Search results for " EPILEPSY"

showing 10 items of 152 documents

Alternating Hemiplegia of Childhood: neurological comorbidities and intrafamilial variability.

2022

Abstract Background Alternating of Childhood (AHC) is an uncommon and complex disorder characterized by age of onset before 18 months with recurrent hemiplegia of one or either sides of the body or quadriplegia. The disorder is mainly caused by mutations in ATP1A3 gene, and to a lesser extent in ATP1A2 gene. In AHC neurological co-morbidities are various and frequently reported including developmental delay, epilepsy, tonic or dystonic spells, nystagmus,autonomic manifestations with intrafamilial variability. Case presentation Clinical and genetic findings of a couple of twins (Family 1: Case 1 and Case 2) and a couple of siblings (Family 2: Case 3 and Case 4) coming from two different Ital…

MaleEpilepsyAlternating hemiplegia of childhood (AHC)Alternating hemiplegia of childhood (AHC) Case report Comorbidities Epilepsy GRIN2AMutation MissenseInfantHemiplegiaNeurology Behaviour and DevelopmentGRIN2AComorbiditiesCase reportMutationHumansSodium-Potassium-Exchanging ATPaseChildItalian journal of pediatrics
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Benign familial infantile epilepsy associated with KCNQ3 mutation: a rare occurrence or an underestimated event?

2020

Abstract Benign familial infantile epilepsy (BFIE) is the most genetically heterogeneous phenotype among early-onset familial infantile epilepsies. It has an autosomal dominant inheritance pattern with incomplete penetrance. Although PRRT2 is the most mutated gene detected in families with BFIE, other mutations in KCNQ2, SCN2A, and GABRA6 genes have also been described. To date, KCNQ3 mutations have been detected in only four patients with BFIE. Here, we describe the clinical pattern and course of an additional individual with BFIE associated with a novel missense heterozygous KCNQ3 c.1850G>C variant inherited by his unaffected father. The incidence of KCNQ3 mutations among BFIE patients…

MaleGABRA6Mutation Missensemedicine.disease_causeKCNQ3 Potassium ChannelEpilepsymutation.medicineHumansMissense mutationBFIEGeneticsBenign familial infantile epilepsyMutationKCNQ3biologybusiness.industryGenetic heterogeneityInfantGeneral Medicinemedicine.diseasePenetranceEpilepsy Benign NeonatalNeurologybenign familial infantile epilepsybiology.proteinincidenceNeurology (clinical)businessPRRT2
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A novel mutation in KCNQ3-related benign familial neonatal epilepsy: electroclinical features and neurodevelopmental outcome.

2019

Benign familial neonatal epilepsy (BFNE) is caused, in about 5% of families, by mutations in the KCNQ3 gene encoding voltage-gated potassium channel subunits. Usually, newborns with BFNE show a normal neurological outcome, but recently, refractory seizures and/or developmental disability have been reported suggesting phenotype variability associated with KCNQ3-related BFNE. Here, we describe a proband from a BFNE family carrying a novel variant in the KCNQ3 gene. Regarding the paucity of data in the literature, we describe the presented case with a view to further establishing: (1) a genotype/phenotype correlation in order to define a BFNE phenotype associated with favourable outcome; (2) a…

MaleGenotypeelectroclinical featureInfantElectroencephalographygenotype-phenotype correlationSettore MED/39 - Neuropsichiatria InfantileEpilepsy Benign NeonatalKCNQ3 Potassium ChannelKCNQSettore MED/38 - Pediatria Generale E SpecialisticaPhenotypevoltage-gated potassium channelsSettore M-PSI/08 - Psicologia ClinicaHumansbenign familial neonatal epilepsyEpileptic SyndromesEpileptic disorders : international epilepsy journal with videotape
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A novel KCNQ3 mutation in familial epilepsy with focal seizures and intellectual disability

2015

Mutations in the KCNQ2 gene encoding for voltage-gated potassium channel subunits have been found in patients affected with early onset epilepsies with wide phenotypic heterogeneity, ranging from benign familial neonatal seizures (BFNS) to epileptic encephalopathy with cognitive impairment, drug resistance, and characteristic electroencephalography (EEG) and neuroradiologic features. By contrast, only few KCNQ3 mutations have been rarely described, mostly in patients with typical BFNS. We report clinical, genetic, and functional data from a family in which early onset epilepsy and neurocognitive deficits segregated with a novel mutation in KCNQ3 (c.989G>T; p.R330L). Electrophysiological stu…

