Abstracts

Rationale: The neuroanatomical substrates of juvenile myoclonic epilepsy (JME) and the similarity of these with other idiopathic generalized epilepsy (IGE) subsyndromes remain to be determined as there are typically no visible abnormalities on clinical MRI scans. The few existing VBM studies of JME have primarily investigated chronic effects on gray matter concentration, however the presence and degree of such abnormalities at the onset of epilepsy remains to be examined and an overall consensus of affected brain regions has not yet been reached. Consequently, the work presented here employs VBM to investigate the gray and white matter differences between patient groups with a recent diagnosis of JME, patients with non-JME IGE syndromes, and healthy controls. The primary objective of this structural investigation is to address the potential early mechanisms involved with JME and to compare these indications with other IGE subsyndromes.Methods: 19 pediatric epilepsy patients with a recent diagnosis of JME, 45 control subjects and 8 patients with a non-JME IGE diagnosis were selected retrospectively from a participant population with an age range of 8-18 years that had been administered a T1 weighted anatomical MRI scan. SPM5 tools were used to perform VBM analyses with unmodulated and modulated segmented images for the quantification of gray and white matter (GM and WM) concentration and volume respectively. Analysis of covariance using a separate lines design with age as the covariate was performed on a voxel-wise basis and statistical maps were produced after correction for multiple comparisons with a false discovery rate of 5%.Results: The most significant differences were in gray matter concentration (GMC) as determined by comparison of unmodulated segmented images. Significant group differences between JME and non-JME IGE groups indicated a unilateral (left) reduced GMC in the lateral thalamus for the JME group. The lateral thalamus also showed reduced GMC bilaterally for the JME versus control comparison as did the frontal lobes, particularly the superior frontal gyrus and medial frontal regions. There were no regions of increased GMC for JME in either comparison. The only WM concentration (WMC) difference was a unilateral increase in the internal capsule for JME compared to non-JME IGE, however this WMC difference was not seen between JME and control. There were no regions of increased or decreased GM or WM volume able to survive multiple comparisons corrections.Conclusions: Early distinctions can be made between JME patients and those with other IGE subsyndromes based on tissue concentration abnormalities in the lateral thalamus. Although further work is necessary, this work may imply that there are heterogeneous mechanisms surrounding the onset of different IGE syndromes.