Search results for "Ataxia"

showing 10 items of 150 documents

Deciphering exome sequencing data: Bringing mitochondrial DNA variants to light

2019

The expanding use of exome sequencing (ES) in diagnosis generates a huge amount of data, including untargeted mitochondrial DNA (mtDNA) sequences. We developed a strategy to deeply study ES data, focusing on the mtDNA genome on a large unspecific cohort to increase diagnostic yield. A targeted bioinformatics pipeline assembled mitochondrial genome from ES data to detect pathogenic mtDNA variants in parallel with the "in-house" nuclear exome pipeline. mtDNA data coming from off-target sequences (indirect sequencing) were extracted from the BAM files in 928 individuals with developmental and/or neurological anomalies. The mtDNA variants were filtered out based on database information, cohort …

AdultMaleMitochondrial DNAAtaxiaAdolescentDevelopmental Disabilities[SDV]Life Sciences [q-bio]BiologyDNA MitochondrialGenomeHaplogroupYoung Adult03 medical and health sciencesExome SequencingGeneticsmedicineHumansChildExomeGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSAged030304 developmental biologyAged 80 and overGenetics0303 health sciences030305 genetics & heredityInfant NewbornComputational BiologyGenetic VariationInfantMiddle AgedPhenotypeEarly DiagnosisChild PreschoolFemaleNervous System Diseasesmedicine.symptom
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Impaired control of an action after supplementary motor area lesion: A case study

2000

The kinematics of the action formed by reaching-grasping an object and placing it on a second target was studied in a patient who suffered from an acute vascular left brain lesion, which affected the Supplementary Motor Area proper (SMA-proper) (Matelli M, Luppino G. Thalamic input to mesial and superior area 6 in the macaque monkey. Journal of Comparative Neurology 1996;372:59-87, Matelli M, Luppino G, Fogassi L, Rizzolatti G. Thalamic input to inferior area 6 and area 4 in the macaque monkey. Journal of Comparative Neurology 1989;280:468-488), and in five healthy control subjects. The reach kinematics of the controls was affected by the positions of both the reaching-grasping and the plac…

AdultMaleMovement disordersKinematicsCognitive NeuroscienceThalamusAccelerationExperimental and Cognitive PsychologyLateralization of brain functionFunctional LateralityBehavioral NeuroscienceBasal gangliamedicineReaction TimeHumansExperimental Brain ResearchSupplementary motor areaHand StrengthMotor CortexMotor controlReaching-graspingBody movementRecovery of FunctionMiddle AgedMagnetic Resonance ImagingSupplementary motor area properFrontal LobeStrokemedicine.anatomical_structureMotor SkillsSupplementary motor area proper Action Reaching±grasping KinematicsActionArmAtaxiaFemalemedicine.symptomPsychologyNeuroscienceReaching±grasping
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Topodiagnostic implications of hemiataxia: An MRI-based brainstem mapping analysis

2007

The topodiagnostic implications of hemiataxia following lesions of the human brainstem are only incompletely understood. We performed a voxel-based statistical analysis of lesions documented on standardised MRI in 49 prospectively recruited patients with acute hemiataxia due to isolated unilateral brainstem infarction. For statistical analysis individual MRI lesions were normalised and imported in a three-dimensional voxel-based anatomical model of the human brainstem. Statistical analysis revealed hemiataxia to be associated with lesions of three distinct brainstem areas. The strongest correlation referred to ipsilateral rostral and dorsolateral medullary infarcts affecting the inferior ce…

AdultMalePathologymedicine.medical_specialtyAtaxiaInferior cerebellar peduncleCognitive NeuroscienceFunctional LateralityBrain IschemiaLesionCerebellumPonsImage Processing Computer-AssistedmedicineHumansProspective StudiesmriAgedAged 80 and overMedulla OblongataPontine BaseSpinocerebellar tractbusiness.industryataxiaDorsal spinocerebellar tractCerebral Infarctionataxia; brain mapping; brain stem; mriAnatomyMiddle AgedMagnetic Resonance ImagingPonsParesismedicine.anatomical_structureNeurologySpinocerebellar Tractsbrain mappingFemaleBrainstemmedicine.symptombrain stembusinessNeuroImage
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Pancreatic encephalopathy: a 7-year follow-up case report and review of the literature

2003

Pancreatic encephalopathy is a rare complication of acute pancreatitis. Clinical features include focal neurological signs and acute onset of dementia. This picture can fluctuate over time: cyclic progression with remission and relapses has been described. We present the case of a 43-year-old man who, after an acute episode of pancreatitis, experienced five relapses, with alternating focal signs. The patient has improved, but cognitive impairment persists after a 7-year follow-up.

