Posttraumatic epilepsy (PTE) represents about 2 3% of all the etiologies of epilepsy. The so called early seizures , which appear in the first week after the traumatic brain injury (TBI), are related to the severity of the injury; they do not have an strictly epileptic mechanism, but they become a risk factor to the development of PTE. PTE appears in 5% of all the patients suffering from all TBI, and in 15 20% of the patients suffering from a severe TBI. However, the endpoint uses to be to use antiepileptic drugs (AEDs) as prophylactic treatment in all well established PTE. The efficacy of classic antiepileptic drugs (Phenobarbital, Phenytoin, Carbamazepine, Valproate acid) to control the kindling effect has not been confirmed yet as a prophylactic treatment for PTE. Prophylactic efficacy of other drugs, like lipid peroxidation inhibitors, neuroprotectors (especially antioxidants), glutamic receptor blockers, NMDA receptor blockers, and drugs that modulate apoptosis via caspasas inhibition; however, they constitute new ways of therapeutic investigation with a strong experimental basis. Our recommended therapeutic strategy is not to administrate AEDs indiscriminately, but analyzing risk factors, designing a careful prevention for late seizures using AEDs with proven efficacy in partial seizures and with the best achievable tolerability; being also attentive to the possible use of new drugs in the future, like lipid peroxidation inhibitors, and drugs designed to inhibit other excitotoxic, ionic or oxidative processes.