Abstract

Post traumatic epilepsy is defined by recurrent seizures secondary to brain injury following head trauma and represent the most frequent cause of epilepsy in young adults. Most post traumatic epilepsies start within two years from trauma, but in some cases may present several years after the brain injury. Severe traumatic brain injuries tend to correlate with an increased risk of developing early and late post-traumatic seizures. A cranial trauma creates a potentially epileptogenic brain damage through a number of different mechanisms. Several structural, physiological and biochemical modifications occur in a brain after a head injury that promote oxidative stress mechanisms and excitotoxic mechanisms. Current evidence shows that prophylactic use of antiepileptic drugs prevent the occurrence of early post-traumatic seizure but does not influence the incidence of post-traumatic epilepsy. Some authors propose treatment with antioxidant drugs in acute phase of severe traumatic brain injuries in order to prevent early tissue changes established in the traumatized tissue.

Highlights

  • Post-traumatic epilepsy (PTE) is a form of symptomatic epilepsy defined by the presence of recurrent seizures secondary to traumatic brain injury [1]

  • We distinguish from immediate post-traumatic seizures (PTSs) which occur within 24 hours after injury, early seizures which occur within a week after injury and late seizures which occur after one week after injury

  • Immediate and early seizures belong to the group of provoked seizures and they do not define epilepsy since they are not underlying a pathogenic mechanism that chronically predisposes the patient to manifest epileptic seizures [2]

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Summary

Introduction

Post-traumatic epilepsy (PTE) is a form of symptomatic epilepsy defined by the presence of recurrent seizures secondary to traumatic brain injury [1]. PTE epidemiology mainly uses frequency rates of epilepsy in traumatized patients and rates of “incidence ratio” between population with head injury and general population.

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Conclusion

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