Abstract
Dimethyl sulfoxide (DMSO) is widely used as a solvent in endovascular embolization procedures, yet its potential neurotoxic effects remain underexplored. In this correspondence, we highlight emerging evidence suggesting that DMSO exposure may contribute to the development of hydrocephalus through mechanisms involving ependymal damage and astrocyte apoptosis. Drawing on recent experimental findings, we propose that DMSO-induced neuroinflammation may play a role in post-embolization complications. We urge the research community to consider hydrocephalus as a possible, though unproven, outcome of DMSO exposure and to include it in long-term safety assessments of embolic agents.