MaleGenotype-phenotype correlationmedicine.medical_specialtyNeurologyBenign familial neonatal seizuresMutantGenotype-phenotype correlationsmedicine.disease_causeMutagenesiKCNQ3 Potassium ChannelEpilepsyKCNQBenign Familial Neonatal Seizures KCNQ cognitive impairment voltage-gated potassium channels epilepsy mutagenesis genotype-phenotype correlationsSeizuresSettore M-PSI/08 - Psicologia ClinicaIntellectual DisabilityIntellectual disabilitymedicineHumansKCNQ2 Potassium ChannelVoltage-gated potassium channelBenign familial neonatal seizuresGenetic Predisposition to DiseaseGenetic TestingChildGenetic testingGeneticsMutationEpilepsymedicine.diagnostic_testGenetic heterogeneitybusiness.industryMedicine (all)Benign familial neonatal seizures; Cognitive impairment; Epilepsy; Genotype-phenotype correlations; KCNQ; Mutagenesis; Voltage-gated potassium channels; Child; Female; Genetic Testing; Humans; Intellectual Disability; KCNQ2 Potassium Channel; KCNQ3 Potassium Channel; Male; Mutation; Pedigree; Seizures; Genetic Predisposition to Disease; Neurology (clinical); Neurology; Medicine (all)Benign familial neonatal seizuremedicine.diseaseSeizureSettore MED/39 - Neuropsichiatria InfantilePedigreeCognitive impairmentNeurologyMutagenesisMutationFemaleNeurology (clinical)businessVoltage-gated potassium channelsHuman
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Mutations in the Neuronal Vesicular SNARE VAMP2 Affect Synaptic Membrane Fusion and Impair Human Neurodevelopment

2019

VAMP2 encodes the vesicular SNARE protein VAMP2 (also called synaptobrevin-2). Together with its partners syntaxin-1A and synaptosomal-associated protein 25 (SNAP25), VAMP2 mediates fusion of synaptic vesicles to release neurotransmitters. VAMP2 is essential for vesicular exocytosis and activity-dependent neurotransmitter release. Here, we report five heterozygous de novo mutations in VAMP2 in unrelated individuals presenting with a neurodevelopmental disorder characterized by axial hypotonia (which had been present since birth), intellectual disability, and autistic features. In total, we identified two single-amino-acid deletions and three non-synonymous variants affecting conserved resid…

MaleHeterozygoteAdolescentVesicle-Associated Membrane Protein 2neuronal exocytosisynaptopathyautismsynaptobrevinMembrane FusionExocytosisR-SNARE ProteinsProtein DomainsReportIntellectual DisabilityGeneticsHumansAutistic DisorderChildGenetics (clinical)NeuronsNeurotransmitter Agentsneurodevelopmental disordersvesicle fusionBrainautism; epilepsy; movement disorders; neurodevelopmental disorders; neuronal exocytosis; SNARE; synaptobrevin; synaptopathy; VAMP2; vesicle fusionneuronal exocytosisLipidsMagnetic Resonance Imagingneurodevelopmental disorderautism epilepsy movement disorders neurodevelopmental disorders neuronal exocytosis SNARE synaptobrevin synaptopathy VAMP2 vesicle fusion Genetics Genetics (clinical)Phenotypeautism; epilepsy; movement disorders; neurodevelopmental disorders; neuronal exocytosis; SNARE; synaptobrevin; synaptopathy; VAMP2; vesicle fusion; Genetics; Genetics (clinical)VAMP2SNAREChild PreschoolMutationSynapsesMuscle Hypotoniaepilepsymovement disordersFemalesense organsmovement disorder
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TBC1D24-TLDc-related epilepsy exercise-induced dystonia: rescue by antioxidants in a disease model

2019

Genetic mutations in TBC1D24 have been associated with multiple phenotypes, with epilepsy being the main clinical manifestation. The TBC1D24 protein consists of the unique association of a Tre2/Bub2/Cdc16 (TBC) domain and a TBC/lysin motif domain/catalytic (TLDc) domain. More than 50 missense and loss-of-function mutations have been described and are spread over the entire protein. Through whole genome/exome sequencing we identified compound heterozygous mutations, R360H and G501R, within the TLDc domain, in an index family with a Rolandic epilepsy exercise-induced dystonia phenotype (http://omim.org/entry/608105). A 20-year long clinical follow-up revealed that epilepsy was self-limited in…

