Search results for "Muscular Diseases"

showing 10 items of 203 documents

Novel slow-skeletal myosin (MYH7) mutation in the original myosin storage myopathy kindred

2006

Abstract Myosin storage myopathy (OMIM 608358), a congenital myopathy characterised by subsarcolemmal, hyaline-like accumulations of myosin in Type I muscle fibres, was first described by Cancilla and Colleagues in 1971 [Neurology 1971;21:579–585] in two siblings as ‘familial myopathy with probable lysis of myofibrils in type I muscle fibres'. Two mutations in the slow skeletal myosin heavy chain gene ( MYH7 ) have recently been associated with the disease in other families. We have identified a novel heterozygous Leu1793Pro mutation in MYH7 in DNA from paraffin sections of one of the original siblings. This historical molecular analysis confirms the original cases had myosin storage myopat…

MaleHeterozygotemacromolecular substancesMyosinsBiologymedicine.disease_causeMuscular DiseasesMyofibrilsMyosinmedicineHumansMyopathyGeneGenetics (clinical)GeneticsMutationMyosin Heavy ChainsMyosin storage myopathyDNAExonsmedicine.diseaseMolecular biologyCongenital myopathyMuscle Fibers Slow-TwitchNeurologyChild PreschoolMutationPediatrics Perinatology and Child HealthFemaleMYH7Neurology (clinical)medicine.symptomMyofibrilCardiac MyosinsNeuromuscular Disorders
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Estimation of the prevalence and incidence of motor neuron diseases in two Spanish regions: Catalonia and Valencia

2021

AbstractAccording to the degree of upper and lower motor neuron degeneration, motor neuron diseases (MND) can be categorized into amyotrophic lateral sclerosis (ALS), primary lateral sclerosis (PLS) or progressive muscular atrophy (PMA). Although several studies have addressed the prevalence and incidence of ALS, there is a high heterogeneity in their results. Besides this, neither concept has been previously studied in PLS or PMA. Thus, the objective of this study was to estimate the prevalence and incidence of MND, (distinguishing ALS, PLS and PMA), in the Spanish regions of Catalonia and Valencia in the period 2011–2019. Two population-based Spanish cohorts were used, one from Catalonia …

MaleMalalties neuromuscularsGene ExpressionSuperoxide Dismutase-10302 clinical medicinePrevalence030212 general & internal medicineAmyotrophic lateral sclerosisEstimation theoryPrimary Lateral Sclerosismedia_commonMotor neuronsMotor Neuronseducation.field_of_studyMultidisciplinaryIncidenceIncidence (epidemiology)QRMiddle AgedProgressive muscular atrophyNeuromuscular diseasesmedicine.anatomical_structureNeurones motoresNeurologyMedicineFemaleRiskSciencemedia_common.quotation_subjectPopulationBiologyArticleMuscular Atrophy Spinal03 medical and health sciencesmedicineHumansMotor Neuron DiseaseEspanyaEstimació Teoria de l'educationAgedEstimationSelection biasMotor neurons -- DiseasesModels StatisticalC9orf72 ProteinAmyotrophic Lateral SclerosisMotor neuronmedicine.diseaseRisk factorsSpainNeurones motores -- MalaltiesMutationBiomarkers030217 neurology & neurosurgeryDemography
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Children with special health care needs attending emergency department in Italy: analysis of 3479 cases

2020

Abstract Background Although children with special health care needs (CSHCN) represent a minority of the population, they go through more hospitalizations, more admissions to the Emergency Department (ED), and receive a major number of medical prescriptions, in comparison to general pediatric population. Objectives of the study were to determine the reasons for admission to the ED in Italian CSHCN, and to describe the association between patient’s demographic data, clinical history, and health services requirements. Methods Ad hoc web site was created to collect retrospective data of 3479 visits of CSHCN to the ED in 58 Italian Hospitals. Results Seventy-two percent of patients admitted to …

