2008
Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status
Waxman SG. Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status. Nature Reviews Neurology 2008, 4: 159-169. PMID: 18227822, DOI: 10.1038/ncpneuro0735.Peer-Reviewed Original Research
2007
Schwann cells and their precursors for repair of central nervous system myelin
Kocsis JD, Waxman SG. Schwann cells and their precursors for repair of central nervous system myelin. Brain 2007, 130: 1978-1980. PMID: 17626033, DOI: 10.1093/brain/awm161.Peer-Reviewed Original Research
2006
Axonal conduction and injury in multiple sclerosis: the role of sodium channels
Waxman SG. Axonal conduction and injury in multiple sclerosis: the role of sodium channels. Nature Reviews Neuroscience 2006, 7: 932-941. PMID: 17115075, DOI: 10.1038/nrn2023.Peer-Reviewed Original ResearchConceptsAxonal degenerationSodium channelsChannel isoformsDistinct pathophysiological rolesKey PointsMultiple sclerosisMultiple neurological deficitsRelapsing-remitting courseRestoration of conductionDegeneration of axonsCerebellar Purkinje neuronsVoltage-gated sodium channelsContext of demyelinationNeurological deficitsProgressive courseMultiple sclerosisAxonal conductionDisease progressionNav1.8 channelsConduction failurePathophysiological rolePurkinje neuronsCNS axonsFiring patternsLoss of coordinationAberrant expression
2005
Characterizing the Mechanisms of Progression in Multiple Sclerosis: Evidence and New Hypotheses for Future Directions
Frohman E, Filippi M, Stuve O, Waxman S, Corboy J, Phillips J, Lucchinetti C, Wilken J, Karandikar N, Hemmer B, Monson N, De Keyser J, Hartung H, Steinman L, Oksenberg J, Cree B, Hauser S, Racke M. Characterizing the Mechanisms of Progression in Multiple Sclerosis: Evidence and New Hypotheses for Future Directions. JAMA Neurology 2005, 62: 1345-1356. PMID: 16157741, DOI: 10.1001/archneur.62.9.1345.Peer-Reviewed Original ResearchMeSH KeywordsDisease ProgressionGeneticsHumansImmune SystemModels, BiologicalMultiple SclerosisNeurosciencesConceptsMultiple sclerosisProgression of MSCause of progressionMechanisms of progressionMS exacerbationDisease courseInflammatory cascadeClinical manifestationsTherapeutic strategiesDisease processTreatment interventionsEvidence-based observationsEmergence of disabilityProgressionDiseasePotential mechanismsTreatment effectsSclerosisProgressive stagesNovel research initiativesExacerbationTherapyIllnessMajor advancementsExpert perspectives
2004
Sodium channel blockers and axonal protection in neuroinflammatory disease
Waxman S. Sodium channel blockers and axonal protection in neuroinflammatory disease. Brain 2004, 128: 5-6. PMID: 15596795, DOI: 10.1093/brain/awh353.Peer-Reviewed Original Research
2002
Axotomy does not up-regulate expression of sodium channel Nav1.8 in Purkinje cells
Black J, Dusart I, Sotelo C, Waxman S. Axotomy does not up-regulate expression of sodium channel Nav1.8 in Purkinje cells. Brain Research 2002, 101: 126-131. PMID: 12007840, DOI: 10.1016/s0169-328x(02)00200-0.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsAxotomyCerebellumDisease Models, AnimalFemaleGanglia, SpinalGene Expression RegulationImmunohistochemistryMultiple SclerosisNAV1.8 Voltage-Gated Sodium ChannelNeurons, AfferentNeuropeptidesPurkinje CellsRatsRats, WistarRNA, MessengerSodium ChannelsUp-RegulationZebrafish ProteinsConceptsMultiple sclerosisPurkinje cellsSensory neuron-specific sodium channelsDorsal root ganglion neuronsAberrant expressionSodium channelsHuman multiple sclerosisPrimary sensory neuronsSodium channel Nav1.8Specific sodium channelsCerebellar Purkinje cellsGanglion neuronsSensory neuronsAxotomySurgical modelSodium channel transcriptsExperimental modelCerebellar functionChannel transcriptsNeuronsSitu hybridizationCellsExpressionNav1.8Sclerosis
2001
Transcriptional channelopathies: An emerging class of disorders
Waxman S. Transcriptional channelopathies: An emerging class of disorders. Nature Reviews Neuroscience 2001, 2: 652-659. PMID: 11533733, DOI: 10.1038/35090026.Peer-Reviewed Original ResearchConceptsNerve injuryMultiple sclerosisSodium channel geneTranscriptional channelopathiesChannel transcriptionPeripheral nerve injurySpinal sensory neuronsChannel genesExperimental nerve injuryFamily of disordersAction potential conductionAutoimmune channelopathiesDemyelinated nervesNeuropathic painDemyelinating conditionMotor abnormalitiesNeurotrophic factorClass of disordersSensory neuronsCalcium channelsChannel expressionCerebellar ataxiaPurkinje cellsPotential conductionChannelopathiesAcquired channelopathies in nerve injury and MS
Waxman S. Acquired channelopathies in nerve injury and MS. Neurology 2001, 56: 1621-1627. PMID: 11428390, DOI: 10.1212/wnl.56.12.1621.Peer-Reviewed Original ResearchMeSH KeywordsAxonsHumansMultiple SclerosisNeuralgiaParesthesiaPeripheral Nerve InjuriesPeripheral NervesPurkinje CellsSodium ChannelsConceptsNerve injurySodium channelsSensory neuron-specific sodium channelsSodium channel geneChannel genesPeripheral nerve injurySpinal sensory neuronsPathophysiology of MSSubtype-specific drugsDistinct sodium channelsVoltage-gated sodium channelsSpecific sodium channelsAxonal transectionGenetic channelopathyPrototype disorderSensory neuronsPurkinje cellsTherapeutic opportunitiesChannelopathiesAbnormal expressionInjuryMolecular changesHyperexcitabilityCellsTransection
2000
Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis
Black J, Dib-Hajj S, Baker D, Newcombe J, Cuzner M, Waxman S. Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 11598-11602. PMID: 11027357, PMCID: PMC17246, DOI: 10.1073/pnas.97.21.11598.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBrainEncephalomyelitis, Autoimmune, ExperimentalHumansImmunohistochemistryMiceMultiple SclerosisNeurons, AfferentSodium ChannelsConceptsExperimental allergic encephalomyelitisMultiple sclerosisAllergic encephalomyelitisClinical abnormalitiesChannel expressionPurkinje cellsTrigeminal ganglion neuronsBrains of micePeripheral nervous systemSodium channel expressionIon channel expressionCerebellar Purkinje cellsAbnormal repertoiresAxonal degenerationControl miceGanglion neuronsControl subjectsMouse modelNormal brainAnimal modelsNervous systemNeurological diseasesSodium channelsProtein expressionAbnormal patternsDo ‘demyelinating’ diseases involve more than myelin?
