page_title: Post-traumatic epilepsy
section_title: Treatment
hierarchical_section_title: Post-traumatic epilepsy / Treatment
caption_attribution_description: Space-filling model of carbamazepine. Created using ACD/ChemSketch 10.0, Accelrys DS Visualizer Pro 1.6 and GIMP.
context_page_description: Post-traumatic epilepsy is a form of acquired epilepsy that results from brain damage caused by physical trauma to the brain. A person with PTE suffers repeated post-traumatic seizures more than a week after the initial injury. PTE is estimated to constitute 5% of all cases of epilepsy and over 20% of cases of acquired epilepsy.
  It is not known how to predict who will develop epilepsy after TBI and who will not. However, the likelihood that a person will develop PTE is influenced by the severity and type of injury; for example penetrating injuries and those that involve bleeding within the brain confer a higher risk. The onset of PTE can occur within a short time of the physical trauma that causes it, or months or years after. People with head trauma may remain at a higher risk for post-traumatic seizures than the general population even decades after the injury. PTE may be caused by several biochemical processes that occur in the brain after trauma, including overexcitation of brain cells and damage to brain tissues by free radicals.
context_section_description: Antiepileptic drugs may be given to prevent further seizures; these drugs completely eliminate seizures for about 35% of people with PTE. However, antiepileptics only prevent seizures while they are being taken; they do not reduce the occurrence once the patient stops taking the drugs. Medication may be stopped after seizures have been controlled for two years. PTE is commonly difficult to treat with drug therapy, and antiepileptic drugs may be associated with side effects.  The antiepileptics carbamazepine and valproate are the most common drugs used to treat PTE; phenytoin may also be used but may increase risk of cognitive side effects such as impaired thinking.  Other drugs commonly used to treat PTE include clonazepam, phenobarbitol, primidone, gabapentin, and ethosuximide.  Among antiepileptic drugs tested  for seizure prevention after TBI (phenytoin, sodium valproate, carbamazepine, phenobarbital), no evidence from randomized controlled trials has shown superiority of one over another.
  People whose PTE does not respond to medication may undergo surgery to remove the epileptogenic focus, the part of the brain that is causing the seizures. However surgery for PTE may be more difficult than it is for epilepsy due to other causes, and is less likely to be helpful in PTE than in other forms of epilepsy. It can be particularly difficult in PTE to localize the epileptic focus, in part because TBI may affect diffuse areas of the brain. Difficulty locating the seizure focus is seen as a deterrent to surgery. However, for people with sclerosis in the mesial temporal lobe (in the inner aspect of the temporal lobe), who comprise about one third of people with intractable PTE, surgery is likely to have good outcome.  When there are multiple epileptic foci or the focus cannot be localized, and drug therapy is not effective, vagus nerve stimulation is another option for treating PTE.
  People with PTE have follow-up visits, in which health care providers monitor neurological and neuropsychological function and assess the efficacy and side effects of medications.  As with sufferers of other types of epilepsy, PTE sufferers are advised to exercise caution when performing activities for which seizures could be particularly risky, such as rock climbing.
caption: Carbamazepine, commonly used to treat PTE
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