Electrocorticographic–Histopathologic Correlations Implying Epileptogenicity of Dysembryoplastic Neuroepithelial Tumor

  • KAGAWA Kota
    Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, Hiroshima University
  • IIDA Koji
    Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, Hiroshima University
  • KAKITA Akiyoshi
    Department of Pathology, Brain Research Institute, University of Niigata
  • KATAGIRI Masaya
    Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, Hiroshima University
  • NISHIMOTO Takeshi
    Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, Hiroshima University
  • HASHIZUME Akira
    Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, Hiroshima University
  • KIURA Yoshihiro
    Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, Hiroshima University
  • HANAYA Ryosuke
    Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University
  • SUGIYAMA Kazuhiko
    Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, Hiroshima University
  • ARIHIRO Koji
    Department of Pathology, Graduate School of Biomedical Sciences, Hiroshima University
  • ARITA Kazunori
    Department of Neurosurgery, Graduate School of Medical and Dental Sciences, Kagoshima University
  • KURISU Kaoru
    Department of Neurosurgery, Graduate School of Biomedical and Health Sciences, Hiroshima University

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Abstract

Based on intracranial-video electroencephalography (EEG), histopathological features, and postoperative seizure outcome, we elucidated the epileptogenicity in patients with dysembryoplastic neuroepithelial tumor (DNT). Five patients (P1–P5) pathologically diagnosed with DNT underwent intracranial-video EEG to identify the ictal onset zone and irritative zone. We evaluated the correlations of ictal onset zone and irritative zone with the magnetic resonance imaging-visible lesion (MRI-lesion) and their histopathological features. Intracranial-video EEG located the ictal onset zone adjacent to the MRI-lesion margin in four patients with complex/simple forms of DNT subcategory, and on the MRI-lesion in P3 with a nonspecific DNT form. The irritative zone extended to surrounding regions of the ictal onset zone in all patients. Histopathologically, MRI-lesions were characterized by specific glioneuronal elements, whereas the ictal onset zone and irritative zone were represented with dysplastic cortex accompanying oligodendroglia-like cells in four (P1, P2, P4, and P5) of five patients. Cortical dysplasia was identified with typical histopathologic features in the irritative zone remote from the MRI-lesion in P5. P3, with a nonspecific form, indicated prominent component of dysplastic cortex with oligodendroglia-like cells scattered in the MRI-lesion. Lesionectomy of MRI-lesion with additional cortical resections (including the ictal onset zone and irritative zone) yielded postoperative seizure freedom (Engel Class I) in P3, P4, and P5, while P1 and P2 (with only lesionectomy) experienced postoperative residual seizure (Class II and III in each patient). Our results suggest the intrinsic epileptogenicity of DNT. The topographical correlation indicated that the dysplastic cortex accompanying oligodendroglia-like cells was more epileptogenic than the specific glioneuronal elements itself. Meticulous intracranial-video EEG analysis delineating the MRI nonvisible ictal onset zone and the irritative zone may yield better seizure outcome.

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