Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum
Identifieur interne : 000335 ( Istex/Corpus ); précédent : 000334; suivant : 000336Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum
Auteurs : Chellamani Harini ; Rohit R. Das ; Sanjay P. Prabhu ; Kanwaljit Singh ; Amit Haldar ; Masanori Takeoka ; Ann M. Bergin ; Tobias Loddenkemper ; Sanjeev V. KothareSource :
- Journal of Neuroimaging [ 1051-2284 ] ; 2015-09.
Abstract
PURPOSE: T2‐hyperintense signal changes in corpus callosum (CC) have been described in epilepsy and encephalitis/encephalopathy. Little is known about their pathophysiology. The aim of this study was to examine the clinical presentation and evolution of CC lesions and relationship to seizures. METHODS: We identified 12 children among 29,634 patients from Radiology Database. We evaluated following characteristics: seizures and accompanying medical history, antiepileptic drug usage, presenting symptoms, and radiological evolution of lesions. RESULTS: CC lesions were seen in patients with prior diagnosis of epilepsy (n = 5) or in those with new onset seizures (n = 3), or with encephalitis/encephalopathy without history of seizures (n = 4). Seizure clustering or disturbances of consciousness were the main presenting symptoms. No relationship was observed between CC lesion and AEDs. On imaging, ovoid lesions at presentation resolved on follow up imaging and linear lesions persisted. DTI showed that the fibers passing through splenial lesions originated from the posterior parietal cortex and occipital cortex bilaterally. CONCLUSION: In patients with seizures, no clear relationship was demonstrated between seizure characteristics or AED use with CC lesions. Ovoid lesions resolved and may have different pathophysiologic mechanism when compared to linear lesions that persisted.
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DOI: 10.1111/jon.12190
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Das</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Indiana State University, IN, Indianapolis</mods:affiliation></affiliation></author><author><name sortKey="Prabhu, Sanjay P" sort="Prabhu, Sanjay P" uniqKey="Prabhu S" first="Sanjay P." last="Prabhu">Sanjay P. Prabhu</name><affiliation><mods:affiliation>Department of Radiology, Boston Children's Hospital and Harvard Medical School, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Singh, Kanwaljit" sort="Singh, Kanwaljit" uniqKey="Singh K" first="Kanwaljit" last="Singh">Kanwaljit Singh</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation></affiliation><affiliation><mods:affiliation>Lurie Center, Massachusetts General Hospital for Children, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Haldar, Amit" sort="Haldar, Amit" uniqKey="Haldar A" first="Amit" last="Haldar">Amit Haldar</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Takeoka, Masanori" sort="Takeoka, Masanori" uniqKey="Takeoka M" first="Masanori" last="Takeoka">Masanori Takeoka</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Bergin, Ann M" sort="Bergin, Ann M" uniqKey="Bergin A" first="Ann M." last="Bergin">Ann M. 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Kothare</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation></affiliation><affiliation><mods:affiliation>New York University Medical Center, Comprehensive Epilepsy Center, Langone Medical School, NY</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8BFC5FF6B031FDD352E3AB750EB4BFA19B4960ED</idno><date when="2015" year="2015">2015</date><idno type="doi">10.1111/jon.12190</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-RQWK7R3P-X/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000335</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000335</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum</title><author><name sortKey="Harini, Chellamani" sort="Harini, Chellamani" uniqKey="Harini C" first="Chellamani" last="Harini">Chellamani Harini</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: chellamani.harini@childrens.harvard.edu</mods:affiliation></affiliation></author><author><name sortKey="Das, Rohit R" sort="Das, Rohit R" uniqKey="Das R" first="Rohit R." last="Das">Rohit R. Das</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Indiana State University, IN, Indianapolis</mods:affiliation></affiliation></author><author><name sortKey="Prabhu, Sanjay P" sort="Prabhu, Sanjay P" uniqKey="Prabhu S" first="Sanjay P." last="Prabhu">Sanjay P. Prabhu</name><affiliation><mods:affiliation>Department of Radiology, Boston Children's Hospital and