Search results for "Seizure"

showing 10 items of 203 documents

NBEA : developmental disease gene with early generalized epilepsy phenotypes

2018

Abstract: NBEA is a candidate gene for autism, and de novo variants have been reported in neurodevelopmental disease (NDD) cohorts. However, NBEA has not been rigorously evaluated as a disease gene, and associated phenotypes have not been delineated. We identified 24 de novo NBEA variants in patients with NDD, establishing NBEA as an NDD gene. Most patients had epilepsy with onset in the first few years of life, often characterized by generalized seizure types, including myoclonic and atonic seizures. Our data show a broader phenotypic spectrum than previously described, including a myoclonic-astatic epilepsy-like phenotype in a subset of patients. Ann Neurol 2018;84:796-803

Male0301 basic medicineCarrier Proteins/geneticsCandidate geneDiseaseNeurodevelopmental Disorders/geneticsEpilepsy0302 clinical medicineNerve Tissue Proteins/geneticsChildAtonic seizureGeneticsddc:618PhenotypePhenotypeNeurologyChild PreschoolEpilepsy GeneralizedFemaleNEUROBEACHINRare cancers Radboud Institute for Health Sciences [Radboudumc 9]AdolescentGenotypeGeneralized/geneticsNerve Tissue ProteinsBiologyPATIENTArticle03 medical and health sciencesAll institutes and research themes of the Radboud University Medical CentermedicineJournal ArticleHumansGeneralized epilepsyAUTISMPreschoolGeneSPECTRUMNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]EpilepsyDELETIONNBEA encodes neurobeachinmedicine.diseaseFRAMEWORK030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsNeurodevelopmental DisordersDE-NOVO MUTATIONSMutationAutismNeurology (clinical)Human medicineCarrier Proteins030217 neurology & neurosurgeryAnnals of neurology
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Pyridoxine dependent epilepsies: new therapeutical point of view

2017

Abstract Pyridoxine dependent epilepsies (PDEs) are rare autosomal recessive disorders with onset in neonatal period. Seizures are typically not responsive to conventional antiepileptic drugs, but they cease after parental pyridoxine administration. Atypical forms are characterized partly response to pyridoxine and a late onset of symptoms (up to the age of three years). Prevalence is variable and it has rarely been described. The genes involved in PDEs are the gene encoding for the Alpha-aminoadipic-semialdehyde dehydrogenase (ALDH7A1) and PROSC gene, which encodes a pyridoxal-5-phosphate binding protein. Mutations in the gene encoding for the pyridoxal-5′-phosphate oxidase enzyme (PNPO) a…

Male0301 basic medicineNew therapeutical approachTreatment outcomePNPOBioinformaticsSeverity of Illness IndexEpilepsy0302 clinical medicineLetter to the EditorAnticonvulsant drugsDrugs-resistant seizuresBrain Diseases MetabolicIncidencelcsh:RJ1-570PyridoxineElectroencephalographyPyridoxine dependent epilepsiesPrognosisPyridoxaminephosphate OxidaseTreatment OutcomeChild PreschoolHypoxia-Ischemia BrainConventional anticonvulsant drugAnticonvulsantsFemalemedicine.drugmedicine.medical_specialtyLate onsetRisk Assessment03 medical and health sciencesDrugs-resistant seizureSeizuresInternal medicinePyridoxine administrationmedicineHumansGenetic Predisposition to DiseaseGeneEpilepsyPyridoxaminephosphate Oxidasebusiness.industryInfantlcsh:PediatricsPyridoxinemedicine.disease030104 developmental biologyEndocrinologyConventional anticonvulsant drugsbusiness030217 neurology & neurosurgeryItalian Journal of Pediatrics
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Pathology-selective antiepileptic effects in the focal freeze-lesion rat model of malformation of cortical development

2021

Malformations of cortical development (MCD) represent a group of rare diseases with severe clinical presentation as epileptic and pharmacoresistant encephalopathies. Morphological studies in tissue from MCD patients have revealed reduced GABAergic efficacy and increased intracellular chloride concentration in neuronal cells as important pathophysiological mechanisms in MCD. Also, in various animal models, alterations of GABAergic inhibition have been postulated as a predominant factor contributing to perilesional hyperexcitability. Along with this line, the NKCC1 inhibitor bumetanide has been postulated as a potential drug for treatment of epilepsy, mediating its antiepileptic effect by red…

