Search results for "Demyelinating Diseases"

showing 10 items of 28 documents

Intrathecal B-cell accumulation and axonal damage distinguish MRI-based benign from aggressive onset in MS.

2019

ObjectiveWe explored the incremental value of adding multiple disease activity biomarkers in CSF and serum for distinguishing MRI-based benign from aggressive MS in early disease course.MethodsNinety-three patients diagnosed with clinically isolated syndrome (CIS) or early MS were divided into 3 nonoverlapping severity groups defined by objective MRI criteria. Ninety-seven patients with noninflammatory neurologic disorders and 48 patients with other inflammatory neurologic diseases served as controls. Leukocyte subsets in the CSF were analyzed by flow cytometry. CSF neurofilament light chain (NfL) and chitinase-3-like protein 1 (CHI3L1) levels were measured by ELISA. Serum NfL levels were e…

0301 basic medicineAdultMalePathologymedicine.medical_specialtyAdolescent41medicine.medical_treatmentCHI3L1ArticleFlow cytometryCohort Studies03 medical and health sciencesYoung Adult0302 clinical medicineText miningMultiple Sclerosis Relapsing-RemittingNeurofilament ProteinsMedicineHumansB cellAgedCD20Aged 80 and overB-LymphocytesClinically isolated syndromebiologymedicine.diagnostic_testbusiness.industryMultiple sclerosisImmunotherapyMiddle Agedmedicine.diseaseMagnetic Resonance ImagingAxons030104 developmental biologymedicine.anatomical_structureCross-Sectional StudiesNeurologybiology.proteinDisease ProgressionFemaleNeurology (clinical)business030217 neurology & neurosurgeryDemyelinating DiseasesNeurology(R) neuroimmunologyneuroinflammation
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Flow cytometric analysis of T cell/monocyte ratio in clinically isolated syndrome identifies patients at risk of rapid disease progression.

2015

Background: Multiple sclerosis is a chronic inflammatory central nervous system disease diagnosed by clinical presentation and characteristic magnetic resonance imaging findings. The role of cerebrospinal fluid (CSF) analysis has been emphasized in particular in the context of differential diagnosis in patients with a first episode suggestive of multiple sclerosis. Objective: We investigated here the potential additional value of analysis of CSF cellularity by fluorescence activated cell sorting (FACS) in the setting of a routine diagnostic work-up in our inpatient clinic. Methods: CSF cells from back-up samples from patients with suspected chronic inflammatory central nervous system disord…

0301 basic medicineCD4-Positive T-LymphocytesMalePathologyTime FactorsLipopolysaccharide ReceptorsCell SeparationCD8-Positive T-LymphocytesMonocytes0302 clinical medicineCerebrospinal fluidCerebrospinal FluidClinically isolated syndromemedicine.diagnostic_testMiddle AgedFlow CytometryPrognosisMagnetic Resonance Imagingmedicine.anatomical_structurePhenotypeNeurologyDisease ProgressionFemaleAdultmedicine.medical_specialtyMultiple SclerosisAdolescentT cellImmunophenotypingCentral nervous system disease03 medical and health sciencesYoung AdultPredictive Value of TestsmedicineHumansB cellAgedbusiness.industryMonocyteMultiple sclerosisOligoclonal BandsMagnetic resonance imagingmedicine.diseaseAntigens CD20030104 developmental biologyImmunologyNeurology (clinical)business030217 neurology & neurosurgeryBiomarkersDemyelinating DiseasesMultiple sclerosis (Houndmills, Basingstoke, England)
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The quality of cortical network function recovery depends on localization and degree of axonal demyelination

2016

AbstractMyelin loss is a severe pathological hallmark common to a number of neurodegenerative diseases, including multiple sclerosis (MS). Demyelination in the central nervous system appears in the form of lesions affecting both white and gray matter structures. The functional consequences of demyelination on neuronal network and brain function are not well understood. Current therapeutic strategies for ameliorating the course of such diseases usually focus on promoting remyelination, but the effectiveness of these approaches strongly depends on the timing in relation to the disease state. In this study, we sought to characterize the time course of sensory and behavioral alterations induced…

0301 basic medicinePathologymedicine.medical_specialtyImmunologyCentral nervous systemSensationMedizinSensory systemBiologyAdaptive ImmunityWhite matter03 medical and health sciencesBehavioral NeuroscienceCuprizoneMice0302 clinical medicineWhite matter lesionmedicineBiological neural networkAnimalsRemyelinationGray MatterPathologicalMyelin SheathCerebral CortexBehavior AnimalEndocrine and Autonomic SystemsMultiple sclerosisLysophosphatidylcholinesThalamocortical systemRecovery of Functionmedicine.diseaseWhite MatterElectrodes ImplantedMice Inbred C57BLGray matter lesion030104 developmental biologymedicine.anatomical_structureRemyelinationDemyelinationTonotopyNerve NetNeuroscience030217 neurology & neurosurgeryDemyelinating Diseases
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Recovery from Toxic-Induced Demyelination Does Not Require the NG2 Proteoglycan

