S L Venance

Summary

Affiliation: University of Western Ontario
Country: Canada

Publications

  1. ncbi request reprint The primary periodic paralyses: diagnosis, pathogenesis and treatment
    S L Venance
    Department of Clinical Neurological Sciences, London Health Sciences Centre, London, ON, Canada
    Brain 129:8-17. 2006
  2. ncbi request reprint SCN4A-associated hypokalemic periodic paralysis merits a trial of acetazolamide
    S L Venance
    Neuromuscular Disease Center, Department of Neurology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642 8673, USA
    Neurology 63:1977. 2004
  3. ncbi request reprint Expression profile of FSHD supports a link between retinal vasculopathy and muscular dystrophy
    R J Osborne
    Department of Neurology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642 8673, USA
    Neurology 68:569-77. 2007

Collaborators

Detail Information

Publications3

  1. ncbi request reprint The primary periodic paralyses: diagnosis, pathogenesis and treatment
    S L Venance
    Department of Clinical Neurological Sciences, London Health Sciences Centre, London, ON, Canada
    Brain 129:8-17. 2006
    ..Moreover, understanding the skeletal muscle channelopathies will hopefully lead to insights into the more common central nervous system channel diseases such as migraine and epilepsy...
  2. ncbi request reprint SCN4A-associated hypokalemic periodic paralysis merits a trial of acetazolamide
    S L Venance
    Neuromuscular Disease Center, Department of Neurology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642 8673, USA
    Neurology 63:1977. 2004
  3. ncbi request reprint Expression profile of FSHD supports a link between retinal vasculopathy and muscular dystrophy
    R J Osborne
    Department of Neurology, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642 8673, USA
    Neurology 68:569-77. 2007
    ..Previous work has suggested that muscle degeneration in FSHD results from increased expression of genes proximal to the deletion, including FRG1...