Male0301 basic medicinePathologymedicine.medical_specialtyZonisamideInhibitory postsynaptic potentialCryosurgeryLesion03 medical and health sciencesEpilepsyOrgan Culture Techniques0302 clinical medicineSodium Potassium Chloride Symporter InhibitorsDevelopmental NeuroscienceSeizuresmedicineAnimals4-AminopyridineRats WistarBumetanideCerebral Cortexbusiness.industryCarbamazepinemedicine.diseaseRatsMicrogyrusMalformations of Cortical Development030104 developmental biologyNeurologyGABAergicAnticonvulsantsmedicine.symptombusiness030217 neurology & neurosurgeryBumetanidemedicine.drugExperimental Neurology
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The landscape of epilepsy-related GATOR1 variants

2019

Purpose:\ud \ud To define the phenotypic and mutational spectrum of epilepsies related to DEPDC5, NPRL2 and NPRL3 genes encoding the GATOR1 complex, a negative regulator of the mTORC1 pathway.\ud \ud Methods:\ud \ud We analyzed clinical and genetic data of 73 novel probands (familial and sporadic) with epilepsy-related variants in GATOR1-encoding genes and proposed new guidelines for clinical interpretation of GATOR1 variants.\ud \ud Results:\ud \ud The GATOR1 seizure phenotype consisted mostly in focal seizures (e.g., hypermotor or frontal lobe seizures in 50%), with a mean age at onset of 4.4 years, often sleep-related and drug-resistant (54%), and associated with focal cortical dysplasia…

Male0301 basic medicineProbandDEPDC5SUDEP030105 genetics & heredityBioinformaticsLoss of Function Mutation/geneticsEpilepsyINDEL MutationLoss of Function MutationmTORC1 pathwayGenetics(clinical)ChildGenetics (clinical)Multiprotein Complexes/geneticsBrugada SyndromeDNA Copy Number VariationBrugada syndromeINDEL Mutation/geneticsGTPase-Activating ProteinsNPRL3SeizureDEPDC5PhenotypePedigree3. Good healthBrugada Syndrome/geneticsChild PreschoolFemaleHumanSignal TransductionDNA Copy Number VariationsAdolescentSeizures/complicationsMechanistic Target of Rapamycin Complex 1/geneticsDNA Copy Number Variations/geneticsMechanistic Target of Rapamycin Complex 1Tumor Suppressor Proteins/geneticsArticleFocal cortical dysplasia03 medical and health sciencesSeizuresGTPase-Activating Proteins/geneticsmedicineHumansGenetic Predisposition to DiseaseDEPDC5; Focal cortical dysplasia; Genetic focal epilepsy; mTORC1 pathway; SUDEPGenetic focal epilepsyEpilepsy/complicationsRepressor Proteins/geneticsEpilepsybusiness.industryGTPase-Activating ProteinTumor Suppressor ProteinsInfant NewbornCorrectionInfantRepressor ProteinCortical dysplasiamedicine.diseaseddc:616.8Repressor Proteins030104 developmental biologyFrontal lobe seizures[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMultiprotein ComplexesMultiprotein ComplexeSignal Transduction/geneticsHuman medicinebusiness
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The FAAH inhibitor URB597 suppresses hippocampal maximal dentate afterdischarges and restores seizure-induced impairment of short and long-term synap…

2017

Synthetic cannabinoids and phytocannabinoids have been shown to suppress seizures both in humans and experimental models of epilepsy. However, they generally have a detrimental effect on memory and memory-related processes. Here we compared the effect of the inhibition of the endocannabinoid (eCB) degradation versus synthetic CB agonist on limbic seizures induced by maximal dentate activation (MDA) acute kindling. Moreover, we investigated the dentate gyrus (DG) granule cell reactivity and synaptic plasticity in naïve and in MDA-kindled anaesthetised rats. We found that both the fatty acid amide hydrolase (FAAH) inhibitor URB597 and the synthetic cannabinoid agonist WIN55,212-2 displayed AM…

