Search results for "ENCEPHALOPATHY"

showing 10 items of 186 documents

Variable impact on mortality of AIDS-defining events diagnosed during combination antiretroviral therapy : not all AIDS-defining conditions are creat…

2009

Contains fulltext : 80963.pdf (Publisher’s version ) (Open Access) BACKGROUND: The extent to which mortality differs following individual acquired immunodeficiency syndrome (AIDS)-defining events (ADEs) has not been assessed among patients initiating combination antiretroviral therapy. METHODS: We analyzed data from 31,620 patients with no prior ADEs who started combination antiretroviral therapy. Cox proportional hazards models were used to estimate mortality hazard ratios for each ADE that occurred in >50 patients, after stratification by cohort and adjustment for sex, HIV transmission group, number of antiretroviral drugs initiated, regimen, age, date of starting combination antiretrovir…

MaleInfectious diseases and international health [NCEBP 13]Lymphoma030312 virologyEsophageal candidiasisCohort Studies0302 clinical medicineInterquartile range030212 general & internal medicineAIDS-RelatedLymphoma AIDS-Related0303 health sciencesMortality rateProgressive multifocal leukoencephalopathyHazard ratioPrognosis3. Good healthPathogenesis and modulation of inflammation [N4i 1]Infectious DiseasesCombinationDrug Therapy CombinationFemaleInfection and autoimmunity [NCMLS 1]HumanMicrobiology (medical)Adultmedicine.medical_specialtyPrognosiAnti-HIV Agentsantiretroviral therapyInfectious DiseaseArticleAIDS-Related Opportunistic Infection03 medical and health sciencesAcquired immunodeficiency syndrome (AIDS)Drug TherapyInternal medicinemedicineHumansAIDS-defining eventProportional Hazards ModelsAIDS-Related Opportunistic Infections/diagnosis/ mortality; Acquired Immunodeficiency Syndrome/complications/diagnosis/drug; therapy/ mortality; Adult; Anti-HIV Agents/ therapeutic use; Cohort Studies; Drug Therapy; Combination; Female; Humans; Lymphoma; AIDS-Related/diagnosis/mortality; Male; Prognosis; Proportional Hazards ModelsAcquired Immunodeficiency SyndromeAIDS-Related Opportunistic Infectionsbusiness.industryProportional hazards modelPoverty-related infectious diseases [N4i 3]Anti-HIV Agentmedicine.diseasemortalityConfidence intervalImmunologyProportional Hazards ModelCohort Studiebusiness
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Giant axonal neuropathy and leukodystrophy

1991

Abstract An 11-year-old Persian boy, born to consanguineous parents, manifested a progressive gait abnormality beginning at 5 years of age. A severe cerebellar disorder developed with associated dysfunction of the peripheral nervous system, but no sign of mental impairment. The sensory and motor nerve conduction velocities were greatly reduced, especially in the lower extremities. Cerebrospinal fluid protein was normal. Computed tomography and magnetic resonance imaging revealed leukoencephalopathy, especially in the cerebellum, but also in periventricular areas. The diagnosis of giant axonal neuropathy was established by biopsy of the sural nerve. The few previous histologic examinations h…

MaleIntermediate FilamentsMotor nerveGenes RecessiveSural nerveCerebral VentriclesLeukoencephalopathyConsanguinityDevelopmental NeuroscienceCerebellummedicineHumansCerebellar disorderGliosisPeripheral NervesChildMyelin SheathSpinocerebellar DegenerationsGiant axonal neuropathybusiness.industryLeukodystrophyAnatomymedicine.diseaseMagnetic Resonance ImagingAxonsMicroscopy Electronmedicine.anatomical_structurenervous systemNeurologyPeripheral nervous systemPediatrics Perinatology and Child HealthGait abnormalityNeurology (clinical)medicine.symptomHereditary Sensory and Motor NeuropathybusinessPediatric Neurology
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A de novo heterozygous mutation in KCNC2 gene implicated in severe developmental and epileptic encephalopathy

