Patients surviving ischemic stroke often express delayed epileptic syndromes. Late poststroke seizures occur after a latency period lasting from several months to years after the insult. These seizures might result from ischemia-induced neuronal death and associated morphological and physiological changes that are only partly elucidated. This review summarizes the long-term morphofunctional alterations observed in animal models of both focal and global ischemia that could explain late-onset seizures and epileptogenesis. In particular, this review emphasizes the change in GABAergic and glutamatergic signaling leading to hyperexcitability and seizure genesis.