Male0301 basic medicinemedicine.medical_treatmentLong-Term Potentiationlcsh:MedicineBrain -- Diseases -- DiagnosisSynaptic TransmissionEpilepsy -- Alternative treatmentchemistry.chemical_compoundEpilepsy0302 clinical medicineFatty acid amide hydrolaselcsh:ScienceTemporal lobe epilepsyInhibitionNeuronal PlasticityMultidisciplinaryLong-term potentiationmedicine.anatomical_structureAnesthesiaBenzamidesHippocampus (Brain)medicine.medical_specialtyArticleAmidohydrolases03 medical and health sciencesSeizuresInternal medicinemedicineAnimalsAuthor CorrectionEpilepsyCannabinoidsDentate gyruslcsh:RURB597medicine.diseaseGranule cellHippocampus (Brain) -- PhysiologyRats030104 developmental biologyEndocrinologychemistryDentate GyrusSynaptic plasticitylcsh:QNeuroplasticityCarbamatesCannabinoid030217 neurology & neurosurgery
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Lamotrigine differently modulates 7-Nitroindazole and L-Arginine influence on Rat Maximal Dentate Gyrus Activation

2007

The effects induced on the maximal dentate gyrus activation (MDA) by administering the anticonvulsant lamotrigine (LTG), the selective inhibitor of neuronal nitric oxide synthase 7-nitroindazole (7-NI) and the precursor of nitric oxide (NO) synthesis L-arginine, alone or in combination, were studied in urethane anaesthetized rats. Either 7-NI or LTG alone administration reduced the number of convulsing animals following angular bundle (AB) stimulation; their combined treatment induced a further increase of the anticonvulsant effect as also demonstrated by the decrease of MDA and afterdischarge (AD) durations in the animals still responding to AB stimulation. On the contrary, the injection o…

Male7-NitroindazoleIndazolesArgininemedicine.medical_treatmentStimulationPharmacologyLamotrigineArginineLamotrigineNitric OxideSettore BIO/09 - FisiologiaNitric oxidechemistry.chemical_compoundSeizuresmedicineAnimalsEnzyme InhibitorsRats WistarBiological PsychiatryTriazinesDentate gyrusElectric StimulationRatsPsychiatry and Mental healthAnticonvulsantNeurologychemistryDentate GyrusAnticonvulsantsNeurology (clinical)Neuronal Nitric Oxide Synthasemedicine.drugLAMOTRIGINE NITRIC OXIDE EPILEPSY CONTROL
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Connexin-30 mRNA Is Up-Regulated in Astrocytes and Expressed in Apoptotic Neuronal Cells of Rat Brain Following Kainate-Induced Seizures

2002

Glial connexins (Cxs) make an extensively interconnected functional syncytium created by a network of gap junctions between astrocytes and oligodendrocytes. Among Cxs expressed in the brain, Cx30 is expressed in grey matter astrocytes, as shown at the protein level by immunoistochemistry. In the present study we aimed to perform a detailed study of the regional distribution of Cx30 mRNA in the adult and postnatal developing rat brain, analyzing its expression by in situ hybridization, and determining its cell type localization by double labeling. Recently, it has been suggested that neuronal activity may control the level of intercellular communication between astrocytes through gap junctio…

MaleAgingCell typeGene ExpressionConnexinApoptosisKainate receptorCell CommunicationIn situ hybridizationGrey matterBiologyConnexinsCellular and Molecular NeuroscienceStatus EpilepticusSeizuresExcitatory Amino Acid AgonistsmedicineAnimalsPremovement neuronal activityRNA MessengerRats WistarMolecular BiologyNeuronsSyncytiumKainic AcidGap junctionBrainCell BiologyImmunohistochemistryRatsUp-RegulationCell biologymedicine.anatomical_structureAnimals NewbornAstrocytesNeuroscienceMolecular and Cellular Neuroscience
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Cellular expression of connexins in the rat brain: neuronal localization, effects of kainate-induced seizures and expression in apoptotic neuronal ce…

