RELATIONS BETWEEN EEG SEIZURE MORPHOLOGY, INTERHEMISPHERIC SPREAD, AND MESIAL TEMPORAL ATROPHY IN BITEMPORAL EPILEPSY

Citation
F. Spanedda et al., RELATIONS BETWEEN EEG SEIZURE MORPHOLOGY, INTERHEMISPHERIC SPREAD, AND MESIAL TEMPORAL ATROPHY IN BITEMPORAL EPILEPSY, Epilepsia, 38(12), 1997, pp. 1300-1314
Citations number
26
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00139580
Volume
38
Issue
12
Year of publication
1997
Pages
1300 - 1314
Database
ISI
SICI code
0013-9580(1997)38:12<1300:RBESMI>2.0.ZU;2-8
Abstract
Purpose: A strong relation exists between lateralization of seizure on set in temporal-lobe epilepsy and atrophic mesial structures measured by volumetric magnetic resonance imaging (MRI). We examined whether th is relation extended to subregions of the mesial temporal lobe and whe ther the trend for seizures to spread contralaterally could be related to the localization of atrophy. Methods: We analyzed 362 seizures (wi th and without clinical signs) from 23 patients having bitemporal epil epsy in whom intracerebral electrodes were implanted for presurgical e valuation. Patients had measurements of hippocampal and amygdala volum es, including comparison with normal controls. We assessed on EEG the laterialization and localization of seizure onset and the trend to spr ead to the contralateral side (proportion of seizures that spread for each patient). We included all seizures, independent of the presence o f clinical manifestations, These features a ere related to presence an d localization of atrophy. Results: Among the 19 patients with mesial atrophy, agreement between side of prevalent seizure onset and predomi nant atrophy was found in 10 (53%). From 99 seizures starting in a tem poral lobe with atrophy limited to the hippocampus, 67% started simult aneously in amygdala and hippocampus, 20% in hippocampus, and 13% in a mygdala. From 137 seizures starting in a temporal lobe with amygdala a nd hippocampal atrophy, 47% started in amygdala and hippocampus, 48% i n hippocampus, and 5% in amygdala. The trend to spread was 45% to the most atrophic side and 62% to the normal or less atrophic side. Conclu sions: When examining amygdala and hippocampus in this group of patien ts with bitemporal epilepsy, regions of seizure onset did not correspo nd to regions of predominant atrophy. The likelihood that seizures spr ead contralaterally was not influenced by atrophy in the region target ed by the spread. Precise relation between mesial temporal atrophy and seizures remain to be elucidated.