Thalamic atrophy in childhood absence epilepsy

Epilepsia. 2006 Feb;47(2):399-405. doi: 10.1111/j.1528-1167.2006.00435.x.


Purpose: Patients with childhood absence epilepsy (CAE) have normal clinical magnetic resonance imaging (MRI) studies. The presence of abnormalities in corticothalamic networks has been suggested to be the functional basis of absence seizure generation. We assessed whether structural grey and white matter volume changes of these areas occurred in patients with absence seizures by using optimized voxel-based morphometry (VBM).

Methods: We recruited 13 patients with a clinical and EEG diagnosis of CAE (mean age at examination, 17 +/- 8 years) and compared them with a consecutive series of 109 controls (mean age, 29 +/- 9 years). The 3 tesla MRI examination included a 3D T(1)-weighted sequence, which was analyzed with an optimized VBM protocol using the SPM2 package. The threshold was set at p < 0.05, corrected for multiple comparisons.

Results: Compared with controls, CAE patients showed areas of grey matter decrease in both thalami and in the subcallosal gyrus. White matter decrease was found in the extranuclear subcortical area and in the white matter of the basal forebrain. Grey and white matter increase was restricted to small clusters of cortical and subcortical areas.

Conclusions: Evidence exists of subcortical grey and white matter volume reduction in CAE patients. Bilateral thalamic atrophy may be either a result of damage from seizures (as in hippocampal sclerosis) or a reflection of a primary underlying pathology as the cause of absence seizures.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Atrophy
  • Brain Mapping
  • Cerebral Cortex / pathology
  • Dominance, Cerebral
  • Electroencephalography
  • Epilepsy, Absence / pathology*
  • Female
  • Humans
  • Image Interpretation, Computer-Assisted
  • Magnetic Resonance Imaging / statistics & numerical data*
  • Male
  • Prosencephalon / pathology
  • Temporal Lobe / pathology
  • Thalamus / pathology*