<?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.neurologic.theclinics.com/?rss=yes"><title>Neurologic Clinics</title><description>Neurologic Clinics RSS feed: Current Issue. 
 
  Neurologic Clinics  updates you on the latest trends in patient management; keeps you up to date on the newest advances; 
and provides a sound basis for choosing treatment options. Each issue focuses on a single topic in neurology and is presented under the 
direction of an experienced guest editor.</description><link>http://www.neurologic.theclinics.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2009 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:issn>0733-8619</prism:issn><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:publicationDate>November 2009</prism:publicationDate><prism:copyright> © 2009 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.neurologic.theclinics.com/article/PIIS0733861909000826/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000838/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000735/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000462/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS073386190900053X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000528/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000474/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000450/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000565/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000504/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000498/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000449/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000541/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000486/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000516/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000553/abstract?rss=yes"/><rdf:li rdf:resource="http://www.neurologic.theclinics.com/article/PIIS0733861909000760/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000826/abstract?rss=yes"><title>Table of Contents</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000826/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0733-8619(09)00082-6</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>vii</prism:startingPage><prism:endingPage>x</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000838/abstract?rss=yes"><title>Forthcoming Pages</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000838/abstract?rss=yes</link><description></description><dc:title>Forthcoming Pages</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0733-8619(09)00083-8</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>xi</prism:startingPage><prism:endingPage>xi</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000735/abstract?rss=yes"><title>Preface</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000735/abstract?rss=yes</link><description>   The diagnosis and management of patients who have epilepsy have greatly evolved over recent years. This issue of Neurologic Clinics presents state-of-the-art reviews by renowned experts of critical issues that illustrate this evolution and underscore their importance in the care of patients. The first six papers focus on the interrelationships between seizures and psychological, neuropsychological, and hormonal factors. The next five papers discuss pharmacologic treatment selection, drug resistance, approaches to localizing seizure onset, and deep brain stimulation as a possible non-pharmacological intervention. The final two papers present an update on the genetics of idiopathic epilepsies and a thought-provoking approach to sudden, unexpected death in epilepsy.</description><dc:title>Preface</dc:title><dc:creator>Steven C. Schachter</dc:creator><dc:identifier>10.1016/j.ncl.2009.09.017</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>xiii</prism:startingPage><prism:endingPage>xiii</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000462/abstract?rss=yes"><title>Determinants of Quality of Life in People with Epilepsy</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000462/abstract?rss=yes</link><description>This article reviews evidence of quality of life (QOL) determinants in people affected by epilepsy, including detractors and promoters. Emerging factors of particular significance for QOL are highlighted, including seizure frequency, medication side effects, psychological comorbidity, and stigma and discrimination. This article also examines the role of resilience, interpreted in its widest sense, for promoting good QOL, even in the presence of poorly controlled seizures. The importance of addressing both clinical and wider psychosocial issues is highlighted and some possible directions for future research into QOL in epilepsy are suggested.