2007
Channel, neuronal and clinical function in sodium channelopathies: from genotype to phenotype
Waxman SG. Channel, neuronal and clinical function in sodium channelopathies: from genotype to phenotype. Nature Neuroscience 2007, 10: 405-409. PMID: 17387329, DOI: 10.1038/nn1857.Peer-Reviewed Original ResearchConceptsSodium channel functionClinical manifestationsClinical statusNeuronal functionChannel functionPositive clinical manifestationsSodium channelsIon channel mutationsNegative clinical manifestationsNeuronal hyperexcitabilityNeuronal hypoexcitabilityNeuronal activityClinical functionNervous systemSodium channelopathiesChannelopathiesChannel mutationsManifestationsCell backgroundPhysiological propertiesStatusHyperexcitabilityHypoexcitabilitySeizuresParalysis
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 perspectives