eMedicine Specialties > Neurology > Seizures and Epilepsy

Posttraumatic Epilepsy

Author: Ewa Posner, MD, MRCP, Consultant Pediatrician, Department of Pediatrics, University Hospital of North Durham, UK
Coauthor(s): Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Contributor Information and Disclosures

Updated: Oct 22, 2009

Introduction

Background

Posttraumatic epilepsy (PTE) refers to a recurrent seizure disorder, the cause of which is believed to be injury to the brain. This injury can be a result of head trauma or a sequel to an operation on the brain. The term PTE must be differentiated from the term posttraumatic seizure (PTS), which signifies any seizure that occurs as a sequel to brain injury. If the seizures occur within 24 hours of the injury, they are called immediate PTSs. A PTS that occurs within 1 week of injury is termed early PTS, and a seizure that occurs more than 1 week after injury is termed late PTS. About 20% of people who have 1 late PTS never have any more, and these people should not be described as having PTE.

Pathophysiology

The mechanism by which trauma to the brain tissue leads to recurrent seizures is unknown. Cortical lesions 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. In the pathophysiology of the PTE kindling model of epilepsy, damage by free radicals caused by iron deposition from extravasated blood and damage by excitotoxicity due to accumulation of glutamate have been postulated. Animal studies suggest that blood brain barrier is disrupted in PTE and this is likely to contribute to the generation of seizures.

Some natural antioxidants, such as alpha-tocopherol and condensed tannins, have been demonstrated to be prophylactic for the occurrence of epileptic discharge in the iron-injected animal brain.1 Studies suggest that antioxidants like phosphate diester of vitamin E and C, vanillyl alcohol, and melatonin may be useful alternative medications for preventing PTE.

Frequency

United States

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. 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. 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.

International

The data above are based on studies from the United States and Europe. In Japan, the occurrence of PTE is approximately 150,000 annually; 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.2

Mortality/Morbidity

Approximately 80% of first PTS occur within 2 years of the injury.

Age

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 adults.

Clinical

History

The seizures are usually partial (focal) or generalized tonic-clonic. Often, both types coexist. Most early PTS are partial seizures, whereas most late PTS, especially when part of PTE, are generalized and either primary or secondary.

Physical

No specific findings are noted on physical examination.

Causes

By definition, PTE is a result of injury to the brain. Recent data suggest that neuroimaging and genomic information (eg, haptoglobin genotypes, apolipoprotein E levels) may be helpful in predicting an individual's risk for PTE. Early PTSs are more common in children younger than 5 years, in patients with focal neurologic deficits, and in patients with a linear or depressed skull fracture than in others.

Factors that increase the risk of PTE are as follows:

  • Severity of trauma
  • Penetrating head injuries
  • Intracranial hematoma
  • Depressed skull fracture
  • Hemorrhagic contusion
  • Coma lasting more than 24 hours
  • Early PTS

More on Posttraumatic Epilepsy

Overview: Posttraumatic Epilepsy
Differential Diagnoses & Workup: Posttraumatic Epilepsy
Treatment & Medication: Posttraumatic Epilepsy
Follow-up: Posttraumatic Epilepsy
References
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References

  1. Mori A, Yokoi I, Noda Y, Willmore LJ. Natural antioxidants may prevent posttraumatic epilepsy: a proposal based on experimental animal studies. Acta Med Okayama. Jun 2004;58(3):111-8. [Medline].

  2. Skandsen T, Ivar Lund T, Fredriksli O, Vik A. Global outcome, productivity and epilepsy 3--8 years after severe head injury. The impact of injury severity. Clin Rehabil. Jul 2008;22(7):653-62. [Medline].

  3. Hudak AM, Trivedi K, Harper CR, Booker K, Caesar RR, Agostini M, et al. Evaluation of seizure-like episodes in survivors of moderate and severe traumatic brain injury. J Head Trauma Rehabil. Jul-Aug 2004;19(4):290-5. [Medline].

  4. Temkin NR, Dikmen SS, Wilensky AJ. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. N Engl J Med. Aug 23 1990;323(8):497-502. [Medline].

  5. Milligan TA, Hurwitz S, Bromfield EB. Efficacy and tolerability of levetiracetam versus phenytoin after supratentorial neurosurgery. Neurology. Aug 26 2008;71(9):665-9. [Medline].

  6. Angeleri F, Majkowski J, Cacchio G, et al. Posttraumatic epilepsy risk factors: one-year prospective study after head injury. Epilepsia. Sep 1999;40(9):1222-30. [Medline].

  7. Annegers JF, Hauser WA, Coan SP, et al. A population-based study of seizures after traumatic brain injuries. N Engl J Med. Jan 1 1998;338(1):20-4. [Medline].

  8. Beghi E. Overview of studies to prevent posttraumatic epilepsy. Epilepsia. 2003;44 Suppl 10:21-6. [Medline].

  9. Chang BS, Lowenstein DH. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. Jan 14 2003;60(1):10-6. [Medline].

  10. Chang BS, Lowenstein DH. Practice parameter: antiepileptic drug prophylaxis in severe traumatic brain injury: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. Jan 14 2003;60(1):10-6. [Medline].

  11. D'Ambrosio R, Perucca E. Epilepsy after head injury. Curr Opin Neurol. Dec 2004;17(6):731-5. [Medline].

  12. Frey LC. Epidemiology of posttraumatic epilepsy: a critical review. Epilepsia. 2003;44 Suppl 10:11-7. [Medline].

  13. Garga N, Lowenstein DH. Posttraumatic epilepsy: a major problem in desperate need of major advances. Epilepsy Curr. Jan-Feb 2006;6(1):1-5. [Medline].

  14. Schierhout G, Roberts I. Anti-epileptic drugs for preventing seizures following acute traumatic brain injury. Cochrane Database Syst Rev. 2001;CD000173. [Medline].

  15. Temkin NR. Prophylactic Anticonvulsants After Neurosurgery. Epilepsy Curr. Jul 2002;2(4):105-107. [Medline].

  16. Temkin NR, Dikmen SS, Anderson GD, et al. Valproate therapy for prevention of posttraumatic seizures: a randomized trial. J Neurosurg. Oct 1999;91(4):593-600. [Medline].

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Further Reading

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Keywords

PTE, head injury, head trauma, posttraumatic seizure, PTS, traumatic brain injury, TBI

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Contributor Information and Disclosures

Author

Ewa Posner, MD, MRCP, Consultant Pediatrician, Department of Pediatrics, University Hospital of North Durham, UK
Ewa Posner, MD, MRCP is a member of the following medical societies: European Paediatric Neurology Society and Royal College of Paediatrics and Child Health
Disclosure: Nothing to disclose.

Coauthor(s)

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

Medical Editor

Joseph F Hulihan, MD, Vice President, Medical Affairs, Ortho-McNeil Janssen Scientific Affairs, LLC
Joseph F Hulihan, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, American Headache Society, and American Medical Association
Disclosure: Johnson & Johnson Salary Employment; Johnson & Johnson Stock Employment

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Jose E Cavazos, MD, PhD, FAAN, Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, University of Texas Health Science Center at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center; Director of the Epilepsy Center, Audie L Murphy Veterans Affairs Medical Center
Jose E Cavazos, MD, PhD, FAAN is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, and Society for Neuroscience
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
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, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
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, and American Medical Association
Disclosure: Nothing to disclose.

 
 
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