2003

The identification of connexins (Cxs) expressed in neuronal cells represents a crucial step for understanding the direct communication between neurons and between neuron and glia. In the present work, using a double-labelling method combining in situ hybridization for Cx mRNAs with immunohistochemical detection for neuronal markers, we provide evidence that, among cerebral connexins (Cx26, Cx32, Cx36, Cx37, Cx40, Cx43, Cx45 and Cx47), only Cx45 and Cx36 mRNAs are localized in neuronal cells in both developing and adult rat brain. In order to establish whether connexin expression is influenced in vivo by abnormal neuronal activity, we examined the short-term effects of kainate-induced seizur…

MaleAgingTime FactorsgliaHippocampusConnexinbrain developmentKainate receptorApoptosisIn situ hybridizationBiologyConnexinsgap junctionbrain development; gap junction; gliaSeizuresTubulinmedicineExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingPremovement neuronal activityAnimalsRNA MessengerOrganic ChemicalsRats WistarIn Situ HybridizationFluorescent DyesNeuronsMessenger RNAKainic AcidReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceGap junctionBrainGene Expression Regulation DevelopmentalFluoresceinsImmunohistochemistryCell biologyRatsmedicine.anatomical_structurenervous systemAnimals NewbornPhosphopyruvate HydrataseAutoradiographysense organsNeuronNeuroscienceDensitometryThe European journal of neuroscience
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Anticonvulsant effects of carbenoxolone in genetically epilepsy prone rats (GEPRs).

2004

Carbenoxolone (CBX), the succinyl ester of glycyrrhetinic acid, is an inhibitor of gap junctional intercellular communication. Systemic administration of CBX was able to decrease the seizure severity score and to increase the latency time of seizure onset in genetically epilepsy prone rats (GEPRs). In particular, intravenous or intraperitoneal administration of carbenoxolone (5-30 mg/kg) produced a dose-dependent and significant reduction in the clonic and tonic phases of the audiogenic seizures in GEPRs. The anticonvulsant doses were not associated with an impairment of motor coordination. The bilateral microinjection of CBX (0.001-0.50 microg/0.5 microl) into the inferior colliculi, the s…

MaleAudiogenic seizuremedicine.medical_treatmentGap junctionGEPR-9sCarbenoxoloneSubstantia nigraPharmacologyConnexinConnexinsRats Sprague-DawleyCellular and Molecular NeuroscienceEpilepsyMedicineAnimalsMicroinjectionPharmacologyEpilepsybusiness.industrymedicine.diseaseMotor coordinationRatsAnticonvulsantAnesthesiaSystemic administrationCarbenoxoloneAnticonvulsantsFemalebusinessPars reticulataGEPR-3medicine.drugNeuropharmacology
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Myocardial infarction following convulsive and nonconvulsive seizures

2009

Abstract Myocardial infarction (MI) has been rarely reported in association with seizures, and only of convulsive type. Methods We describe a series of five patients observed over a 4-year period, who presented MI immediately following seizures, either convulsive or nonconvulsive. Results Patient 1 had pre-existent coronary disease (CD) and presented multiple focal nonconvulsive seizures. Patient 2 had no CD, normal coronary angiography and presented secondary generalized convulsive seizures. Patient 3 had no history of CD, normal angiography and had a first single convulsive seizure. Patient 4 had severe CD and suffered from a single convulsive event. Patient 5 had a partial and a generali…

MaleCoronary angiographyGeneralized seizures; Myocardial infarction; Partial seizures; Sudden deathClinical NeurologySudden deathConvulsive seizureEpilepsySeizuresGeneralized seizuresmedicineHumansIn patientMyocardial infarctionAgedAged 80 and overPartial seizuresmedicine.diagnostic_testbusiness.industrySudden deathGeneral MedicineMiddle Agedmedicine.diseaseMyocardial infarctionConvulsive SeizuresNeurologyAnesthesiaAngiographyEpilepsy GeneralizedFemaleNeurology (clinical)businessSeizure
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