</description><dc:title>Determinants of Quality of Life in People with Epilepsy</dc:title><dc:creator>Ann Jacoby, Dee Snape, Gus A. Baker</dc:creator><dc:identifier>10.1016/j.ncl.2009.06.003</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>843</prism:startingPage><prism:endingPage>863</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS073386190900053X/abstract?rss=yes"><title>Depression and Epilepsy: A Review of Multiple Facets of Their Close Relation</title><link>http://www.neurologic.theclinics.com/article/PIIS073386190900053X/abstract?rss=yes</link><description>Depressive disorders are the most frequent psychiatric comorbidity in patients with epilepsy (PWE). Although they are typically considered a psychiatric disorder, ample data suggest that depressive disorders are a neurologic disorder with psychiatric clinical manifestations. Patients with epilepsy whose seizures originate in temporal and frontal lobes have the highest prevalence of comorbid depressive disorders. Not only are patients with epilepsy at higher risk of developing depression but also patients with depression are at higher risk of developing epilepsy. This article reviews these data, the clinical manifestations of depressive disorders in PWE, and their significant impact on the suicidal risk and quality of life.</description><dc:title>Depression and Epilepsy: A Review of Multiple Facets of Their Close Relation</dc:title><dc:creator>Andres M. Kanner</dc:creator><dc:identifier>10.1016/j.ncl.2009.08.002</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>865</prism:startingPage><prism:endingPage>880</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000528/abstract?rss=yes"><title>The Emerging Architecture of Neuropsychological Impairment in Epilepsy</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000528/abstract?rss=yes</link><description>A new literature is now under way, one linking cognitive abnormalities directly to indices of structural, functional, metabolic, and other neurobiologic markers of cerebral integrity, independent of their association with clinical epilepsy characteristics. These trends are reviewed in this article. The focus is on temporal lobe epilepsy (TLE) as a model with which to address the core points because this form of localization-related epilepsy has been very carefully studied from both a cognitive and imaging standpoint. Some pertinent historical issues are touched on first, followed by more detailed reviews of the cognitive and neuroimaging abnormalities that have been found in TLE, followed by an overview of studies examining direct structure-function relationships in TLE and other epilepsies.</description><dc:title>The Emerging Architecture of Neuropsychological Impairment in Epilepsy</dc:title><dc:creator>Bruce P. Hermann, Jack J. Lin, Jana E. Jones, Michael Seidenberg</dc:creator><dc:identifier>10.1016/j.ncl.2009.08.001</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>881</prism:startingPage><prism:endingPage>907</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000474/abstract?rss=yes"><title>The Etiology of Psychogenic Non-Epileptic Seizures: Toward a Biopsychosocial Model</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000474/abstract?rss=yes</link><description>Psychogenic non-epileptic seizures (PNES) are one of the most common differential diagnoses of epilepsy. PNES are poorly understood and often sub-optimally treated. This article summarizes current knowledge about the etiology of PNES. Through describing the interactions of predisposing, precipitating, perpetuating, and triggering factors, an integrated biopsychosocial model of a complex disorder is developed. PNES emerge as a dissociative response to a range of different stressors in vulnerable individuals. Once established, maintaining factors turn a temporary disturbance into a chronically disabling disorder.</description><dc:title>The Etiology of Psychogenic Non-Epileptic Seizures: Toward a Biopsychosocial Model</dc:title><dc:creator>Markus Reuber</dc:creator><dc:identifier>10.1016/j.ncl.2009.06.004</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>909</prism:startingPage><prism:endingPage>924</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000450/abstract?rss=yes"><title>Predicting Seizures: A Behavioral Approach</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000450/abstract?rss=yes</link><description>This article reviews the clinical evidence for seizure prediction. The epilepsy cycle is considered, including the interictal, preictal, ictal, and postictal phases. Evidence suggesting that the preictal phase can sometimes be identified based on neurophysiologic signals, premonitory features, the presence of trigger factors, or self-report is discussed. Diary studies have shown that seizures are not randomly distributed in time and that a subgroup of persons with epilepsy can predict an impending seizure. Paper diary data and preliminary analysis of electronic diary data suggest that seizure prediction is feasible.