Director, Neuroscience and Regeneration Research Center

Neurology

Stephen Waxman is an expert in the field of Neurology. He studied medicine at Albert Einstein College of Medicine of Yeshiva University. He has 21 awards "Paul B. Magnuson Award for Outstanding Achievement in Rehabilitation Research", "W.I. McDonald Award", "William S Middleton Award (highest scientific honor of the Dept of Veterans Affairs, presented at Ceremonies at the U.S. Capitol)", "Annual Review Prize (Premier Award of the Society; previous awardees include J.C. Eccles, A.F. Huxley, A.L. Hodgkin)", "Ohio State University", "Honorary member", "Reingold Award", "Norman Allen Award", "Dystel Prize for Research on Multiple Sclerosis", "Landmark Award for Biomedical Research", "Wartenberg Award", "Honorary Senior Fellow", "Elected Member", "Elected to Institute of Medicine", "The Adrian Lecture (Xth International Congress of Clinical Neurophysiology)", "Listed in The Best Doctors in America", "Member", "Distinguished Alumnus Award", "Fellow", "Research Career Development Award" and "Trygve Tuve Memorial Award for Outstanding Contributions in the Biomedical Sciences". Stephen Waxman is also a published doctor. He has 101 publication published. The most recent publication is: Inherited erythromelalgia due to mutations in SCN9A: natural history, clinical phenotype and somatosensory profile.