Harvard Medical School, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Singh, Kanwaljit" sort="Singh, Kanwaljit" uniqKey="Singh K" first="Kanwaljit" last="Singh">Kanwaljit Singh</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation></affiliation><affiliation><mods:affiliation>Lurie Center, Massachusetts General Hospital for Children, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Haldar, Amit" sort="Haldar, Amit" uniqKey="Haldar A" first="Amit" last="Haldar">Amit Haldar</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Takeoka, Masanori" sort="Takeoka, Masanori" uniqKey="Takeoka M" first="Masanori" last="Takeoka">Masanori Takeoka</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Bergin, Ann M" sort="Bergin, Ann M" uniqKey="Bergin A" first="Ann M." last="Bergin">Ann M. Bergin</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Loddenkemper, Tobias" sort="Loddenkemper, Tobias" uniqKey="Loddenkemper T" first="Tobias" last="Loddenkemper">Tobias Loddenkemper</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation></affiliation></author><author><name sortKey="Kothare, Sanjeev V" sort="Kothare, Sanjeev V" uniqKey="Kothare S" first="Sanjeev V." last="Kothare">Sanjeev V. Kothare</name><affiliation><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation></affiliation><affiliation><mods:affiliation>New York University Medical Center, Comprehensive Epilepsy Center, Langone Medical School, NY</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Neuroimaging</title><title level="j" type="alt">JOURNAL OF NEUROIMAGING</title><idno type="ISSN">1051-2284</idno><idno type="eISSN">1552-6569</idno><imprint><biblScope unit="vol">25</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="824">824</biblScope><biblScope unit="page" to="831">831</biblScope><biblScope unit="page-count">8</biblScope><date type="published" when="2015-09">2015-09</date></imprint><idno type="ISSN">1051-2284</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1051-2284</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">PURPOSE: T2‐hyperintense signal changes in corpus callosum (CC) have been described in epilepsy and encephalitis/encephalopathy. Little is known about their pathophysiology. The aim of this study was to examine the clinical presentation and evolution of CC lesions and relationship to seizures. METHODS: We identified 12 children among 29,634 patients from Radiology Database. We evaluated following characteristics: seizures and accompanying medical history, antiepileptic drug usage, presenting symptoms, and radiological evolution of lesions. RESULTS: CC lesions were seen in patients with prior diagnosis of epilepsy (n = 5) or in those with new onset seizures (n = 3), or with encephalitis/encephalopathy without history of seizures (n = 4). Seizure clustering or disturbances of consciousness were the main presenting symptoms. No relationship was observed between CC lesion and AEDs. On imaging, ovoid lesions at presentation resolved on follow up imaging and linear lesions persisted. DTI showed that the fibers passing through splenial lesions originated from the posterior parietal cortex and occipital cortex bilaterally. CONCLUSION: In patients with seizures, no clear relationship was demonstrated between seizure characteristics or AED use with CC lesions. Ovoid lesions resolved and may have different pathophysiologic mechanism when compared to linear lesions that persisted.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Chellamani Harini MD</name><affiliations><json:string>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</json:string><json:string>E-mail: chellamani.harini@childrens.harvard.edu</json:string></affiliations></json:item><json:item><name>Rohit R. Das MD, MPH</name><affiliations><json:string>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</json:string><json:string>Department of Neurology, Indiana State University, IN, Indianapolis</json:string></affiliations></json:item><json:item><name>Sanjay P. Prabhu MBBS</name><affiliations><json:string>Department of Radiology, Boston Children's Hospital and Harvard Medical School, Harvard Medical School, MA, Boston</json:string></affiliations></json:item><json:item><name>Kanwaljit Singh MD, MPH</name><affiliations><json:string>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</json:string><json:string>Lurie Center, Massachusetts General Hospital for Children, Harvard Medical School, MA, Boston</json:string></affiliations></json:item><json:item><name>Amit Haldar