Widespread cortical thinning in children with frontal lobe epilepsy.

PURPOSE: Spread of seizure activity outside the frontal lobe due to cortico-cortical connections can result in alteration in the cortex beyond the frontal lobe in children with intractable frontal lobe epilepsy (FLE). The aim of this study was to identify regions of reduced cortical thickness in children with intractable FLE. METHODS: High-resolution volumetric T(1)-weighted imaging was performed on 17 children with FLE, who were being evaluated for epilepsy surgery, and 26 age-matched healthy controls. The cortical thickness of 12 patients with left FLE and 5 patients with right FLE was compared to controls. The clusters of cortical thinning were regressed against age of seizure onset, duration of epilepsy, seizure frequency, and number of medications. KEY FINDINGS: In children with left FLE, cortical thinning was present in the left superior frontal, paracentral, precuneus, cingulate, inferior parietal, supramarginal, postcentral, and superior temporal gyri, as well as in the right superior and middle frontal, medial orbitofrontal, supramarginal, postcentral, banks of superior temporal sulcus, and parahippocampal gyri. In children with right FLE, cortical thinning was present in the right precentral, postcentral, transverse temporal, parahippocampal, lingual, and lateral occipital gyri, as well as in the left superior frontal, inferior parietal, postcentral, superior temporal, posterior cingulate, and lingual gyri. In children with left FLE, following exclusion of one outlier, there was no significant association between age at seizure onset, duration of epilepsy, seizure frequency and number of medications with clusters of cortical thinning. In children with right FLE, age at seizure onset, duration of epilepsy, frequency of seizures, and number of medications were not associated with clusters of cortical thinning within the right and left hemispheres. SIGNIFICANCE: Cortical changes were present in the frontal and extrafrontal cortex in children with intractable FLE. These changes may be related to spread of seizure activity, large epileptogenic zones involving both frontal and extrafrontal lobes, and development of secondary epileptogenic zones that over time lead to cortical abnormality. Further studies correlating cortical changes with neurocognitive measures are needed to determine if the cortical changes relate to cognitive function.

Longitudinal brain volumes in children with intractable partial seizures.

Cross sectional studies in children with epilepsy have reported variable changes in brain volume. The study hypothesis was that seizures result in injury to the developing brain, which is manifested as a reduction in brain volume. The aim was to evaluate the gray and white matter volumes longitudinally in children with partial epilepsy. All patients had two magnetic resonance scans, 1-7 years apart. The total, cerebral, and hemispheric gray and white matter volumes of 20 children with intractable partial epilepsy were measured. The correlation between change in volume and age at epilepsy onset and duration of epilepsy were assessed. There were no significant differences in total, cerebral, or hemispheric gray and white matter volumes with time. Up to six patients exhibited greater than 10% volume loss in total, cerebral, or hemispheric gray or white matter. There were no significant correlations between change in volume and age or duration of epilepsy. The findings suggest that volume loss does not occur in the shorter-term monitoring of children with partial seizures. It is possible that volume loss could become evident with long-term monitoring of children with epilepsy. Alternatively, brain volume may be an insensitive measure of alteration in brain structure secondary to epilepsy, and that other imaging techniques, such as diffusion tensor imaging, may be more sensitive for detecting microstructural changes induced by recurrent seizures.

Diffusion tensor imaging identifies changes in normal-appearing white matter within the epileptogenic zone in tuberous sclerosis complex.

PURPOSE: To evaluate diffusion tensor imaging (DTI) indices of (i) cortical tubers and (ii) normal-appearing subcortical white matter adjacent to cortical tubers within the epileptogenic zone and non-epileptogenic zone. METHODS: Twelve children with tuberous sclerosis complex underwent MRI, DTI and magnetoencephalography (MEG). Regions of interest (ROIs) were placed within cortical tubers and normal-appearing subcortical white matter adjacent to cortical tubers within MEG identified epileptogenic zone and non-epileptogenic zone. Fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (lambda(parallel)) and radial diffusivity (lambda(perpendicular)) were calculated. RESULTS: 26 out of 104 cortical tubers were in the epileptogenic zone. FA of cortical tubers in the epileptogenic zone was significantly lower than non-epileptogenic zone (p=0.015). There were no significant differences between MD (p=0.896), lambda(parallel) (p=0.672) and lambda(perpendicular) (p=0.651) of cortical tubers in the epileptogenic and non-epileptogenic zone. In normal-appearing subcortical white matter within the epileptogenic zone, FA was lower (p=0.001) and lambda(perpendicular) (p=0.011) was higher than non-epileptogenic zone. There were no significant differences between MD (p=0.110) and lambda(parallel) (p=0.735) of normal-appearing subcortical white matter within the epileptogenic and non-epileptogenic zone. CONCLUSION: DTI changes in normal-appearing white matter within the epileptogenic zone could represent abnormal white matter related to MRI-occult dysplastic cortex or ictal/interictal activity.

Diffusion tensor tractography detection of functional pathway for the spread of epileptiform activity between temporal lobe and Rolandic region.

PURPOSE: The aim of the study was to assess the connectivity between magnetoencephalographic (MEG) dipoles in the temporal lobe and Rolandic region in children with temporal lobe epilepsy using diffusion tensor imaging (DTI) tractography. METHODS: Six pediatric patients with intractable focal epilepsy had MEG performed, which showed MEG dipoles over both temporal and Rolandic regions in a unilateral hemisphere. DTI tractography was performed on each patient. Six control subjects were studied for comparison. Two volumes of interest (VOIs) that encompassed the MEG dipoles were drawn, one placed in temporal lobe and the other in Rolandic region. Similar VOIs were placed in the contralateral side in the patients and on both sides in controls. Fractional anisotropy (FA) and trace of the external capsules were compared between patients and controls. RESULTS: In all patients, a tractography pathway traversing through the external capsule, connecting the temporal and Rolandic MEG dipoles, was visualized. However, on the contralateral hemisphere in each patient, there was no evidence of a similar fiber tract. There was no corresponding tractography pathway identified in either hemisphere within the controls. There were no significant differences in FA and trace between the seizure focus side and contralateral side in the patients. There was no significant difference in FA, but a difference in trace between patients and controls. CONCLUSION: We have found aberrant tractography pathway traversing through the external capsule, connecting two distant foci of epileptiform activity. Chronic interictal epileptogenic discharge could play a causal role in the de novo organization of these tracts.