نتایج جستجو برای: scn1a

تعداد نتایج: 569  

Journal: :Seizure 2011
A. A. Mhanni J. N. Hartley W. G. Sanger A. E. Chudley E. L. Spriggs

Mutations in the SCN1A gene can cause a variety of dominantly inherited epilepsy syndromes. Severe phenotypes usually result from loss of function mutations, whereas missense mutations cause a milder phenotype by altering the sodium channel activity. We report on a novel missense variant (p.Val1379Leu) in the SCN1A gene segregating in an autosomal dominant pattern in a family exhibiting a varia...

2017
Lynette G. Sadleir Emily I. Mountier Deepak Gill Suzanne Davis Charuta Joshi Catherine DeVile Manju A. Kurian Simone Mandelstam Elaine Wirrell Katherine C. Nickels Hema R. Murali Gemma Carvill Candace T. Myers Heather C. Mefford Ingrid E. Scheffer

OBJECTIVE To define a distinct SCN1A developmental and epileptic encephalopathy with early onset, profound impairment, and movement disorder. METHODS A case series of 9 children were identified with a profound developmental and epileptic encephalopathy and SCN1A mutation. RESULTS We identified 9 children 3 to 12 years of age; 7 were male. Seizure onset was at 6 to 12 weeks with hemiclonic s...

Afshin Borhani-Haghighi, Katayoon Javidnia Mehrdad Emami Negar Azarpira, Rahimeh Rahjoo Razieh Berahmand, Soha Namazi,

Objective (s): From a genetic point of view, epilepsy is a polygenic multifactorial syndrome. The SCN1A and B genes belong to a family of genes that provide instructions for making sodium channels. Understanding the relevance of SCN1A and SCN1B gene polymorphisms to plasma concentration of carbamazepine (CBZ) and its active metabolite carbamazepine 10, 11 epoxide (CBZE), may shed more light on ...

Journal: :Pharmacogenomics 2013
Batoul Sadat Haerian Larry Baum Patrick Kwan Hui Jun Tan Azman Ali Raymond Zahurin Mohamed

AIM Approximately a third of newly diagnosed epilepsy patients do not respond to antiepileptic drugs (AEDs). Evidence suggests that low penetrance variants in the genes of drug targets such as voltage-gated sodium channels may be involved in drug responsiveness. To examine this hypothesis, we compared data from two epilepsy cohorts from Malaysia and Hong Kong, as well as a meta-analysis from pu...

Journal: :Epilepsy currents 2013
Jennifer A Kearney

Commentary Dravet syndrome is an infant-onset epileptic encephalopathy characterized by generalized clonic, tonic–clonic, or hemi-clonic seizures. Patients subsequently develop other types of seizures, including myoclonic, absence, or partial seizures. Seizures are often refractory to conventional antiepileptic drugs and lack ofadequate seizure control is correlated with poor outcomes. Developm...

Journal: :PLoS Genetics 2009
Christel Depienne Delphine Bouteiller Boris Keren Emmanuel Cheuret Karine Poirier Oriane Trouillard Baya Benyahia Chloé Quelin Wassila Carpentier Sophie Julia Alexandra Afenjar Agnès Gautier François Rivier Sophie Meyer Patrick Berquin Marie Hélias Isabelle Py Serge Rivera Nadia Bahi-Buisson Isabelle Gourfinkel-An Cécile Cazeneuve Merle Ruberg Alexis Brice Rima Nabbout Eric LeGuern

Dravet syndrome (DS) is a genetically determined epileptic encephalopathy mainly caused by de novo mutations in the SCN1A gene. Since 2003, we have performed molecular analyses in a large series of patients with DS, 27% of whom were negative for mutations or rearrangements in SCN1A. In order to identify new genes responsible for the disorder in the SCN1A-negative patients, 41 probands were scre...

Journal: :Orvosi hetilap 2015
Judit Bene Kinga Hadzsiev Katalin Komlósi Erzsébet Kövesdi Petra Mátyás Béla Melegh

Severe myoclonic epilepsy in infancy (Dravet's syndrome) is a very rare form of epilepsy. Mutations of SCN1A gene encoding voltage-gated sodium channel alpha-1 subunit are major causes of the autosomal dominant disorder. Most cases are associated with a de novo point mutation, but some patients have copy number variations. The protein encoded by the SCN1A gene plays a role in the generation and...

2013
Nienke E. Verbeek Nicoline A. T. van der Maas Floor E. Jansen Marjan J. A. van Kempen Dick Lindhout Eva H. Brilstra

OBJECTIVES To determine the prevalence of Dravet syndrome, an epileptic encephalopathy caused by SCN1A-mutations, often with seizure onset after vaccination, among infants reported with seizures following vaccination. To determine differences in characteristics of reported seizures after vaccination in children with and without SCN1A-related Dravet syndrome. METHODS Data were reviewed of 1,26...

Journal: :Brain : a journal of neurology 2007
Louise A Harkin Jacinta M McMahon Xenia Iona Leanne Dibbens James T Pelekanos Sameer M Zuberi Lynette G Sadleir Eva Andermann Deepak Gill Kevin Farrell Mary Connolly Thorsten Stanley Michael Harbord Frederick Andermann Jing Wang Sat Dev Batish Jeffrey G Jones William K Seltzer Alison Gardner Grant Sutherland Samuel F Berkovic John C Mulley Ingrid E Scheffer

The relationship between severe myoclonic epilepsy of infancy (SMEI or Dravet syndrome) and the related syndrome SMEI-borderland (SMEB) with mutations in the sodium channel alpha 1 subunit gene SCN1A is well established. To explore the phenotypic variability associated with SCN1A mutations, 188 patients with a range of epileptic encephalopathies were examined for SCN1A sequence variations by de...

Journal: :The Journal of General Physiology 2006
Carlos G. Vanoye Christoph Lossin Thomas H. Rhodes Alfred L. George

Mutations in genes encoding neuronal voltage-gated sodium channel subunits have been linked to inherited forms of epilepsy. The majority of mutations (>100) associated with generalized epilepsy with febrile seizures plus (GEFS+) and severe myoclonic epilepsy of infancy (SMEI) occur in SCN1A encoding the NaV1.1 neuronal sodium channel alpha-subunit. Previous studies demonstrated functional heter...

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