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Updated: Apr 19, 2026

A Model of Epileptogenesis in Rhinal Cortex-Hippocampus Organotypic Slice Cultures
Published on: March 18, 2021
[Histopathologic features of epileptogenic brain lesions in infants and children]
1Department of Pathology, University of Niigata. kakita@bri.niigata-u.ac.jp
Insights
Histopathological findings in intractable epilepsy vary by age at seizure onset. Infantile onset is linked to cortical malformations, while juvenile and adult onset show hippocampal sclerosis, tumors, and other lesions.
Area of Science:
- Neurology
- Pathology
- Epileptology
Context:
- Intractable epilepsy presents diverse histopathological findings.
- Understanding these lesions is crucial for diagnosing and treating epilepsy.
- Age at seizure onset is a key factor influencing lesion type.
Purpose:
- To analyze the histopathological features of surgical epilepsy specimens.
- To correlate lesion types with age at seizure onset in 600 patients.
- To elucidate the pathomechanisms and clinical relevance of epilepsy-associated lesions.
Summary:
- Retrospective review of 600 intractable epilepsy surgical specimens.
- Patients categorized into infantile, juvenile, and adolescent/adult onset groups.
- Infantile onset predominantly showed cortical malformations (e.g., FCD type II a/b, tuberous sclerosis).
- Juvenile/adult onset frequently exhibited hippocampal sclerosis, tumors, FCD type I, and vascular lesions.
- FCD type III a was common in patients with hippocampal sclerosis across age groups.
- Tumor types included dysembryoplastic neuroepithelial tumors, gangliogliomas, and astrocytomas.
Impact:
- Highlights age-dependent variations in epilepsy-associated histopathology.
- Provides insights into the pathomechanisms underlying different epilepsy types.
- Informs clinical relevance and potential therapeutic strategies for intractable epilepsy.
Abstract:
I retrospectively reviewed the histopathologic features of surgical specimens taken consecutively from 600 patients with intractable epilepsy, and showed the scope of variation in lesions responsible for epileptogenesis. The patients were divided into three groups on the basis of age at seizure onset: 94 patients with infantile onset (before 1 year of age), 307 patients with juvenile onset (between 1 and 12 years of age), and 199 patients with adolescent/adult onset (at 13 years of age or beyond). In the infant group, seizure duration was significantly shorter than in the other groups, and malformations caused by abnormalities of cortical development, including focal cortical dysplasia (FCD) type II a/b, tuberous sclerosis, hemimegalencephaly, and polymicrogyria were predominant, whereas in the juvenile and adolescent/adult groups, other lesions such as hippocampal sclerosis (HS), tumors, FCD type I, and vascular lesions were frequently observed. FCD type III a was noted in nearly half of patient with HS in both juvenile and adolescent/adult groups. The causative tumors included dysembryoplastic neuroepithelial tumors, gangliogliomas, astrocytomas, and other glioneuronal and glial tumors. Thus, various histopathological entities and types, showing clear predominance depending on the age at seizure onset, were observed in patients with epilepsy. These features appear to provide information on the pathomechanisms of the lesions and their clinical relevance in affected patients.
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