THE AMYGDALA AND INTRACTABLE TEMPORAL-LOBE-EPILEPSY - A QUANTITATIVE MAGNETIC-RESONANCE-IMAGING STUDY

Citation
W. Vanpaesschen et al., THE AMYGDALA AND INTRACTABLE TEMPORAL-LOBE-EPILEPSY - A QUANTITATIVE MAGNETIC-RESONANCE-IMAGING STUDY, Neurology, 47(4), 1996, pp. 1021-1031
Citations number
76
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00283878
Volume
47
Issue
4
Year of publication
1996
Pages
1021 - 1031
Database
ISI
SICI code
0028-3878(1996)47:4<1021:TAAIT->2.0.ZU;2-9
Abstract
Objective: To establish a quantitative MRI technique using T-2 relaxat ion time mapping to study systematically the amygdala in patients with intractable temporal lobe epilepsy (TLE). Background: Identification of a focal abnormality on MRI in patients with intractable TLE is impo rtant, because outcome from surgery depends largely on the removal of the underlying pathology. Hippocampal sclerosis (HS) is the most commo n cause of intractable TLE, but epileptogenic lesions can be confined to the amygdala. Methods: Twenty control subjects and 82 patients with intractable TLE were studied. Patients who had foreign tissue lesions visible on routine MRI were excluded. All subjects had a hippocampal T-2 map and volumetry and an amygdala T-2 (AT2) map. Results: Forty-fo ur of the 82 patients (54%) had an abnormal AT2, which was bilateral i n 18. Forty-four patients (54%) had unilateral HS on MRI, 25 (57%) of whom had an abnormal AT2. Seven patients (8%) had bilateral HS, four o f whom had an abnormal AT2. Thirty-one patients (38%) had normal quant itative hippocampal measures, 15 of whom had an abnormal AT2, which wa s bilateral in seven. Fluid attenuated inversion recovery (FLAIR) imag ing, where appropriate, confirmed that the increased AT2 signal was du e to parenchymal changes. Neuropathologic correlates of an increased A T2 included microdysgenesis in one and gliosis in three patients. Pati ents with an isolated AT2 abnormality were significantly older at the onset of habitual epilepsy and rarely had a history of febrile convuls ions, in comparison with patients who had HS. An isolated AT2 abnormal ity correlated well with interictal EEG findings. Conclusions: The com bination of AT2 mapping and FLAIR is a sensitive method to detect lesi ons that are not seen on routine MRI in the amygdalae of patients with intractable TLE. Further correlational studies will be required to de fine the role of this technique in the presurgical evaluation of patie nts with intractable TLE.