Variable expressivity of a novel mutation in the SCN1A gene leading to an autosomal dominant seizure disorder

Seizure. 2011 Nov;20(9):711-2. doi: 10.1016/j.seizure.2011.06.014. Epub 2011 Jul 19.

Abstract

Mutations in the SCN1A gene can cause a variety of dominantly inherited epilepsy syndromes. Severe phenotypes usually result from loss of function mutations, whereas missense mutations cause a milder phenotype by altering the sodium channel activity. We report on a novel missense variant (p.Val1379Leu) in the SCN1A gene segregating in an autosomal dominant pattern in a family exhibiting a variable epilepsy phenotype ranging from generalized epilepsy with febrile seizures during infancy to a well controlled seizure disorder in adulthood. This report supports the importance of SCN1A mutation analysis in families in which seizure disorders segregate in an autosomal dominant fashion.

Publication types

  • Case Reports

MeSH terms

  • Child, Preschool
  • Epilepsy / diagnosis
  • Epilepsy / genetics*
  • Gene Expression Regulation
  • Genes, Dominant*
  • Genetic Variation / genetics*
  • Humans
  • Leucine / genetics
  • Male
  • Mutation, Missense / genetics*
  • NAV1.1 Voltage-Gated Sodium Channel
  • Nerve Tissue Proteins / biosynthesis
  • Nerve Tissue Proteins / genetics*
  • Pedigree
  • Seizures, Febrile / diagnosis
  • Seizures, Febrile / genetics
  • Sodium Channels / biosynthesis
  • Sodium Channels / genetics*
  • Valine / genetics

Substances

  • NAV1.1 Voltage-Gated Sodium Channel
  • Nerve Tissue Proteins
  • SCN1A protein, human
  • Sodium Channels
  • Leucine
  • Valine