Reduced cortical thickness in children with new-onset seizures.

BACKGROUND AND PURPOSE: Children with new-onset seizures may have antecedent neurobiologic alterations that predispose them to developing seizures. Our aim was to evaluate hippocampal and thalamic volumes and lobar cortical thickness of children with new-onset seizures. MATERIALS AND METHODS: Twenty-nine children with new-onset seizures and normal MR imaging findings were recruited. Ten patients had generalized seizures, 19 had partial seizures, and 15 were on antiepileptic medications. Twenty-three age-matched healthy controls were also recruited. Hippocampal and thalamic volumes and lobar cortical thickness, including frontal, medial temporal, lateral temporal, parietal, cingulate, and occipital cortical thickness, were assessed by using volumetric T1-weighted imaging and were compared between patients and controls. RESULTS: There were no significant differences in hippocampal and thalamic volumes of patients with new-onset seizures, including the subgroups with generalized and partial seizures and those on and off antiepileptic medications, compared with controls (P > .01). There was significant reduction in cortical thickness in right cingulate (P = .004), right medial temporal (P = .006), and left frontal (P = .007) cortices in patients with new-onset seizures. Patients with generalized seizures did not demonstrate a significant reduction in cortical thickness (P > .01). Patients with partial seizures demonstrated a significant reduction in cortical thickness in the right frontal (P = .008), right parietal (P = .003), and left frontal (P = .007) cortices. There were no significant differences in cortical thickness among patients on or off antiepileptic medications (P > .01). CONCLUSIONS: We found reduced cortical thickness in children with new-onset seizures. Further studies are necessary to elucidate the neurobiologic relevance of these structural changes.

Abnormal axial diffusivity in the deep gray nuclei and dorsal brain stem in infantile spasm treated with vigabatrin.

We evaluated the DTI changes in the deep gray nuclei and dorsal brain stem, which demonstrated abnormal T2 and/or diffusion signal intensity, in 6 patients with infantile spasm treated with vigabatrin compared with 6 age-matched controls. Regions of interest were placed in the globi pallidi, thalami, and dorsal brain stem; FA, trace, D(‖), and D(⊥) were measured. Patients on vigabatrin had significantly lower FA in both globi pallidi (P = .01) and the dorsal brain stem (P < .01), significantly lower trace in both globi pallidi (P = .01) and the thalami (P = .02 and .01 for right and left, respectively), and significantly lower D(‖) in both globi pallidi (P ≤ .01), the thalami (P < .01), and the dorsal brain stem (P = .03). There were no significant differences in D(⊥) of the globi pallidi, thalami, or dorsal brain stem in patients compared with controls. The findings suggest that axonal changes play a greater role in the observed abnormal signal intensity, with lesser contribution from myelin changes.