of Fe, and also decreased in the liver, kidney and muscle after inhalation of O(2). MG increased only in the brain. This finding suggested that the reactive oxygen species(O(2)(-), H(2)O(2), ・OH) were most effective there, because oxygen consumpution in the brain was much more than in the other organs.
en-copyright=
kn-copyright=

en-aut-name=WatanabeSeigo
en-aut-sei=Watanabe
en-aut-mei=Seigo
kn-aut-name=渡邊省吾
kn-aut-sei=渡邊
kn-aut-mei=省吾
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部附属分子細胞医学研究施設神経情報学部門
en-keyword=hyperoxygenation
kn-keyword=hyperoxygenation
en-keyword=iron ion
kn-keyword=iron ion
en-keyword=guanidino compounds
kn-keyword=guanidino compounds
en-keyword=methylganidine
kn-keyword=methylganidine
en-keyword=free radicals
kn-keyword=free radicals
END

start-ver=1.4
cd-journal=joma
no-vol=105
cd-vols=
no-issue=11-12
article-no=
start-page=977
end-page=986
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1993
dt-pub=19931231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Developmental changes in the serotonergic system in El mouse brain
kn-title=成長およびけいれん準備性獲得に伴う El マウス脳内セロトニン代謝の変動に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=El mice manifest epileptiform seizures which are gradually elicited by tossing stimulation once a week from 5 to 10 weeks of ages. It was reported that brain monoamines, especially serotonin (5-HT), are important factors in seizure susceptivity. In this study, we observed changes in brain 5-HT and its metabolite, 5-hydroxyindolacetic acid (5-HIAA), and its metabolic enzymes, tryptophan hydroxylase (Trp-OHase) and monoamine oxidase-A (MAO-A) , during growth with and without tossing stimulation. In non-stimulated El mice, the 5-HT level was lower at 6 and 7 weeks than that in other ages, and the 5-HIAA level was generally lower in older mice. In stimulated El mice, the 5-HT level was higher after the first stimulation, lower at 8 weeks, and then higher again at 10 weeks. However, 5-HIAA levels were generally higher in older mice. The Trp-OHase activity was higher at 8 and 10 weeks, and the MAO-A activity was higher at 8 weeks compared to that of non-stimulated El mice. These findings suggest that a disordered release and metabolism of 5-HT influences the development of the epileptiform seizures induced by tossing stimulation.
en-copyright=
kn-copyright=

en-aut-name=SuyamaKeiko
en-aut-sei=Suyama
en-aut-mei=Keiko
kn-aut-name=陶山ケイ子
kn-aut-sei=陶山
kn-aut-mei=ケイ子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部分子細胞医学研究施設神経情報学部門
en-keyword=El mouse seizures
kn-keyword=El mouse seizures
en-keyword=serotonin
kn-keyword=serotonin
en-keyword=5-hydroxyindolacetic acid
kn-keyword=5-hydroxyindolacetic acid
en-keyword=tryptophan hydroxylase
kn-keyword=tryptophan hydroxylase
en-keyword=monoamine oxidase-A
kn-keyword=monoamine oxidase-A
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=1-2
article-no=
start-page=103
end-page=115
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199402
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Immunohistocemical analysis of glutamic acid, γ-aminobutyric acid, and glial fibrillary acidic protein positive cells in the hippocampus of E1 mice
kn-title=E1マウスの海馬におけるグルタミン酸,γ-アミノ酪酸及び glial fibrillary acidic protein の免疫組織化学的研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Glutamic acid, γ-aminobutyric acid and glial fibrillary accidic protenin positive cells in the hippocampus of E1 mice and ddY mice were examined immunohistochemically. The shape of glutamic acid positive cells in CA1, CA2, CA3 and CA4 of hippocampus were expanded compar-ed to that of ddY mice. There was a space between cells and cells containing glutamic acid and the nucleus of such cells was larger in the CA1 of E1 mice than that of ddY mice. The glutamic acid cells were irregular and the nucleus was larger in the gyrus dentantus of E1 mice than that of ddY mice. There was an intermittence in the process of glutamic acid cells in the area of of str. radiatum of E1 mice. γ-Aminobutyric acid-posititve cells seemed to be expanded in CA1 of CA2, CA3, and CA4 and gyrus dentatus and there was space between such cells in the CA1 of E1 mice. Large γ-aminobutyric acid positive cells, which were located close to the gyrus dentatus in ddY mice, were not found in E1 mice. The number of γ-aminobutyric acid-positive cells was lower in E1 mice than in ddY mice. A greater number of glial fibrillary acidic protein postive cells was found in the area of the hippocampus in E1 mice than in ddY mice. These results suggest that E1 mice are genetically epileptic mice.
en-copyright=
kn-copyright=

