Magnetoencephalographic Findings on Patients Having Symptomatic Localization‐Related Epilepsy with Dysembryoplastic Neuroepithelial Tumor as the Epileptogenic Lesion

Abstract

Purpose: Dysembryoplastic neuroepithelial tumor (DNT) is one of the major pathologies that are related to the epileptogenicity in patients having symptomatic localization‐related epilepsy (SLE). Histopathological definition of DNT is as follows: (I) intracortical locations, (2) multinodular architecture, (3)heterogeneous cellular composition with astrocytes, oligodendrocytes, and neurons, and (4) foci of cortical dysplasia. There are many glial cells and very few neurons at the center of the MRI lesion of DNT, which shows low intensity in TI image and high in T2. This characteristic is in contrast with that of focal cortical dysplasia (FCD), with MRI lesions that show iso‐intensity in TI image and high in T2, wherein are found many giant neurons pathologically. Epileptogenicity related to FCD is supposed to be intrinsic, that is, to exist within the MRI lesion, because of existence of these giant new rons. We have previously confirmed that spike‐dipoles estimated by magnetoencephalography (MEG) in SLE patients with FCD are distributed within the MRI lesion, suggesting the intrinsic epileptogenicity of FCD. We, therefore, suppose that epileptogenicity related to DNT should exist in the foci of cortical dysplasia, which are rather distant from the center of the MRI lesion, and hypothesized that spike‐dipoles in SLE patients with DNT would be distributed out of the center of the MRI lesion. This study was performed to test the hypothesis. Methods: Subjects of this study were composed of 1 I SLE patients who underwent surgical treatment and received good outcome for seizure reduction, and histopathological diagnosis of DNT was confirmed postoperatively. Three patients were female and 8 were male. Age at the MEG study ranged from I to 35 years. As to the epileptic syndrome, 3 were frontal lobe epilepsy (FLE), 7 were temporal (TLE), and I patient was parietal (PLE). The lobe i n which DNT was found and from which the seizure was supposed to originate were the same in all of the patients. MEG measurement and dipole fitting of interictal spikes were performed using a 37+37‐channel dual sensor system (Biomag‐netic Technologies Inc.; San Diego, California, USA) preoperatively. Estimated spike‐dipoles were overlaid on the preoperative MRI image, and the topographical relationship between spike‐dipoles and MRI lesion was examined in each patient. Results: Estimated spike‐dipoles were distributed at the marginal area around thc MRI lesion in all of the FLE patients and 20 of the TLE patients. In the PLE patient spike‐dipoles were distributed at a rather distant area from the MRI lesion, although within the same lobe. Four of the TLE patients showed extended distribution of spike‐dipoles around the MRI lesion. One patient with TLE was found to have DNT only after surgery. This patient's spike‐dipoles were distributed in a pattern characteristic of the mesial type of TLE. Conclusions: Spike‐dipoles estimated by MEC were distributed not within the MRI lesion but in a marginal area surrounding the lesion, or rather a distant area of the cortex in the majority of cases. This result supports our hypothesis that epileptogenicity of DNT exists not at the center of the lesion, but around its margin.