MaleModels Molecular0301 basic medicineProtein ConformationAmino Acid Motifsalpha-TocopherolMutantCrystallography X-RayPHENOTYPECompound heterozygosityAntioxidantsAnimals Genetically ModifiedEpilepsy0302 clinical medicineCatalytic DomainDrosophila ProteinsMissense mutationoxidative stressChildTLDC DOMAINVITAMIN-EExome sequencingSequence DeletionNeuronsDystoniaGeneticsexercise-induced dystoniaTBC1D24GTPase-Activating ProteinsANNOTATIONSEpilepsy RolandicPhenotypeRecombinant ProteinsPedigree3. Good healthRolandic epilepsyDystoniaDrosophila melanogasterChild PreschoolFemaleSettore MED/26 - NeurologiaSynaptic VesiclesDrosophila melanogasterPROTEIN STABILITYLife Sciences & BiomedicineLocomotionAdolescentPhysical ExertionMutation MissenseClinical NeurologyPREDICTIONSBiology03 medical and health sciencesmedicineAnimalsHumansAmino Acid SequenceCOMPARTMENToxidative streScience & TechnologySequence Homology Amino AcidMUTATIONSNeurosciencesInfantBiological TransportDEGRADATIONmedicine.diseasebiology.organism_classificationAcetylcysteineDisease Models AnimalOxidative Stress030104 developmental biologyrab GTP-Binding ProteinsSEIZURESNeurosciences & NeurologyNeurology (clinical)Reactive Oxygen SpeciesSequence Alignment030217 neurology & neurosurgery
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Clinical Significance of Rare Copy Number Variations in Epilepsy A Case-Control Survey Using Microarray-Based Comparative Genomic Hybridization

2012

Objective To perform an extensive search for genomic rearrangements by microarray-based comparative genomic hybridization in patients with epilepsy. Design Prospective cohort study. Setting Epilepsy centers in Italy. Patients Two hundred seventy-nine patients with unexplained epilepsy, 265 individuals with nonsyndromic mental retardation but no epilepsy, and 246 healthy control subjects were screened by microarray-based comparative genomic hybridization. Main Outcomes Measures Identification of copy number variations (CNVs) and gene enrichment. Results Rare CNVs occurred in 26 patients (9.3%) and 16 healthy control subjects (6.5%) (P = .26). The CNVs identified in patients were larger (P = …

MaleOncologyendocrine system diseasesMicroarrayGene DosagePreschool Cohort Studies Computational Biology Diagnostic and Statistical Manual of Mental Disorders EpilepsyBioinformaticsPolymerase Chain ReactionFluorescence Intellectual DisabilityCohort StudiesEpilepsySettore MED/38 - Pediatria Generale E SpecialisticaGene DuplicationProspective StudiesCopy-number variationAge of OnsetChildProspective cohort studyIn Situ Hybridization Fluorescenceepidemiology/genetics Nucleic Acid Hybridization Polymerase Chain Reaction Prospective Studies Young AdultGene RearrangementNucleic Acid HybridizationMiddle AgedControl subjectsMagnetic Resonance ImagingDiagnostic and Statistical Manual of Mental Disordersgenetics Female Gene Deletion Gene Dosage Gene Duplication Gene Rearrangement Genome-Wide Association Study Humans In Situ HybridizationItalyRare Copy Number Variations EpilepsyChild PreschoolFemaleepidemiology/genetics ItalyAdultmedicine.medical_specialtyAdolescentBiologyYoung AdultAdolescent Adult Age of Onset Aged Child ChildArts and Humanities (miscellaneous)Intellectual DisabilityInternal medicinemental disordersmedicineHumansIn patientClinical significanceepidemiology Magnetic Resonance Imaging Male Microarray Analysis Middle Aged Nervous System DiseaseAgedEpilepsyComputational BiologyMicroarray Analysismedicine.diseaseSettore MED/03 - Genetica MedicaNeurology (clinical)Nervous System DiseasesGene DeletionGenome-Wide Association StudyComparative genomic hybridization
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Modulatory effects of nitric oxide-active drugs on the anticonvulsant activity of lamotrigine in an experimental model of partial complex epilepsy in…

2007

Abstract Background The effects induced by administering the anticonvulsant lamotrigine, the preferential inhibitor of neuronal nitric oxide synthase 7-nitroindazole and the precursor of NO synthesis L-arginine, alone or in combination, on an experimental model of partial complex seizures (maximal dentate gyrus activation) were studied in urethane anaesthetized rats. The epileptic activity of the dentate gyrus was obtained through the repetitive stimulation of the angular bundle and maximal dentate gyrus activation latency, duration and post-stimulus afterdischarge duration were evaluated. Results Either Lamotrigine (10 mg kg-1) or 7-nitroindazole (75 mg kg-1) i.p. administration had an ant…