en-aut-name=SuhMoon-Suk
en-aut-sei=Suh
en-aut-mei=Moon-Suk
kn-aut-name=徐文錫
kn-aut-sei=徐
kn-aut-mei=文錫
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部分子細胞医学研究施設神経情報学部門
en-keyword=E1マウス
kn-keyword=E1マウス
en-keyword=グルタミン酸
kn-keyword=グルタミン酸
en-keyword=γ-アミノ酪酸
kn-keyword=γ-アミノ酪酸
en-keyword=免疫組織化学
kn-keyword=免疫組織化学
en-keyword=海馬
kn-keyword=海馬
END

start-ver=1.4
cd-journal=joma
no-vol=109
cd-vols=
no-issue=1-2
article-no=
start-page=1
end-page=6
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1997
dt-pub=19970228
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Cerebral dysgenesis and psychomotor retardation in neonatal epilepsy
kn-title=新生児期発症のてんかんにおける脳形成障害および心身障害についての検討
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=A clinical and neuroradiological study was carried out to clarify the relationship among cerebral dysgenesis, psychomotor retardation and neonatal epilepsy. Twenty-one cases with epilepsy developed within four weeks after birth were selected among 770 in-patients with childhood epilepsy. They consisted of one benign familial neonatal convulsion, nine of early myoclonic encephalopathy, four of Ohtahara syndrome, six of symptomatic localizationrelated epilepsy, and one of undetermined epilepsy. Seven cases with non specific types of epilepsies were investigated in detail. They developed into four of frontal lobe epilepsy, one of temporal lobe epilepsy and one severe epilepsy with multiple independent spike foci. Psychomotor retardation was observed in six of seven cases, and cerebral dysgenesis was considered to be important as an etiological factor. Proton MR spectroscopy revealed the decrease in the ratio of N-acetylaspartate/choline in the area with heterotopic gray matter and in the side of hemimegalencephaly, contrasted with a contralateral area without lesions. These findings can be inferred to reflect the decreased numbers of neuronal cell population or reduced metabolism in the lesions.
en-copyright=
kn-copyright=

en-aut-name=SanadaSatoshi
en-aut-sei=Sanada
en-aut-mei=Satoshi
kn-aut-name=真田敏
kn-aut-sei=真田
kn-aut-mei=敏
aut-affil-num=1
ORCID=

en-aut-name=OkaEiji
en-aut-sei=Oka
en-aut-mei=Eiji
kn-aut-name=岡鍈次
kn-aut-sei=岡
kn-aut-mei=鍈次
aut-affil-num=2
ORCID=

en-aut-name=OhtaharaShunsuke
en-aut-sei=Ohtahara
en-aut-mei=Shunsuke
kn-aut-name=大田原俊輔
kn-aut-sei=大田原
kn-aut-mei=俊輔
aut-affil-num=3
ORCID=

en-aut-name=KawaharaMichiko
en-aut-sei=Kawahara
en-aut-mei=Michiko
kn-aut-name=河原道子
kn-aut-sei=河原
kn-aut-mei=道子
aut-affil-num=4
ORCID=

en-aut-name=SakaeKatsuyoshi
en-aut-sei=Sakae
en-aut-mei=Katsuyoshi
kn-aut-name=栄勝美
kn-aut-sei=栄
kn-aut-mei=勝美
aut-affil-num=5
ORCID=

en-aut-name=HirakiYoshio
en-aut-sei=Hiraki
en-aut-mei=Yoshio
kn-aut-name=平木祥夫
kn-aut-sei=平木
kn-aut-mei=祥夫
aut-affil-num=6
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部小児神経科