</description><dc:title>Predicting Seizures: A Behavioral Approach</dc:title><dc:creator>Sheryl R. Haut, Richard B. Lipton</dc:creator><dc:identifier>10.1016/j.ncl.2009.06.002</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>925</prism:startingPage><prism:endingPage>940</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000565/abstract?rss=yes"><title>Hormonal Aspects of Epilepsy</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000565/abstract?rss=yes</link><description>The interactions between hormones, epilepsy, and the medications used to treat epilepsy are complex, with tri-directional interactions which affect both men and women in various ways. Abnormalities of baseline endocrine status occur more commonly in people with epilepsy, and are most often described for the sex steroid hormone axis. Common symptoms include sexual dysfunction, decreased fertility, premature menopause, and polycystic ovarian syndrome. Antiepileptic drugs (AEDs) and hormones have a bidirectional interaction, with a decrease in the efficacy of hormonal contraceptive agents with some AEDs and a decrease in the concentration and efficacy of other AEDs with hormonal contraceptives. Endogenous hormones can influence seizure severity and frequency, resulting in catamenial patterns of epilepsy. However, this knowledge can be used to develop hormonal strategies to improve seizure control in people with epilepsy.</description><dc:title>Hormonal Aspects of Epilepsy</dc:title><dc:creator>Page B. Pennell</dc:creator><dc:identifier>10.1016/j.ncl.2009.08.005</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>941</prism:startingPage><prism:endingPage>965</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000504/abstract?rss=yes"><title>Selection of Antiepileptic Drugs in Adults</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000504/abstract?rss=yes</link><description>Epilepsy affects approximately 50 million people worldwide, with an annual incidence of 50 to 70 cases per 100,000 population. The condition can strike at any time of life, with an immediate impact on everyday activities and routine. Key to optimal management is swift referral to an epilepsy specialist, appropriate investigation, and timely institution of antiepileptic drug therapy. In the past 20 years, the explosion of 13 new agents into the marketplace has greatly increased the potential for therapeutic intervention. This article explores the rationale for treatment selection in adults with epilepsy.</description><dc:title>Selection of Antiepileptic Drugs in Adults</dc:title><dc:creator>Linda J. Stephen, Martin J. Brodie</dc:creator><dc:identifier>10.1016/j.ncl.2009.06.007</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>967</prism:startingPage><prism:endingPage>992</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000498/abstract?rss=yes"><title>Teratogenic Effects of Antiepileptic Medications</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000498/abstract?rss=yes</link><description>During the last few years epilepsy and pregnancy registries and other large scale observational studies have provided new information on the teratogenic effects of the most frequently used antiepileptic drugs (AEDs). The prevalence of major congenital malformations associated with exposure to carbamazepine or lamotrigine appears to be only marginally increased from the expected, while malformation rates with valproate have been reported to be 2 to 4 times higher. Recent studies also suggest that compared with carbamazepine, lamotrigine and phenytoin, exposure to valproate in utero may be associated with poorer postnatal cognitive development. However, adverse outcomes with valproate appear to be dose-related, and doses below 800-1,000 mg/day might not be associated with worse outcome than with other AEDs. Information on the teratogenic potential of other newer generation AEDs than lamotrigine is still insufficient.</description><dc:title>Teratogenic Effects of Antiepileptic Medications</dc:title><dc:creator>Torbjörn Tomson, Dina Battino</dc:creator><dc:identifier>10.1016/j.ncl.2009.06.006</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>993</prism:startingPage><prism:endingPage>1002</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000449/abstract?rss=yes"><title>Identification of Pharmacoresistant Epilepsy</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000449/abstract?rss=yes</link><description>There is no single definition of pharmacoresistant (intractable, refractory) epilepsy. Prospective identification of pharmacoresistance is complicated by the variability of its appearance across different types of epilepsy and the variability of seizure control within a given patient over time. Failure of informative trials of two appropriate antiepileptic drugs has been recommended as a threshold that should trigger referral for evaluation at a comprehensive epilepsy center. Maximizing seizure control is imperative for reducing the risks and consequences of epilepsy, including the cognitive and psychiatric comorbidities and even sudden death.