damage. 89]10111213 Current guidelines (AHA/ASA 2023, ESO 2024) recommend integrating molecular biomarkers, advanced neuroimaging, and AI-based models for risk assessment and optimal therapy selection (Table 1). 6,7,141516 PathoPhysiology o f Cerebral edemaOver the past decade, understanding of molecular processes underlying cerebral edema formation has significantly expanded (Table 2).Particularly important are the roles of AQP4 in regulating water homeostasis and SUR1-TRPM4 introduCtion Ischemic stroke remains one of the leading causes of mortality and long-term disability worldwide. 1,2 In a significant number of patients, the disease is complicated by the development of space-occupying cerebral edema, which may lead to rapid neurological deterioration, brain herniation, and death. 1,2 Traditionally, the management of cerebral edema was largely supportive, and decompressive craniectomy (DC) reserved only for life-threatening cases. 3]5 However, evidence from randomized controlled trials and meta-analyses (e.g., DESTINY-II, HAMLET, DECIMAL) has clearly confirmed the role of DC in reducing mortality and improving functional outcomes. 34]5 In recent years, advances in neuroimaging, neurocritical care, and translational pharmacology have paved the way for a personalized approach to the management of postischemic edema.Radiomics and artificial intelligence (AI) algorithms now enable early prediction of malignant cerebral edema (MCE). 6,7Studies from 2023 to 2025 demonstrate that combined models incorporating clinical and radiomic parameters can accurately identify patients at high risk of MCE. 6,7Additionally, genetic variations in aquaporin-4 (AQP4) and sulfonylurea receptor 1-transient receptor potential melastatin 4 (SUR1-TRPM4) channels and increased expression of matrix metalloproteinase (MMP)-9, S100B, and microribonucleic acids (microRNAs) play a key role in the progression of edema and blood-brain barrier (BBB)
Dostović et al. (2026) studied this question.