AdultMalePediatricsmedicine.medical_specialtyNeurologyRemission SpontaneousEncephalopathyDermatologyNeuropsychological TestsDiagnosis DifferentialRecurrencemedicineHumansDementiaNeuroradiologyBrain Diseasesbusiness.industryElectrodiagnosisGeneral Medicinemedicine.diseaseMagnetic Resonance ImagingSurgeryParesisPsychiatry and Mental healthPancreatitisAcute DiseaseAmylasesChronic DiseaseDisease ProgressionAcute pancreatitisPancreatitisAtaxiaNeurology (clinical)NeurosurgeryCognition DisordersComplicationbusinessFollow-Up StudiesNeurological Sciences
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Chronic T cell leukemia with unusual cellular characteristics in ataxia telangiectasia

1986

Abstract A 27-year-old male patient with ataxia telangiectasia (AT) developed atypical chronic lymphocytic leukemia with increasing bone marrow infiltration in the absence of organomegaly. One-third of the leukemia cells expressed a mature suppressor/cytotoxic T cell phenotype (T3+ T4- T6- T8+ T10-), two-thirds demonstrated additional helper/inducer T cell- associated antigens (T3+ T4+ T6- T8+ T10-), and a small fraction reacted with a natural killer (NK) cell-specific monoclonal antibody (Leu 11+). The proliferative response to stimulation in vitro with lectins and various monoclonal antibodies resembled the proliferation pattern of mature thymocytes: The cells responded to phytohemaggluti…

AdultMaleReceptor complexChronic lymphocytic leukemiaT cellT-LymphocytesImmunologyBiochemistryAtaxia TelangiectasiaAntigenmedicineCytotoxic T cellHumansLeukemiabiologyAntibody-Dependent Cell CytotoxicityCell BiologyHematologymedicine.diseaseMolecular biologyKiller Cells NaturalLeukemiamedicine.anatomical_structurePhenotypeConcanavalin AKaryotypingAtaxia-telangiectasiaImmunologyChronic Diseasebiology.proteinLymphocyte Culture Test MixedCell DivisionBlood
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GAA trinucleotide repeat expansion in variant Friedreich's ataxia families.

1997

Phenotypic variants in Friedreich's ataxia include late onset, preservation of the lower limbs tendon reflexes, and slow progression. We describe clinical and electrophysiological features from three families with Friedreichlike phenotypes. Friedreich's ataxia diagnosis was confirmed by finding two allelic expansions of the GAA trinucleotide repeat at the X25 gene. In family 1 both patients had a late-onset phenotype with preservation of knee and ankle jerks, lack of cardiomyopathy, and preserved H reflex. One of them did not have electrophysiologic evidence of sensory axonal neuropathy. Patients from family 2 showed variability in the age of onset, and 2 out of 3 affected children had hype…

AdultMaleReflex Stretchcongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtySensory axonal neuropathyAtaxiaPhysiologyGenetic LinkageAction PotentialsLate onsetBiologyH-ReflexCellular and Molecular NeuroscienceDegenerative diseaseTrinucleotide RepeatsPhysiology (medical)medicineHumansNeurons AfferentChildAllelesLegGenetic VariationDNACardiomyopathy Hypertrophicmedicine.diseasePedigreePeripheral neuropathyFriedreich AtaxiaReflexDisease ProgressionFemaleNeurology (clinical)medicine.symptomAge of onsetTrinucleotide repeat expansionMusclenerve
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Glutathione levels in blood from ataxia telangiectasia patients suggest in vivo adaptive mechanisms to oxidative stress

2007

Objective: To evaluate an in vivo pro-oxidant state in patients with ataxia telangiectasia (AT). Methods: A set of oxidative stress endpoints were measured in 9 AT homozygotes, 16 AT heterozygotes (parents) and 83 controls (grouped in age ranges as for patients and parents, respectively). The following analytes were measured: (a) leukocyte 8-hydroxy-2-deoxyguanosine (8-OHdG); (b) blood glutathione (GSSG and GSH); and (c) plasma levels of glyoxal (Glx) and methylglyoxal (MGlx). Results: AT patients displayed a significant decrease in blood GSSG (p=0.012) and in MGlx plasma concentrations (P=0.012). A nonsignificant decrease in the GSSG:GSH ratio (p = 0.1) and a non-significant increase in 8-…

AdultMalemedicine.medical_specialtyAdolescentglyoxalClinical Biochemistryataxia telengiectasiamedicine.disease_causeAtaxia Telangiectasiachemistry.chemical_compoundIn vivoInternal medicinemethylglyoxalmedicineHumansataxia telangectasiaoxidative stressglutathioneChildoxidative streMethylglyoxalDeoxyguanosine8-Hydroxy-2'-deoxyguanosineHeterozygote advantageGeneral MedicineGlutathionePyruvaldehydemedicine.diseaseAdaptation Physiological8-Hydroxy-2'-deoxyguanosineEndocrinologychemistryBiochemistryChild PreschoolAtaxia-telangiectasiaFemaleataxia telangectasia; oxidative stress; glutathione; glyoxal; methylglyoxal; 8-Hydroxy-2'-deoxyguanosineOxidative stressTarget organDNA DamageClinical Biochemistry
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Central motor conduction time by magnetic stimulation of the cortex and peripheral nerve conduction follow-up studies in Friedreich's ataxia.