affil-num=2
en-affil=
kn-affil=岡山大学医学部小児神経科

affil-num=3
en-affil=
kn-affil=岡山大学医学部小児神経科

affil-num=4
en-affil=
kn-affil=岡山大学医学部放射線科

affil-num=5
en-affil=
kn-affil=岡山大学医学部放射線科

affil-num=6
en-affil=
kn-affil=岡山大学医学部放射線科
en-keyword=新生児期
kn-keyword=新生児期
en-keyword=局在関連性てんかん
kn-keyword=局在関連性てんかん
en-keyword=心身障害
kn-keyword=心身障害
en-keyword=脳形成障害
kn-keyword=脳形成障害
en-keyword=MR スペクトロスコピー
kn-keyword=MR スペクトロスコピー
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=7-8
article-no=
start-page=799
end-page=809
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=An electroclinical study on latent epilepsy in childhood
kn-title=小児期の潜在性てんかんの脳波に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Clinical and electroencephalographic studies were carried out to clarify the characteristics of latent epilepsy (LE) in children and to obtain criteria for treatment. LE was defined as a condition manifesting epileptic EEG abnormalities without any clinical epilepsy, febrile convulsion or other seizures. Three hundred and thirty-nine children with LE seen at the Department of Child Neurology, Okayama University Hospital were divided into four groups by their etiological backgrounds (e. g., organic brain damage and convulsive predisposition) and were compared with 149 controls with clinical epilepsy. Clinical epileptic seizures appeared in 14 (4.1%) of the 339 children during follow-up of two months to 19 years. Thirteen of the 14 cases belonged to the organic brain damage group. The EEG findings in children susceptible to clinical seizures consisted of slow spike-wave, generalized cortico-subcortical discharges, multiple focal cortical discharges, focal discharges with forcal slow wave, and discharges activated by hyperventilation.
The EEG findings in children not disposed to develop clinical epilepsy consisted of sharp wave, small sharp wave, Rolandic spike, parietal focal spike, and photo-sensitivity discharges in adolescence. Convulsive and epileptic predisposition was not regarded as a risk factor in clinical epilepsy. On the basis of these findings, criteria for antiepileptic drug therapy for LE were proposed.
en-copyright=
kn-copyright=

en-aut-name=OhnoShigeru
en-aut-sei=Ohno
en-aut-mei=Shigeru
kn-aut-name=大野繁
kn-aut-sei=大野
kn-aut-mei=繁
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部小児神経学教室
en-keyword=潜在性てんかん
kn-keyword=潜在性てんかん
en-keyword=てんかん
kn-keyword=てんかん
en-keyword=てんかん波
kn-keyword=てんかん波
en-keyword=抗てんかん剤
kn-keyword=抗てんかん剤
en-keyword=脳波
kn-keyword=脳波
END

start-ver=1.4
cd-journal=joma
no-vol=106
cd-vols=
no-issue=7-8
article-no=
start-page=757
end-page=762
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1994
dt-pub=199408
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Influence of the combined treatment with phenytoin or valproate on serum concentration of carbamazepine
kn-title=血清中カルバマゼピン濃度に及ぼすフェニトインおよびバルプロ酸併用の影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To clarify the pharmacokinetic interaction in poly-therapy for epilepsy, the serum concentration of carbamazepine (CZB) was measured in epileptic patients to whom CBZ had been prescribed chronically with or without phenytoin (PHT) and sodium valproate (VPA). The serum CBZ concentrations increased with increasing doses of CBZ, but increased less at higher doses. Chiliren (<12 yrs) showed lower serum CBZ concentrations than patients 12 years old and older. The L/D ratios (L : CBZ level, D : dose/body weight) were significantly decreased by the combined treatment with PHT and VPA in a dose-dependent manner, probably due to an induction of metabolizing enzyme. These findings suggest that especially in the case of change of the drug therapy from mono-therapy to mono therapy, careful monitoring of serum concentration is necessary.
en-copyright=
kn-copyright=

en-aut-name=KishimaMiyuki
en-aut-sei=Kishima
en-aut-mei=Miyuki
kn-aut-name=鬼嶋みゆき
kn-aut-sei=鬼嶋
kn-aut-mei=みゆき
aut-affil-num=1
ORCID=

en-aut-name=YaoKazuhisa
en-aut-sei=Yao
en-aut-mei=Kazuhisa
kn-aut-name=矢尾和久
kn-aut-sei=矢尾
kn-aut-mei=和久
aut-affil-num=2
ORCID=

en-aut-name=YasuharaKanako
en-aut-sei=Yasuhara
en-aut-mei=Kanako
kn-aut-name=安原加奈子
kn-aut-sei=安原
kn-aut-mei=加奈子
aut-affil-num=3
ORCID=