</description><dc:title>Identification of Pharmacoresistant Epilepsy</dc:title><dc:creator>Anne T. Berg</dc:creator><dc:identifier>10.1016/j.ncl.2009.06.001</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1003</prism:startingPage><prism:endingPage>1013</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000541/abstract?rss=yes"><title>Localization in Epilepsy</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000541/abstract?rss=yes</link><description>Pharmacologic therapy represents the first line of treatment of epilepsy and is effective in most patients. However, about 20% to 30% of cases develop intractable seizures that cannot be controlled by medication alone. In such cases, surgical intervention is considered for therapeutic, often curative purposes. Dynamic spatiotemporal variability in the epileptic focus renders seizure localization a challenge to the clinician. Many diagnostic modalities have been developed to identify different aspects of the epileptic focus. Older techniques are being increasingly supplemented by a variety of anatomic and functional imaging modalities that can help clarify discrepancies. Invasive electroencephalography remains the gold standard for identifying epileptic foci and guiding the surgeon to successful resections.</description><dc:title>Localization in Epilepsy</dc:title><dc:creator>Dimitris G. Placantonakis, Theodore H. Schwartz</dc:creator><dc:identifier>10.1016/j.ncl.2009.08.004</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1015</prism:startingPage><prism:endingPage>1030</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000486/abstract?rss=yes"><title>Therapeutic Brain Stimulation for Epilepsy</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000486/abstract?rss=yes</link><description>Deep brain stimulation (DBS) for epilepsy is a functional therapy that avoids many of the adverse effects associated with antiepileptic drug therapy and resective brain surgery. DBS is a relatively new therapy, and only recently has controlled evidence shown its efficacy. This article concentrates on clinical studies of DBS for epilepsy.</description><dc:title>Therapeutic Brain Stimulation for Epilepsy</dc:title><dc:creator>Juliana Lockman, Robert S. Fisher</dc:creator><dc:identifier>10.1016/j.ncl.2009.06.005</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1031</prism:startingPage><prism:endingPage>1040</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000516/abstract?rss=yes"><title>Advances on the Genetics of Mendelian Idiopathic Epilepsies</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000516/abstract?rss=yes</link><description>Genetic factors play an increasingly recognized role in idiopathic epilepsies. Since 1995, positional cloning strategies in multi-generational families with autosomal dominant transmission have revealed 11 genes (KCNQ2, KCNQ3, CHRNA4, CHRNA2, CHRNB2, SCN1B, SCN1A, SCN2A, GABRG2, GABRA1, and LGI1) and numerous loci for febrile seizures and epilepsies. To date, all genes with the exception of LGI1 (leucine-rich glioma inactivated 1), encode neuronal ion channel or neurotransmitter receptor subunits. Molecular approaches have revealed great genetic heterogeneity, with the vast majority of genes remaining to be identified. One of the major challenges is now to understand phenotype–genotype correlations. This review focuses on the current knowledge on the molecular basis of these rare Mendelian autosomal dominant forms of idiopathic epilepsies.</description><dc:title>Advances on the Genetics of Mendelian Idiopathic Epilepsies</dc:title><dc:creator>Stéphanie Baulac, Michel Baulac</dc:creator><dc:identifier>10.1016/j.ncl.2009.07.001</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1041</prism:startingPage><prism:endingPage>1061</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000553/abstract?rss=yes"><title>Sudden Unexpected Death in Epilepsy (SUDEP): Update and Reflections</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000553/abstract?rss=yes</link><description>This article addresses aspects of sudden unexpected death in epilepsy, reflecting on current knowledge and questions that need answers to quantify, monitor, and reduce risk. A brief overview is followed by a discussion of definitions, drug treatment, genetic susceptibility, mechanisms in relation to seizure monitoring units and supervision, with some suggestions for the way forward.</description><dc:title>Sudden Unexpected Death in Epilepsy (SUDEP): Update and Reflections</dc:title><dc:creator>Lina Nashef, Philippe Ryvlin</dc:creator><dc:identifier>10.1016/j.ncl.2009.08.003</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1063</prism:startingPage><prism:endingPage>1074</prism:endingPage></item><item rdf:about="http://www.neurologic.theclinics.com/article/PIIS0733861909000760/abstract?rss=yes"><title>Index</title><link>http://www.neurologic.theclinics.com/article/PIIS0733861909000760/abstract?rss=yes</link><description></description><dc:title>Index</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0733-8619(09)00076-0</dc:identifier><dc:source>Neurologic Clinics 27, 4 (2009)</dc:source><dc:date>2009-11-01</dc:date><prism:publicationName>Neurologic Clinics</prism:publicationName><prism:publicationDate>2009-11-01</prism:publicationDate><prism:volume>27</prism:volume><prism:number>4</prism:number><prism:issueIdentifier>S0733-8619(09)X0004-6</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1075</prism:startingPage><prism:endingPage>1085</prism:endingPage></item></rdf:RDF>