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  <Article>
    <Journal>
      <PublisherName>Elsevier BV</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2589-9864</Issn>
      <Volume>31</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Investigation of the relationship between 0.5–1200 Hz signal characteristics of cortical high-frequency oscillations and epileptogenicity through multivariate analysis</ArticleTitle>
    <FirstPage LZero="delete">100776</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Shibata</LastName>
        <Affiliation>Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroki</FirstName>
        <LastName>Tsuchiya</LastName>
        <Affiliation>Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mari</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyuki</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masao</FirstName>
        <LastName>Matsuhashi</LastName>
        <Affiliation>Department of Epilepsy, Movement Disorders and Physiology, Graduate School of Medicine, Kyoto University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Pediatric Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
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    <Abstract>Fast ripples (FRs) (250–500 Hz) on the electroencephalogram (EEG) are closely related to epileptogenicity and are important to determine cortical regions resected in epilepsy surgery. However, FR-related epileptogenicity may be variable, and may depend on information associated with FRs. We enrolled nine epilepsy patients who had undergone intracranial 5 kHz-sampling-rate EEG for surgical treatment and had final Engel class I outcomes. Three electrodes were selected from each epileptogenic area (EA) and the unlikely EA (the region outside the EA) in each patient. Up to 100 candidate FRs were automatically detected from interictal nocturnal EEG at each of the selected electrodes and were visually reviewed independently by two researchers. Multivariate logistic regression analysis was performed using the frequency and log-power value of the corresponding FRs, presence of concurrent spike, ripple, very-high-frequency oscillations (vHFO)1 (500–600 Hz), and vHFO2 (600–1200 Hz), and whether the timing of the spectral peak of corresponding FRs was in the peak–trough or trough–peak transition of each slow activity (0.5–1, 1–2, 2–3, 3–4, and 4–8 Hz) as independent variables. Factors significantly related to epileptogenicity were FR power, the concurrent presence of spike and vHFO2, coupling with 0.5–1 and 1–2 Hz slow waves in the peak–trough transition, and coupling with 3–4 and 4–8 Hz slow waves in the trough–peak transition. Multifactorial analysis of FRs may increase their usefulness, potentially leading to improved treatment outcomes in epilepsy surgery.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Phase-amplitude coupling</Param>
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        <Param Name="value">Ripple</Param>
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        <Param Name="value">Very high-frequency oscillations</Param>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier BV</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0387-7604</Issn>
      <Volume>46</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2024</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Exploration of urine metabolic biomarkers for new-onset, untreated pediatric epilepsy: A gas and liquid chromatography mass spectrometry-based metabolomics study</ArticleTitle>
    <FirstPage LZero="delete">180</FirstPage>
    <LastPage>186</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomoyuki</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daisuke</FirstName>
        <LastName>Saigusa</LastName>
        <Affiliation>Laboratory of Biomedical and Analytical Sciences, Faculty of Pharma-Science, Teikyo University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takushi</FirstName>
        <LastName>Inoue</LastName>
        <Affiliation>Department of Pediatric Neurology, NHO Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chiho</FirstName>
        <LastName>Tokorodani</LastName>
        <Affiliation>Department of Pediatrics, Kochi Health Sciences Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mari</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Rie</FirstName>
        <LastName>Michiue</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Atsushi</FirstName>
        <LastName>Mori</LastName>
        <Affiliation>Department of Neurology, Shiga Medical Center for Children</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Eiji</FirstName>
        <LastName>Hishinuma</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naomi</FirstName>
        <LastName>Matsukawa</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Shibata</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroki</FirstName>
        <LastName>Tsuchiya</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
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    <Abstract>Objective: The discovery of objective indicators for recent epileptic seizures will help confirm the diagnosis of epilepsy and evaluate therapeutic effects. Past studies had shortcomings such as the inclusion of patients under treatment and those with various etiologies that could confound the analysis results significantly. We aimed to minimize such confounding effects and to explore the small molecule biomarkers associated with the recent occurrence of epileptic seizures using urine metabolomics.&lt;br&gt;
Methods: This is a multicenter prospective study. Subjects included pediatric patients aged 2 to 12 years old with new-onset, untreated epilepsy, who had had the last seizure within 1 month before urine collection. Controls included healthy children aged 2 to 12 years old. Those with underlying or chronic diseases, acute illnesses, or recent administration of medications or supplements were excluded. Targeted metabolome analysis of spot urine samples was conducted using gas chromatography (GC)- and liquid chromatography (LC)-tandem mass spectrometry (MS/MS).&lt;br&gt;