en-aut-name=SuemaruKatsuya
en-aut-sei=Suemaru
en-aut-mei=Katsuya
kn-aut-name=末丸克矢
kn-aut-sei=末丸
kn-aut-mei=克矢
aut-affil-num=4
ORCID=

en-aut-name=FurunoKatsushi
en-aut-sei=Furuno
en-aut-mei=Katsushi
kn-aut-name=古野勝志
kn-aut-sei=古野
kn-aut-mei=勝志
aut-affil-num=5
ORCID=

en-aut-name=OishiRyozo
en-aut-sei=Oishi
en-aut-mei=Ryozo
kn-aut-name=大石了三
kn-aut-sei=大石
kn-aut-mei=了三
aut-affil-num=6
ORCID=

en-aut-name=GomitaYutaka
en-aut-sei=Gomita
en-aut-mei=Yutaka
kn-aut-name=五味田裕
kn-aut-sei=五味田
kn-aut-mei=裕
aut-affil-num=7
ORCID=

en-aut-name=OhtaharaShunsuke
en-aut-sei=Ohtahara
en-aut-mei=Shunsuke
kn-aut-name=大田原俊輔
kn-aut-sei=大田原
kn-aut-mei=俊輔
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部附属病院薬剤部

affil-num=2
en-affil=
kn-affil=岡山大学医学部附属病院薬剤部

affil-num=3
en-affil=
kn-affil=岡山大学医学部附属病院薬剤部

affil-num=4
en-affil=
kn-affil=岡山大学医学部附属病院薬剤部

affil-num=5
en-affil=
kn-affil=岡山大学医学部附属病院薬剤部

affil-num=6
en-affil=
kn-affil=岡山大学医学部附属病院薬剤部

affil-num=7
en-affil=
kn-affil=岡山大学医学部附属病院薬剤部

affil-num=8
en-affil=
kn-affil=岡山大学医学部小児神経学教室
en-keyword=カルバマゼピン
kn-keyword=カルバマゼピン
en-keyword=フェニトイン
kn-keyword=フェニトイン
en-keyword=バルプロ酸
kn-keyword=バルプロ酸
en-keyword=血清中濃度
kn-keyword=血清中濃度
en-keyword=薬物相互作用
kn-keyword=薬物相互作用
END

start-ver=1.4
cd-journal=joma
no-vol=107
cd-vols=
no-issue=7-8
article-no=
start-page=131
end-page=141
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=19950831
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Adenosines as preventive preparations of post-traumatic epilepsy
kn-title=アデノシン関連物質による外傷性てんかん発症予防に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=As oxidation of neural membranes by reactive oxygen species (ROS), especially hydroxyl radicals (・OH), is involved in the biochemical pathogenesis of post-traumatic epilepsy, post-traumatic epilepsy is thought to be prevented by treatment with ROS scavengers. In the present study, I first examined the effects of adenosine (Ado), 2-chloroadenosine (CI-Ado) and guanosine on ・OH and superoxide anion (O(-)(2)), generated by the Fenton reagent and the hypoxanthine-xanthine oxidase system, respectively, using electron spin resonance spectrometry. I also examined the effecta of Ado and Cl-Ado on the occurrence of epileptic discharges on the electrocorticogram (ECoG) induced by FeCl(3) injection (500nmol) into the sensorimotor cortex of rats, i.e., a model of an experimental post-traumatic epilepsy. Although O(-)(2) was not scavenged, ・OH were scavenged by Ado and Cl-Ado dose-dependently. The scavenging activity of Ado was 4 times stronger then thst of Cl-Ado. On the ECoG of rats given FeCl(3), sporadic spike discharges, polyspikes and/or ictal patterns started to be observed 15-90 min after the injection. Epileptic discharges did not appear or their occurrence was delayed by the intraperitioneal injection of Ado (5mg/kg) or Cl-Ado (1mg/kg) 30 min prior to the FeCl(3) injection, although Cl-Ado showed a chronotropic action. Thus Ado and Ci-Ado may be useful in the prevention and the attenuation of progression of post-traumatic epilepsy by scavenging ・OH and by their anticonvulsant effect.
en-copyright=
kn-copyright=

