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Localizing value of ecstatic phenomenon in epilepsy surgery: A systematic review.

Sep 2026 · Epileptic disorders · 0 citations · 63 references
Medicine

Abstract

Objective

A systematic review was conducted to synthesize current anatomo-clinical correlations of ecstatic symptoms in focal epilepsy, aiming to provide evidence-based guidance for interpreting this ictal semiology during presurgical evaluation.

Methods

We searched PubMed and Web of Science using terms related to ecstatic experience (e.g., ecstatic, bliss, mystical, time dilation) combined with epilepsy, seizure, or aura. This was supplemented by manual screens of review bibliographies and AI-assisted queries. Of 926 selected papers, 33 were retained for localization analysis. We included studies from which lateralization and localization data could be reliably extracted and evaluated. From the extracted data, 51 patients were initially identified. The definitive analysis, however, was restricted to 9 patients who met "high" or "very high" confidence criteria for the correct delineation of the epileptogenic zone (EZ). A secondary analysis of the symptomatogenic zone (SZ) was conducted, drawing on data from 9 patients and identifying 14 sublobar localizations.

Results

For the EZ, the highest level of evidence pointed to various subregions of the temporal lobe, particularly the anterior, basal or mesial regions, identified in 6 of the 9 high-quality cases. For the SZ, the insular lobe was the most frequently identified region, particularly the dorsal anterior portion, which accounted for 9 of the 14 identified localizations.

Significance

Evidence from the highest-quality surgical series and individual case reports consistently demonstrates that the EZ for ecstatic seizures resides in the temporal lobe or, in approximately one-third of cases, extra-temporal structures (insulo-opercular or orbitofrontal cortex). In contrast, data from direct electrical stimulation, intracranial recordings, and ictal single-photon emission computed tomography (SISCOM) strongly point to the insular cortex as the symptom-generating zone. This review is limited by the relatively low number of eligible patients with sufficient electro-clinical data and the high risk of bias in the existing literature.

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