MaleMetabolic diseaseHospitalization rateCongenital skeletal conditionHospitalization rateChildren with special health care needs; Congenital skeletal condition; Emergency department; Hospitalization rate; Isolated CNS malformation; Metabolic diseases; Multiple AED therapy; Neuromuscular diseases; Syndromic disorders; True isolated microcephaly0302 clinical medicineClinical historyMedicineChildeducation.field_of_studyNeuromuscular diseaseSettore MED/38Disabled ChildrenHospitalizationNeuromuscular diseasesSettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICAItalyChild PreschoolFemaleChildren with special health care needEmergency Service Hospitalmedicine.medical_specialtyAdolescentPopulationTriage CodeChildren with special health care needsSyndromic disordersChildren with special health care needs03 medical and health sciencesPharmacotherapy030225 pediatricsHumansMedical prescriptioneducationRetrospective StudiesHealth Services Needs and DemandSyndromic disorderEmergency departmentTrue isolated microcephalybusiness.industryResearchInfant NewbornInfantMetabolic diseases030208 emergency & critical care medicineEmergency departmentChildren with special health care needs Congenital skeletal conditionsEmergency department Hospitalization rate Isolated CNS malformation Metabolic diseases Multiple AED therapy Neuromuscular diseases Syndromic disorders True isolated microcephalyFamily medicineChronic DiseaseMultiple AED therapyIsolated CNS malformationbusinessFacilities and Services UtilizationItalian Journal of Pediatrics
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Actin-related myopathy without any missense mutation in the ACTA1 gene.

2004

Actinopathies are defined by missense mutations in the ACTA1 gene coding for sarcomeric actin, of which some 70 families have, so far, been identified. Often, but not always, muscle fibers carry large patches of actin filaments. Many such patients also have nemaline myopathy, qualifying actinopathies as a subgroup of nemaline myopathies. This article concerns a then newborn, now 21/2-year-old boy, the first and single child of nonconsanguineous parents, who was born floppy, requiring immediate postnatal assisted ventilation. A quadriceps muscle biopsy revealed large patches of thin myofilaments reacting at light and electron microscopic levels with antibodies against actin but only a few s…

MaleMyofilamentBiopsyDNA Mutational AnalysisMutation MissenseGene mutationBiologymedicine.disease_cause03 medical and health sciences0302 clinical medicineNemaline myopathyMuscular Diseases030225 pediatricsmedicineMissense mutationHumansPoint MutationMyopathyMuscle SkeletalActinMutationInfantmedicine.diseaseMolecular biologyCongenital myopathyActinsPediatrics Perinatology and Child HealthNeurology (clinical)medicine.symptom030217 neurology & neurosurgeryJournal of child neurology
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Childhood neuromuscular disease with rimmed vacuoles

1986

A 5-year-old boy suffered from a slowly progressive non-familial neuromuscular disease, clinically marked by generalised muscle weakness, atrophy and hypotonia, a "myopathic" EMG and mildly elevated CK values. His gastrocnemius muscle showed marked myopathy, type I fibre predominance, and numerous "rimmed" vacuoles. This boy's condition is regarded as a childhood neuromuscular disease with rimmed vacuoles.

MaleNeuromuscular diseasemedicine.diagnostic_testbusiness.industryMusclesRimmed vacuolesMuscle weaknessNeuromuscular DiseasesAnatomymedicine.diseaseHypotoniaOrganoidsGastrocnemius muscleAtrophyChild PreschoolVacuolesPediatrics Perinatology and Child HealthBiopsymedicineHumansmedicine.symptombusinessMyopathyEuropean Journal of Pediatrics
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Expanding the clinical spectrum of hereditary fibrosing poikiloderma with tendon contractures, myopathy and pulmonary fibrosis due to FAM111B mutatio…