Results: We enrolled 17 patients and 21 controls. Among 172 metabolites measured by GC/MS/MS and 41 metabolites measured by LC/MS/MS, only taurine was consistently reduced in the epilepsy group. This finding was subsequently confirmed by the absolute quantification of amino acids. No other metabolites were consistently altered between the two groups.&lt;br&gt;
Conclusions: Urine metabolome analysis, which covers a larger number of metabolites than conventional biochemistry analyses, found no consistently altered small molecule metabolites except for reduced taurine in epilepsy patients compared to healthy controls. Further studies with larger samples, subjects with different ages, expanded target metabolites, and the investigation of plasma samples are required.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">Amino acids</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Gas chromatography</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Liquid chromatography</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Mass spectrometry</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">New-onset epilepsy</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>136</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2024</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>進行性ミオクローヌスてんかんについて</ArticleTitle>
    <FirstPage LZero="delete">22</FirstPage>
    <LastPage>25</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
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    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">難治てんかん</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">ミオクローヌス</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">失調</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">知的退行</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">ポリグラフ</Param>
      </Object>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>135</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2023</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>小児神経学と小児期発症難病</ArticleTitle>
    <FirstPage LZero="delete">116</FirstPage>
    <LastPage>122</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">指定難病</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">小児慢性特定疾患</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">発達性てんかん性脳症</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">先天性代謝異常症</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>77</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2023</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Effective Epilepsy Surgery for Post-Traumatic West Syndrome Following Abusive Head Trauma</ArticleTitle>
    <FirstPage LZero="delete">561</FirstPage>
    <LastPage>566</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hiroki</FirstName>
        <LastName>Tsuchiya</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Shibata</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tatsuya</FirstName>
        <LastName>Sasaki</LastName>
        <Affiliation>Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takushi</FirstName>
        <LastName>Inoue</LastName>
        <Affiliation>Department of Pediatrics, National Hospital Organization Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Isao</FirstName>
        <LastName>Date</LastName>
        <Affiliation>Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyuki</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Case Report</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/65980</ArticleId>
    </ArticleIdList>
    <Abstract>West syndrome, an infantile developmental and epileptic encephalopathy with a deleterious impact on long-term development, requires early treatment to minimize developmental abnormality; in such cases, epilepsy surgery should be considered a powerful therapeutic option. We describe a 10-month-old female admitted with West syndrome associated with a hemispheric lesion following abusive head trauma. Her seizures were suppressed by hemispherotomy at 12 months of age, leading to developmental improvement. Surgical treatment of West syndrome following traumatic brain injury has not been reported previously but is worth considering as a treatment option, depending on patient age and brain plasticity.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">abusive head trauma</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">developmental and epileptic encephalopathy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">epilepsy surgery</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">epileptic spasms</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">hemispherotomy</Param>
      </Object>
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  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>135</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2023</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>第65回日本小児神経学会学術集会の開催報告</ArticleTitle>
    <FirstPage LZero="delete">98</FirstPage>
    <LastPage>99</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Pediatrics (Child Neurology), Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier BV</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1059-1311</Issn>
      <Volume>107</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2023</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Comprehensive study of metabolic changes induced by a ketogenic diet therapy using GC/MS- and LC/MS-based metabolomics</ArticleTitle>
    <FirstPage LZero="delete">52</FirstPage>
    <LastPage>59</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Mari</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyuki</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Paediatrics (Child Neurology), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daisuke</FirstName>
        <LastName>Saigusa</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Eiji</FirstName>
        <LastName>Hishinuma</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naomi</FirstName>
        <LastName>Matsukawa</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Shibata</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroki</FirstName>
