Subcortical gray matter changes in pediatric patients with new-onset juvenile myoclonic epilepsy.

Objective: The objective of the study was to identify the relationship between subcortical gray matter (GM) volumes and juvenile myoclonic epilepsy (JME).

Methods: We analyzed the brain magnetic resonance imaging (MRI) scans that were performed during the time of the diagnosis of epilepsy by using voxel-based morphometry (VBM) method. The volumetric three-dimensional sequence was used for structural investigation. The volumes of the thalamus, caudate nucleus, pallidum, and putamen were measured in both hemispheres of patients with JME, patients with generalized tonic-clonic seizures alone (GTCS) (as a disease control group) and healthy controls (HCs). All patients were drug-naïve, and treatment had been started after evaluating MRI results.

Results: Fifteen patients with JME (9 females, mean age = 16.1 ± 3.2), 18 patients with GTCS (10 females, mean age = 15.5 ± 2.9), and 43 HCs (24 females, mean age = 15.9 ± 2.8) were included in the analysis. No significant difference was found for relative globus pallidus, caudate, and putamen volumes among the groups with JME, GTCS, and the HC group. The relative left and right thalamic volumes were significantly different between groups (Kruskal-Wallis rank test, p = 0.007, p = 0.001). In pairwise comparisons, both right and left relative thalamic volumes were lower in patients with JME than in HCs (right thalamus: means: 0.521 ± 0.066 vs. 0.597 ± 0.058, p < 0.001; left thalamus: means: 0.526 ± 0.088 vs. 0.605 ± 0.057, p < 0.001, Bonferroni post hoc corrections) and in patients with JME than in patients with GTCS (right thalamus: means: 0.521 ± 0.066 vs. 0.578 ± 0.066, p = 0.03; left thalamus: means: 0.526 ± 0.088 vs. 0.592 ± 0.068, p = 0.01, Bonferroni post hoc corrections), whereas there was no significant difference between the HCs and patients with GTCS (right thalamus: means: 0.597 ± 0.058 vs. 0.578 ± 0.066, p = 0.8; left thalamus: means: 0.605 ± 0.057 vs. 0.592 ± 0.068, p = 0.999, Bonferroni post hoc corrections).

Conclusion: This study allowed us to know that microstructural abnormalities exist from the disease onset, and the thalamus might play a critical role in the pathogenesis of JME.