2015

Background Hereditary Fibrosing Poikiloderma (HFP) with tendon contractures, myopathy and pulmonary fibrosis (POIKTMP [MIM 615704]) is a very recently described entity of syndromic inherited poikiloderma. Previously by using whole exome sequencing in five families, we identified the causative gene, FAM111B (NM_198947.3), the function of which is still unknown. Our objective in this study was to better define the specific features of POIKTMP through a larger series of patients. Methods Clinical and molecular data of two families and eight independent sporadic cases, including six new cases, were collected. Results Key features consist of: (i) early-onset poikiloderma, hypotrichosis and hypoh…

MalePathologyMyopathyPulmonary FibrosisMedicine/Public HealthCell Cycle ProteinsGrowthHypotrichosisContracturesTendons030207 dermatology & venereal diseases0302 clinical medicineFibrosisPulmonary fibrosisSerineGenetics(clinical)Pharmacology (medical)TrypsinExomeChildGenetics (clinical)FAM111BSkinMedicine(all)0303 health sciencesMicroscopyMuscle WeaknessMusclesSkin Diseases GeneticGeneral MedicineMiddle AgedMagnetic Resonance ImagingMuscle atrophy3. Good healthMuscular AtrophyTissuesLiverChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtyContractureAdolescentMolecular Sequence DataPoikiloderma03 medical and health sciencesPoikilodermaMuscular DiseasesmedicineHumansAdiposisAmino Acid SequenceCysteineExocrine pancreatic insufficiencyMyopathyMuscle Skeletal030304 developmental biologyMuscle contractureHypohidrosisSclerosisbusiness.industryResearchInfantProteinsmedicine.diseaseFibrosisGenesMutationSkin AbnormalitiesHypotrichosisExocrine Pancreatic Insufficiencybusiness
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Clinical spectrum time course in anti jo-1 positive antisynthetase syndrome: Results from an international retrospective multicenter study

2015

Anti Jo-1 antibodies are the main markers of the antisynthetase syndrome (ASSD), an autoimmune disease clinically characterized by the occurrence of arthritis, myositis, and interstitial lung disease (ILD). These manifestations usually co-occur (for practical purpose complete forms) in the same patient, but cases with only 1 or 2 of these findings (for practical purpose incomplete forms) have been described. In incomplete forms, the ex novo occurrence of further manifestations is possible, although with frequencies and timing not still defined. The aim of this international, multicenter, retrospective study was to characterize the clinical time course of anti Jo-1 positive ASSD in a large c…

MalePathologyNeurologyAnti Jo-1:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Epidemiologic Study Characteristics as Topic::Epidemiologic Studies::Case-Control Studies::Retrospective Studies [Medical Subject Headings]MedizinArthritisAntisynthetase syndrome:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Primates::Haplorhini::Catarrhini::Hominidae::Humans [Medical Subject Headings]AntinuclearMasculinoMyositis:Persons::Persons::Age Groups::Adult::Aged [Medical Subject Headings]Medicine (all)Interstitial lung diseaseFemeninoGeneral MedicineMiddle Aged:Diseases::Musculoskeletal Diseases::Muscular Diseases::Myositis [Medical Subject Headings]HumanosAnticuerpos antinuclearesAntibodies Antinuclear:Diseases::Musculoskeletal Diseases::Joint Diseases::Arthritis [Medical Subject Headings]Female:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Blood Proteins::Immunoproteins::Immunoglobulins::Antibodies::Autoantibodies::Antibodies Antinuclear [Medical Subject Headings]Adultmedicine.medical_specialty:Check Tags::Male [Medical Subject Headings]AntibodiesNOEstudios retrospectivosInternal medicinemedicineHumansRisk factorAdult; Aged; Antibodies Antinuclear; Arthritis; Female; Humans; Male; Middle Aged; Myositis; Retrospective Studies; Medicine (all):Persons::Persons::Age Groups::Adult [Medical Subject Headings]AgedRetrospective StudiesArtritisMyositisbusiness.industryArthritisRetrospective cohort study:Persons::Persons::Age Groups::Adult::Middle Aged [Medical Subject Headings]Anti Jo-1 Antisynthetase Syndromemedicine.diseaseDermatologyRheumatology:Check Tags::Female [Medical Subject Headings]Miositisantisynthetase syndromebusiness
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A new familial congenital myopathy in children with desmin and dystrophin reacting plaques.

