Abstracts

NE with an extratemporal or temporal structural lesion may be associated with hippocampal sclerosis (dual pathology). The usefulness of MR spectroscopy for the detection of hippocampal damage in temporal lobe epilepsy has been well established. Therefore, the aims of this study were: 1. To determine the frequency of hippocampal damage in NE with and without structural lesion. 2. To study if NE with EEG evidence for neocortical temporal seizure onset (NE-T) is more frequently associated with hippocampal damage than NE with extratemporal seizure onset (NE-ET) 2. To assess the value of hippocampal damage in the lateralization of NE.
We studied 16 patients with NE (7 NE-T, 9 NE-ET; mean age 25.4[plusmn]8.2) and 16 controls (mean age 28.1[plusmn]8.2). Eight NE patients had MR visible lesions, 8 had normal MRI. Spectroscopic measurements were done with a 2D MRSI sequence (TR/TE = 1800/135 ms) using PRESS volume pre-selection (15 mm axial, 60 mm left-right, 100 mm anterior-posterior) with 24x24 phase encoding steps and a 210 mm² FOV angulated along the long axis of the hippocampus, covering both hippocampi. Hippocampal voxels were selected on a T1 weighted FLASH image and their position in the hippocampus indicated with a number ranging from 1 for the most anterior in the head to 6 for the most posterior in the tail of the hippocampus. At each position 2 hippocampal voxels (medial and lateral) were selected. In controls, mean[plusmn]SD NAA/(Cr+Cho) for each voxel were calculated and voxels with NAA/(Cr+Cho) [le] (mean in controls [ndash]2SD in controls) were defined as [ldquo]pathological[rdquo] in patients.
10/16 patients had at least one voxel (mean 2.2, range 1-5) with an abnormally low NAA/(Cr+Cho) in one hippocampus. In 8/10 of those patients the ipsilateral hippocampus was affected, in one patient with bilateral frontal seizure onsets the left hippocampus was affected and in one patient with right temporal neocortical seizure onsets, the left hippocampus was affected. Five patients with abnormally low hippocampal NAA/(Cr+Cho) had a MR visible lesion and 5 had normal MRI (Fisher[rsquo]s Exact Test: p=0.7). Four, i.e. 57% of all NE-T patients, had evidence for hippocampal damage as did 6, i.e., 67% of all NE-ET (Fisher[lsquo]s Exact Test: p=0.8).
Evidence for unilateral hippocampal damage, i.e., pathologically low NAA/(Cr+Cho), was demonstrated in 62.5% of the NE patients. Hippocampal NAA/(Cr+Cho) reductions were found with the same frequency in NE with structural lesions as in NE without structural lesions and were not more frequent in NE with temporal lobe seizure onsets than in NE with extratemporal lobe onsets. In 80%, NAA/(Cr+Cho) was reduced in the hippocampus ipsilateral to the neocortical seizure focus, therefore, hippocampal abnormalities might be helpful for focus lateralization in NE.
[Supported by: NIH Grant R01-NS31966 to KDL.]