Publications

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• The cerebellar channelopathy of Multiple sclerosis.
• Inherited erythromelalgia due to mutations in SCN9A: natural history, clinical phenotype and somatosensory profile.
• Neurology-the next 10 years.
• Virus-Mediated Knockdown of Nav1.3 in Dorsal Root Ganglia of STZ-Induced Diabetic Rats Alleviates Tactile Allodynia.
• Ca2+ toxicity due to reverse Na+/Ca2+ exchange contributes to degeneration of neurites of DRG neurons induced by a neuropathy-associated Nav1.7 mutation.
• Correction: Contactin-1 and Neurofascin-155/-186 Are Not Targets of Auto-Antibodies in Multifocal Motor Neuropathy.
• NaV1.9: a sodium channel linked to human Pain.
• Contactin-1 and Neurofascin-155/-186 Are Not Targets of Auto-Antibodies in Multifocal Motor Neuropathy.
• Destruction of paranodal architecture in inflammatory neuropathy with anti-contactin-1 autoantibodies.
• Sodium channel Nav1.7 in vascular myocytes, endothelium, and innervating axons in human skin.
• Painful peripheral neuropathy and sodium channel mutations.
• Human Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons.
• De novo gain-of-function and loss-of-function mutations of SCN8A in patients with intellectual disabilities and Epilepsy.
• Preferential targeting of Nav1.6 voltage-gated Na+ Channels to the axon initial segment during development.
• The Domain II S4-S5 Linker in Nav1.9: A Missense Mutation Enhances Activation, Impairs Fast Inactivation, and Produces Human Painful Neuropathy.
• DENDRITIC SPINE DYSGENESIS CONTRIBUTES TO HYPERREFLEXIA AFTER Spinal CORD INJURY.
• Dendritic spine dysgenesis in neuropathic Pain.
• Sodium channel genes in Pain-related disorders: phenotype-genotype associations and recommendations for clinical use.
• Neuropathic Pain in two-generation twins carrying the sodium channel Nav1.7 functional variant R1150W.
• Characterization of a de novo SCN8A mutation in a patient with epileptic encephalopathy.
• Channelopathies, Painful neuropathy, and diabetes: which way does the causal arrow point?
• Painful neuropathies: the emerging role of sodium channelopathies.
• Paroxysmal itch caused by gain-of-function Nav1.7 mutation.
• Depolarized Inactivation Overcomes Impaired Activation to Produce DRG Neuron Hyperexcitability in a Nav1.7 Mutation in a Patient with Distal Limb Pain.
• The role of sodium channels in Painful diabetic and idiopathic neuropathy.
• Translational Pain research: Lessons from genetics and genomics.
• Dynamics of sodium channel Nav1.5 expression in astrocytes in mouse models of Multiple sclerosis.
• Contribution of sodium channels to lamellipodial protrusion and Rac1 and ERK1/2 activation in ATP-stimulated microglia.
• Physiological and genetic analysis of multiple sodium channel variants in a model of genetic absence Epilepsy.
• A novel de novo mutation of SCN8A (Nav1.6) with enhanced channel activation in a child with epileptic encephalopathy.
• Gain-of-function mutations in sodium channel NaV1.9 in Painful neuropathy.
• Voltage-gated sodium channel Nav 1.5 contributes to astrogliosis in an in vitro model of glial injury via reverse Na(+) /Ca(2+) exchange.
• Dynamic-clamp analysis of wild-type human Nav1.7 and erythromelalgia mutant channel L858H.
• Tapered withdrawal of phenytoin removes protective effect in EAE without inflammatory rebound and mortality.
• Nav1.9 expression in magnocellular neurosecretory cells of supraoptic nucleus.
• Inherited Pain: sodium channel Nav1.7 A1632T mutation causes erythromelalgia due to a shift of fast inactivation.
• Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic Pain in human subjects with lingual nerve neuromas.
• Noncanonical roles of voltage-gated sodium channels.
• Multistate structural modeling and voltage-clamp analysis of Epilepsy/autism mutation Kv10.2-R327H demonstrate the role of this residue in stabilizing the channel clos...
• Wound-healing growth factor, basic FGF, induces Erk1/2-dependent mechanical hyperalgesia.
• Differential effect of D623N variant and wild-type Nav1.7 sodium channels on resting potential and interspike membrane potential of dorsal root ganglion neurons.
• The G1662S NaV1.8 mutation in small fibre neuropathy: impaired inactivation underlying DRG neuron hyperexcitability.
• Burn injury-induced mechanical allodynia is maintained by Rac1-regulated dendritic spine dysgenesis.
• Small-Fiber Neuropathy Nav1.8 Mutation Shifts Activation to Hyperpolarized Potentials and Increases Excitability of Dorsal Root Ganglion Neurons.
• Painful Na-channelopathies: an expanding universe.
• Virus-mediated shRNA knockdown of Na(v)1.3 in rat dorsal root ganglion attenuates nerve injury-induced neuropathic Pain.
• A new Na(v)1.7 mutation in an erythromelalgia patient.
• The Na(V)1.7 sodium channel: from molecule to man.
• Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(v)1.7 mutant channel.
• Sodium channel nav1.7 is essential for lowering heat Pain threshold after burn injury.
• Functional profiles of SCN9A variants in dorsal root ganglion neurons and superior cervical ganglion neurons correlate with autonomic symptoms in small fibre neuropathy.
• Na(v)1.8 expression is not restricted to nociceptors in mouse peripheral Nervous system.
• Sodium channels, the electrogenisome and the electrogenistat: lessons and questions from the clinic.
• Extraterritorial temperature Pain threshold abnormalities in subjects with healed thermal injury.
• Maladaptive dendritic spine remodeling contributes to diabetic neuropathic Pain.
• Mesenchymal stem cells: therapeutic outlook for Stroke.
• Intra- and interfamily phenotypic diversity in pain Syndromes associated with a gain-of-function variant of NaV1.7.
• Sodium channels and microglial function.
• Physiological interactions between Nav1.7 and Nav1.8 sodium channels: A computer simulation study.
• Rac1-regulated dendritic spine remodeling contributes to neuropathic Pain after peripheral nerve injury.
• Spinal cord injury, dendritic spine remodeling, and Spinal memory mechanisms.
• Na(V)1.7 accumulates and co-localizes with phosphorylated ERK1/2 within transected axons in early experimental neuromas.
• Gain of function Na(V) 1.7 mutations in idiopathic small fiber neuropathy.
• Novel SCN1A mutation in a proband with malignant migrating partial seizures of infancy.
• Intravenous administration of auto serum-expanded autologous mesenchymal stem cells in Stroke.
• Kinetic modeling of Nav1.7 provides insight into erythromelalgia-associated F1449V mutation.
• Slowly progressive axonal degeneration in a rat model of chronic, nonimmune-mediated demyelination.
• Neuroma removal for neuropathic Pain: efficacy and predictive value of lidocaine infusion.
• Minocycline attenuates mechanical allodynia and central sensitization following Peripheral second-degree burn injury.
• Two Nedd4-binding motifs underlie modulation of sodium channel Nav1.6 by p38 MAPK.
• A sodium channel mutation linked to Epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons.
• Channelopathic Pain: a growing but still small list of model disorders.
• ERK1/2 mitogen-activated protein kinase phosphorylates sodium channel Na(v)1.7 and alters its gating properties.
• Sodium channels in normal and pathological Pain.
• Familial pain Syndromes from mutations of the NaV1.7 sodium channel.
• Erythromelalgia mutation L823R shifts activation and inactivation of threshold sodium channel Nav1.7 to hyperpolarized potentials.
• A sodium channel gene SCN9A polymorphism that increases nociceptor excitability.
• FGF14 N-terminal splice variants differentially modulate Nav1.2 and Nav1.6-encoded sodium channels.
• Dendritic spine remodeling after Spinal cord injury alters neuronal signal processing.
• Voltage-gated sodium channels: therapeutic targets for Pain.
• Sodium channel activity modulates Multiple functions in microglia.
• A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia.
• Mexiletine-responsive erythromelalgia due to a new Na(v)1.7 mutation showing use-dependent current fall-off.
• Regulation of podosome formation in macrophages by a splice variant of the sodium channel SCN8A.
• The ataxia3 mutation in the N-terminal cytoplasmic domain of sodium channel Na(v)1.6 disrupts intracellular trafficking.
• Role of hippocampal sodium channel Nav1.6 in kindling epileptogenesis.
• Early microglial inhibition preemptively mitigates chronic Pain development after experimental spinal cord injury.
• Neuropathic Pain memory is maintained by Rac1-regulated dendritic spine remodeling after spinal cord injury.
• Multiple sodium channel isoforms and mitogen-activated protein kinases are present in Painful human neuromas.
• Paroxysmal extreme Pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable.
• A pore-blocking hydrophobic motif at the cytoplasmic aperture of the closed-state Nav1.7 channel is disrupted by the erythromelalgia-associated F1449V mutation.
• Axonal dysfunction in chronic Multiple sclerosis: meltdown in the membrane.
• Phosphorylation of sodium channel Na(v)1.8 by p38 mitogen-activated protein kinase increases current density in dorsal root ganglion neurons.
• Early treatment suppresses the development of spike-wave Epilepsy in a rat model.
• Locomotor dysfunction and Pain: the scylla and charybdis of fiber sprouting after spinal cord injury.
• Genetics and molecular pathophysiology of Na(v)1.7-related pain Syndromes.
• Disruption of cAMP and prostaglandin E2 transport by multidrug resistance protein 4 deficiency alters cAMP-mediated signaling and nociceptive response.
• Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic Pain disorders.
• Retinal involvement in Multiple sclerosis.
• Sodium channel expression within chronic Multiple sclerosis plaques.

