Seizure termination has been linked to spreading depolarizations (SDs) in experimental models of epilepsy, and SDs have been suggested to protect against seizures. However, the precise mechanisms of seizure-associated SDs remain unclear. Additionally, the co-occurrence of SDs with human seizures remains debated. In this study, we found that SDs are a prominent feature following ictal events in both human clinical recordings and in a rodent model of ictogenesis. Approximately one-third of rodent seizure-like events (SLEs) associated with SDs, while all human seizures analyzed associated with propagating infraslow shifts, indicative of SDs. In rodents, SDs clustered towards the end of ictal events, resulting in significantly shorter SLEs and delayed onset of subsequent SLEs. Interestingly, SLEs with SDs displayed significantly more low gamma activity during ictal events than SLEs that did not end in SDs. Furthermore, we found no significant correlation between [K