Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Posttraumatic Epilepsy

  • Author: David Y Ko, MD; Chief Editor: Selim R Benbadis, MD  more...
 
Updated: Apr 04, 2014
 

Background

Posttraumatic epilepsy (PTE) is a recurrent seizure disorder that apparently results from injury to the brain. This injury may be due to traumatic brain injury (TBI) or to an operation on the brain. There is an increase in PTE due to increasing TBI.[1]

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.

In a patient who is still hospitalized 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.

Next

Pathophysiology

The mechanism by which trauma to 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.

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. 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.

Previous
Next

Etiology

By definition, PTE is a result of injury to the brain. Patient factors that increase susceptibility to PTE include the following[2] :

  • Age younger than 5 years or older than 65 years
  • Chronic alcoholism

Apolipoprotein E epsilon4 genotype has been proposed as a risk factor,[3, 4] but other studies have not found that to be the case.[5, 6]

Injury-related factors that increase the risk of PTE are as follows[7] :

  • Severe trauma
  • Penetrating head injuries
  • Intracranial hematoma
  • Linear or depressed skull fracture
  • Hemorrhagic contusion
  • Coma lasting more than 24 hours
  • Early PTS
  • History of prior TBI as it tends to be cumulative
  • Focal neuroimaging or electroencephalographic abnormalities in the acute postinjury period [8]
Previous
Next

Epidemiology

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.

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.[2, 3]

The incidence of PTS is as high as 50% in military series, as these studies include many patients with penetrating head injuries.[9] 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.[10]

Previous
Next

Prognosis

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.

Previous
Next

Patient Education

As in any seizure disorder, patients must be warned to exercise caution during bathing, swimming, and climbing heights. They should never be alone during these activities. 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.

For patient education information, see the Brain and Nervous System Center, as well as Epilepsy.

Previous
 
 
Contributor Information and Disclosures
Author

David Y Ko, MD Associate Professor of Clinical Neurology, Associate Director, USC Adult Epilepsy Program, Keck School of Medicine of the University of Southern California

David Y Ko, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Headache Society, American Clinical Neurophysiology Society

Disclosure: Received honoraria from UCB for speaking and teaching; Received consulting fee from Lundbeck for consulting; Received consulting fee from Westward for consulting; Received consulting fee from Esai for consulting; Received consulting fee from Supernus for consulting; Received consulting fee from Sunovion for speaking and teaching.

Specialty Editor Board

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 Professor with Tenure, Departments of Neurology, Pharmacology, 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; Co-Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director, San Antonio Veterans Affairs Epilepsy Center of Excellence and Neurodiagnostic Centers, Audie L Murphy Veterans Affairs Medical Center

Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Neurological Association, Society for Neuroscience, American Epilepsy Society

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Brain Sentinel, consultant.<br/>Stakeholder (<5%), Co-founder for: Brain Sentinel.

Chief Editor

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: Cyberonics; Eisai; Lundbeck; Sunovion; UCB; Upsher-Smith<br/>Serve(d) as a speaker or a member of a speakers bureau for: Cyberonics (Livanova); Eisai; Lundbeck; Sunovion; UCB<br/>Received research grant from: Cyberonics (Livanova); GW, Lundbeck; Sunovion; UCB; Upsher-Smith.

Acknowledgements

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)

Nicholas Lorenzo, MD, CPE is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and American College of Physician Executives

Disclosure: Nothing to disclose.

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.

References
  1. Hunt RF, Boychuk JA, Smith BN. Neural circuit mechanisms of post-traumatic epilepsy. Front Cell Neurosci. 2013. 7:89. [Medline]. [Full Text].

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

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

  4. Diaz-Arrastia R, Gong Y, Fair S, Scott KD, Garcia MC, Carlile MC, et al. Increased risk of late posttraumatic seizures associated with inheritance of APOE epsilon4 allele. Arch Neurol. 2003 Jun. 60(6):818-22. [Medline].

  5. Anderson GD, Temkin NR, Dikmen SS, Diaz-Arrastia R, Machamer JE, Farhrenbruch C. Haptoglobin phenotype and apolipoprotein E polymorphism: relationship to posttraumatic seizures and neuropsychological functioning after traumatic brain injury. Epilepsy Behav. 2009 Nov. 16(3):501-6. [Medline].

  6. Chamelian L, Reis M, Feinstein A. Six-month recovery from mild to moderate Traumatic Brain Injury: the role of APOE-epsilon4 allele. Brain. 2004 Dec. 127:2621-8. [Medline].

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

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

  9. Raymont V, Salazar AM, Lipsky R, Goldman D, Tasick G, Grafman J. Correlates of posttraumatic epilepsy 35 years following combat brain injury. Neurology. 2010 Jul 20. 75(3):224-9. [Medline]. [Full Text].

  10. 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. 2008 Jul. 22(7):653-62. [Medline].

  11. 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. 2004 Jul-Aug. 19(4):290-5. [Medline].

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

  13. Löscher W, Brandt C. Prevention or modification of epileptogenesis after brain insults: experimental approaches and translational research. Pharmacol Rev. 2010 Dec. 62(4):668-700. [Medline]. [Full Text].

  14. Pearl PL, McCarter R, McGavin CL, Yu Y, Sandoval F, Trzcinski S, et al. Results of phase II levetiracetam trial following acute head injury in children at risk for posttraumatic epilepsy. Epilepsia. 2013 Jul 22. [Medline].

  15. [Guideline] 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. 2003 Jan 14. 60(1):10-6. [Medline].

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

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

  18. Szaflarski JP, Sangha KS, Lindsell CJ, Shutter LA. Prospective, randomized, single-blinded comparative trial of intravenous levetiracetam versus phenytoin for seizure prophylaxis. Neurocrit Care. 2010 Apr. 12(2):165-72. [Medline].

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

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

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

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

 
Previous
Next
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.