MD, DM</name><affiliations><json:string>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</json:string></affiliations></json:item><json:item><name>Masanori Takeoka MD</name><affiliations><json:string>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</json:string></affiliations></json:item><json:item><name>Ann M. Bergin MD</name><affiliations><json:string>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</json:string></affiliations></json:item><json:item><name>Tobias Loddenkemper MD</name><affiliations><json:string>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</json:string></affiliations></json:item><json:item><name>Sanjeev V. Kothare MD</name><affiliations><json:string>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</json:string><json:string>New York University Medical Center, Comprehensive Epilepsy Center, Langone Medical School, NY</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Splenial lesions</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>corpus callosum</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>encephalitis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>encephalopathy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>antiepileptic drugs</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MRI</value></json:item></subject><articleId><json:string>JON12190</json:string></articleId><arkIstex>ark:/67375/WNG-RQWK7R3P-X</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>PURPOSE: T2‐hyperintense signal changes in corpus callosum (CC) have been described in epilepsy and encephalitis/encephalopathy. Little is known about their pathophysiology. The aim of this study was to examine the clinical presentation and evolution of CC lesions and relationship to seizures. METHODS: We identified 12 children among 29,634 patients from Radiology Database. We evaluated following characteristics: seizures and accompanying medical history, antiepileptic drug usage, presenting symptoms, and radiological evolution of lesions. RESULTS: CC lesions were seen in patients with prior diagnosis of epilepsy (n = 5) or in those with new onset seizures (n = 3), or with encephalitis/encephalopathy without history of seizures (n = 4). Seizure clustering or disturbances of consciousness were the main presenting symptoms. No relationship was observed between CC lesion and AEDs. On imaging, ovoid lesions at presentation resolved on follow up imaging and linear lesions persisted. DTI showed that the fibers passing through splenial lesions originated from the posterior parietal cortex and occipital cortex bilaterally. CONCLUSION: In patients with seizures, no clear relationship was demonstrated between seizure characteristics or AED use with CC lesions. 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ref="https://scientific-publisher.data.istex.fr/ark:/67375/H02-QW5Q88H5-V">Wiley Publishing Ltd</publisher><availability><licence>Copyright © 2014 by the American Society of Neuroimaging</licence></availability><date type="published" when="2015-09"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum</title><title level="a" type="short">Corpus Callosum Lesions in Children</title><author xml:id="author-0000" role="corresp"><persName><forename type="first">Chellamani</forename><surname>Harini</surname><roleName type="degree">MD</roleName></persName><affiliation><orgName type="division">Division of Clinical Neurophysiology</orgName><orgName type="division">Department of Neurology</orgName><orgName type="institution">Boston Children's Hospital, Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Rohit R.</forename><surname>Das</surname><roleName type="degree">MD, MPH</roleName></persName><affiliation><orgName type="division">Division of Clinical Neurophysiology</orgName><orgName type="division">Department of Neurology</orgName><orgName type="institution">Boston Children's Hospital, Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation><affiliation><orgName type="division">Department of Neurology</orgName><orgName type="institution">Indiana State University</orgName><address><settlement>Indianapolis</settlement><region>IN</region></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Sanjay P.