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Showing 1–7 of 7 results
Advanced filters: Author: "Stephen G. Waxman" Clear advanced filters

  • Since the launch ofNature Clinical Practice Neurologyin 2005, we have seen remarkable progress in many areas of neurology research, but what does the future hold? For this special Viewpoint article, we invited a panel of Advisory Board members and other journal contributors to outline their research priorities and predictions for the next 10 years.

    • Ralf Baron
    • Donna M. Ferriero
    • Michael Weller
    Reviews
    Nature Reviews Neurology
    Volume: 11, P: 658-664

  • A sodium channel known for its role in the perception of pain also seems to be necessary for olfaction. The multiple roles of this channel and the diverse effects of its mutations raise intriguing questions. See Article p.186

    • Stephen G. Waxman
    News & Views
    Nature
    Volume: 472, P: 173-174

  • Choi et al. describe the case of a 3 month-old infant who, on the second day of life, had begun to experience painful paroxysmal events starting with tonic contraction of the whole body followed by erythematous harlequin-type color changes. The patient was diagnosed as having paroxysmal extreme pain disorder. The condition was attributed to a mutation in the SCN9A gene, which encodes the voltage-gated sodium channel NaV1.7.

    • Jin-Sung Choi
    • Franck Boralevi
    • Stephen G. Waxman
    Reviews
    Nature Reviews Neurology
    Volume: 7, P: 51-55

  • Axon degeneration is a major contributor to disability in multiple sclerosis, and sodium channels have been shown to have a crucial role in this process. In this article, Waxman reviews the development of the concept of sodium channel blockers as neuroprotectants in multiple sclerosis, and discusses recent attempts to translate this approach from the laboratory to the clinic.

    • Stephen G Waxman
    Reviews
    Nature Clinical Practice Neurology
    Volume: 4, P: 159-169

  • Mutations inSCN9A, which encodes the voltage-gated sodium channel NaV1.7, can lead to severe neuropathic pain in humans. In this Review, Waxman and colleagues examine the mechanistic basis of NaV1.7-linked pain and explore strategies for targeting this channel in pain therapy.

    • Sulayman D. Dib-Hajj
    • Yang Yang
    • Stephen G. Waxman
    Reviews
    Nature Reviews Neuroscience
    Volume: 14, P: 49-62

  • Emerging evidence suggests a role for the voltage-gated sodium channel NaV1.9 in pain. In this Progress article, Dib-Hajj, Black and Waxman analyse the findings from three studies that report mutations in the gene encoding NaV1.9 in pain disorders, and suggest that NaV1.9 may be a potential therapeutic target for pain.

    • Sulayman D. Dib-Hajj
    • Joel A. Black
    • Stephen G. Waxman
    Reviews
    Nature Reviews Neuroscience
    Volume: 16, P: 511-519