MRI Findings in Temporal Lobe Epilepsy—An Analysis of 70 Cases
Authors: Ma Jie , Takeuchi Juji , Kubo Hiroaki , Kawasaki Jun , Kanemoto Kousuke 
Published: August 2009

Purpose: To examine the frequency of hippocampal, cerebral, and cerebellar cortical atrophy in patients with intractable temporal lobe epilepsy (TLE) on reverse T,‐weighted coronal images or on T,‐weighted axial images.

Methods: Eleven control subjects and 70 patients, who had been treated for >5 years with various drugs by trained epileptologists and who still had seizures, were studied. The histories of all patients were studied to determine the age of their first epileptic episodes, perinatal events, febrile convulsions, and other relevant data. One and one‐half T magnetic resonance imaging (MRI) was performed on 70 patients with medically intractable TLE and 1 I control subjects. To examine for atrophy of the hippocampus, the surface areas of each diagonal slice of the hippocampus were measured and summed. The data were compared with the normal control data. The right‐left difference also was calculated. To examine for atrophy of the frontoparietal, temporooccipital and cerebellar cortices, the images were macroscopically estimated by J. T. and J. M.

Results: The values for the summed surface areas of the hippocampus in the 11 control subjects were between 4.1821 and 5.395 cm2. The ratio of the smaller to larger hippocampus ranged from 84.5 to 99%. Hippocampal atrophy was diagnosed when the summed surface areas of the hippocampus were ≥20% smaller than on the contralateral side. When the summed contralateral hippocampus was ≤4.2 cm2. both sides were diagnosed as atrophic. Considering all of the 70 patients with TLE, 42 (60%) showed a ≥20% smaller hippocampus compared with the contralateral side. There were a few patients with a hippocampal atrophy under the 50% ratio. However, the patients with atrophic ratios of 50–60%, 6G70%, and 7G80% were evenly distributed. Of the 140 hemispheres examined, 86 (61.4%) showed mild to severe atrophies in the frontoparietal cortex, 60 (42.9%) in the lateral or basal temporal cortex, 26 (18.7%) in the occipital cortex, and 12 (8.6%) in the cerebellum. In most cases, these atrophic lesions affected both sides and more than one cortical lobe. When the cerebellum was affected, both sides were usually atrophic. A right‐left differential atrophy was observed in four patients in the frontoparietal cortex, in four in the temporal cortex, and in two in the occipital cortex. Severe atrophy was always found on the same side as the more atrophic hippocampus. Severe atrophy was never found in the cerebellum. No clear correlation was found between the atrophy of the hippocampus and the duration of the symptoms of the epileptic seizures.

Conclusions: In this study, more than half of the patients with medically intractable TLE had an atrophy of the hippocampus, probably ipsilateral to the epileptogenic focus, and, therefore, we would consider them as candidates for surgical treatment. The presence of cerebral and cerebellar atrophic lesions, which involved more than one lobe or both sides, was frequently detected in patients with TLE. The cerebral cortical atrophic lesions were bilateral and, in most cases, almost symmetrical. In a few cases, they were asymmetrical and more severe on the same side as the focus. The presence of cerebral atrophic lesions should not be ignored, and it will be helpful in deciding the surgical indication and the extent of the resection of the epileptogenic lesions in the patients with medically intractable TLE.