</forename><surname>Prabhu</surname><roleName type="degree">MBBS</roleName></persName><affiliation><orgName type="division">Department of Radiology</orgName><orgName type="division">Boston Children's Hospital and Harvard Medical School</orgName><orgName type="institution">Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Kanwaljit</forename><surname>Singh</surname><roleName type="degree">MD, MPH</roleName></persName><affiliation><orgName type="division">Division of Clinical Neurophysiology</orgName><orgName type="division">Department of Neurology</orgName><orgName type="institution">Boston Children's Hospital, Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation><affiliation><orgName type="division">Lurie Center</orgName><orgName type="division">Massachusetts General Hospital for Children</orgName><orgName type="institution">Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Amit</forename><surname>Haldar</surname><roleName type="degree">MD, DM</roleName></persName><affiliation><orgName type="division">Division of Clinical Neurophysiology</orgName><orgName type="division">Department of Neurology</orgName><orgName type="institution">Boston Children's Hospital, Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Masanori</forename><surname>Takeoka</surname><roleName type="degree">MD</roleName></persName><affiliation><orgName type="division">Division of Clinical Neurophysiology</orgName><orgName type="division">Department of Neurology</orgName><orgName type="institution">Boston Children's Hospital, Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation></author><author xml:id="author-0006"><persName><forename type="first">Ann M.</forename><surname>Bergin</surname><roleName type="degree">MD</roleName></persName><affiliation><orgName type="division">Division of Clinical Neurophysiology</orgName><orgName type="division">Department of Neurology</orgName><orgName type="institution">Boston Children's Hospital, Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation></author><author xml:id="author-0007"><persName><forename type="first">Tobias</forename><surname>Loddenkemper</surname><roleName type="degree">MD</roleName></persName><affiliation><orgName type="division">Division of Clinical Neurophysiology</orgName><orgName type="division">Department of Neurology</orgName><orgName type="institution">Boston Children's Hospital, Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation></author><author xml:id="author-0008"><persName><forename type="first">Sanjeev V.</forename><surname>Kothare</surname><roleName type="degree">MD</roleName></persName><affiliation><orgName type="division">Division of Clinical Neurophysiology</orgName><orgName type="division">Department of Neurology</orgName><orgName type="institution">Boston Children's Hospital, Harvard Medical School</orgName><address><settlement>Boston</settlement><region>MA</region></address></affiliation><affiliation><orgName type="division">New York University Medical Center</orgName><orgName type="division">Comprehensive Epilepsy Center</orgName><orgName 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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main"><head>ABSTRACT</head><head>PURPOSE</head><p>T2‐hyperintense signal changes in corpus callosum (CC) have been described in epilepsy and encephalitis/encephalopathy. Little is known about their pathophysiology. The aim of this study was to examine the clinical presentation and evolution of CC lesions and relationship to seizures.</p><head>METHODS</head><p>We identified 12 children among 29,634 patients from Radiology Database. We evaluated following characteristics: seizures and accompanying medical history, antiepileptic drug usage, presenting symptoms, and radiological evolution of lesions.</p><head>RESULTS</head><p>CC lesions were seen in patients with prior diagnosis of epilepsy (<hi rend="italic">n</hi> = 5) or in those with new onset seizures (<hi rend="italic">n</hi> = 3), or with encephalitis/encephalopathy without history of seizures (<hi rend="italic">n</hi> = 4). Seizure clustering or disturbances of consciousness were the main presenting symptoms. No relationship was observed between CC lesion and AEDs. On imaging, ovoid lesions at presentation resolved on follow up imaging and linear lesions persisted. DTI showed that the fibers passing through splenial lesions originated from the posterior parietal cortex and occipital cortex bilaterally.</p><head>CONCLUSION</head><p>In patients with seizures, no clear relationship was demonstrated between seizure characteristics or AED use with CC lesions. Ovoid lesions resolved and may have different pathophysiologic mechanism when compared to linear lesions that persisted.