JLE

Epileptic Disorders

MENU

Late-onset epileptic spasms may be cured by focal cortical resective surgery Volume 14, issue 3, September 2012



Figure 1 (S: 15 Î¼V/mm; T: 0.1 sec; H: 35 Hz): Interictal sleep EEG: burst of diffuse asymmetric slow spike-and-waves predominantly in the left frontotemporal area.



Figure 2 Coronal slices of MRI and PET. (A) MRI of the anterior frontal lobe (left: T1; right: Flair) showing a hypersignal in the white matter in the medial part of the left superior frontal gyrus on Flair sequence. (B) Hypometabolism of the medial part of the left superior frontal gyrus as evidenced by FDG-PET (left) and FDG-PET-MRI co-recording which colocalised anatomically with the white matter abnormalities (right).



Figure 3 SEEG with location of the ten electrodes: seven frontal electrodes including two vertical (BM: basal medial with external contact located in the lesion; BL: basal lateral) and five orthogonal (FI: frontal inferior; FA: frontal anterior; FM: frontal medium; MS: supplementary motor area; PM: opercular medium) electrodes, and three orthogonal temporal electrodes (NA: uncus; HA: hippocampus anterior; HP: hippocampus posterior). AC: anterior commissure; PC: posterior commissure. Projection of all electrodes is shown in the sagittal plane (above) and of the seven frontal electrodes in the coronal plane (below). This projection in two single MRI slices does not represent the real trajectory for each electrode, which can only be appreciated with the combination of the two.



Figure 4 Interictal SEEG: infraclinical rhythmic sharp wave discharges on BM 13-18.



Figure 5 Ictal SEEG. (A) First spasm of the cluster: rhythmic sharp wave discharge on the external contacts of electrode BM (BM 13-18) ceases and is followed by a fast activity spreading mainly to FA 1-7 and coinciding with the first spasm of the cluster. (B) Following spasms of the cluster, fast activity becomes longer and more diffuse.