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HOME > J Pathol Transl Med > Volume 30(4); 1996 > Article
Original Article Non-neoplastic Lesions in Temporal Lobe Epilepsy: A Pathologic Review of 64 cases.
Sang Pyo Kim, Kun Young Kwon, Eun Sook Chang, Kwan Kyu Park, Sang Do Yi, Eun Ik Son
Journal of Pathology and Translational Medicine 1996;30(4):281-292
DOI: https://doi.org/
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1Department of Pathology, Keimyung University School of Medicine, 700-310 Taegu, Korea.
2Department of Neurology, Keimyung University School of Medicine, 700-310 Taegu, Korea.
3Department of Neurosurgery, Keimyung University School of Medicine, 700-310 Taegu, Korea.
4Institute for Medical Science, Keimyung University School of Medicine, 700-310 Taegu, Korea.

Temporal lobe epilepsy is characterized by complex partial seizures with either primary intracranial neoplasms or other non-neoplastic lesions. We reviewed 64 cases of surgically resected temporal lobes and amygdalo-hippocampal regions for temporal lobe epilepsy ansed by non-neoplastic lesions to elucidate the incidence and histologic features of each histologic group for a period of 2 years. The patient's age ranged from 12 to 49 years and the ratio of male to female was 42:22. There were 37 cases(57.8%) with single pathology and an additional 20 cases(31.3%) with dual pathology. The emaining 7 cases(10.9%) had no structural alternations. The most common temporal lobe pathology was hippocampal sclerosis in 41 cases(64.1%), diagnosed alone in 21 cases and as dual lesions in 20 cases. The hippocampal neuron loss was most pro,omemt in CA1, followed by CA4, CA3, and CA2. Amygdaloid sclerosis was present in 28 cases(43.8%), lases had 13 dual lesions, 25 cases also had hippocampal sclerosis. The 20 dual lesions showed that 6 cortical dysplasia, 10 microdysgenesis, 1 chronic non-specific inflammatory lesion, and 3 cysticercosis were associated with the various degree of mesial temporal sclerosis. Neuronoglial malformative lesions were identified in 21 cases(32.8%) including 16 dual lesion cases, which composed of 15 microdysgenesis and 6 cortical dysplasia. Neurofilament immunostain for cortical dysplasia revealed abnormally beaded disarray of axons in dysplastic pyramidal cells. The remaining pathologic lesions observed were 1 cysticercosis, 1 chronic non-specific inflammatory lesion, 3 arteriovenous malformation, 2 fibrous nodule, and 1 fibrous adhesions of the arachnoid.

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