2020

Abstract An increasing number of developmental and epileptic encephalopathies have been correlated with variants of ion channel genes, and in particular of potassium channels genes, such as KCNA1, KCNA2, KCNB1, KCNQ2, KCTD7 and KCNT1. Here we report a child with an early severe developmental and epileptic encephalopathy, spastic tetraplegia, opisthotonos attacks. The whole exome sequencing showed the de novo heterozygous variant c.1411G > C (p.Val471Leu) in the KCNC2 gene. Although this is, to our knowledge, the first case of encephalopathy associated with a KCNC2 gene variant, and further confirmatory studies are needed, previous preclinical and clinical evidence seems to suggest that KCNC…

MaleKCNC2 geneKCTD7EncephalopathyBiologyEpilepsyGeneticsmedicineHumansExomeEEGChildGeneExomeSpastic tetraplegiaGenetics (clinical)Exome sequencingGeneticsEpilepsyKv3.2ElectroencephalographyDevelopmental and epileptic encephalopathieGeneral Medicinemedicine.diseaseKCNC2Shaw Potassium ChannelsNGSMutationEuropean Journal of Medical Genetics
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Liver failure caused by light chain deposition disease associated with multiple myeloma.

2012

Acute liver failure is an unusual complication in multiple myeloma. Here, we report a case of multiple myeloma with light chain deposition disease (LCDD) that presented with progressive jaundice due to intrahepatic cholestasis. Diagnosis was made after liver biopsy that showed deposition of kappa light chains occupying perisinusoidal spaces. The patient developed encephalopathy and liver failure and died despite prompt initiation of dexamethasone therapy. The current prognosis of multiple myeloma patients with liver failure due to LCDD is dismal. New therapeutic strategies might improve this condition.

MalePathologymedicine.medical_specialtyEncephalopathyParaproteinemiasCholestasis IntrahepaticImmunoglobulin light chainLight chain deposition diseaseImmunoglobulin kappa-ChainsFatal OutcomeCholestasisInternal MedicineMedicineHumansMultiple myelomaAgedAged 80 and overmedicine.diagnostic_testbusiness.industryGeneral MedicineJaundiceLiver Failure Acutemedicine.diseaseLiver biopsyHepatic Encephalopathymedicine.symptomComplicationbusinessMultiple MyelomaInternal medicine (Tokyo, Japan)
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Progressive necrotic encephalopathy following tacrolimus therapy for liver transplantation.

2009

Previously described neurologic damage induced by immunosuppressive treatments includes transient or reversible central nervous system involvement. We describe a 57-year-old man who underwent liver transplantation and was started on immunosuppressive therapy with tacrolimus (FK506). Six months later, he started complaining of a progressive motor and sensory impairment of the left side, together with cognitive impairment. Brain MRI showed an enlarging lesion of the white matter with peripheral contrast enhancement. PET study indicated severe hypometabolism in the right hemisphere and spectroscopic MRI showed a peak of choline and relative reduction of other metabolites. Findings of CSF exami…

MalePathologymedicine.medical_specialtyNeurologyMagnetic Resonance Spectroscopymedicine.medical_treatmentEncephalopathyDermatologyBrain damageLiver transplantationTacrolimusWhite PeopleWhite matterLesionNecrosisProgressive necrotic encephalopathy liver transplantation.MedicineHumansHepatitis ChronicBrain Diseasesbusiness.industrySettore MED/27 - NeurochirurgiaBrainGeneral MedicineMiddle Agedmedicine.diseaseMagnetic Resonance ImagingTacrolimusLiver TransplantationPsychiatry and Mental healthmedicine.anatomical_structurePositron-Emission TomographyDisease ProgressionSettore MED/26 - NeurologiaNeurology (clinical)Neurosurgerymedicine.symptombusinessImmunosuppressive AgentsFollow-Up StudiesNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Further delineation of eye manifestations in homozygous 15q13.3 microdeletions including TRPM1: a differential diagnosis of ceroid lipofuscinosis.

