2012
Myelin, Impulse Conduction, and the Pathophysiology of Demyelination
Bangalore L, Waxman S. Myelin, Impulse Conduction, and the Pathophysiology of Demyelination. 2012, 529-542. DOI: 10.1093/med/9780199794591.003.0042.Peer-Reviewed Original ResearchPathophysiology of demyelinationNormal brain functionMultiple sclerosisGlial cellsParkinson's diseaseNeurological diseasesAlzheimer's diseasePsychiatric conditionsImpulse conductionBrain functionDiseaseGliaNeuronsBasic biologyCell anatomyConcerted actionCellsDemyelinationSclerosisPathophysiologyStrokeCentral roleBrainMyelin
2010
Sodium channel expression and function in multiple sclerosis
Bangalore L, Black J, Carrithers M, Waxman S. Sodium channel expression and function in multiple sclerosis. 2010, 29-43. DOI: 10.1017/cbo9780511781698.005.Peer-Reviewed Original ResearchMultiple sclerosisRecovery of functionSodium channel expressionHealth care advisorsMechanisms of recoveryNeurorehabilitation programChannel expressionSpecific syndromesTherapeutic interventionsCare advisorsClinical rehabilitationEfficient therapySclerosisDisease mechanismsPatientsCliniciansNeurorehabilitationInterventionBasic scienceSocial participationPathophysiologySyndromeTherapyNeuroplasticity
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
2006
Transcriptional Channelopathies of the Nervous System
Waxman S. Transcriptional Channelopathies of the Nervous System. 2006 DOI: 10.1002/9780470015902.a0006086.Peer-Reviewed Original ResearchSodium channel geneChannel genesTranscriptional channelopathiesSodium channel gene expressionChannel gene expressionGene expressionPeripheral nerve injurySpinal sensory neuronsGenesDysregulated expressionNerve injuryMultiple sclerosisSensory neuronsNervous systemCerebellar functionRecent studiesExpressionChannelopathiesAbstract Recent studiesHyperexcitabilitySclerosisInjuryNeuronsCells
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 ResearchConceptsMultiple sclerosisProgression of MSCause of progressionMechanisms of progressionMS exacerbationDisease courseInflammatory cascadeClinical manifestationsTherapeutic strategiesDisease processTreatment interventionsEvidence-based observationsEmergence of disabilityProgressionDiseasePotential mechanismsTreatment effectsSclerosisProgressive stagesNovel research initiativesExacerbationTherapyIllnessMajor advancementsExpert perspectives7 Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and its Models
Waxman S. 7 Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and its Models. 2005, 101-118. DOI: 10.1016/b978-012738761-1/50008-0.Peer-Reviewed Original ResearchMultiple sclerosisSodium channel subtypesVoltage-gated sodium channelsSodium channelsChannel subtypesDistinct voltage-gated sodium channelsPathophysiology of MSAxonal degenerationTherapeutic strategiesSclerosisFiring patternsExperimental modelMaladaptive roleNeuronal signalingSubtypesMolecular analysisAltered distributionNeuronsRecent studiesMajor contributorPathophysiologyAxonsDegenerationDiseaseImportant role22 Neuronal Blocking Factors in Demyelinating Diseases
Cummins T, Waxman S. 22 Neuronal Blocking Factors in Demyelinating Diseases. 2005, 317-326. DOI: 10.1016/b978-012738761-1/50023-7.Peer-Reviewed Original ResearchVoltage-gated sodium channelsGuillain-Barré syndromeMultiple sclerosisSodium channelsChronic inflammatory demyelinating polyneuropathyInflammatory demyelinating polyneuropathyInflammatory demyelinating diseaseBlocking factorsDemyelinating polyneuropathyDemyelinating diseaseClinical deficitsAxonal degenerationInflammatory diseasesConduction blockSodium currentNitric oxideExperimental modelDiseaseImpulse transmissionSclerosisBiological toxinsDemyelinationFactorsPolyneuropathyCytokines
2003
Multiple Sclerosis
Vollmer T, Preiningerova J, Waxman S. Multiple Sclerosis. 2003 DOI: 10.1038/npg.els.0000192.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
2000
Do ‘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
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
1987
Physiological effects of 4‐aminopyridine on demyelinated mammalian motor and sensory fibers
Bowe C, Kocsis J, Targ E, Waxman S. Physiological effects of 4‐aminopyridine on demyelinated mammalian motor and sensory fibers. Annals Of Neurology 1987, 22: 264-268. PMID: 2821876, DOI: 10.1002/ana.410220212.Peer-Reviewed Original ResearchConceptsSensory fibersClinical trialsAction potentialsPotassium channel blockadeDorsal root axonsCompound action potentialDorsal spinal rootsSingle action potentialMammalian motorIntrathecal injectionMultiple sclerosisSensory dysfunctionVentral rootsSpinal rootsNeuromuscular disordersSpecific fiber typesElectrophysiological responsesSingle stimulusPhysiological effectsTrialsFiber typesResponseParesthesiaSclerosisDysfunction
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