        <LastName>Tsuchiya</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Atsushi</FirstName>
        <LastName>Mori</LastName>
        <Affiliation>Department of Neurology, Shiga Medical Centre for Children</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuji</FirstName>
        <LastName>Fujii</LastName>
        <Affiliation>Department of Paediatrics, Hiroshima City Funairi Citizens Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yukiko</FirstName>
        <LastName>Mogami</LastName>
        <Affiliation>Department of Paediatric Neurology, Osaka Women's and Children's Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chiho</FirstName>
        <LastName>Tokorodani</LastName>
        <Affiliation>Department of Paediatrics, Kochi Health Sciences Centre</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kozue</FirstName>
        <LastName>Kuwahara</LastName>
        <Affiliation>Department of Paediatrics, Ehime Prefectural Central Hospital,</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yurika</FirstName>
        <LastName>Numata-Uematsu</LastName>
        <Affiliation>Department of Paediatrics, Tohoku University School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Inoue</LastName>
        <Affiliation>Department of Neurology, Shiga Medical Centre for Children</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Paediatrics (Child Neurology), Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
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    <Abstract>Objective: The ketogenic diet (KD), a high-fat and low-carbohydrate diet, is effective for a subset of patients with drug-resistant epilepsy, although the mechanisms of the KD have not been fully elucidated. The aims of this observational study were to investigate comprehensive short-term metabolic changes induced by the KD and to explore candidate metabolites or pathways for potential new therapeutic targets.&lt;br&gt;
Methods: Subjects included patients with intractable epilepsy who had undergone the KD therapy (the medium-chain triglyceride [MCT] KD or the modified Atkins diet using MCT oil). Plasma and urine samples were obtained before and at 2–4 weeks after initiation of the KD. Targeted metabolome analyses of these samples were performed using gas chromatography-tandem mass spectrometry (GC/MS/MS) and liquid chromatography-tandem mass spectrometry (LC/MS/MS).&lt;br&gt;
Results: Samples from 10 and 11 patients were analysed using GC/MS/MS and LC/MS/MS, respectively. The KD increased ketone bodies, various fatty acids, lipids, and their conjugates. In addition, levels of metabolites located upstream of acetyl-CoA and propionyl-CoA, including catabolites of branched-chain amino acids and structural analogues of γ-aminobutyric acid and lactic acid, were elevated.&lt;br&gt;
Conclusions: The metabolites that were significantly changed after the initiation of the KD and related metabolites may be candidates for further studies for neuronal actions to develop new anti-seizure medications.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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        <Param Name="value">Amino acids</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Biomarkers</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Intractable epilepsy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Ketone bodies</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Organic acids</Param>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Frontiers Media SA</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1662-5161</Issn>
      <Volume>15</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Exclusion of the Possibility of "False Ripples" From Ripple Band High-Frequency Oscillations Recorded From Scalp Electroencephalogram in Children With Epilepsy</ArticleTitle>
    <FirstPage LZero="delete">696882</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Shibata</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroki</FirstName>
        <LastName>Tsuchiya</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyuki</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences and Okayama University Hospital</Affiliation>
      </Author>
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      <ArticleId IdType="doi"/>
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    <Abstract>Aim Ripple-band epileptic high-frequency oscillations (HFOs) can be recorded by scalp electroencephalography (EEG), and tend to be associated with epileptic spikes. However, there is a concern that the filtration of steep waveforms such as spikes may cause spurious oscillations or "false ripples." We excluded such possibility from at least some ripples by EEG differentiation, which, in theory, enhances high-frequency signals and does not generate spurious oscillations or ringing. Methods The subjects were 50 pediatric patients, and ten consecutive spikes during sleep were selected for each patient. Five hundred spike data segments were initially reviewed by two experienced electroencephalographers using consensus to identify the presence or absence of ripples in the ordinary filtered EEG and an associated spectral blob in time-frequency analysis (Session A). These EEG data were subjected to numerical differentiation (the second derivative was denoted as EEG ''). The EEG '' trace of each spike data segment was shown to two other electroencephalographers who judged independently whether there were clear ripple oscillations or uncertain ripple oscillations or an absence of oscillations (Session B). Results In Session A, ripples were identified in 57 spike data segments (Group A-R), but not in the other 443 data segments (Group A-N). In Session B, both reviewers identified clear ripples (strict criterion) in 11 spike data segments, all of which were in Group A-R (p &lt; 0.0001 by Fisher's exact test). When the extended criterion that included clear and/or uncertain ripples was used in Session B, both reviewers identified 25 spike data segments that fulfilled the criterion: 24 of these were in Group A-R (p &lt; 0.0001). Discussion We have demonstrated that real ripples over scalp spikes exist in a certain proportion of patients. Ripples that were visualized consistently using both ordinary filters and the EEG '' method should be true, but failure to clarify ripples using the EEG '' method does not mean that true ripples are absent. Conclusion The numerical differentiation of EEG data provides convincing evidence that HFOs were detected in terms of the presence of such unusually fast oscillations over the scalp and the importance of this electrophysiological phenomenon.