</p></abstract><textClass><keywords><term xml:id="jon12190-kwd-0001">Splenial lesions</term><term xml:id="jon12190-kwd-0002">corpus callosum</term><term xml:id="jon12190-kwd-0003">encephalitis</term><term xml:id="jon12190-kwd-0004">encephalopathy</term><term xml:id="jon12190-kwd-0005">antiepileptic drugs</term><term xml:id="jon12190-kwd-0006">MRI</term></keywords><keywords rend="articleCategory"><term>Clinical Investigative Study</term></keywords><keywords rend="tocHeading1"><term>ORIGINAL RESEARCH</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-RQWK7R3P-X/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en" xml:id="jon12190"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1552-6569</doi><issn type="print">1051-2284</issn><issn type="electronic">1552-6569</issn><idGroup><id type="product" value="JON"></id></idGroup><titleGroup><title type="main" sort="JOURNAL OF NEUROIMAGING">Journal of Neuroimaging</title><title type="short">Journal of Neuroimaging</title></titleGroup></publicationMeta><publicationMeta level="part" position="09105"><doi>10.1111/jon.2015.25.issue-5</doi><copyright ownership="thirdParty">Copyright © 2015 by the American Society of Neuroimaging</copyright><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2015-09">September/October 2015</coverDate></publicationMeta><publicationMeta level="unit" position="190" type="article" status="forIssue"><doi origin="wiley">10.1111/jon.12190</doi><idGroup><id type="unit" value="JON12190"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Clinical Investigative Study</title><title type="tocHeading1"><i>ORIGINAL RESEARCH</i></title></titleGroup><copyright ownership="thirdParty">Copyright © 2014 by the American Society of Neuroimaging</copyright><eventGroup><event type="manuscriptReceived" date="2014-02-04"></event><event type="manuscriptRevised" date="2014-07-23"></event><event type="manuscriptAccepted" date="2014-09-13"></event><event type="xmlCreated" agent="Aptara" date="2014-11-25"></event><event type="publishedOnlineEarlyUnpaginated" date="2014-12-18"></event><event type="firstOnline" date="2014-12-18"></event><event type="publishedOnlineFinalForm" date="2015-08-14"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.7.5 mode:FullText" date="2016-01-23"></event></eventGroup><numberingGroup><numbering type="pageFirst">824</numbering><numbering type="pageLast">831</numbering></numberingGroup><correspondenceTo><b>Correspondence</b>: Address correspondence to Chellamani Harini, MD, Division of Epilepsy & Clinical Neurophysiology, Boston Children's Hospital, Harvard Medical School, Fegan 9, 300 Longwood Avenue, Boston, MA 02115. E‐mail: <email>chellamani.harini@childrens.harvard.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:JON.JON12190.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum</title><title type="short">Corpus Callosum Lesions in Children</title><title type="shortAuthors">Harini et al</title></titleGroup><creators><creator xml:id="jon12190-cr-0001" creatorRole="author" affiliationRef="#jon12190-aff-0001" noteRef="#jon12190-note-0002" corresponding="yes"><personName><givenNames>Chellamani</givenNames><familyName>Harini</familyName><degrees>MD</degrees></personName></creator><creator xml:id="jon12190-cr-0002" creatorRole="author" affiliationRef="#jon12190-aff-0001 #jon12190-aff-0002" noteRef="#jon12190-note-0002"><personName><givenNames>Rohit R.</givenNames><familyName>Das</familyName><degrees>MD, MPH</degrees></personName></creator><creator xml:id="jon12190-cr-0003" creatorRole="author" affiliationRef="#jon12190-aff-0003"><personName><givenNames>Sanjay P.</givenNames><familyName>Prabhu</familyName><degrees>MBBS</degrees></personName></creator><creator xml:id="jon12190-cr-0004" creatorRole="author" affiliationRef="#jon12190-aff-0001 #jon12190-aff-0004"><personName><givenNames>Kanwaljit</givenNames><familyName>Singh</familyName><degrees>MD, MPH</degrees></personName></creator><creator xml:id="jon12190-cr-0005" creatorRole="author" affiliationRef="#jon12190-aff-0001"><personName><givenNames>Amit</givenNames><familyName>Haldar</familyName><degrees>MD, DM</degrees></personName></creator><creator xml:id="jon12190-cr-0006" creatorRole="author" affiliationRef="#jon12190-aff-0001"><personName><givenNames>Masanori</givenNames><familyName>Takeoka</familyName><degrees>MD</degrees></personName></creator><creator xml:id="jon12190-cr-0007" creatorRole="author" affiliationRef="#jon12190-aff-0001"><personName><givenNames>Ann M.</givenNames><familyName>Bergin</familyName><degrees>MD</degrees></personName></creator><creator xml:id="jon12190-cr-0008" creatorRole="author" affiliationRef="#jon12190-aff-0001"><personName><givenNames>Tobias</givenNames><familyName>Loddenkemper</familyName><degrees>MD</degrees></personName></creator><creator xml:id="jon12190-cr-0009" creatorRole="author" affiliationRef="#jon12190-aff-0001 #jon12190-aff-0005"><personName><givenNames>Sanjeev V.