Post-Traumatic Epilepsy: Incidence and Mechanisms after Brain Injury

Overview/Disease BurdenPost traumatic epilepsy (PTE) is a form of epilepsy that results from brain damage caused by physical trauma to the brain (traumatic brain injury) and is defined as occurrence of more than one seizure related to the injury itself, occurring after one week of traumatic brain injury [1].PTE is the most common cause of acquired epilepsy, comprising around 20% of symptomatic epilepsy cases and 5% of all cases of epilepsy.It is the most common cause of epilepsy with onset in young adulthood.Head injury increases the risk of developing epilepsy by three times as compared to general population [2][3][4][5].The probability of post traumatic epilepsy is estimated to be 0.7% with mild TBI, 1.2% with moderate TBI, and 10% with severe traumatic brain injury over a five year period.The incidence is much higher with penetrating head injuries, as compared to blunt closed head trauma.The prevalence of post-traumatic epilepsy has also been found to have increased over the last 30 years, likely due to an increase in patient survival after severe brain injury [6,7]. Pathophysiology of PTESeizures following TBI can be categorized in three groups based on the time of onset: Immediate, Early and Late onset seizures.Seizures occurring within 24 hours of injury are categorized as Immediate onset and are thought to be due to immediate repercussion impact of the injury that stimulates brain tissue with low seizure threshold [1,6].They are more common in children.Early onset posttraumatic seizures occur within one week of traumatic insult.The mechanism of these seizures is thought to be related to the initial trauma and shearing forces, causing diffuse axonal injury and focal brain injury, caused by direct impact or brain movement inside the skull, or by penetrating wounds.Such mechanisms are followed by secondary axonal injury, due to swelling, retraction, and degeneration of injured neurons.Secondary effects from head trauma like cerebral edema, hemorrhage and contusion, causes alteration in blood brain barrier, damage of tissues due to release of free oxygen radicals and cytokines, the influx of calcium into open ion channels, and the release of excitatory neurotransmitters like glutamate [7][8][9].Incidence depends on the severity of injury and 10-15% of adults and 30 to 35% of children develop early onset seizures after severe TBI.Early PTS is the most significant risk factor for development of PTE in adults [6,10].Nonconvulsive seizures (detected by continuous EEG) are more common than convulsive seizure in first week Abstract Post-traumatic epilepsy can result from traumatic brain injury (TBI) due to a number immediate and chronic changes to the cellular environment in the affected tissues.This form of acquired epilepsy represents 20% of symptomatic epilepsy cases and relates to injury severity.The pathological mechanisms occurring after TBI that give rise to seizure initiation include an early phase (early PTE 1-7 days post-injury) and a late phase which can occur months to years after TBI.The pathological mechanisms at early and late onset PTE differ, and are still poorly understood.Underlying mechanisms are reviewed in the context of epileptogenesis, and prophylactic use of medications is briefly reviewed for both pediatric and adult patients in relation to outcomes.PTE is a concerning adverse health outcome as a consequence of TBI, and should be assessed and monitored with newer advances in bedside point of care technologies.Technologies such as blood biomarker tests and portable EEG devices hold promise for diagnosing and even predicting PTE.