1995

In 5 children with a progressive congenital myopathy representing 3 different families, unusual histological, immunohistochemical and ultrastructural changes in skeletal muscle have been found. Histologically, this myopathy was characterized by the presence of fine hyaline plaques devoid of oxidative as well as ATPase enzyme activities. At the ultrastructural level plaques were composed of helical filaments and amorphous dense material. Helical filament storage corresponded to strong desmin as well as ubiquitin immunoreactivity. In addition they were also dystrophin positive. The exclusive appearance of desmin, ubiquitin and dystrophin positive plaques in muscle specimens from 5 children em…

MalePathologymedicine.medical_specialtyAdolescentImmunocytochemistryBiologyDesminDystrophinMyofibrilsBiopsymedicineHumansMyopathyChildUbiquitinsHyalinemedicine.diagnostic_testMusclesSkeletal muscleNeuromuscular Diseasesmedicine.diseaseCongenital myopathyImmunohistochemistryMicroscopy Electronmedicine.anatomical_structureNeurologyChild Preschoolbiology.proteinDesminFemaleNeurology (clinical)medicine.symptomDystrophinJournal of the neurological sciences
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Infantile neuroaxonal dystrophy: Diagnosis by skin biopsy

1991

A child who shows progressive motor and mental deterioration after the first year of life, who has pyramidal signs, marked muscle hypotonia, but no seizures, suggests to have infantile neuroaxonal dystrophy (INAD). Beyond the age of two years, the EEG also entails characteristic findings. Diagnosis may be obtained by an ultrastructural examination of biopsied skin. The respective clinical and morphological findings are recorded and illustrated from four patients in this report.

MalePathologymedicine.medical_specialtyMuscle HypotoniaBiopsySural nerveInfantile neuroaxonal dystrophyDegenerative diseaseDevelopmental NeuroscienceBiopsyHumansMedicineSkinmedicine.diagnostic_testMental deteriorationbusiness.industryLeukodystrophyInfantPeripheral Nervous System DiseasesNeuromuscular DiseasesGeneral Medicinemedicine.diseaseChild PreschoolPediatrics Perinatology and Child HealthSkin biopsyFemaleNeurology (clinical)businessBrain and Development
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A Paucisymptomatic Neuromuscular Disease Mimicking Type III 5q-SMA With Complex Rearrangements in the SMN Gene

2013

Spinal muscular atrophy is an autosomal-recessive neuromuscular disorder, causing progressive proximal weakness and atrophy of the voluntary muscles. More than 96% of the spinal muscular atrophy patients show a homozygous absence of exons 7 and 8, or exon 7 only, in SMN1, the telomeric copy of the SMN gene. We report a young male patient with neurogenic symptoms and sparse muscle fiber atrophy, suggestive of a mild form of type III spinal muscular atrophy. He was found to be a carrier of intragenic mutations in both copies of the SMN gene, exhibiting a homozygous duplication of exons 7 and 8 in SMN1 and a homozygous deletion of exon 8 as well as a heterozygous deletion of exon 7 in SMN2. H…

MalePathologymedicine.medical_specialtyNeuromuscular diseaseBiopsyDNA Mutational AnalysisSMN1Spinal Muscular Atrophies of ChildhoodBiologyQuadriceps MuscleDiagnosis DifferentialMice03 medical and health sciencesExonAtrophyGene duplicationmedicineAnimalsHumansChildSequence Deletion030304 developmental biology0303 health sciences030305 genetics & heredityNeuromuscular DiseasesSpinal muscular atrophymedicine.diseaseSMA*ImmunohistochemistrySurvival of Motor Neuron 1 ProteinMolecular biologynervous system diseasesSmn geneSurvival of Motor Neuron 2 ProteinMuscular AtrophyPhenotypeMutationPediatrics Perinatology and Child HealthNeurology (clinical)Journal of Child Neurology
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