</givenNames><familyName>Kothare</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="jon12190-aff-0001"><orgDiv>Division of Clinical Neurophysiology</orgDiv><orgDiv>Department of Neurology</orgDiv><orgName>Boston Children's Hospital, Harvard Medical School</orgName><address><city>Boston</city><countryPart>MA</countryPart></address></affiliation><affiliation xml:id="jon12190-aff-0002"><orgDiv>Department of Neurology</orgDiv><orgName>Indiana State University</orgName><address><city>Indianapolis</city><countryPart>IN</countryPart></address></affiliation><affiliation xml:id="jon12190-aff-0003"><orgDiv>Department of Radiology</orgDiv><orgDiv>Boston Children's Hospital and Harvard Medical School</orgDiv><orgName>Harvard Medical School</orgName><address><city>Boston</city><countryPart>MA</countryPart></address></affiliation><affiliation xml:id="jon12190-aff-0004"><orgDiv>Lurie Center</orgDiv><orgDiv>Massachusetts General Hospital for Children</orgDiv><orgName>Harvard Medical School</orgName><address><city>Boston</city><countryPart>MA</countryPart></address></affiliation><affiliation xml:id="jon12190-aff-0005"><orgDiv>New York University Medical Center</orgDiv><orgDiv>Comprehensive Epilepsy Center</orgDiv><orgName>Langone Medical School</orgName><address><countryPart>NY</countryPart></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="jon12190-kwd-0001">Splenial lesions</keyword><keyword xml:id="jon12190-kwd-0002">corpus callosum</keyword><keyword xml:id="jon12190-kwd-0003">encephalitis</keyword><keyword xml:id="jon12190-kwd-0004">encephalopathy</keyword><keyword xml:id="jon12190-kwd-0005">antiepileptic drugs</keyword><keyword xml:id="jon12190-kwd-0006">MRI</keyword></keywordGroup><abstractGroup><abstract type="main"><title type="main">ABSTRACT</title><section xml:id="jon12190-sec-0010"><title type="main">PURPOSE</title><p>T2‐hyperintense signal changes in corpus callosum (CC) have been described in epilepsy and encephalitis/encephalopathy. Little is known about their pathophysiology. The aim of this study was to examine the clinical presentation and evolution of CC lesions and relationship to seizures.</p></section><section xml:id="jon12190-sec-0020"><title type="main">METHODS</title><p>We identified 12 children among 29,634 patients from Radiology Database. We evaluated following characteristics: seizures and accompanying medical history, antiepileptic drug usage, presenting symptoms, and radiological evolution of lesions.</p></section><section xml:id="jon12190-sec-0030"><title type="main">RESULTS</title><p>CC lesions were seen in patients with prior diagnosis of epilepsy (<i>n</i> = 5) or in those with new onset seizures (<i>n</i> = 3), or with encephalitis/encephalopathy without history of seizures (<i>n</i> = 4). Seizure clustering or disturbances of consciousness were the main presenting symptoms. No relationship was observed between CC lesion and AEDs. On imaging, ovoid lesions at presentation resolved on follow up imaging and linear lesions persisted. DTI showed that the fibers passing through splenial lesions originated from the posterior parietal cortex and occipital cortex bilaterally.</p></section><section xml:id="jon12190-sec-0040"><title type="main">CONCLUSION</title><p>In patients with seizures, no clear relationship was demonstrated between seizure characteristics or AED use with CC lesions. Ovoid lesions resolved and may have different pathophysiologic mechanism when compared to linear lesions that persisted.</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="jon12190-note-0001" numbered="no"><p><b>Conflicts of Interest</b>: None of the authors have any conflicts of interest to declare.</p></note><note xml:id="jon12190-note-0002"><p>Chellamani Harini and Rohit R. Das contributed equally.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Corpus Callosum Lesions in Children</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum</title></titleInfo><name type="personal"><namePart type="given">Chellamani</namePart><namePart type="family">Harini</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</affiliation><description>Chellamani Harini and Rohit R. Das contributed equally.</description><affiliation>E-mail: chellamani.harini@childrens.harvard.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rohit R.</namePart><namePart type="family">Das</namePart><namePart type="termsOfAddress">MD, MPH</namePart><affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</affiliation><affiliation>Department of Neurology, Indiana State University, IN, Indianapolis</affiliation><description>Chellamani Harini and Rohit R. Das contributed equally.