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From the Epilepsy Research Group (Drs. Van Paesschen and Duncan), University Department of Clinical Neurology, National Hospital for Neurology and Neurosurgery; and the NMR Unit (Drs. Van Paesschen and Connelly and Ms. Johnson), Great Ormond Street Hospital for Children and Institute of Child Health, London, England.
Approved by the Ethics Committees of the National Hospital for Neurology and Neurosurgery and the Great Ormond Street Hospital for Children.
Presented in part at the 48th annual meeting of the American Academy of Neurology, San Francisco, 1996. This manuscript was selected as the winner of the 1996 Founders Award of the American Academy of Neurology.
Received November 21, 1995. Accepted in final form February 15, 1996.
Address correspondence and reprint requests to Dr. Wim Van Paesschen, University Hospital Gasthuisberg, Department of Neurology, 49 Herestraat, 3000 Leuven, Belgium.
Objective: To establish a quantitative MRI technique using T2 relaxation 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 important, because outcome from surgery depends largely on the removal of the underlying pathology. Hippocampal sclerosis (HS) is the most common 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 T2 map and volumetry and an amygdala T2 (AT2) map. Results: Forty-four of the 82 patients (54%) had an abnormal AT2, which was bilateral in 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 of whom had an abnormal AT2. Thirty-one patients (38%) had normal quantitative hippocampal measures, 15 of whom had an abnormal AT2, which was bilateral in seven. Fluid attenuated inversion recovery (FLAIR) imaging, where appropriate, confirmed that the increased AT2 signal was due to parenchymal changes. Neuropathologic correlates of an increased AT2 included microdysgenesis in one and gliosis in three patients. Patients with an isolated AT2 abnormality were significantly older at the onset of habitual epilepsy and rarely had a history of febrile convulsions, in comparison with patients who had HS. An isolated AT2 abnormality correlated well with interictal EEG findings. Conclusions: The combination of AT2 mapping and FLAIR is a sensitive method to detect lesions that are not seen on routine MRI in the amygdalae of patients with intractable TLE. Further correlational studies will be required to define the role of this technique in the presurgical evaluation of patients with intractable TLE.
NEUROLOGY 1996;47: 1021-1031
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