Certain secondary antiepileptic drugs can rescue hippocampal injury following a critical growth period despite poor anticonvulsant activity and cognitive deficits.

Clinical and experimental studies have shown that many common secondary antiepileptic drugs (AEDs) are ineffective at blocking seizures in adulthood; however, some afford neuroprotection. In early development, certain AEDs cause apoptosis; however, it is unknown whether these drugs are neurotoxic to the juvenile brain following a developmentally regulated proapoptotic period and whether they alter the seizure threshold, seizure-induced neuronal vulnerability, and/or cognitive function. Lamotrigine (LTG), carbamazepine (CBZ), phenytoin (PHT), valproate (VPA), and topiramate (TPM) were systemically administered to rat pups for 7days beginning on postnatal (P) day 14 (P14), then half the animals were injected with kainate (KA) to trigger seizures, an age when the CA1 subregion becomes preferentially sensitive to status epilepticus.