Post-traumatic epilepsy and recovery of function from experimental brain damage: A review

The incidence of post-traumatic epilepsy (PTE), that is, persistent seizure activity following significant head trauma, varies with the type and severity of the head injury, i.e. depressed skull fractures, haematomas, and penetrating head injuries. Many other factors also appear to determine the risks for developing PTE, such as the length of time for which a person is unconscious following the injury, the development of intracranial pressure or haemorrhage, focal neurological signs, location of the injury, and age 1. A common preventative treatment for the recurrence of PTE is the administration of anticonvulsant drugs. The idea of pharmacological prophylaxis of PTE is based on the clinical observation that there is a delay, described by Glotzner 2 as an 'incubation period', between brain injury and the first seizure. Animal studies have been conducted to examine the effects of anticonvulsant drugs on behavioural recovery from brain damage. Animals, including humans, show a remarkable capacity for recovery after brain injury. It is clear that many of the drugs administered to patients after head injury have pronounced effects on neuronal function and could influence the rate or extent of recovery. Although anticonvulsant drugs are commonly given prophylactically to humans following brain injury, there is very little information about their effects upon subsequent behavioural recovery. It has, however been argued by Pellock 3 that overall, there is only an approximate 5% risk, post brain injury, of developing PTE which suggests that the remaining 95% may receive anticonvulsants needlessly. This review will examine what is known about the effects of PTE and anticonvulsant drugs on recovery of function from experimental brain damage, on the basis of several experimental animal studies which have attempted to address this issue over the past 10 years. The review will look first at two animal models: amygdala kindling, which is used as a model for human epilepsy; and a model of neurological effects of brain damage. PTE, anticonvulsants and recovery of function following experimental brain damage will then be discussed.