Hippocampal region asymmetry assessed by 1H-MRS in rolandic epilepsy

Staffan Lundberg1, Jan Weis, Orvar Eeg-Olofsson

  • 1Department of Women's and Children's Health, Section for Pediatrics, Slovak Academy of Sciences, Bratislava, Slovakia. staffan.lundberg@kbh.uu.se

Epilepsia
|February 1, 2003
PubMed

Insights

Children with rolandic epilepsy (RE) show abnormal hippocampal neuronal function, indicated by altered N-acetylaspartate (tNAA) levels. This magnetic resonance spectroscopy study highlights metabolic changes in the hippocampus of RE patients.

Area of Science:

  • Neuroscience
  • Pediatric Neurology
  • Medical Imaging

Background:

  • Rolandic epilepsy (RE) is a common childhood epilepsy syndrome.
  • Previous studies indicated hippocampal abnormalities in children with RE using MRI.
  • Further investigation into metabolic changes within the hippocampus is warranted.

Purpose of the Study:

  • To analyze metabolic changes in the hippocampal region of children with rolandic epilepsy using proton magnetic resonance spectroscopy (1H-MRS).
  • To compare hippocampal metabolic profiles between children with RE and healthy controls.

Main Methods:

  • Proton magnetic resonance spectroscopy (1H-MRS) was performed on 13 children with RE and 15 healthy controls.
  • Voxel placement included the head and body of the hippocampus.
  • Metabolite ratios (tNAA/tCr, Glx/tCr, tCho/tCr) and asymmetry indices (AIs) were calculated.

Main Results:

  • A significantly higher tNAA/tCr asymmetry index was observed in the hippocampal regions of children with RE compared to controls (p < 0.001).
  • No significant differences in Glx/tCr or tCho/tCr asymmetry were found between groups.
  • Lateralization of epileptiform activity correlated with lower tNAA/tCr ratios in most RE patients.

Conclusions:

  • Altered tNAA/tCr ratios in the hippocampus suggest abnormal neuronal function in children with rolandic epilepsy.
  • Hippocampal asymmetry, measured by tNAA/tCr, is a significant finding in RE.
  • Findings support the role of hippocampal metabolic alterations in the pathophysiology of RE.
Abstract