ABSTRACT
Traumatic brain injury (TBI) is a recognized risk factor for acute and delayed seizures. Head injury sequelae account for 10-20% of all symptomatic epilepsies and 5% of all epilepsies. Since only an unidentifi ed group of individuals will develop post-TBI seizures, treatments to prevent this phenomenon cannot be targeted to the at risk population. The process of epileptogenesis has been studied in clinical settings as well as in experimental models with the aim of understanding strategies to prevent secondary events after head trauma. Whether insight in these mechanisms will also provide better understanding of epilepsy in general remains unknown, but recent fi ndings suggest an overall link between ictogenesis and mechanisms of delayed epileptogenesis after TBI. Whether these common pathways relate to seizures or comorbidities of the epileptic pathology is unclear. We will review accepted as well as recent hypotheses addressing the mechanisms of epileptogenesis following traumatic brain injury.
