About half of PTE cases go into remission, but cases that occur later may have a smaller chance of doing so. Epidemiology
Studies have found that the incidence of PTE ranges between 1.9 and more than 30% of those with TBI, varying by severity of injury and by the amount of time after TBI for which the studies followed subjects.Brain trauma is one of the strongest predisposing factors for epilepsy development, and is an especially important factor in young adults. Young adults, who are at the highest risk for head injury, also have the highest rate of PTE, which is the largest cause of new-onset epilepsy cases in young people. Children have a lower risk for developing epilepsy; 10% of children with severe TBI and 16–20% of similarly injured adults develop PTE. Being older than 65 is also a predictive factor in the development of epilepsy after brain trauma. One study found PTE to be more common in male TBI survivors than in females. History
Records of PTE exist from as early as 3000 BC. Trepanation, in which a hole is cut in the skull, may have been used to treat PTE in ancient cultures. In the early 19th century, the surgeons Baron Larrey and WC Wells each reported having performed the operation for PTE. The French-educated American surgeon Benjamin Winslow Dudley (1785–1870) performed six trepanations for PTE between the years of 1819 and 1832 in Kentucky and had good results despite the unavailability of antisepsis.
Status epilepticus, a continuous seizure or multiple seizures in rapid succession, is especially strongly correlated with the development of PTE; status seizures occur in 6% of all TBIs but are associated with PTE 42% of the time, and quickly halting a status seizure reduces chances of PTE development. Pathophysiology
For unknown reasons, trauma can cause changes in the brain that lead to epilepsy. There are a number of proposed mechanisms by which TBI causes PTE, more than one of which may be present in a given person. In the period between a brain injury and onset of epilepsy, brain cells may form new synapses and axons, undergo apoptosis or necrosis, and experience altered gene expression. In addition, damage to particularly vulnerable areas of the cortex such as the hippocampus may give rise to PTE.Blood that gathers in the brain after an injury may damage brain tissue and thereby cause epilepsy. Products that result from the breakdown of hemoglobin from blood may be toxic to brain tissue. The "iron hypothesis" holds that PTE is due to damage by oxygen free radicals, the formation of which is catalyzed by iron from blood. Animal experiments using rats have shown that epileptic seizures can be produced by injecting iron into the brain. Iron catalyzes the formation of hydroxyl radicals by the Haber-Weiss reaction; such free radicals damage brain cells by peroxidizing lipids in their membranes.