<?xml version="1.0" encoding="UTF-8"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.seizure-journal.com//inpress?rss=yes"><title>Seizure: European Journal of Epilepsy - Articles in Press</title><description>Seizure: European Journal of Epilepsy RSS feed: Articles in Press. 
 Seizure - European Journal of Epilepsy  is an international journal providing a forum for the publication of papers on all topics 
related to epilepsy and seizure disorders. 
These topics include the basic sciences related to the condition itself, the differential 
diagnosis, natural history and epidemiology of seizures, and the investigation and practical management of epilepsy (including drug treatment, 
neurosurgery and non-medical and behavioural treatments).  
 
The journal also reflects the social and psychological burden and impact 
of epilepsy on the person who has it, his family and society, and the methods and ideas that may help to alleviate such handicaps and 
stigma as the condition may cause. The aim of the journal is to share and disseminate knowledge between all disciplines that work in 
the field of epilepsy 

 
 
  
 
 



</description><link>http://www.seizure-journal.com//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 British Epilepsy Association. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Seizure: European Journal of Epilepsy</prism:publicationName><prism:issn>1059-1311</prism:issn><prism:publicationDate>2010-03-04</prism:publicationDate><prism:copyright> © 2010 British Epilepsy Association. Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.seizure-journal.com/article/PIIS1059131110000336/abstract?rss=yes"/><rdf:li rdf:resource="http://www.seizure-journal.com/article/PIIS1059131110000324/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.seizure-journal.com/article/PIIS1059131110000336/abstract?rss=yes"><title>Post-traumatic seizures—A prospective study from a tertiary level trauma center in a developing country - Corrected Proof</title><link>http://www.seizure-journal.com/article/PIIS1059131110000336/abstract?rss=yes</link><description>Abstract: Rationale: No large studies till date are available from India on post-traumatic seizures (PTS).Methods: This is a prospective observational study of 520 patients with traumatic brain injury (TBI) (July 2007–2008). Patients admitted after 24h of injury, with Glasgow coma scale (GCS)≤4 were excluded.Results: At a median follow-up of 386 days, 59 (11.4%) patients developed PTS. Incidence of immediate, early and late onset seizure were 6.5%, 2.1% and 2.7% respectively. In children, incidence of PTS was 18.3%. On univariate analysis, females, of age &lt;10 years, with associated medical problems and with delayed loss of consciousness and poor GCS (&lt;9), following fall from height, had significantly higher odds of PTS. On multivariate analysis, the risk of PTS was 3.7 times higher in patients who had fallen from height, 4.4 times higher in associated medical problems, and 3.7 times higher in severe head injury (GCS&lt;9) at presentation. PTS was associated with poor Glasgow outcome score and higher incidence of behavioral abnormality on follow up. 32% patient with PTS developed recurrent delayed seizures. Seizure recurrence was significantly higher in late onset PTS. PTS affected overall outcome of the patients in severe head injury.Conclusion: The risk of PTS was higher in patients who sustained fall from height, in GCS&lt;9, and associated medical problems. About 1/3rd of the patients with early PTS developed recurrent delayed seizures.</description><dc:title>Post-traumatic seizures—A prospective study from a tertiary level trauma center in a developing country - Corrected Proof</dc:title><dc:creator>Amit Thapa, Sarat P. Chandra, Sumit Sinha, V. Sreenivas, Bhawani S. Sharma, Manjari Tripathi</dc:creator><dc:identifier>10.1016/j.seizure.2010.02.004</dc:identifier><dc:source>Seizure: European Journal of Epilepsy (2010)</dc:source><dc:date>2010-03-04</dc:date><prism:publicationName>Seizure: European Journal of Epilepsy</prism:publicationName><prism:publicationDate>2010-03-04</prism:publicationDate></item><item rdf:about="http://www.seizure-journal.com/article/PIIS1059131110000324/abstract?rss=yes"><title>Anterior striatum with dysmorphic neurons associated with the epileptogenesis of focal cortical dysplasia - Corrected Proof</title><link>http://www.seizure-journal.com/article/PIIS1059131110000324/abstract?rss=yes</link><description>Abstract: The epileptogenesis of the striatum is unknown. We describe the case of a 12-year-old girl with intractable epilepsy who was treated by surgical interventions. Magnetic resonance imaging (MRI) showed ambiguous corticomedullary boundary in the left frontal lobe, and magnetoencephalography (MEG) revealed spike dipoles in the vicinity of the left ventral striatum. The epileptic seizures disappeared after partial resection of the frontal lobe, but recurred within 2 months and remained intractable. Neuropathological examination confirmed the presence of focal cortical dysplasia in the resected brain tissue. Ictal single photon emission computed tomography at this period displayed hyperperfusion of the left anterior striatum. At the second surgery, intraoperative electrocorticography exhibited spike discharges from the anterior striatum. After the removal of this structure and adjacent brain tissues, the patient remains seizure-free for 33 months, without any neurological deficits. Histopathological examination of the resected tissue revealed a large number of dysmorphic neurons distributed widely in the cerebral cortex, subcortical white matter, striatum, and insular cortex. These findings suggest that microscopic dysplasia of basal ganglia can accompany certain cases of focal cortical malformations, and may play a critical role in the epileptogenesis through their interaction with cortical structures.</description><dc:title>Anterior striatum with dysmorphic neurons associated with the epileptogenesis of focal cortical dysplasia - Corrected Proof</dc:title><dc:creator>Takanobu Kaido, Taisuke Otsuki, Yuu Kaneko, Akio Takahashi, Akiyoshi Kakita, Hitoshi Takahashi, Yoshiaki Saito, Eiji Nakagawa, Kenji Sugai, Masayuki Sasaki</dc:creator><dc:identifier>10.1016/j.seizure.2010.02.003</dc:identifier><dc:source>Seizure: European Journal of Epilepsy (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Seizure: European Journal of Epilepsy</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate><prism:section>CASE REPORT</prism:section></item></rdf:RDF>