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">epilepsy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">child</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">scalp EEG</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">false ripple</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">high-frequency oscillation (HFO)</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">fast oscillation (FO)</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0887-8994</Issn>
      <Volume>113</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Pyridoxal in the Cerebrospinal Fluid May Be a Better Indicator of Vitamin B6–dependent Epilepsy Than Pyridoxal 5′-Phosphate</ArticleTitle>
    <FirstPage LZero="delete">33</FirstPage>
    <LastPage>41</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomoyuki</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Hyodo</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kosei</FirstName>
        <LastName>Hasegawa</LastName>
        <Affiliation>Department of Pediatrics, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Taikan</FirstName>
        <LastName>Oboshi</LastName>
        <Affiliation>Department of Pediatric Neurology, Osaka Women’s and Children’s Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsumi</FirstName>
        <LastName>Imai</LastName>
        <Affiliation>Department of Pediatrics, NHO Shizuoka Institute of Epilepsy and Neurological Disorders</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoko</FirstName>
        <LastName>Ishihara</LastName>
        <Affiliation>Department of Pediatrics, Fujita Health University School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuri</FirstName>
        <LastName>Dowa</LastName>
        <Affiliation>Department of Neurology, Gunma Children’s Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takayoshi</FirstName>
        <LastName>Koike</LastName>
        <Affiliation>Department of Pediatrics, NHO Shizuoka Institute of Epilepsy and Neurological Disorders</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toshiyuki</FirstName>
        <LastName>Yamamoto</LastName>
        <Affiliation>Institute of Clinical Genomics, Tokyo Women’s Medical University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Shibasaki</LastName>
        <Affiliation>Department of Neonatology, Kanagawa Children’s Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroko</FirstName>
        <LastName>Shimbo</LastName>
        <Affiliation>Clinical Institute, Kanagawa Children’s Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tetsuhiro</FirstName>
        <LastName>Fukuyama</LastName>
        <Affiliation>Department of Pediatrics, Shinshu University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kyoko</FirstName>
        <LastName>Takano</LastName>
        <Affiliation>Center for Medical Genetics, Shinshu University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Shiraku</LastName>
        <Affiliation>Department of Pediatrics, JA Toride Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Saoko</FirstName>
        <LastName>Takeshita</LastName>
        <Affiliation>Department of Pediatrics, Yokohama City University Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tohru</FirstName>
        <LastName>Okanishi</LastName>
        <Affiliation>Department of Child Neurology, Comprehensive Epilepsy Center, Seirei Hamamatsu General Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shimpei</FirstName>
        <LastName>Baba</LastName>
        <Affiliation>Department of Child Neurology, Comprehensive Epilepsy Center, Seirei Hamamatsu General Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaya</FirstName>
        <LastName>Kubota</LastName>
        <Affiliation>Division of Neurology, National Center for Child Health and Development</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shin-ichiro</FirstName>
        <LastName>Hamano</LastName>
        <Affiliation>Division of Neurology, Saitama Children’s Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background&lt;/br&gt;
We aimed to demonstrate the biochemical characteristics of vitamin B6–dependent epilepsy, with a particular focus on pyridoxal 5′-phosphate and pyridoxal in the cerebrospinal fluid.&lt;/br&gt;
Methods&lt;/br&gt;
Using our laboratory database, we identified patients with vitamin B6–dependent epilepsy and extracted their data on the concentrations of pyridoxal 5′-phosphate, pyridoxal, pipecolic acid, α-aminoadipic semialdehyde, and monoamine neurotransmitters. We compared the biochemical characteristics of these patients with those of other epilepsy patients with low pyridoxal 5′-phosphate concentrations.&lt;/br&gt;
Results&lt;/br&gt;
We identified seven patients with pyridoxine-dependent epilepsy caused by an ALDH7A1 gene abnormality, two patients with pyridoxal 5′-phosphate homeostasis protein deficiency, and 28 patients with other epilepsies with low cerebrospinal fluid pyridoxal 5′-phosphate concentrations. Cerebrospinal fluid pyridoxal and pyridoxal 5′-phosphate concentrations were low in patients with vitamin B6–dependent epilepsy but cerebrospinal fluid pyridoxal concentrations were not reduced in most patients with other epilepsies with low cerebrospinal fluid pyridoxal 5′-phosphate concentrations. Increase in 3-O-methyldopa and 5-hydroxytryptophan was demonstrated in some patients with vitamin B6–dependent epilepsy, suggestive of pyridoxal 5′-phosphate deficiency in the brain.&lt;/br&gt;
Conclusions&lt;/br&gt;
