Acute encephalopathy in children with Dravet syndrome

Epilepsia. 2012 Jan;53(1):79-86. doi: 10.1111/j.1528-1167.2011.03311.x. Epub 2011 Nov 16.

Abstract

Purpose: The occurrence of acute encephalopathy in children with Dravet syndrome has been reported sporadically. This study clarified the features of acute encephalopathy in children with Dravet syndrome.

Methods: Through the mailing list of the Annual Zao Conference on Pediatric Neurology, we collected 15 patients with clinically diagnosed Dravet syndrome, who had acute encephalopathy, defined as a condition with decreased consciousness with or without other neurologic symptoms, such as seizures, lasting for >24 h in association with infectious symptoms.

Key findings: There were seven boys and eight girls. A mutation of the SCN1A gene was present in nine (truncation in six and missense in three). The frequency of seizures during the 3 months before the onset of acute encephalopathy was monthly in seven children and none in three. The median age at the onset of acute encephalopathy was 44 months (range 8-184 months). All children had status epilepticus followed by coma as the initial manifestation. Two different distributions of brain lesions were observed on diffusion-weighted images during the acute phase: cerebral cortex-dominant lesions with or without deep gray matter involvement and subcortical-dominant lesions. Four children died; nine survived with severe sequelae, and two had moderate sequelae.

Significance: We must be aware that acute encephalopathy is an important complication in children with Dravet syndrome, and associated with fulminant clinical manifestations and a poor outcome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Disease
  • Cerebral Cortex / pathology*
  • Child
  • Child, Preschool
  • Female
  • Humans
  • Infant
  • Intellectual Disability / etiology*
  • Intellectual Disability / pathology*
  • Intellectual Disability / physiopathology
  • Lennox Gastaut Syndrome
  • Magnetic Resonance Imaging*
  • Male
  • Mutation
  • NAV1.1 Voltage-Gated Sodium Channel
  • Nerve Tissue Proteins / genetics*
  • Seizures / complications*
  • Seizures / genetics
  • Seizures / pathology
  • Sodium Channels / genetics*
  • Spasms, Infantile / etiology*
  • Spasms, Infantile / pathology*
  • Spasms, Infantile / physiopathology
  • Syndrome

Substances

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

Supplementary concepts

  • Epileptic encephalopathy, Lennox-Gastaut type