Search results for "PRRT2"

showing 4 items of 4 documents

PRRT2 mutations are the major cause of benign familial infantile seizures.

2012

Mutations in PRRT2 have been described in paroxysmal kinesigenic dyskinesia (PKD) and infantile convulsions with choreoathetosis (PKD with infantile seizures), and recently also in some families with benign familial infantile seizures (BFIS) alone. We analyzed PRRT2 in 49 families and three sporadic cases with BFIS only of Italian, German, Turkish, and Japanese origin and identified the previously described mutation c.649dupC in an unstable series of nine cytosines to occur in 39 of our families and one sporadic case (77% of index cases). Furthermore, three novel mutations were found in three other families, whereas 17% of our index cases did not show PRRT2 mutations, including a large fami…

AdultMaleAdolescentChoreoathetosisNerve Tissue ProteinsBiologymedicine.disease_causeSeizures FebrileInfantile seizures03 medical and health sciencesEpilepsy0302 clinical medicineGeneticsmedicineHumansChildGenetics (clinical)030304 developmental biologyAgedGenetics0303 health sciencesMutationBenign familial infantile epilepsyEpilepsyPRRT2; EpilepsyInfantMembrane ProteinsParoxysmal dyskinesiaMiddle Agedmedicine.diseaseMajor genePedigreeChild PreschoolMutationPRRT2medicine.symptomSpasms Infantile030217 neurology & neurosurgeryPRRT2Human mutation
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Benign nocturnal alternating hemiplegia of childhood

2018

Objective: To describe the clinical spectrum of benign nocturnal alternating hemiplegia of childhood (BNAHC) including long-term follow-up data of previously published cases and to propose an underlying genetic cause of this disorder. Methods: We studied the medical data of two novel patients, reviewed the literature on BNAHC, and gathered information of the most recent follow-up of published cases regarding the course of episodes, further development, attempted drugs, ancillary investigations, and sequelae. Results: All patients, i.e. two novel cases and twelve patients identified in the literature (13 boys, 1 girl, age at onset four months to three years), experienced episodes of hemipleg…

0301 basic medicineMaleExome sequencingPediatricsmedicine.medical_specialtyHeterozygoteHemiplegiaNerve Tissue ProteinsPATIENTSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]03 medical and health sciences0302 clinical medicinePRRT2 MUTATIONSmedicineHumansIctalPAROXYSMAL KINESIGENIC DYSKINESIAFamily historyPRRT2 geneExome sequencingCryingbusiness.industryAlternating hemiplegia of childhoodInfantMembrane ProteinsGeneral MedicineParoxysmal dyskinesiamedicine.diseaseDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]GENESleep deprivation030104 developmental biologyPhenotypeTreatment OutcomeSYNAPTIC-TRANSMISSIONMigraineMIGRAINEChild PreschoolPediatrics Perinatology and Child HealthDisease ProgressionNeurology (clinical)medicine.symptombusinessINFANTILE CONVULSIONS030217 neurology & neurosurgeryGene DeletionBenign nocturnal alternating hemiplegia of childhoodEuropean Journal of Paediatric Neurology
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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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PRRT2 gene variant in a child with dysmorphic features, congenital microcephaly, and severe epileptic seizures: genotype-phenotype correlation?

2019

Abstract Background Mutations in Proline-rich Transmembrane Protein 2 (PRRT2) have been primarily associated with individuals presenting with infantile epilepsy, including benign familial infantile epilepsy, benign infantile epilepsy, and benign myoclonus of early infancy, and/or with dyskinetic paroxysms such as paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia, and exercise-induced dyskinesia. However, the clinical manifestations of this disorder vary widely. PRRT2 encodes a protein expressed in the central nervous system that is mainly localized in the pre-synaptic neurons and is involved in the modulation of synaptic neurotransmitter release. The anomalous functio…

0301 basic medicineMaleMicrocephalyMutation MissenseCase ReportNerve Tissue ProteinsBioinformaticsRisk AssessmentSeverity of Illness Index03 medical and health sciences0302 clinical medicineRare DiseasesSeizuresmedicineHumansGenetic Predisposition to DiseaseGenetic TestingExome sequencingGenetic Association StudiesBenign familial infantile epilepsyDysmorphic featuresbusiness.industryEpileptic encephalopathylcsh:RJ1-570InfantMembrane Proteinslcsh:PediatricsParoxysmal dyskinesiamedicine.diseaseBody Dysmorphic DisordersPrognosisPRRT2 mutationMagnetic Resonance Imaging030104 developmental biologyDyskinesiaMicrocephalymedicine.symptomPRRT2 mutation Dysmorphic features Microcephaly Epileptic encephalopathybusinessMyoclonus030217 neurology & neurosurgeryPRRT2Benign infantile epilepsy
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