Schools

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• Albert Einstein College of Medicine of Yeshiva University

• Boston City Hospital

• Harvard University

Conditions Treated

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• Brain and Nervous System Cancer (incl. Gliomas, Astrocytoma, Schwannoma, Medulloblastoma, Chordoma)
• Carpal Tunnel Syndrome
• Cerebrovascular Disease
• Convulsions
• View All

Doctors Specialties

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• Neurology

Accepted Insurances

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Awards

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• Paul B. Magnuson Award for Outstanding Achievement in Rehabilitation Research
• W.I. McDonald Award
• William S Middleton Award (highest scientific honor of the Dept of Veterans Affairs, presented at Ceremonies at the U.S. Capitol)
• Annual Review Prize (Premier Award of the Society; previous awardees include J.C. Eccles, A.F. Huxley, A.L. Hodgkin)
• Ohio State University
• Honorary member
• Reingold Award
• Norman Allen Award
• Dystel Prize for Research on Multiple Sclerosis
• Landmark Award for Biomedical Research
• Wartenberg Award
• Honorary Senior Fellow
• Elected Member
• Elected to Institute of Medicine
• The Adrian Lecture (Xth International Congress of Clinical Neurophysiology)
• Listed in The Best Doctors in America
• Member
• Distinguished Alumnus Award
• Fellow
• Research Career Development Award
• Trygve Tuve Memorial Award for Outstanding Contributions in the Biomedical Sciences

Education

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• Yale University
• Boston University Medical Center
• Albert Einstein College of Medicine of Yeshiva University
• Harvard College

Drug Facts

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NPI NUMBER		1750305041
NPPES Provider LastName		WAXMAN
NPPES Provider FirstName		STEPHEN
NPPES Provider ZIPCode		100163083
NPPES Provider State		NY
Specialty Description		Internal Medicine
Total Claim Count		881.0
Distinct Opioid Count		0.0
Opioid Claim Count		0.0
Percent Opioid Claims		0.0

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Medicare Facts

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National Provider Identifier [NPI]	1750305041
Last Name Of The Provider	WAXMAN
First Name Of The Provider	STEPHEN
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