Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum
Identifieur interne : 000335 ( Istex/Curation ); précédent : 000334; suivant : 000336Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum
Auteurs : Chellamani Harini [États-Unis] ; Rohit R. Das [États-Unis] ; Sanjay P. Prabhu [États-Unis] ; Kanwaljit Singh [États-Unis] ; Amit Haldar [États-Unis] ; Masanori Takeoka [États-Unis] ; Ann M. Bergin [États-Unis] ; Tobias Loddenkemper [États-Unis] ; Sanjeev V. Kothare [États-Unis]Source :
- 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 wicri:level="2"><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston</wicri:cityArea></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 wicri:level="3"><mods:affiliation>Department of Radiology, Boston Children's Hospital and Harvard Medical School, Harvard Medical School, MA, Boston</mods:affiliation><country>États-Unis</country><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName><wicri:orgArea>Department of Radiology, Boston Children's Hospital and Harvard Medical School, Harvard Medical School, MA</wicri:orgArea></affiliation></author><author><name sortKey="Singh, Kanwaljit" sort="Singh, Kanwaljit" uniqKey="Singh K" first="Kanwaljit" last="Singh">Kanwaljit Singh</name><affiliation wicri:level="2"><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston</wicri:cityArea></affiliation><affiliation wicri:level="3"><mods:affiliation>Lurie Center, Massachusetts General Hospital for Children, Harvard Medical School, MA, Boston</mods:affiliation><country>États-Unis</country><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName><wicri:orgArea>Lurie Center, Massachusetts General Hospital for Children, Harvard Medical School, MA</wicri:orgArea></affiliation></author><author><name sortKey="Haldar, Amit" sort="Haldar, Amit" uniqKey="Haldar A" first="Amit" last="Haldar">Amit Haldar</name><affiliation wicri:level="3"><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation><country>États-Unis</country><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName><wicri:orgArea>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA</wicri:orgArea></affiliation></author><author><name sortKey="Takeoka, Masanori" sort="Takeoka, Masanori" uniqKey="Takeoka M" first="Masanori" last="Takeoka">Masanori Takeoka</name><affiliation wicri:level="3"><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation><country>États-Unis</country><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName><wicri:orgArea>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA</wicri:orgArea></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 wicri:level="3"><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation><country>États-Unis</country><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName><wicri:orgArea>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA</wicri:orgArea></affiliation></author><author><name sortKey="Loddenkemper, Tobias" sort="Loddenkemper, Tobias" uniqKey="Loddenkemper T" first="Tobias" last="Loddenkemper">Tobias Loddenkemper</name><affiliation wicri:level="3"><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA, Boston</mods:affiliation><country>États-Unis</country><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName><wicri:orgArea>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, MA</wicri:orgArea></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 wicri:level="2"><mods:affiliation>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston</wicri:cityArea></affiliation><affiliation wicri:level="2"><mods:affiliation>New York University Medical Center, Comprehensive Epilepsy Center, Langone Medical School, NY</mods:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>New York University Medical Center, Comprehensive Epilepsy Center, Langone Medical School</wicri:cityArea></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></record>Pour manipuler ce document sous Unix (Dilib)
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