Marked accumulation of oligodendroglia‐like cells in temporal lobe epilepsy with amygdala enlargement and hippocampal sclerosis. Issue 2 (25th August 2017)

• Record Type: Journal Article
• Authors: Sone, Daichi; Ikemura, Masako; Saito, Yuko; Taniguchi, Go; Kunii, Naoto
• Is Part Of: Neuropathology. Volume 38:Issue 2(2018)
• Page Start: 154
• Page End: 158
• Publication Date: 2017-08-25
• Subjects: amygdala enlargement -- hippocampal sclerosis -- malformation of cortical development -- oligodendroglia‐like cells -- temporal lobe epilepsy; Nervous system -- Diseases -- Periodicals; Nervous system -- Pathophysiology -- Periodicals; 616.8047
• DOI: 10.1111/neup.12410
• Languages: English
• ISSNs: 0919-6544

Abstract

Abstract : Although an increasing number of cases of temporal lobe epilepsy (TLE) with ipsilateral amygdala enlargement (AE) have been reported, there are few pathological reports, and no clear consensus has been established. Oligodendroglia or oligodendroglia‐like cells (OLCs) have recently attracted attention in epilepsy studies. Here, we report the clinical and pathological findings of a 40‐year‐old male TLE patient with AE and hippocampal sclerosis, in whom histopathological study demonstrated remarkable clustering of OLCs around the uncus. The patient began to have refractory seizures at the age of 14, and preoperative MRI revealed left amygdala enlargement and left hippocampal atrophy. Other examinations were consistent with left mesial temporal epileptogenicity. He underwent surgical resection and achieved seizure freedom. Histopathological study of the amygdala showed swollen neurons with relatively large bodies and thick neurites, accompanied by vacuolar degeneration in the background. Additionally, there were marked clusters of OLCs with round nuclei and densely stained chromatin around the uncus. The OLCs were Olig2‐positive. In the hippocampus, severe cell loss in CA1 and granule cell dispersion in the dentate gyrus were found. These findings may provide some insights for further pathological investigations of TLE with non‐neoplastic AE.