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J Neurol Neurosurg Psychiatry 84:364 doi:10.1136/jnnp-2012-304098
  • Editorial commentary

No gain – no pain?

  1. Michelle A Farrar2
  1. 1Faculty of Medicine, Translational Neuroscience Facility, School of Medical Science, University of New South Wales, New South Wales, Sydney, Australia
  2. 2Sydney Children's Hospital and School of Women's and Children's Health, University of New South Wales, Sydney, New South Wales, Australia
  1. Correspondence to Dr Cindy Shin-Yi Lin, Faculty of Medicine, Translational Neuroscience Facility, School of Medical Science, University of New South Wales, NSW 2052 Sydney, Australia; c.lin{at}unsw.edu.au
  • Received 17 September 2012
  • Revised 17 September 2012
  • Accepted 17 September 2012
  • Published Online First 21 November 2012

Pain is one of the most pervasive symptoms in clinical medicine and always presents a challenge, both in terms of diagnosis and management. Abnormal voltage gated sodium channels (VGSCs) are emerging as key determinants in painful neuropathies. Genetic, metabolic or immunological factors have independently been demonstrated to alter ion channel properties, providing insight into complex pathophysiological mechanisms in pain. Specifically, modification of the Nav 1.7 isoform, encoded by the SCN9A gene, can profoundly impact pain sensitivity.1 Nav 1.7 is expressed in the peripheral nervous system in sensory and sympathetic neurons. Activating mutations in SCN9A produce severe pain due to gain-of-function in …

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