Waxman S. Do ‘demyelinating’ diseases involve more than myelin? Nature Medicine 2000, 6: 738-739. PMID: 10888913, DOI: 10.1038/77450.Peer-Reviewed Original Research
1993
Peripheral nerve abnormalities in multiple sclerosis
Waxman S. Peripheral nerve abnormalities in multiple sclerosis. Muscle & Nerve 1993, 16: 1-5. PMID: 8380899, DOI: 10.1002/mus.880160102.Peer-Reviewed Original Research
1988
Evoked potentials in suspected multiple sclerosis: Diagnostic value and prediction of clinical course
Hume A, Waxman S. Evoked potentials in suspected multiple sclerosis: Diagnostic value and prediction of clinical course. Journal Of The Neurological Sciences 1988, 83: 191-210. PMID: 3128646, DOI: 10.1016/0022-510x(88)90068-8.Peer-Reviewed Original ResearchConceptsSilent lesionsMultiple sclerosisOptic neuritisIsolated optic neuritisDefinite multiple sclerosisEP abnormalitiesMS suspectsClinical deteriorationBrainstem auditoryClinical courseVisual EPsChance of deteriorationNeurologic disordersOnly abnormalityNormal EPsPatientsAuditory EPsClinical diagnosisDiagnostic valueLesionsSclerosisNeuritisChronicAbnormalitiesFollow
1986
Different effects of 4-aminopyridine on sensory and motor fibers: pathogenesis of paresthesias.
Kocsis J, Bowe C, Waxman S. Different effects of 4-aminopyridine on sensory and motor fibers: pathogenesis of paresthesias. Neurology 1986, 36: 117-20. PMID: 3001584, DOI: 10.1212/wnl.36.1.117.Peer-Reviewed Original Research
1983
Major morbidity related to hyperthermia in multiple sclerosis
Waxman S, Geschwind N. Major morbidity related to hyperthermia in multiple sclerosis. Annals Of Neurology 1983, 13: 348-348. PMID: 6847156, DOI: 10.1002/ana.410130331.Peer-Reviewed Original Research
1982
Membranes, Myelin, and the Pathophysiology of Multiple Sclerosis
Waxman S. Membranes, Myelin, and the Pathophysiology of Multiple Sclerosis. New England Journal Of Medicine 1982, 306: 1529-1533. PMID: 7043271, DOI: 10.1056/nejm198206243062505.Peer-Reviewed Original Research
1981
Basic and clinical electrophysiology of demyelinating diseases.
Ritchie J, Waxman S, Waksman B. Basic and clinical electrophysiology of demyelinating diseases. Neurology 1981, 31: 1308-10. PMID: 6287348, DOI: 10.1212/wnl.31.10.1308.Peer-Reviewed Original ResearchClinicopathological correlations in multiple sclerosis and related diseases.
Waxman S. Clinicopathological correlations in multiple sclerosis and related diseases. Advances In Neurology 1981, 31: 169-82. PMID: 7325041.Peer-Reviewed Original Research
1978
Conduction through demyelinated plaques in multiple sclerosis: computer simulations of facilitation by short internodes.
Waxman S, Brill M. Conduction through demyelinated plaques in multiple sclerosis: computer simulations of facilitation by short internodes. Journal Of Neurology Neurosurgery & Psychiatry 1978, 41: 408. PMID: 660202, PMCID: PMC493046, DOI: 10.1136/jnnp.41.5.408.Peer-Reviewed Original Research
1977
Conduction in Myelinated, Unmyelinated, and Demyelinated Fibers
Waxman S. Conduction in Myelinated, Unmyelinated, and Demyelinated Fibers. JAMA Neurology 1977, 34: 585-589. PMID: 907529, DOI: 10.1001/archneur.1977.00500220019003.Peer-Reviewed Original Research