Post-traumatic epilepsy

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Post-traumatic epilepsy
MeSH D004834

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Overview

Post-traumatic epilepsy (PTE) is a clinical syndrome in which a person suffers repeated late post-traumatic seizures (PTS), seizures that result from traumatic brain injury (TBI), or brain damage caused by physical trauma.[1] PTE is estimated to be responsible for 5% of all cases of epilepsy.[2] According to another estimate, 20% of cases of symptomatic epilepsy in the general population are PTE.[3]

A person who has a seizure or seizures due to trauma does not necessarily have PTE, which is a form of epilepsy and is a chronic condition. However, the terms PTS and PTE may be used interchangeably in medical literature.[4] Medical articles usually define PTE as "one or more unprovoked seizures occurring after head trauma", but more recently the definition of all types of epilepsy has been narrowed to include only conditions in which more than one unprovoked seizure occur.[5]

PTE may be caused by several biochemical processes that occur in the brain after trauma, including excitotoxicity and damage to brain tissues by free radicals.[3] The likelihood that a person will develop PTE, which may occur years after the physical trauma that causes it, is influenced by the severity of the injury.

As with other forms of epilepsy, seizures may be generalized or partial.[6] In the time period shortly after head trauma, seizures are commonly generalized, while partial seizures increase in prevalence with increasing time after the injury.[7]

Pathophysiology

For unknown reasons, trauma can cause changes in the brain that lead to epilepsy.[8] There are a number of proposed mechanisms by which TBI causes PTE, more than one of which may be present in a given patient.[3]

In PTE, neurons die, and cavitarian necrosis occurs.[7]

The kindling hypothesis suggests that new neural connections are formed in the brain and cause an increase in excitability.[7] Synapses are reorganized in the hippocampus.[8] Neurons that are in a hyperexcitable state due to trauma may create an epileptic focus in the brain that leads to seizures.[4]

Blood that gathers in the brain after an injury may damage brain tissue and thereby cause epilepsy.[3] Products that result from the breakdown of hemoglobin from blood may be toxic to brain tissue.[3] The "iron hypothesis" holds that PTE is due to damage by oxygen free radicals, the formation of which is catalyzed by iron from blood.[7] Animal experiments using rats have shown that epileptic seizures can be produced by injecting iron into the brain.[3] Iron leads to the formation of hydroxyl radicals by the Haber-Weiss reaction.[3] Free radicals damage brain cells by peroxidizing lipids in their membranes.[9]

The iron from blood also reduces the activity of an enzyme called nitric oxide synthase, another factor thought to contribute to PTE.[7]

Excitotoxicity is another possible factor in the etiology of PTE.[10] TBI causes excessive amounts of the neurotransmitter glutamate to be released, which may be related to seizure development.[4] In addition, the release of inhibitory neurotransmitters such as GABA may be reduced.[3] Overactivation of the biochemical receptors that bind excitatory neurotransmitters like glutamate leads to the formation of free radicals, and it can cause excitotoxicity.[3] Brain cells are damaged due to overexcitation of the receptors for excitatory amino acids on the membranes of neurons.[3] A chronic epileptogenic focus may follow excitotoxicity from excessive release of excitatory neurotransmitters that occurs during seizures.[3]

Diagnosis

Witnessing a seizure is the most effective way to diagnose PTE.[4] EEG is a tool used to diagnose a seizure disorder, but a large portion of people with PTE may not have the abnormal "epileptiform" EEG findings used to diagnose the disorder.[4] However, while EEG is not useful for predicting who will develop PTE, it can be useful to localize the epileptic focus, to determine severity, and to predict whether a person will suffer more seizures if they stop taking antiepileptic medications.[3]

Magnetic resonance imaging (MRI) is performed in people with PTE, and CT scanning can be used if MRI is unavailable to detect brain lesions.[3]

Prevention

Prevention of PTE involves preventing TBI in general. Antiepileptic drugs can prevent early PTS but studies have failed to show that prophylactic use of antiepileptic drugs prevents the development of PTE.[1][11] Therefore, the drugs are recommended to prevent late seizures only for people in whom PTE has already been diagnosed, not as a preventative measure.[12] However, it has been proposed that a narrow window of about one hour after TBI may exist during which administration of antiepileptics could prevent epileptogenesis and PTE.[10]

