Significance of mesial temporal atrophy in relation to intracranial ictal and interictal stereo EEG abnormalities

Abstract

We studied 31 consecutive patients with temporal and extratemporal epilepsy who underwent presurgical evaluation with stereotaxic depth EEG (SEEG) to assess the relationships between amygdalo-hippocampal (AM-HF) atrophy and the location of SEEG seizure onset and SEEG interictal abnormalities. Scalp EEG recordings with sphenoidal electrodes had shown bitemporal ictal or interictal epileptic abnormalities in all. Patients underwent high quality MRI scans, including MRI volumetric measurements of mesial temporal structures. None had foreign tissue lesions. The final conclusions of the SEEG investigation coincided with the lateralization obtained by MRI volumetric measurements in the eight patients who had significant unilateral atrophy of the amygdala, hippocampus or both (> 2 SD below the mean of controls). In these patients with unilateral atrophy, all or > 75% of clinical seizures originated from the atrophic side. The seven patients with bilateral, but significantly asymmetrical, mesial atrophy had bilateral seizure onsets with > 70% originating from the more atrophic side in four, from the less atrophic side in two, and without predominance in one. The one patient with severe bilateral symmetrical atrophy had seizures originating equally from both sides. Five patients had no atrophy on MRI, but depth electrodes revealed predominant unilateral ictal temporal onsets in four of them. There was no significant correlation between the frequency of SEEG interictal spikes and the amount of AM-HF atrophy. However, we found a significant correlation between the severity of SEEG background disturbance in AM and HF and the degree of atrophy of these structures. Patients with unilateral atrophy were more frequently free of seizures after surgery than those with bilateral or no atrophy (P < 0.05). We conclude that unilateral mesial atrophy predicts ipsilateral mesial SEEG seizure onset despite bitemporal extracranial EEG foci. However, in patients with significant bilateral mesial atrophy, SEEG seizures may originate from either side, even in the presence of significant asymmetry. Finally, the identification of unilateral mesial atrophy has prognostic importance.

Results of surgery in patients with bilateral independent temporal lobe spiking (BITLS) with normal MRI or bilateral mesial temporal sclerosis (MTS) investigated with bilateral subdural grids

“…This compares badly with the results obtained in our patients and those from other series with unilateral MTS (89% seizure-free) [10][11][12][13][14] or even bilateral MTS (Group II; 80% seizurefree). Some of Group I patients might prove not to have TLE despite clinical and neurophysiological clues suggestive of a temporal lobe onset.…”

Relations Between EEG Seizure Morphology, Interhemispheric Spread, and Mesial Temporal Atrophy in Bitemporal Epilepsy

“…Volumetric MRI measurements of AM and HF were performed in all patients, according to the protocol described by Watson et al (5,17,20). MRI scans were obtained on a I .5-T Philips Gyroscan (Philips Medical Systems, Eindhoven, The Netherlands).…”

“…Volumes were compared with those of a control population of 30 age-matched healthy volunteers. The anatomic guidelines for identification and segmentation of the AM and HF were those described by Watson et al (17) 1. seven patients with unilateral seizure onset (patients l , 4, 16, 18, 19, 22, 23); 2. nine patients with bilateral independent seizure onset but with >60% of seizures starting from one side (patients 5,6,9,10,11,13,14,17,20); 3. six patients with bilateral independent onset without prevalent side (patients 2, 3, 7, 12, 15, 21); and 4. one patient with simultaneous bilateral onset in most (71%) of his seizures (patient 8).…”

Epileptiform synchronization in the rat insular and perirhinal cortices in vitro

“…Furthermore, animais subjected to single episodes or a short series of seizures experience cell loss and synaptic rearrangement (Bengzon et al, 1997;Holmes and Ben-Ari, 1998;Haas et al, 2001). Combined MRI and EEG studies of TLE patients show that sites of epileptiform discharge onset tend to localize to the sa me brain regions exhibiting volumetric reductions (Cendes et al, 1996;Watson et al, 1997;Cendes et al, 2000;Bernasconi et al, 2003;Vossler et al, 2004). Many have therefore revised old theories to suggest instead that an initial insult causing subtle reactive changes can lead to recurrent temporal lobe seizures, which subsequently cause the global structural changes commonly associated with TLE (Ben-Ari, 1985;Holmes and Ben-Ari, 1998).…”