Glucose Transporter 1 Deficiency: A Treatable Cause of Opsoclonus and Epileptic Myoclonus

Pediatr Neurol. 2015 Oct;53(4):364-6. doi: 10.1016/j.pediatrneurol.2015.05.019. Epub 2015 Jun 12.

Abstract

Background: Epileptic myoclonus in infancy is associated with various pathological conditions. In the absence of an identifiable central nervous system lesion, an underlying metabolic genetic cause is often suspected.

Patients: We describe two infants with glucose transporter 1 deficiency syndrome who presented with epileptic myoclonus. One infant presented with an electroclinical phenotype mimicking benign myoclonic epilepsy of infancy; the other infant had a novel mutation and presented with opsoclonus and epileptic myoclonus with a robust response to high-dose steroids. Both infants began the ketogenic diet after the diagnosis of glucose transporter 1 deficiency syndrome, with good yet variable treatment responses.

Conclusions: These infants demonstrate that an evaluation for glucose transporter 1 deficiency syndrome is warranted in patients presenting with an electroclinical picture compatible with benign myoclonic epilepsy of infancy as well as in patients with intractable epilepsy who demonstrate a significant response to steroid therapy.

Keywords: GLUT1; developmental delays; epilepsy; myoclonus; opsoclonus.

Publication types

  • Case Reports

MeSH terms

  • Carbohydrate Metabolism, Inborn Errors / complications
  • Carbohydrate Metabolism, Inborn Errors / diet therapy*
  • Carbohydrate Metabolism, Inborn Errors / physiopathology*
  • Diet, Ketogenic
  • Epilepsies, Myoclonic / diet therapy*
  • Epilepsies, Myoclonic / etiology
  • Epilepsies, Myoclonic / physiopathology*
  • Female
  • Humans
  • Infant
  • Monosaccharide Transport Proteins / deficiency*
  • Ocular Motility Disorders / diet therapy*
  • Ocular Motility Disorders / etiology
  • Ocular Motility Disorders / physiopathology*

Substances

  • Monosaccharide Transport Proteins

Supplementary concepts

  • Glut1 Deficiency Syndrome