2016

NG2 cells are defined as CNS cells expressing chondroitin sulfate proteoglycan nerve/glia antigen. The vast majority of NG2-positive cells also express platelet-derived growth factor receptor alpha (PDGFRα) and are oligodendroglial progenitors (OPC). In addition a subpopulation of pericytes expresses NG2, but is positive for PDGF receptor beta (PDGFRβ) [1]. NG2-positive OPC comprise approximately 5% of the cells in the CNS where they are evenly distributed in grey and white matter [2, 3]. NG2-positive OPC form synapses with neurons [4–6] and react to brain injury with proliferation, as has been shown in several animal models as well as in human demyelinating and degenerative diseases [7–9].…

0301 basic medicineReceptor Platelet-Derived Growth Factor alphaCellular differentiationlcsh:MedicineGene ExpressionMice TransgenicOLIG203 medical and health scienceschemistry.chemical_compoundCuprizone0302 clinical medicineCell MovementExtracellularmedicineAnimalsRemyelinationAntigenslcsh:ScienceCells CulturedCell ProliferationMice KnockoutMultidisciplinarybiologyMicrogliaReverse Transcriptase Polymerase Chain ReactionStem Cellslcsh:RBrainCorrectionCell DifferentiationImmunohistochemistryCell biologyMicroscopy ElectronOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemchemistryChondroitin sulfate proteoglycanCell cultureImmunologybiology.proteinlcsh:QProteoglycans030217 neurology & neurosurgeryPlatelet-derived growth factor receptorDemyelinating DiseasesPloS one
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Increased structural white and grey matter network connectivity compensates for functional decline in early multiple sclerosis

2016

Background: The pathology of multiple sclerosis (MS) consists of demyelination and neuronal injury, which occur early in the disease; yet, remission phases indicate repair. Whether and how the central nervous system (CNS) maintains homeostasis to counteract clinical impairment is not known. Objective: We analyse the structural connectivity of white matter (WM) and grey matter (GM) networks to understand the absence of clinical decline as the disease progresses. Methods: A total of 138 relapsing–remitting MS patients (classified into six groups by disease duration) and 32 healthy controls were investigated using 3-Tesla magnetic resonance imaging (MRI). Networks were analysed using graph the…

AdultMale0301 basic medicineMultiple SclerosisModularity (biology)DiseaseGrey matterBiologyNerve Fibers MyelinatedYoung Adult03 medical and health sciences0302 clinical medicineImage Processing Computer-AssistedmedicineHumansGray MatterMultiple sclerosisMiddle Agedmedicine.diseaseNetwork dynamicsWhite MatterPathology of multiple sclerosisWhite (mutation)Diffusion Tensor Imaging030104 developmental biologymedicine.anatomical_structureNeurologyFemaleNeurology (clinical)Nerve NetAdaptationNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesMultiple Sclerosis Journal
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Diagnosis of multiple sclerosis: a multicentre study to compare revised McDonald-2010 and Filippi-2010 criteria

2018

MRI has been formally included in the diagnostic work-up of patients with a suspicion of multiple sclerosis (MS) in 2001, to demonstrate disease dissemination in space (DIS) and time (DIT) and to exclude alternative diagnoses.1 Over time, these criteria have been modified to simplify their use and to clarify specific aspects (eg, spinal cord findings).2 One aspect marginally analysed in the diagnostic work-up of patients with clinically isolated syndrome (CIS) is the role of intracortical lesions (ICLs), which are a prominent feature of MS and contribute to disability and cognitive impairment.2 A single-centre study3 showed that inclusion of ICL for the evaluation of DIS in CIS increased th…

AdultMalemedicine.medical_specialtyMultiple SclerosisTime Factorsmultiple sclerosis030218 nuclear medicine & medical imagingCohort Studies03 medical and health sciencesYoung Adult0302 clinical medicineMedicineHumansMRI; multiple sclerosisProspective StudiesMedical diagnosisProspective cohort studymriCerebral CortexClinically isolated syndromemedicine.diagnostic_testbusiness.industryMultiple sclerosisBrainMagnetic resonance imagingMiddle Agedmedicine.diseaseInstitutional review boardMagnetic Resonance ImagingSurgeryPsychiatry and Mental healthSpinal CordCohortSurgeryFemaleNeurology (clinical)Radiologybusiness030217 neurology & neurosurgeryMRICohort studyDemyelinating Diseases
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Paradoxical heat sensation in patients with multiple sclerosis

1996

Temperature thresholds were determined in 16 patients with probable or definite multiple sclerosis, in six patients with possible but unconfirmed multiple sclerosis and in 34 healthy subjects, using the method of limits and the thermal sensory limen (TSL) of the MarStock technique. A significant proportion of the patients had thresholds outside the 2.5 SD range for normal subjects, both for warmth detection threshold and TSL. In addition, 10 patients with probable or definite multiple sclerosis and one patient with possible multiple sclerosis reported a paradoxical heat sensation, i.e. a sensation of warmth elicited by a cold stimulus. This illusion was almost exclusively observed with the …