MalePARTIAL COMPLEX EPILEPSYIndazolesArgininemedicine.medical_treatmentLamotriginePharmacologyArginineLamotrigineNitric OxideSettore BIO/09 - Fisiologialcsh:RC321-571Nitric oxideCellular and Molecular Neurosciencechemistry.chemical_compoundEpilepsy Complex PartialmedicineAnimalsDrug InteractionsEnzyme InhibitorsRats Wistarlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryNitric oxide Lamotrigine epilepsy controlbiologyTriazinesExperimental modelGeneral NeuroscienceDentate gyruslcsh:QP351-495BrainElectric StimulationRatsNitric oxide synthaseDisease Models Animallcsh:Neurophysiology and neuropsychologyAnticonvulsantnervous systemchemistryDentate Gyrusbiology.proteinAnticonvulsantsNitric Oxide SynthaseResearch Articlemedicine.drugBMC Neuroscience
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Rufinamide in children and adults with Lennox-Gastaut syndrome: first Italian multicenter experience

2010

This is the first multicenter Italian experience with rufinamide as an adjunctive drug in children, adolescents and adults with Lennox-Gastaut syndrome. The patients were enrolled in a prospective, add-on, open-label treatment study from 11 Italian centers for children and adolescent epilepsy care. Forty-three patients (26 males, 17 females), aged between 4 and 34 years (mean 15.9 ± 7.3, median 15.0), were treated with rufinamide for a mean period of 12.3 months (range 3-21 months). Twenty patients were diagnosed as cryptogenic and 23 as symptomatic. Rufinamide was added to the baseline therapy at the starting dose of 10mg/kg body weight, evenly divided in two daily doses and then increased…

MalePediatricsLennox-Gastaut syndromeAtypical absence seizuresRufinamideLennox–Gastaut syndrome; Rufinamide; Orphan drug; Pediatrics; Epilepsy; Drop attacksInfantilePediatricsSpasmsEpilepsyRufinamideDrop attacks; Epilepsy; Lennox-Gastaut syndrome; Orphan drug; Pediatrics; Rufinamide; Adolescent; Adult; Anticonvulsants; Child; Child Preschool; Drug Therapy Combination; Female; Humans; Intellectual Disability; Italy; Lennox Gastaut Syndrome; Male; Spasms Infantile; Treatment Outcome; Triazoles; Valproic Acid; Young Adult; Neurology (clinical); NeurologyChildPediatricValproic AcidDrop attacksGeneral MedicineSettore MED/39 - Neuropsichiatria InfantileTreatment OutcomeItalyNeurologyAnesthesiaChild PreschoolCombinationVomitingAnticonvulsantsDrug Therapy CombinationFemalemedicine.symptomSpasms Infantilemedicine.drugAdultmedicine.medical_specialtyAdolescentClinical NeurologyIrritabilityYoung AdultDrug TherapyIntellectual DisabilitymedicineHumanspediatrics epilepsyPreschoolAdverse effectLennox–Gastaut syndrome; rufinamide; orphan drug; pediatrics epilepsy; drop attacks; refractory epilepsy.EpilepsyOrphan drugbusiness.industryLennox Gastaut SyndromeValproic Acidrefractory epilepsyTriazolesmedicine.diseaseNeurology (clinical)businessLennox–Gastaut syndromeLennox–Gastaut syndrome
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Benign myoclonic epilepsy in infancy: neuropsychological and behavioural outcome

2003

Benign myoclonic epilepsy in infancy (BMEI) is a rare syndrome of idiopathic generalized epilepsies with onset below 3 years of age. It has been reported that BMEI is associated with a good prognosis, however, recently some studies suggest less favourable neuropsychological outcome. We report a long-term follow-up of seven patients with BMEI. Seizure outcome and neuropsychological, cognitive, and behavioural evolution were discussed for each of them. At the end of follow-up, 86% of children showed neuropsychological and intellectual disorders: two children had mental retardation, three patients achieved a borderline IQ and one normal but low IQ. All but one displayed neuropsychological disa…

MalePediatricsmedicine.medical_specialtyDevelopmental DisabilitiesEpilepsies MyoclonicNeuropsychological TestsBorderline intellectual functioningCognitionDevelopmental NeurosciencemedicineRare syndromeHumansAge of OnsetPsychiatryChildNeuropsychological outcomeBenign myoclonic epilepsy in infancyNeuropsychologyLanguage impairmentBehavioural outcomeCognitionElectroencephalographyGeneral Medicinemedicine.diseaseFine motor skillOnset ageChild PreschoolPediatrics Perinatology and Child HealthMyoclonic epilepsyFemaleNeurology (clinical)Good prognosisPsychology
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