en-aut-name=TomaJunji
en-aut-sei=Toma
en-aut-mei=Junji
kn-aut-name=当真純二
kn-aut-sei=当真
kn-aut-mei=純二
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部附属分子細胞医学研究施設神経情報学部門
en-keyword=adenosine
kn-keyword=adenosine
en-keyword=chloroadenosine
kn-keyword=chloroadenosine
en-keyword=radical scavenger
kn-keyword=radical scavenger
en-keyword=post-traumatic epilepsy
kn-keyword=post-traumatic epilepsy
en-keyword=experimental epilepsy
kn-keyword=experimental epilepsy
END

start-ver=1.4
cd-journal=joma
no-vol=107
cd-vols=
no-issue=7-8
article-no=
start-page=99
end-page=109
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=19950831
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=An electroclinical study of localization-related epilepsies occurring before 6 months of age
kn-title=生後6ヵ月未満発症の局在関連性てんかんに関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=To clarify the characteristics of localization-related epilepsies occurring before 6 monthes of age, I carried out an electroclinical study on 28 cases which had been followed up for more than one year after the onset. The subjects were divided into two groups : the controlled group (8 cases) and the refractory group (20 cases). The controlled group was defined as the subjects whose seizures were suppressed within one year after the onset and the other subjects were classified into the refractory group. The characteristies of the refractory group were as follows : Most cases had serious underlying pathologies. The seizure type of most cases was simple partial seizure or complex partial seizure or complex partial seizure without secondary generalization. The inter-ictal EEG showed focal abnormalities and severe dysrrythmia on the basic pattern associated with mulitifocal spikes in most cases. Some cases developed West syndrome after localization-related epilepsies, and generalized seizures or pseudoabsences appeared later in some other cases. 
 In conclusion, a comprehensive assessment and an intensive follow-up of clinical and EEG manifestations are of great value for determining the prognosis localization-related epilepsies occurring in early infancy.
en-copyright=
kn-copyright=

en-aut-name=OhmoriIori
en-aut-sei=Ohmori
en-aut-mei=Iori
kn-aut-name=大守伊織
kn-aut-sei=大守
kn-aut-mei=伊織
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部小児神経学教室
en-keyword=局在関連性てんかん
kn-keyword=局在関連性てんかん
en-keyword=難治てんかん
kn-keyword=難治てんかん
en-keyword=予後
kn-keyword=予後
en-keyword=脳波
kn-keyword=脳波
en-keyword=乳児期
kn-keyword=乳児期
END

start-ver=1.4
cd-journal=joma
no-vol=110
cd-vols=
no-issue=1-6
article-no=
start-page=39
end-page=51
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1998
dt-pub=19980625
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Analysis of ictal EEGs in West syndrome
kn-title=West 症候群の発作時脳波に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Although tonic spasms (TS) observed in West syndrome(WS) are regarded as generalized seizures, the mechanism of their occurrence has not yet been fully elucidated. We analyzed ictal EEGs of TS to determine the mechanism and to clarify the role of cortical pathology in the occurrence of TS. Of 53 infants with WS, we classified cryptogenic cases as Group Ⅰ. Symptomatic cases were classified into 2 groups : Group Ⅱ consisted of those without partial seizures during the period of WS and Group 3 consisted of those with partial seizures. We analyzed 7283 ictal EEGs of TS regarding the following 5 points : 1) patterns of ictal EEGs, 2) frequency of isolated TS, 3) asymmetry of ictal EEGs, 4) spasm-spasm intervals, and 5) duration of ictal EEGs of each TS. We concluded that the asymmetry of ictal EEGs and the "rhythmic slow activity" immediately following ictal EEGs of TS were related to cortical pathology. Since "rhythmic slow activities" were often observed in Group Ⅲ and appeared at the same regions as those in ictal EEGs of concomittant partial seizures, they were considered to be peculiar EEG patterns related to cortical pathologic lesions.
en-copyright=
kn-copyright=

en-aut-name=AsanoTakashi
en-aut-sei=Asano
en-aut-mei=Takashi
kn-aut-name=浅野孝
kn-aut-sei=浅野
kn-aut-mei=孝
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部小児神経学講座
en-keyword=West 症候群
kn-keyword=West 症候群
en-keyword=発作時脳波
kn-keyword=発作時脳波
en-keyword=Tonic spasms
kn-keyword=Tonic spasms
en-keyword=部分発作
kn-keyword=部分発作
END