2014

The 15q13.3 heterozygous microdeletion is a fairly common microdeletion syndrome with marked clinical variability and incomplete penetrance. The average size of the deletion, which comprises six genes including CHRNA7, is 1.5 Mb. CHRNA7 has been identified as the gene responsible for the neurological phenotype in this microdeletion syndrome. Only seven patients with a homozygous microdeletion that includes at least CHRNA7, and is inherited from both parents have been described in the literature. The aim of this study was to further describe the distinctive eye manifestations from the analysis in the three French patients diagnosed with the classical 1.5 Mb homozygous microdeletion. Patients…

MalePathologymedicine.medical_specialtygenetic structuresalpha7 Nicotinic Acetylcholine ReceptorEncephalopathyTRPM Cation ChannelsChromosome DisordersBiologyBlindnessEyePupilNeuronal Ceroid-LipofuscinosesNight BlindnessSeizuresIntellectual DisabilityRetinal DystrophiesGeneticsmedicineElectroretinographyMyopiaHumansEye AbnormalitiesChildGenetics (clinical)TRPM1Genetic Association StudiesCongenital stationary night blindnessGeneticsChromosomes Human Pair 15DystrophyEye Diseases HereditaryGenetic Diseases X-LinkedOptic NerveMicrodeletion syndromemedicine.diseasePenetranceChild PreschoolFemalesense organsDifferential diagnosisChromosome DeletionAmerican journal of medical genetics. Part A
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Mathematical models for the diffusion magnetic resonance signal abnormality in patients with prion diseases

2014

In clinical practice signal hyperintensity in the cortex and/or in the striatum on magnetic resonance (MR) diffusion-weighted images (DWIs) is a marker of sporadic Creutzfeldt–Jakob Disease (sCJD). MR diagnostic accuracy is greater than 90%, but the biophysical mechanisms underpinning the signal abnormality are unknown. The aim of this prospective study is to combine an advanced DWI protocol with new mathematical models of the microstructural changes occurring in prion disease patients to investigate the cause of MR signal alterations. This underpins the later development of more sensitive and specific image-based biomarkers. DWI data with a wide a range of echo times and diffusion weightin…

MalePathologysCJD sporadic Creutzfeldt–Jakob diseaseROI region of interestPrion diseasePrPSc prion protein scrapieElectroencephalographyFOV field of viewlcsh:RC346-429Prion DiseasesADC apparent diffusion coefficientTI inversion timeRPE rapidly progressive encephalopathyAged 80 and overTE echo timeBrain Mappingmedicine.diagnostic_testBrainRegular ArticleMiddle AgedBIC Bayesian information criterionTR repetition timemedicine.anatomical_structureNeurologylcsh:R858-859.7FemaleMPRAGE magnetization-prepared rapid acquisition gradient-echoAbnormalitySS-SE single shot spin-echoAdultmedicine.medical_specialtyCognitive NeuroscienceCreutzfeldt–Jakob diseaseCNR contrast to noise ratioEPI echo-planar imagingNeuropathologyPrPC prion protein cellularGrey matterSpongiform degenerationlcsh:Computer applications to medicine. Medical informaticsEEG electroencephalogramDiffusion MRINeuroimagingImage Interpretation Computer-AssistedmedicineHumansRadiology Nuclear Medicine and imaginglcsh:Neurology. Diseases of the nervous systemAgedCJD Creutzfeldt–Jakob diseaseGSS Gerstmann–Sträussler–Scheinker syndromebusiness.industryDWI diffusion weighted imagingDiffusion MRI; Biophysical models; Creutzfeldt-Jakob disease; Prion disease; Spongiform degenerationMagnetic resonance imagingModels TheoreticalHyperintensityCreutzfeldt-Jakob diseaseDiffusion Magnetic Resonance ImagingNeurology (clinical)businessBiophysical modelsDiffusion MRINeuroImage: Clinical
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Childhood-onset CADASIL: clinical, imaging, and neurocognitive features.

2010

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is a progressive neurodegenerative condition, associated with mutations in the notch3 gene. Symptoms include migraine with aura, mood disorders, progressive cognitive decline, subcortical ischemic strokes, dementia, and premature death. We present an 8-year-old boy with attention and behavioral difficulties, as well as a family history of the condition. Magnetic resonance imaging revealed subcortical foci of increased T2 hyperintensity, and sequencing of the notch3 gene revealed 1 previously reported mutation and 1 novel sequence variant. Neurocognitive assessment revealed deficits in sever…

