Encephalopathy and SCN1A mutations

Epilepsia. 2011 Apr;52(4):e26-30. doi: 10.1111/j.1528-1167.2011.03019.x. Epub 2011 Mar 22.

Abstract

We describe three children with genetically different sodium channel alpha 1 subunit (SCN1A) mutation associated epilepsy who experienced a sudden and sustained neurologic regression following status epilepticus in two and acute sepsis in one. Neuroimaging showed evidence of cerebral ischemia in one, but the other two cases showed cerebellar signal abnormalities. The selectivity of cerebellar white matter change suggests a different mechanism of injury or increased susceptibility of this brain region to injury in at least some patients with SCN1A mutations. This report adds to the spectrum and mechanism of acute neurologic deterioration and functional deficit associated with SCN1A mutations, which remains to be fully understood.

Publication types

  • Case Reports

MeSH terms

  • Brain Ischemia / diagnosis
  • Brain Ischemia / genetics*
  • Cerebellar Diseases / diagnosis
  • Cerebellar Diseases / genetics*
  • Child, Preschool
  • Epilepsy / diagnosis
  • Epilepsy / genetics*
  • Fatal Outcome
  • Humans
  • Intellectual Disability / diagnosis
  • Intellectual Disability / genetics
  • Lennox Gastaut Syndrome
  • Male
  • NAV1.1 Voltage-Gated Sodium Channel
  • Nerve Tissue Proteins / genetics*
  • Sodium Channels / genetics*
  • Spasms, Infantile / diagnosis
  • Spasms, Infantile / genetics

Substances

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

Supplementary concepts

  • Epileptic encephalopathy, Lennox-Gastaut type