The most common measures of traumatic brain injury (TBI) severity include the Glasgow Coma Scale (GCS), the duration of loss of consciousness (LOC), and the duration of post-traumatic amnesia (PTA). Post-traumatic seizures are usually divided into three categories: immediate, early seizures, and late seizures. Early seizures have a different pathogenesis than late seizures; early post-traumatic seizure (PTS) are thought to be due to mechanical damage to neurons, related to extravasated blood, brain swelling, and perioperative events from cerebral manipulation or stress from general anaesthesia and metabolic factors. The relative risks of epilepsy are raised twofold after a mild head injury and sevenfold after severe head injury, risks are slightly greater in women than in men, and are increased with older age at time of injury. Structural imaging has shown promise for improving prediction of PTS risk. Phenytoin has the most evidence to support its use to reduce early post-traumatic seizures.

Open head injuries (OHI) may be classified according to the dynamics of trauma into perforating and penetrating: perforating injuries occur when an object enters and exits the skull, while penetrating injuries occur when the object does not exit the cranial vault. Two types of mechanism for brain damages are described in OHIs: primary and secondary. The diagnosis of post-traumatic epilepsy requires at least two seizures after head injury. Post-traumatic seizures are usually partial at onset even if secondary generalization may be rapid enough to simulate generalized seizures from onset. About 25% of seizures are focal, 50% focal with secondary generalization, while 25% are generalized. The number of damaged brain lobes may be a predictive factor to evaluate the volume of brain loss. Antiepileptic drugs (AEDs) should be administered to all patients with OHI, in both early and late post-injury phases, especially if a significant loss of brain tissue has occurred.