MalePediatricsmedicine.medical_specialtyCADASILNeuropsychological TestsLeukoencephalopathymedicineHumansClinical imagingAge of OnsetCADASILChildReceptor Notch3medicine.diagnostic_testReceptors NotchBrainGenetic VariationMagnetic resonance imagingSequence Analysis DNAmedicine.diseaseMagnetic Resonance ImagingPediatrics Perinatology and Child HealthMutationNeurology (clinical)Age of onsetPsychologyCognition DisordersNeuroscienceNeurocognitiveJournal of child neurology
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NEXMIF encephalopathy: an X-linked disorder with male and female phenotypic patterns

2021

Contains fulltext : 231688.pdf (Publisher’s version ) (Closed access) PURPOSE: Pathogenic variants in the X-linked gene NEXMIF (previously KIAA2022) are associated with intellectual disability (ID), autism spectrum disorder, and epilepsy. We aimed to delineate the female and male phenotypic spectrum of NEXMIF encephalopathy. METHODS: Through an international collaboration, we analyzed the phenotypes and genotypes of 87 patients with NEXMIF encephalopathy. RESULTS: Sixty-three females and 24 males (46 new patients) with NEXMIF encephalopathy were studied, with 30 novel variants. Phenotypic features included developmental delay/ID in 86/87 (99%), seizures in 71/86 (83%) and multiple comorbidi…

MalePediatricsmedicine.medical_specialtyINTELLECTUAL DISABILITYAutism Spectrum DisorderEncephalopathyNerve Tissue ProteinsILAE COMMISSIONMOSAICISMEpilepsy/geneticsCLASSIFICATIONEpilepsyBrain Diseases/geneticsGenes X-LinkedSeizuresIntellectual disabilityGenotypemedicineHumansdevelopmental and epileptic encephalopathyMYOCLONIAAtonic seizureGenetics (clinical)Brain Diseasesddc:618Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]KIAA2022business.industryMUTATIONSmedicine.diseasePhenotypeAutism Spectrum Disorder/geneticsGenes X-Linked/geneticsAutism spectrum disorderintellectual disabilityNEXMIFAutismepilepsyFemaleINACTIVATIONHuman medicineSeizures/geneticsbusinessPOSITION PAPERGenetics in Medicine
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Proteomic signature of the Dravet syndrome in the genetic Scn1a-A1783V mouse model.

2021

Abstract Background Dravet syndrome is a rare, severe pediatric epileptic encephalopathy associated with intellectual and motor disabilities. Proteomic profiling in a mouse model of Dravet syndrome can provide information about the molecular consequences of the genetic deficiency and about pathophysiological mechanisms developing during the disease course. Methods A knock-in mouse model of Dravet syndrome with Scn1a haploinsufficiency was used for whole proteome, seizure, and behavioral analysis. Hippocampal tissue was dissected from two- (prior to epilepsy manifestation) and four- (following epilepsy manifestation) week-old male mice and analyzed using LC-MS/MS with label-free quantificati…

MaleProteomics0301 basic medicineProteomeHippocampusEpilepsies MyoclonicHaploinsufficiencyScn1aHippocampusSynaptic TransmissionElevated Plus Maze TestEpilepsyMice0302 clinical medicineTandem Mass Spectrometry11-beta-Hydroxysteroid Dehydrogenase Type 1Genetic epilepsyCarbon-Nitrogen LigasesGene Knock-In TechniquesGliosisNeuronal PlasticityBehavior AnimalEpileptic encephalopathyImmunohistochemistryAstrogliosisNeurologyProteomeDisease ProgressionFemaleHaploinsufficiencySignal TransductionRC321-571Dopamine and cAMP-Regulated Phosphoprotein 32Neovascularization PhysiologicNeurosciences. Biological psychiatry. NeuropsychiatryBiologyNitric Oxide03 medical and health sciencesDravet syndromemedicineAnimalsHyperthermiaSocial Behaviorras-GRF1Proteomic Profilingmedicine.diseaseVascular Endothelial Growth Factor Receptor-2NAV1.1 Voltage-Gated Sodium ChannelDisease Models Animal030104 developmental biologyRotarod Performance TestSynaptic plasticityEpileptic Encephalopathy ; Genetic Epilepsy ; Mice ; Proteome ; Scn1aCalcium-Calmodulin-Dependent Protein Kinase Type 2Open Field TestNeuroscience030217 neurology & neurosurgeryChromatography Liquid
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