Posttraumatic epilepsy (PTE) is a recurrent seizure disorder that apparently results from injury to the brain.  This injury may be due to multiple types of head insults often labled traumatic brain injury (TBI). There is an increase in PTE due to increasing TBI. 
PTE must be differentiated from posttraumatic seizures (PTS), which is a broader-spectrum term and signifies seizures that occur as a sequel to brain injury. Seizures that occur within 24 hours after brain injury are called immediate PTS. PTS that occur within 1 week after injury are termed early PTS, and seizures that occur more than 1 week after injury are termed late PTS. About 20% of people who have a single late posttraumatic seizure never have any further seizures, and these people should not be labeled as having PTE. The former definition of epilepsy required 2 unprovoked seizures, but the updated definition of epilepsy can be met with 1 unprovoked seizure and high likelihood of another. This blurrs the definition of PTS and PTE, but it is important to differentiate between the two. As PTS is a provoked seizure it is different than unprovoked seizure, but late PTS may be hard to differentiate from PTE.
In a patient who had a seizure after a recent head injury, investigation of a seizure should focus on determining whether an intracranial bleed or a change in clinical condition (eg, hyponatremia) has caused the seizure (see Workup). Early PTS should be treated promptly, but treatment for late PTS is not mandatory (see Treatment and Management)
Go to Epilepsy and Seizures for an overview of this topic.
The mechanism by which trauma to brain tissue leads to recurrent seizures is unknown because there are so many different types of head insults and the excitatory cascade is a series of complex processes. Cortical lesions with cortical dysfunction seem important in the genesis of the epileptic activity. Early seizures are likely to have a different pathogenesis than late seizures; early PTS are thought to be a nonspecific response to the physical insult.
The PTE kindling model of epilepsy postulates that iron deposition from extravasated blood leads to damage by free radicals, and the accumulation of glutamate leads to damage by excitotoxicity. Animal studies suggest that disruption of the blood-brain barrier is likely to contribute to the generation of seizures in PTE.
New information suggests that inflammation and immune system alteration may be contributing to the development of seizures and epilepsy. The TBI that leads to PTE in humans is probably the best model for studying epileptogenesis, but even then it is difficult to do so. This offers an opportunity to intervene with therapry to decrease the developement of PTE.
By definition, PTE is a result of injury to the brain. Patient factors that increase susceptibility to PTE include the following  :
Age younger than 5 years or older than 65 years
Injury-related factors that increase the risk of PTE are as follows  :
Penetrating head injuries
Linear or depressed skull fracture
Coma lasting more than 24 hours
History of prior TBI as it tends to be cumulative
Focal neuroimaging or electroencephalographic abnormalities in the acute postinjury period 
Although the incidence of epilepsy in the general population is estimated at 0.5-2%, the incidence of PTS for all types of head injuries is 2-2.5% in civilian populations and is higher in the military due to higher-velocity projectiles. This incidence increases to 5% in hospitalized neurosurgical patients. When only severe head injuries (usually Glasgow Coma Scale score < 9) are considered, the incidence is 10-15% for adults and 30-35% for children.
In the United States, the incidence of brain injury is highest among young adults; this is reflected in the incidence of PTE in the relevant age group. Early PTS are more common in children, while late PTS are more common in older adults. [3, 4]
The incidence of PTS is as high as 50% in military series, as these studies include many patients with penetrating head injuries.  The incidence of seizures (excluding early seizures) after uncomplicated mild head injury is the same in the military population as in the general population.
In Japan, approximately 150,000 cases of PTE occur each year; this equals 10% of all hospitalized patients with head injury and 1% of all outpatients with head injury. In a study from Norway, the incidence of PTE in a mixed age group of patients with severe head injuries was 23%, and there was significant correlation with severity of injury and intracranial surgery. 
Approximately 80% of first PTS occur within 2 years of the injury. The risk of PTS decreases with time and reaches the normal value for the population at 5 years after the head injury. About half the patients who develop late PTS have 3 or fewer seizures and go into spontaneous remission thereafter.
As in any seizure disorder with alteration of awarness, patients must be warned to exercise caution during bathing (showers are safer), swimming, and climbing heights. They should never be alone during these activities. Other practical issues come into play such as cooking with open flame, operating dangerous equipment, and so on. In all situations, appropriate steps should be taken to ensure the safety of the person if a seizure occurs. Patients must also be counseled about the limitations in obtaining or retaining a driver’s license.
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David Y Ko, MD Associate Professor of Clinical Neurology, Loma Linda University School of Medicine
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Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS, FAES Professor with Tenure, Departments of Neurology, Neuroscience, and Physiology, Assistant Dean for the MD/PhD Program, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio
Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS, FAES is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, American Neurological Association, Society for Neuroscience
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Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, American Medical Association
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Acorda, Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion, Upsher-Smith.<br/>Serve(d) as a speaker or a member of a speakers bureau for: Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion.<br/>Received research grant from: Acorda, Livanova, Greenwich, Lundbeck, Sepracor, Sunovion, UCB, Upsher-Smith.
Nicholas Lorenzo, MD, CPE Chairman and CEO, Neurology Specialists and Consultants; Senior Vice President, Founding Executive Director, Continuing Medical Education, Gannett Education (Division Gannett Healthcare Group)
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Ewa Posner, MD, MRCP Consultant Pediatrician, Department of Pediatrics, University Hospital of North Durham, UK
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