start-ver=1.4
cd-journal=joma
no-vol=107
cd-vols=
no-issue=7-8
article-no=
start-page=69
end-page=78
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=19950831
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Effect of zonisamide on neurotransmitter release from hippocampal slice of E1 mice : A study of neurotransmitter release using an improved experimemtal system
kn-title=改良型神経伝達物質放出測定装置によるE1マウス海馬切片よりの神経伝達物質放出と抗てんかん薬ゾニサミドの影響に関する研究
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Using an experimental apparatus for estimating neurotransmitter release from brain slices, which involved an improved type of perfusion chamber and more well-controlled tube lines than the previous one were aspartic acid and γ-aminobutyric acid (GABA) release from hippocampal slices from epileptic E1 mice estimated more exactly and stably. Zonisamide had no effect on the aspartic acid release from hippocampal slices of E1 mice by zonisamide. However, zonisamide accelerated dose dependently GABA release from hippocampal slices of non-stimulated E1 mice, though no such acceleration was observed in stimulated E1 mice, i. e., repeatedly convulsed E1 mice.
en-copyright=
kn-copyright=

en-aut-name=EndoAtsushi
en-aut-sei=Endo
en-aut-mei=Atsushi
kn-aut-name=遠藤敦
kn-aut-sei=遠藤
kn-aut-mei=敦
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部附属分子細胞医学研究施設神経情報学部門
en-keyword=E1マウス
kn-keyword=E1マウス
en-keyword=アスパラギン酸
kn-keyword=アスパラギン酸
en-keyword=γ-アミノ酪酸
kn-keyword=γ-アミノ酪酸
en-keyword=ゾニサミド
kn-keyword=ゾニサミド
en-keyword=けいれん
kn-keyword=けいれん
END

start-ver=1.4
cd-journal=joma
no-vol=116
cd-vols=
no-issue=3
article-no=
start-page=251
end-page=255
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2005
dt-pub=20050131
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=West 症候群の薬物療法
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=大塚頌子
kn-aut-sei=大塚
kn-aut-mei=頌子
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯学総合研究所　発達神経病態学
en-keyword=West症候群
kn-keyword=West症候群
en-keyword=点頭てんかん
kn-keyword=点頭てんかん
en-keyword=薬物療法
kn-keyword=薬物療法
en-keyword=予後
kn-keyword=予後
END

start-ver=1.4
cd-journal=joma
no-vol=119
cd-vols=
no-issue=1
article-no=
start-page=41
end-page=47
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=An animal model of status epilepticus induced by massed electrical stimulations to the deep prepiriform cortex
kn-title=深部前梨状葉皮質の間欠的電気刺激によるてんかん発作重積モデル
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Hippocampal damage induced by status epilepticus (SE) has been suggested as the developmental pathway of temporal lobe epilepsy. We developed an experimental model of SE induced by massed electrical stimulations into the deep prepiriform cortex. Stimulations under aminophylline pretreatment more effectively induced SE than those in the absence of aminophylline. Most SE episodes included secondary generalized seizures. Cresyl violet staining indicated neuronal degeneration in CA1 and CA3, 1-2 weeks after the SE. Mild neuronal loss was observed 8 weeks after the SE, although there were no obvious histological changes in the hilus. Immunoreactivity for GluR1, a subunit of the AMPA receptors, was reduced in CA3 and the hilus starting 1 week after SE, indicating a discrepancy between the distributions of neuronal damage and the GluR1 decrement. The present model serves as a useful model of SE. Further improvement of this method will make it an effective tool for understanding the developmental process of temporal lobe epilepsy.
en-copyright=
kn-copyright=

