Brain Damage During New-Onset Refractory Status Epilepticus
Simmen, C. F.; Stattmann, M.; Togni, C.; Eisele, A.; Hortobagyi, T.; Schubert, K. M.; Braun, A. A.; Casagrande, F.; Ferreira Atuesta, C.; Briel, N.; Schmick, A.; Herwerth, M.; Lasne, A.; Mock, N.; Appenzeller, S.; Loosli, S.; Liu, R.; Duncan, J. S.; Rajakulendran, S.; Walker, M. C.; Neligan, A.; Kilmer, J.; Prados Carrasco, F.; Kunst, S.; Fearns, N.; Dimitriadis, K.; Schmidbauer, M. L.; Fisch, U.; Sutter, R.; Rueegg, S.; Bosque Varela, P.; Kuchukhidze, G.; Trinka, E.; Zelano, J.; Akel, S.; Zetterberg, H.; De Stefano, P.; Seeck, M.; Fluegel, D.; Zieglgaensberger, D.; Schaper, F. L. W. V. J.; Tu
Show abstract
Status epilepticus (SE) has long been linked to neuronal damage in experimental and animal studies, yet direct human evidence remains scarce. The risk of seizure-induced brain injury is central to the definition, urgency, treatment, and prognosis of SE. We studied 2,055 longitudinal MRI scans from 559 individuals, including 33 patients with new-onset refractory SE (NORSE) across multiple centres, to quantify grey matter volume changes during and after SE. We demonstrate a rapid, widespread, and irreversible decline in grey matter volume during NORSE, exceeding normal aging by 80-fold and Alzheimers disease by 20-fold. Fluid biomarkers confirmed marked neurodegeneration during NORSE, correlated with grey matter volume reduction, and returned to low levels after SE. Accelerated atrophy was linked to longer SE duration, poorer long-term outcome, and cryptogenic aetiology. These findings underscore the urgency of treating SE to limit brain damage and provide a framework for evaluating potentially neuroprotective interventions in humans.
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