AdultMalemedicine.medical_specialtyMultiple Sclerosismedicine.medical_treatmentCentral nervous systemSensory systemAudiologyStimulus (physiology)Central nervous system diseaseSensationHumansMedicineThermal grill illusionbusiness.industryMultiple sclerosisMiddle Agedmedicine.diseasemedicine.anatomical_structureSensory ThresholdsNerve blockFemaleNeurology (clinical)businessNeuroscienceBody Temperature RegulationDemyelinating DiseasesBrain
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Evaluation of carpal tunnel syndrome in patients with polyneuropathy

1997

The difference between the median nerve latency to the second lumbrical muscle and the ulnar nerve latency to the second interosseous muscle (L-I DIFF) was tested in a prospective study to discriminate whether prolonged distal motor latency of the median nerve in patients with polyneuropathy (PNP) reflects an additional carpal tunnel syndrome (CTS). We investigated 92 patients (107 hands) with CTS, 30 patients (34 hands) with PNP, 22 patients (27 hands) with CTS and coexisting PNP (PNP+CTS), and 77 controls (87 hands). L-I DIFF was significantly prolonged in both the CTS and PNP+CTS patients as compared to PNP patients and controls. It proved to be the most specific test to differentiate be…

Adultinorganic chemicalsmedicine.medical_specialtyPhysiologyNeural ConductionNerve conduction velocityCellular and Molecular NeurosciencePhysiology (medical)medicineHumansheterocyclic compoundsIn patientNeurons AfferentProspective cohort studyUlnar nerveCarpal tunnel syndromeUlnar NerveAgedMotor Neuronsmedicine.diagnostic_testbusiness.industryMiddle Agedmedicine.diseaseCarpal Tunnel SyndromeMedian nerveMedian Nervenervous system diseasesSurgeryenzymes and coenzymes (carbohydrates)Evaluation Studies as TopicNerve conduction studyNeurology (clinical)businessPolyneuropathyDemyelinating DiseasesMuscle & Nerve
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Mesenchymal stromal-cell transplants induce oligodendrocyte progenitor migration and remyelination in a chronic demyelination model.

2013

Demyelinating disorders such as leukodystrophies and multiple sclerosis are neurodegenerative diseases characterized by the progressive loss of myelin that may lead toward a chronic demyelination of the brain’s white matter, impairing normal axonal conduction velocity and ultimately causing neurodegeneration. Current treatments modifying the pathological mechanisms are capable of ameliorating the disease; however, frequently, these therapies are not sufficient to repress the progressive demyelination into a chronic condition and permanent loss of function. To this end, we analyzed the effect that bone marrow-derived mesenchymal stromal cell (BM-MSC) grafts exert in a chronically demyelinate…

Cancer ResearchPathologymedicine.medical_specialtyNeurogenesisImmunologyNeural ConductionBiologyMesenchymal Stem Cell TransplantationModels Biologicaltrophic releaseCuprizoneMiceCellular and Molecular NeuroscienceMyelinNerve FibersCell MovementmedicineSubependymal zoneAnimalsNerve Growth FactorsStem Cell NicheProgenitor cellRemyelinationMyelin Sheathdemyelinating mouse modelMultiple sclerosisMesenchymal stem cellCell DifferentiationMesenchymal Stem CellsCell Biologymedicine.diseaseAxonsOligodendrocyteTransplantationDisease Models AnimalOligodendrogliaremyelinationmedicine.anatomical_structureChronic DiseaseDentate GyrusImmunologyoligodendrocyte activationOriginal Articlemesenchymal stromal cellsGenèticaDemyelinating Diseases
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IkappaB kinase 2 determines oligodendrocyte loss by non-cell-autonomous activation of NF-kappaB in the central nervous system

2011

The IκB kinase complex induces nuclear factor kappa B activation and has recently been recognized as a key player of autoimmunity in the central nervous system. Notably, IκB kinase/nuclear factor kappa B signalling regulates peripheral myelin formation by Schwann cells, however, its role in myelin formation in the central nervous system during health and disease is largely unknown. Surprisingly, we found that brain-specific IκB kinase 2 expression is dispensable for proper myelin assembly and repair in the central nervous system, but instead plays a fundamental role for the loss of myelin in the cuprizone model. During toxic demyelination, inhibition of nuclear factor kappa B activation by …

Central Nervous SystemBlotting WesternIκB kinaseBiologyddc:616.07Myelin assemblyMicroglia/cytology/metabolismNerve Regeneration/physiologyDemyelinating Diseases/chemically induced/metabolism03 medical and health sciencesMyelinCuprizoneMice0302 clinical medicineCentral Nervous System/cytology/metabolismmedicineAnimalsRemyelinationCHUKMyelin Sheath030304 developmental biologyAstrocytes/cytology/metabolismMyelin Sheath/metabolism0303 health sciencesReverse Transcriptase Polymerase Chain ReactionSignal Transduction/physiologyI-Kappa-B KinaseNF-kappa BI-kappa B Kinase/metabolismOriginal ArticlesOligodendrocyte3. Good healthCell biologyI-kappa B KinaseNerve RegenerationOligodendrogliamedicine.anatomical_structureOligodendroglia/metabolismAstrocytesNF-kappa B/metabolismNeurogliaNeurology (clinical)MicrogliaNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesSignal Transduction
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