Stroke is a severe clinical issue for global public health, representing the third leading cause of death and a major cause of disability in developed countries. Progresses in the pharmacological treatment of the acute stroke have given rise to a significant decrease in its mortality rate. However, as a result, there has been an increasing number of stroke survivors living with disability worldwide. Poststroke epilepsy (PSE) is a common clinical complication following stroke. Seizures can arise in close temporal association with stroke damage and/or after a variably longer interval. Overall, PSE have a good prognosis; in fact, its responding rate to antiepileptic drugs (AEDs) is higher than other types of epilepsy. However, regarding pharmacological treatment, some issues are still unresolved. To this aim, a deeper understanding of mechanisms underlying the transformation of infarcted tissue into an epileptic focus or better from a nonepileptic brain to an epileptic brain is also mandatory for PSE. However, studying epileptogenesis in patients with PSE clearly has several limitations and difficulties; therefore, modeling PSE is crucial. Until now, different experimental models have been used to study the etiopathology of cerebrovascular stroke with or without infarction, but few studies focused on poststroke epileptogenesis and PSE. In this review, we show a brief overview on the features emerging from preclinical research into experimental PSE, which could affect the discovery of biomarkers and therapy strategies for poststroke epileptogenesis. This article is part of the Special Issue "Seizures & Stroke".
Keywords: Animal models; Antiepileptic drugs; Disease-modifying treatment; Poststroke epilepsy; Poststroke epileptogenesis; Poststroke seizures.
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