en-aut-name=KoyamaFumihiko
en-aut-sei=Koyama
en-aut-mei=Fumihiko
kn-aut-name=小山文彦
kn-aut-sei=小山
kn-aut-mei=文彦
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大岡山大学大学院医歯薬学総合研究科 精神神経病態学
en-keyword=けいれん発作重積(status epilepticus)
kn-keyword=けいれん発作重積(status epilepticus)
en-keyword=深部前梨状葉皮質(deep prepiriform cortex)
kn-keyword=深部前梨状葉皮質(deep prepiriform cortex)
en-keyword=反復電気刺激(massed electrical stimulations)
kn-keyword=反復電気刺激(massed electrical stimulations)
en-keyword=AMPA型受容体(AMPA receptors)
kn-keyword=AMPA型受容体(AMPA receptors)
en-keyword=ラット(rat)
kn-keyword=ラット(rat)
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=マウスの電気生理学的手法を用いたてんかんの新しい評価方法と抗てんかん薬の影響
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=MurakamiAya
en-aut-sei=Murakami
en-aut-mei=Aya
kn-aut-name=村上理
kn-aut-sei=村上
kn-aut-mei=理
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=てんかん性スパズムの発作時脳波におけるガンマ律動のスペクトル特性
kn-title=Spectral characteristics of EEG gamma rhythms associated with epileptic spasms
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=InoueTakushi
en-aut-sei=Inoue
en-aut-mei=Takushi
kn-aut-name=井上拓志
kn-aut-sei=井上
kn-aut-mei=拓志
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=10
cd-vols=
no-issue=2
article-no=
start-page=69
end-page=76
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2000
dt-pub=20000324
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=An experimental study on the relation of T2-signal high intensity in MRI to histopathological changes in the kainic acid model of temporal lobe epilepsy in rats.
kn-title=ラットにおけるカイニン酸けいれん発作重積後のMRI所見と病理所見の関係
en-subtitle=
kn-subtitle=
en-abstract=The relation of T2-signal high intensity areas observed in temporal lobe epilepsy to histopathological changes in limbic structures was examined in the rat kainic acid (KA) model of epilepsy. Male 8-week-old Sprague-Dawley rats were injected with 10mg/kg(i.p.) of KA or saline (control). Repetitive generalized convulsions (stage 3, or stage 4,5 seizures of amygdala kindled seizures) lasted for 3 to 4 hrs. were induced by KA injection in all rats. MRI was recorded on the day before the KA injection and 1, 2, 4, 8 weeks after the injection by fluid-attenuated inversion recovery method under deep pentobarbital anesthesia. Following the last MRI recording, rats were perfused with 4% paraformaldehyde (PFA) from left cardiac ventricle, post-fixed overnight in 4% PFA and brains were embedded in parafin. Coronal brain sections (6μm) were stained with cresyl violet, or mouse anti-GFAP antibody followed by biotinylated goat anti-mouse IgG and avidin-biotin-peroxidase (vectastain ABC kit). Irregularshaped moderate to severe high T2-signal areas were observed in bilateral piriform and entorhinal cortex in MRI. These high T2-signal areas were ovserved from 1 week after the KA injection to 8 weeks after the injection, and were more prominent in rats elicited stage 4 or 5 seizures than in rats elicited stage 3 seizures. Loss of pyramidal neurons and increased GFAP immunoreactivity were observed in piriform cortex, entorhinal cortex, CA1, subiculum, and hilus of dentate gyrus. The increase of GFAP immunoreactivity, but not the intensity of neuronal loss, in piriform and entorhinal cortex was almost correponded to the size and intensity of T2-signal. However, the increase of GFAP immunoreactivity in hippocampus was not detected as the increase of T2-signal in MRI. These findings indicate that astroglial reactions in piriform and entorhinal cortex are more sensitive to T2-weighted MRI than those in hippocampus.
kn-abstract=側頭葉てんかんでは，てんかん焦点に一致してMRI T2高信号領域が見られ，FLAIR法でこれがより明瞭になるが，このMRI所見と病理組織学的変化との関係は必ずしもはっきりしていない。そこで，Sprague－Dawleyラットにカイニン酸（KA）でけいれん発作重積状態を起こし，経時的にMRIを記録するとともに，ニッスル染色，GFAP免疫染色での病理組織学的変化を調べて両者の関係について検討した。KA群では，MRIで1～8週間後のいずれにおいてもpiriform cortexからentorhinal cortexにかけて不整形のT2高信号領域がみられたが，stage3のけいれん発作しか出現しなかったラットではstage4，5が出現したラットに比べて程度が弱かった。組織学的には，CA1，subiculum，piriform cortex，entorhinal cortexで神経細胞の消失，濃染細胞の増加と萎縮，GFAP免疫反応の増強が見られたが，piriform cortex，entorhinal cortexでの神経細胞消失の程度はT2信
号の程度と相関せず，GFAP免疫反応が増強した領域に一致して高信号がみられた。しかし，海馬のGFAP免疫反応増強はMRI所見に反映されず，これはMRIの解像度の限界にもよると考えられた。
en-copyright=
kn-copyright=

en-aut-name=SakiyamaJunko
en-aut-sei=Sakiyama
en-aut-mei=Junko
kn-aut-name=﨑山順子
kn-aut-sei=﨑山
kn-aut-mei=順子
aut-affil-num=1
ORCID=