Low cerebrospinal fluid pyridoxal concentrations may be a better indicator of pyridoxal 5′-phosphate deficiency in the brain in vitamin B6–dependent epilepsy than low cerebrospinal fluid pyridoxal 5′-phosphate concentrations. This finding is especially helpful in individuals with suspected pyridoxal 5′-phosphate homeostasis protein deficiency, which does not have known biomarkers.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">ALDH7A1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">PLPBP</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">PLPHP</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">PROSC</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Pyridoxal 5′-phosphate homeostasis protein deficiency</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Pyridoxine-dependent epilepsy</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1328-8067</Issn>
      <Volume>62</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Laboratory changes during adrenocorticotropic hormone therapy associated with renal calcified lesions</ArticleTitle>
    <FirstPage LZero="delete">587</FirstPage>
    <LastPage>592</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Miyahara</LastName>
        <Affiliation>Department of Pediatrics, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyuki</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kosei</FirstName>
        <LastName>Hasegawa</LastName>
        <Affiliation>Department of Pediatrics, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mari</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Child Neurology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Makio</FirstName>
        <LastName>Oka</LastName>
        <Affiliation>Department of Child Neurology, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hirokazu</FirstName>
        <LastName>Tsukahara</LastName>
        <Affiliation>Department of Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background&lt;/br&gt;
Renal calcified lesions are known as one of the complications during adrenocorticotropic hormone (ACTH) therapy for intractable epilepsy. However, laboratory changes during the therapy or laboratory features of high‐risk cases with renal calcified lesions are yet to be clarified.&lt;/br&gt;
Methods&lt;/br&gt;
In this study, 43 patients with West syndrome aged ≤2 years were included. We retrospectively reviewed age and body mass index at the beginning of ACTH therapy, as well as the amount of fluid intake, daily urinary volume, and laboratory data during therapy. In addition, we studied the urinary sediment of the cases with renal calcified lesions diagnosed by computed tomography.

Results
After initiating ACTH treatment, urinary calcium (Ca)/creatinine ratio and urinary pH increased within 2 weeks. Urinary crystals and renal tubular epithelial cells (RTECs) in urinary sediment were frequently found in most cases. Urinary Ca levels, proteinuria or frequency of urinary crystals, and number of RTECs in the urinary sediment were significantly higher in patients with epithelial casts (ECs) or hematuria than in patients without these findings. Among the seven patients who underwent abdominal CT, ECs or hematuria were found only in those with renal calcified lesions. These findings suggested that patients with ECs or hematuria were more likely to have calcified lesions.&lt;/br&gt;
Conclusions&lt;/br&gt;
The risk of renal calcified lesions increased after 2 weeks of ACTH treatment. Abnormal findings in urinary sediments might be an early sign of renal calcification during ACTH therapy.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">adrenocorticotropic hormone therapy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">calcium</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">crystal</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">renal tubular epithelial cell</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">urinary sediment</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>74</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Metabolic Profiling of the Cerebrospinal Fluid in Pediatric Epilepsy</ArticleTitle>
    <FirstPage LZero="delete">65</FirstPage>
    <LastPage>72</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomoyuki</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daisuke</FirstName>
        <LastName>Saigusa</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Hyodo</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiko</FirstName>
        <LastName>Umeda</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Reina</FirstName>
        <LastName>Saijo</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Seizo</FirstName>
        <LastName>Koshiba</LastName>
        <Affiliation>Tohoku Medical Megabank Organization, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Hospital</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/57955</ArticleId>
    </ArticleIdList>
    <Abstract> To characterize metabolic profiles within the central nervous system in epilepsy, we performed gas chromatography-tandem mass spectrometry (GC-MS/MS)-based metabolome analysis of the cerebrospinal fluid (CSF) in pediatric patients with and without epilepsy. The CSF samples obtained from 64 patients were analyzed by GC-MS/MS. Multivariate analyses were performed for two age groups, 0-5 years of age and 6-17 years of age, to elucidate the effects of epilepsy and antiepileptic drugs on the metabolites. In patients aged 0-5 years (22 patients with epilepsy, 13 without epilepsy), epilepsy patients had reduced 2-ketoglutaric acid and elevated pyridoxamine and tyrosine. In patients aged 6-17 years (12 with epilepsy, 17 without epilepsy), epilepsy patients had reduced 1,5-anhydroglucitol. Valproic acid was associated with elevated 2-aminobutyric acid, 2-ketoisocaproic acid, 4-hydroxyproline, acetylglycine, methionine, N-acetylserine, and serine. Reduced energy metabolism and alteration of vitamin B6 metabolism may play a role in epilepsy in young children. The roles of 1,5-anhydroglucitol in epilepsy in older children and in levetiracetam and zonisamide treatment remain to be explained. Valproic acid influenced the levels of amino acids and related metabolites involved in the metabolism of serine, methionine, and leucine.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">antiepileptic drugs</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">gas chromatography-tandem mass spectrometry</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">metabolome analysis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">metabolomics</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>128</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2016</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>脳波：小児てんかんにおける古くて新しい検査</ArticleTitle>
