Traumatic brain injury is one of the most common causes of morbidity and mortality, with posttraumatic epilepsy and functional disability being its major sequelae. Once posttraumatic epilepsy has developed, it remits less often than previously reported. Patients with penetrating head trauma have a very high incidence of posttraumatic epilepsy because of dural tear with intracerebral blood and metallic fragments. Several animal models have been used to explore the structural, chemical, and physiologic changes that are responsible for seizures in traumatic brain injury. Animal studies suggested 2 potential mechanisms of epileptogenesis in patients with head injury: occurrence of disinhibition and development of new functional excitatory connectivity. Possibly, reorganization of astrocytes may, along with dendritic sprouting and new synapse formation, form the structural basis for recurrent excitation in the epileptic brain. Structural imaging abnormalities on magnetic resonance imaging have been assessed as a biomarker to predict the risk of posttraumatic epilepsy following traumatic brain injury. Hippocampal volume deficit and inferior temporal cortex thinning predict early posttraumatic epilepsy. Genetic studies have suggested there is a significant genetic contribution to the development of posttraumatic epilepsy. Abnormalities in neuronal glutamate transporter genes were found to be associated with increased risk of epileptogenesis following severe traumatic brain injury. Epileptiform abnormalities in EEG performed in the acute period following traumatic brain injury predict first-year posttraumatic epilepsy. No effective prophylaxis for posttraumatic epilepsy currently exists. Levetiracetam is now considered a preferred drug over phenytoin because use of phenytoin was associated with longer length of hospital stay and more dizziness. Vagus nerve stimulation should be considered in patients with medically refractory posttraumatic epilepsy who are not good candidates for resection. Long-term mortality is higher in patients with posttraumatic epilepsy than in other patients with traumatic brain injury. In this article, the author summarizes the current data on epileptogenesis of posttraumatic epilepsy. The author also provides updated information on the epidemiology, clinical features, differential diagnosis, and management of posttraumatic epilepsy.
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• Posttraumatic seizures may occur almost simultaneously with head injury or be delayed for several years.
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• Once posttraumatic epilepsy has developed, it remits less often than previously reported.
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• Patients with posttraumatic epilepsy appear to have a higher mortality rate than patients with traumatic brain injury without epilepsy.
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• Posttraumatic epilepsy appears in many cases as temporal lobe epilepsy that possibly originates from the hippocampus.
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• Neither phenytoin nor any other antiepileptic drugs have proven valuable for preventing the development of late posttraumatic epilepsy.
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• The most effective way to prevent posttraumatic epilepsy is to prevent head trauma.
Historical note and terminology
Hippocrates (460 BC to 357 BC), in "Injuries of the Head," observed that a wound of 1 side of the head could cause convulsions on the other side of the body. By the time of the Renaissance, physicians were aware of the potential for head injuries to cause both acute convulsions and chronic epilepsy (83). In the 19th century, John Hughlings Jackson provided a detailed description of the association between the character of epileptic attacks and the location of causative head injury wounds (80). Penfield and colleagues extended Jackson's observations relating injury location to symptomatology and recognized meningocerebral scar formation in the pathophysiology of posttraumatic epilepsy (65; 68; 67; 66).
Military conflicts have been a major cause of head injuries throughout recorded history, and studies of posttraumatic epilepsy have been conducted following World War I (04), World War II (94; 88; 89; 90), the Korean War (93), and the Vietnam War (09; 77; 78). Studies of posttraumatic epilepsy in nonmilitary personnel have been fewer and reported most extensively by Jennett and colleagues (38; 34; 35; 36; 37) and later by several other groups (18; 19; 54; 46; 82).