NEURONAL LOSS AND GLIOSIS OF THE AMYGDALOID NUCLEUS IN TEMPORAL-LOBE EPILEPSY - A QUANTITATIVE-ANALYSIS OF 70 SURGICAL SPECIMENS

Although clinical and electrophysiological evidence indicates that the amygdaloid body plays an important role in the pathogenesis of tempor al lobe epilepsy, there are very few detailed data on histopathologica l changes in this nucleus in epilepsy patients. In the present study w e have examined the lateral nucleus of the amygdaloid body in 70 surgi cal specimens from patients with temporal lobe epilepsy and in 10 cont rol specimens with respect to neuronal density and gliosis. The result s were compared to the neuronal loss in the hippocampal formation. Our goal was to examine the pathological alterations of the amygdaloid bo dy and their correlation with other morphological changes in temporal lobe epilepsy. In epilepsy patients with Ammon's horn sclerosis or foc al lesions of the temporal lobe, the neuronal density of the lateral a mygdaloid nucleus was significantly decreased as compared to normal co ntrols (P < 0.001). Overall, the mean volumetric density in epilepsy p atients was reduced to 59% of that in normal individuals. There was no correlation between the neuronal density in the lateral amygdaloid nu cleus and that in the different segments of the hippocampal formation or to the age at onset or the duration of epilepsy, The neuronal loss of the amygdaloid nucleus correlated well with the presence of fibrill ary gliosis. Our findings demonstrate that the amygdaloid body is seve rely altered in most patients with temporal lobe epilepsy and that the se changes are independent of those in the hippocampus. The presence o f neuronal loss and gliosis in the amygdaloid nucleus of patients with focal lesions but no Ammon's horn sclerosis is compatible with an inv olvement of the amygdala in secondary epileptogenesis.