Marked accumulation of oligodendroglia‐like cells in temporal lobe epilepsy with amygdala enlargement and hippocampal sclerosis

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.

Transient epileptic amnesia complex syndrome and epileptic cognitive impairment resembling Alzheimer's disease: Should the concept of epilepsy be extended?

“…There are various reasons why neurons in the brain may acquire epileptogenic properties. In late-onset epilepsy in older people without obvious structural abnormalities, several conditions such as inflammation, autoantibodies, sclerosis, microvascular disorders, and neurodegenerative diseases have been postulated as etiologies [17][18][19][20]. We suspect that in these patients, the abnormal discharges may be caused by the following process: (1) A small number of neurons initiate abnormal discharges due to certain causes/ mechanisms.…”

Quantitative cellular pathology of the amygdala in temporal lobe epilepsy and correlation with magnetic resonance imaging volumetry, tissue microstructure, and sudden unexpected death in epilepsy risk factors

“…83 We also explored evidence of tau pathology in this series, particularly as a previous report identified tau accumulation in glial cells in AE. 84 There is also evidence for neuronal tau accumulation and phosphorylation in the hippocampus and neocortex in TLE with aging, 13 and furthermore, experimental data suggest that tau reduction reduces SUDEP risk in Dravet models. 14 Using three common pTau antibodies in AD research, we noted variable neuronal more than glial accumulation in the amygdala that correlated with the age of patients but not with MRI measures or SUDEP risk factors.…”

Management of elderly-onset epilepsy: A narrative review

“…However, there is limited information on the underlying pathology of TLE with AE, as only a few cases require surgical intervention. Pathological findings from a small number of surgical cases have included cortical dys-plasia, low-grade glioma, nonspecific gliosis, and accumulation of oligodendroglia-like cells, indicating a heterogeneous disease background [35]. Sone et al [36] found that methionine PET uptake increased in 27% of TLE-AE cases [34].…”