1998

A follow-up clinical study, peripheral motor and sensory nerve conduction velocities and central motor conduction by magnetic stimulation of the cortex were performed in 13 patients with classical Friedreich's ataxia (FA) phenotype, for a period of 9-12 years. Clinical worsening was unrelated to peripheral nerve abnormalities. The amplitude of the nerve action potentials and delayed conduction velocity remained unchanged for several years. Central motor conduction times were abnormal in all patients. Clinical conditions worsened significantly between successive examinations with significant increments in threshold and significant decrement of the amplitude of motor evoked potentials. The re…

AdultMalemedicine.medical_specialtyAtaxiaAdolescentNeural ConductionMotor nerveElectromyographyNerve conduction velocityMagneticsSural NerveTrinucleotide RepeatsInternal medicineCerebellumPhysical StimulationReaction TimeMedicineHumansNeurons AfferentPeripheral NervesChildMuscle SkeletalNeural ConductionMotor Neuronsmedicine.diagnostic_testbusiness.industryElectromyographyGeneral NeurosciencePyramidal CellsMotor CortexMiddle AgedMedian Nervemedicine.anatomical_structureFriedreich AtaxiaPeripheral nervous systemCardiologyDisease ProgressionFemaleNeurology (clinical)medicine.symptomH-reflexbusinessNeuroscienceSensory nerveFollow-Up StudiesElectroencephalography and clinical neurophysiology
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Acetyl-dl-leucine in Niemann-Pick type C

2015

Objective: To assess the effects of the modified amino acid acetyl-dl-leucine (AL) on cerebellar ataxia, eye movements, and quality of life of patients with Niemann-Pick type C (NP-C) disease. Methods: Twelve patients with NP-C disease were treated with AL 3 g/d for 1 week and then with 5 g/d for 3 weeks with a subsequent washout period of 1 month. The Scale for the Assessment and Rating of Ataxia (SARA), the Spinocerebellar Ataxia Functional Index (SCAFI), the modified Disability Rating Scale (mDRS), EuroQol 5Q-5D-5L, and the visual analog scale (VAS) were administered. Measurements took place at baseline, after 1 month of therapy, and after 1 month of washout. Results: The SARA score chan…

AdultMalemedicine.medical_specialtyAtaxiaAdolescentVisual analogue scaleYoung AdultQuality of lifeLeucineInterquartile rangemedicineHumansCerebellar ataxiabusiness.industryWashoutNiemann-Pick Disease Type CDisability Rating Scalemedicine.diseaseSurgeryAnesthesiaQuality of LifeSpinocerebellar ataxiaFemaleNeurology (clinical)medicine.symptombusinessNeurology
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Progressive cerebellar ataxia, proximal neurogenic weakness and ocular motor disturbances: hexosaminidase A deficiency with late clinical onset in fo…

1997

Tay-Sachs disease is a genetically determined neurodegenerative disorder, resulting from mutations of the hexosaminidase (Hex) A gene coding for the alpha-subunit of beta-D-N-acetyl-hexosaminidase. Clinically, there is severe encephalomyelopathy leading to death within the first few years of life. Hex A activity is usually absent in tissue and body fluids of these patients. Juvenile and adult Hex A deficiencies are less severe but rare variants with some residual Hex A activity. All these variants are most prevalent among Ashkenazi Jews. We describe a non-Jewish family in which four adult brothers and sisters had markedly reduced Hex A activities and onset of symptoms in the second decade o…

AdultMalemedicine.medical_specialtyAtaxiaCerebellar AtaxiaEye MovementsBiopsyNeural ConductionCompound heterozygosityNuclear FamilyHexosaminidase AInternal medicinemedicineHumansHexosaminidaseAge of OnsetMotor Neuron DiseaseSkinMuscle WeaknessTay-Sachs Diseaseintegumentary systemTay-Sachs diseaseSpinal muscular atrophyDNAExonsmedicine.diseaseMagnetic Resonance ImagingAshkenazi jewsbeta-N-AcetylhexosaminidasesPedigreecarbohydrates (lipids)EndocrinologyPhenotypeNeurologyOculomotor MusclesCerebellar atrophyFemaleNeurology (clinical)Age of onsetmedicine.symptomPsychologyJournal of the neurological sciences
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