ArticleEpilepsia2026
The interacting etiologies of hippocampal sclerosis in epilepsy: A scoping review.
Article in Epilepsia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Acute and longitudinal magnetic resonance imaging abnormalities in antibody-mediated encephalitis.Brain communications · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to the International League Against Epilepsy classification, mesial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) is considered an epilepsy syndrome. Several etiologies may precede HS, but there is little overview in the literature about these etiologies. We conducted a scoping review to systematically search, select, analyze, and synthesize the existing knowledge about the etiology of HS in patients with epilepsy. MEDLINE, Embase, Web of Science Core Collection, and Cochrane Library were searched using a systematic search strategy. Relevant data were selected according to strict criteria. A bibliometric analysis was done by VOSviewer software. A total of 907 studies were selected and classified. The main classes of etiologies we found are prolonged (febrile) seizures, genetic predisposition, infection, autoimmunity, trauma, neurodegeneration, developmental aspects, toxins (e.g., domoic acid), and hypertensive events (e.g., Posterior reversible encephalopathy syndrome), with several interactions between different etiologies. Autoimmunity and neurodegeneration were the most recently described etiologies. We found that the etiology of MTLE-HS is complex, with several risk factors influencing susceptibility and a heterogenous pathophysiology between patients. Future, prospective studies addressing the interactions of these etiologies in the development of HS are warranted. A better understanding of the interacting etiologies of MTLE-HS could have a major impact on the development of more precise diagnostic biomarkers, preventive strategies, and treatment options for this epilepsy syndrome.
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