    <FirstPage LZero="delete">183</FirstPage>
    <LastPage>189</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Child Neurology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract/>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">頭皮脳波</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">点頭てんかん</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">てんかん外科</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">高周波振動</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">時間・周波数分析</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>66</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Successful Treatment of Epilepsy by Resection of Periventricular Nodular Heterotopia</ArticleTitle>
    <FirstPage LZero="delete">487</FirstPage>
    <LastPage>492</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Agari</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tadahiro</FirstName>
        <LastName>Mihara</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichi</FirstName>
        <LastName>Baba</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naotaka</FirstName>
        <LastName>Usui</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kiyohito</FirstName>
        <LastName>Terada</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Fumihiro</FirstName>
        <LastName>Nakamura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kazumi</FirstName>
        <LastName>Matsuda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Isao</FirstName>
        <LastName>Date</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Case Report</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/49045</ArticleId>
    </ArticleIdList>
    <Abstract>We report on a case of successful surgical treatment of drug-resistant epilepsy associated with a solitary lesion of periventricular nodular heterotopia (PNH). In the reported patient, intracranial ictal electroencephalography disclosed that seizures did not originate from the heterotopic nodules. However, the seizures were completely suppressed by lesionectomy of PNH alone. Epileptogenesis associated with PNH likely involves a very complex network between PNH and the surrounding cortex, and the disruption of this network may be an effective means of curing intractable, PNH-associated epilepsy.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">periventricular nodular heterotopia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">epilepsy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">surgery</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">ictal electroencephalography</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>66</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2012</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Dravet Syndrome : A Genetic Epileptic Disorder</ArticleTitle>
    <FirstPage LZero="delete">369</FirstPage>
    <LastPage>376</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Mari</FirstName>
        <LastName>Akiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuhiro</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoko</FirstName>
        <LastName>Ohtsuka</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Review</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/48961</ArticleId>
    </ArticleIdList>
    <Abstract>Dravet syndrome (DS), or severe myoclonic epilepsy in infancy, is one of the most severe types of genetic epilepsy. It is characterized by the initial occurrence of febrile or afebrile seizures that often evolve into status epilepticus in infants with normal development, and by the subsequent appearance of myoclonic and/or atypical absence seizures as well as complex partial seizures. The key feature that characterizes DS is fever sensitivity, although photosensitivity and pattern-sensitivity are also often seen. The prognosis is unfavorable in most cases. Seizures become drug-resistant and persist, with many patients suffering from motor and cognitive impairment. Mutations of SCN1A, which encodes the voltage-gated sodium channel NaV1.1, are the most frequent genetic cause of this syndrome. SCN1A mutations and/or microchromosomal rearrangements involving SCN1A are detected in about 85% of patients. Mutations of PCDH19 have also been reported in female patients with clinical findings compatible with DS. PCDH19 mutations might account for 5% of overall DS cases. Thirty years after its first description, DS is considered as a model of channelopathy. This survey reviews recent developments in the research literature on DS, focusing on the clinical course, as well as its genetic causes.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Dravet syndrome</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">long-term outcome</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">SCN1A</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">PCDH19</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>岡山医学会</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0030-1558</Issn>
      <Volume>123</Volume>
      <Issue>2</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2011</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>成人期に達したDravet症候群の長期経過に関する研究</ArticleTitle>
    <FirstPage LZero="delete">91</FirstPage>
    <LastPage>95</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Mari</FirstName>
        <LastName>Akiyama</LastName>
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