We aimed to determine whether lesion connectivity to previously published adult-derived epilepsy risk networks, identified in adult stroke patients, is associated with post-stroke epilepsy (PSE) in pediatric stroke patients.

PSE is a common and potentially debilitating sequelae of pediatric stroke. Recent lesion-network mapping work has identified distributed brain networks associated with epilepsy outcomes in adult ischemic stroke patients (Schaper et al., 2023).

We analyzed neuroimaging data from 328 children enrolled in the Vascular Effects of Infection in Pediatric Stroke (VIPS I) study. Lesion network mapping was used to estimate the connectivity of each pediatric patient’s lesion with previously published adult-derived epilepsy risk networks. We used independent samples unequal variance t-tests to compare mean intra-lesion network connectivity scores between children who developed epilepsy (n = 40) and those who did not (n = 288), and we used logistic regression to evaluate whether lesion-connectivity scores provide unique predictive power when accounting for other known risk factors for PSE.

Pediatric patients with epilepsy showed stronger lesion connectivity with the adult-derived functional (t[64.85]=6.03, p<0.001) and structural (t[56.11]=4.64, p<0.001) epilepsy networks than those without epilepsy. The fit of logistic regression models that included lesion volume, age, and presence of acute seizures as predictors was significantly improved when functional (p=0.005), structural (p= p=0.01), or both structural and functional (p=0.02) connectivity scores were added to the models, and the addition of connectivity scores also improved classification performance in cross-validation analyses.

Lesion connectivity to brain networks associated with post-stroke epilepsy in adult patients also predicts children at higher risk of PSE, suggesting common underlying network mechanisms across age groups. Lesion-network connectivity provided unique predictive power beyond that afforded by age of onset, lesion size, or presence of acute post-stroke seizures, supporting the conclusion that damage to specific brain networks uniquely contributes to the development of post-stroke epilepsy.