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sanjay P.</namePart><namePart type="family">Prabhu</namePart><namePart type="termsOfAddress">MBBS</namePart><affiliation>Department of Radiology, Boston Children's Hospital and Harvard Medical School, Harvard Medical School, MA, Boston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kanwaljit</namePart><namePart type="family">Singh</namePart><namePart type="termsOfAddress">MD, MPH</namePart><affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</affiliation><affiliation>Lurie Center, Massachusetts General Hospital for Children, Harvard Medical School, MA, Boston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Amit</namePart><namePart type="family">Haldar</namePart><namePart type="termsOfAddress">MD, DM</namePart><affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Masanori</namePart><namePart type="family">Takeoka</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ann M.</namePart><namePart type="family">Bergin</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tobias</namePart><namePart type="family">Loddenkemper</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sanjeev V.</namePart><namePart type="family">Kothare</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</affiliation><affiliation>New York University Medical Center, Comprehensive Epilepsy Center, Langone Medical School, NY</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2015-09</dateIssued><dateCreated encoding="w3cdtf">2014-11-25</dateCreated><dateCaptured encoding="w3cdtf">2014-02-04</dateCaptured><dateValid encoding="w3cdtf">2014-09-13</dateValid><copyrightDate encoding="w3cdtf">2015</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>PURPOSE: T2‐hyperintense signal changes in corpus callosum (CC) have been described in epilepsy and encephalitis/encephalopathy. Little is known about their pathophysiology. The aim of this study was to examine the clinical presentation and evolution of CC lesions and relationship to seizures. METHODS: We identified 12 children among 29,634 patients from Radiology Database. We evaluated following characteristics: seizures and accompanying medical history, antiepileptic drug usage, presenting symptoms, and radiological evolution of lesions. RESULTS: CC lesions were seen in patients with prior diagnosis of epilepsy (n = 5) or in those with new onset seizures (n = 3), or with encephalitis/encephalopathy without history of seizures (n = 4). Seizure clustering or disturbances of consciousness were the main presenting symptoms. No relationship was observed between CC lesion and AEDs. On imaging, ovoid lesions at presentation resolved on follow up imaging and linear lesions persisted. DTI showed that the fibers passing through splenial lesions originated from the posterior parietal cortex and occipital cortex bilaterally. CONCLUSION: In patients with seizures, no clear relationship was demonstrated between seizure characteristics or AED use with CC lesions. Ovoid lesions resolved and may have different pathophysiologic mechanism when compared to linear lesions that persisted.</abstract><subject><genre>keywords</genre><topic>Splenial lesions</topic><topic>corpus callosum</topic><topic>encephalitis</topic><topic>encephalopathy</topic><topic>antiepileptic drugs</topic><topic>MRI</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neuroimaging</title></titleInfo><titleInfo type="abbreviated"><title>Journal of Neuroimaging</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Clinical Investigative Study</topic><topic>ORIGINAL RESEARCH</topic></subject><identifier type="ISSN">1051-2284</identifier><identifier type="eISSN">1552-6569</identifier><identifier type="DOI">10.1111/(ISSN)1552-6569</identifier><identifier type="PublisherID">JON</identifier><part><date>2015</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>824</start><end>831</end><total>8</total></extent></part></relatedItem><relatedItem type="references" displayLabel="jon12190-cit-0001"><titleInfo><title>Corpus callosotomy</title></titleInfo><name type="personal"><namePart type="given">AA</namePart><namePart type="family">Asadi‐Pooya</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Sharan</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Nei</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Asadi‐Pooya AA, Sharan A, Nei M, et al. 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