Posttraumatic Epilepsy

Posttraumatic Epilepsy

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Posttraumatic epilepsy (PTE) is a recurrent seizure disorder that apparently results from injury to the brain. [1] 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. [2]

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 [3] :

Age younger than 5 years or older than 65 years

Chronic alcoholism

Apolipoprotein E epsilon4 genotype has been proposed as a risk factor, [4, 5] but other studies have not found that to be the case. [6, 7]

Injury-related factors that increase the risk of PTE are as follows [8] :

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 [9]

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. [10] 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. [11]

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.

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

Lucke-Wold BP, Nguyen L, Turner RC, Logsdon AF, Chen YW, Smith KE, et al. Traumatic brain injury and epilepsy: Underlying mechanisms leading to seizure. Seizure. 2015 Dec. 33:13-23. [Medline].

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

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

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

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].

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].

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].

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].

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].

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].

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].

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].

Wilson CD, Burks JD, Rodgers RB, Evans RM, Bakare AA, Safavi-Abbasi S. Early and Late Post-Traumatic Epilepsy in the Setting of Traumatic Brain Injury: A Review of Anti-Epileptic Management. World Neurosurg. 2017 Nov 28. [Medline].

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].

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].

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].

[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].

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

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

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].

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

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].

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].

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].

David Y Ko, MD Associate Professor of Clinical Neurology, Loma Linda University School of Medicine

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

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: SK<br/>Serve(d) as a speaker or a member of a speakers bureau for: Eisai, Lundbeck, Sunovion, Supernus, UCB.

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

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.

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)

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.

Posttraumatic Epilepsy

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