en-aut-name=OkamotoMotoi
en-aut-sei=Okamoto
en-aut-mei=Motoi
kn-aut-name=岡本基
kn-aut-sei=岡本
kn-aut-mei=基
aut-affil-num=2
ORCID=

en-aut-name=KitamuraYoshihiro
en-aut-sei=Kitamura
en-aut-mei=Yoshihiro
kn-aut-name=北村吉宏
kn-aut-sei=北村
kn-aut-mei=吉宏
aut-affil-num=3
ORCID=

en-aut-name=YamadaNorihito
en-aut-sei=Yamada
en-aut-mei=Norihito
kn-aut-name=山田了士
kn-aut-sei=山田
kn-aut-mei=了士
aut-affil-num=4
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学医学部保健学科検査技術科学専攻

affil-num=2
en-affil=
kn-affil=岡山大学医学部保健学科検査技術科学専攻

affil-num=3
en-affil=
kn-affil=岡山療護センター

affil-num=4
en-affil=
kn-affil=岡山大学医学部医学科神経精神医学講座
en-keyword=カイニン酸 (kainic acid)
kn-keyword=カイニン酸 (kainic acid)
en-keyword=MRI
kn-keyword=MRI
en-keyword=FLAIR法 (FLAIR)
kn-keyword=FLAIR法 (FLAIR)
en-keyword=神経細胞死 (neuronal death)
kn-keyword=神経細胞死 (neuronal death)
en-keyword=GFAP
kn-keyword=GFAP
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2007
dt-pub=20070323
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=深部前梨状葉皮質の間欠的電気刺激によるてんかん発作重積モデル
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=KoyamaFumihiko
en-aut-sei=Koyama
en-aut-mei=Fumihiko
kn-aut-name=小山文彦
kn-aut-sei=小山
kn-aut-mei=文彦
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2004
dt-pub=20041231
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=小児期の潜因性局在関連性てんかんにおける抗てんかん薬減量, 断薬後の再発に関する研究
kn-title=Prognosis after withdrawal of antiepileptic drugs in childhood-onset cryptogenic localization-related epilepsies
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=OhtaHodaka
en-aut-sei=Ohta
en-aut-mei=Hodaka
kn-aut-name=太田穂高
kn-aut-sei=太田
kn-aut-mei=穂高
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1992
dt-pub=19920930
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=ラットてんかんモデルにおける脳線条体中でのモノアミン放出の経時変化と,各種薬物の影響について 脳内透析法を用いた実験
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=加太英明
kn-aut-sei=加太
kn-aut-mei=英明
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=1995
dt-pub=19950325
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=鉄イオン誘導てんかんラット及び自然発症てんかんE1マウスの脳内における±)-1-amino-1,3-cyclopentane-trans-dicarboxyli cacidtrans-ACPD) によるinositol triphosphoric acid 生成に関する研究
kn-title=(±)-1-AMINO-1,3-CYCLOPENTANE-TRANS-DICARBOXYKIC ACID (TRANS-ACPD) INDUCED INOSITOL TRIPHOSPHORIC ACID FORMATION IN THE BRAIN OF IRON-INDUCED EPILEPTIC RATS AND EPILEPTIC EL MICE
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=
en-aut-sei=
en-aut-mei=
kn-aut-name=門脇大
kn-aut-sei=門脇
kn-aut-mei=大
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学
END

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en-title=てんかん発作発現機序に関する実験的研究 第1編:キンドリング刺激中の脳波変化:GABA性抑制の虚脱と rhythmic synchronous burst の発現) 第2編:キンドリング刺激中の脳波変化:Ⅱ.自発および誘発電位の比較) 第3編:キンドリング刺激中の脳波変化:Ⅲ.刺激扁桃核に対する薬理学的操作)
kn-title=第1編　:　Kindling　induced　changes　in　EEG　recorded　during　stimulation　from　the　site　of　stimulation　:　Collapse　of　GABA－mediated　inhibition　and　onset　of　rhythmic　synchronous　burst　　第2編　:　Kindling-induced　changes　in　the　EEG　recorded　during　stimulation　from　the　site　of　stimulation　:　Ⅱ.　Comparison　between　spontaneous　and　evoked　potentials　　第3編　:　Kindling－inducedcd　changes　in　EEG　recorded　during　stimulation　from　the　site　of　stimulation　:　Ⅲ.　Direct　pharmacological　manipulations　of　the　kindled　amygdala
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