Treatment

People with PTE may be given antiepileptic drugs to prevent further seizures.[10] However, though antiepileptics prevent seizures while they are being taken, they do not reduce their occurrence once the patient stops taking the drugs.[1] Antiepileptic drugs may be associated with adverse side effects.[12]

People whose PTE does not respond to medication may undergo surgery to remove the epileptogenic focus, the part of the brain that is causing the seizures, but this may be more difficult than it is for epilepsy due to other causes.[10] Surgery is less likely to be helpful in PTE than in other forms of epilepsy because the epileptogenic focus is less localized.[3]

People with PTE have followup visits, in which health care providers monitor neurological and neuropsychological function and assess the efficacy and side effects of medications.[3] As with sufferers of other types of epilepsy, PTE sufferers are advised to exercise caution when performing activities for which seizures could be particularly risky, such as rock climbing.[10]

Prognosis

The prognosis for epilepsy due to trauma is worse than that for epilepsy of undetermined cause.[13] People with PTE are thought to have shorter life expectancies than people with brain injury who do not suffer from seizures.[4] One study found that, compared to people with similar structural brain injuries but without PTE, people with PTE take longer to recover from the injury, have more cognitive and motor problems, and perform worse at everyday tasks.[4] This finding may suggest that PTE is an indicator of a more severe brain injury, rather than a complication that itself worsens outcome.[4] Another study found that PTE was associated with worse social and functional outcomes but did not worsen patients' rehabilitation or return to work.[3] PTE may be associated with a higher incidence of stroke.[4]

About half of PTE cases go into remission.[13] Most PTE sufferers have their first seizure within two years of the TBI; the number may be 80 to 90% or more.[3] Cases of PTE that occur later may have a smaller chance of going into remission.[13]

Epidemiology

Young adults, who are at the highest risk for head injury, also have the highest rate of PTE.[3] One study found PTE to be more common in male TBI survivors than their female counterparts.[4]

Genetics may play a role in the risk that a person will develop PTE; people with the ApoE-ε4 allele may be at higher risk for PTE.[11] The haptoglobin Hp2-2 allele may be another genetic risk factor, possibly because it binds hemoglobin poorly and thus allows more iron to escape and damage tissues.[11]

Risks

It is not clear why some patients get PTE while others with very similar injuries do not.[5] Genes may contribute to a susceptibility to PTE, but most studies have found that having family members with epilepsy does not significantly increase the risk of PTS.[5]

The more severe the brain trauma is, the more likely a person is to suffer late PTE.[7] Evidence suggests that mild head injuries do not confer an increased risk of developing PTE, while more severe types do.[13] In simple mild TBI, the risk for PTE has a standardized incidence ratio of 1.5.[14] About half of sufferers of severe neurotrauma experience PTE.[7] Other estimates place the risk of PTE at 5% for all TBI patients and 15 to 20% for severe TBI.[15]

People who suffer depressed skull fractures, penetrating head trauma, early PTS, and intracerebral and subdural haematomas due to the TBI are especially likely to suffer late PTE, which occurs in more than a 30% of people with any one of these findings.[7] About 50% of patients with penetrating head trauma develop PTE.[3][13] Intracranial hematomas are one of the most important risk factors for PTE.[16] Subdural hematoma confers a higher risk of PTE than does epidural hematoma, possibly because it causes more damage to brain tissue.[3]

The risk that a person will develop PTE is heightened if PTS occur, but occurrence of PTS does not mean that development of epilepsy is certain to occur.[13] However, many of the risk factors for both PTE and early PTS are the same, so it is unknown whether PTS is a risk factor in and of itself.[11] A person who has one late seizure is at even greater risk for having another than one who has early PTS.[3]

Damage to tissues from surgery can cause PTE.[10] Repeated intracranial surgery confers a high risk for late PTE, possibly because these patients are likely to have factors associated with worse brain trauma such as large hematomas or cerebral swelling.[3]

References

  1. 1.0 1.1 1.2 Pagni CA, Zenga F (2005). "Posttraumatic Epilepsy with Special Emphasis on Prophylaxis and Prevention". Acta Neurochirurgica. 93: 27–34. PMID 15986723.
  2. Teasell R, Bayona N, Lippert C, Villamere J, Hellings C (2007). "Post-traumatic Seizure Disorder Following Acquired Brain Injury". Brain Injury. 21 (2): 201–214. doi:10.1080/02699050701201854. PMID 17364531.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 3.17 3.18 3.19 3.20 3.21 Agrawal A, Timothy J, Pandit L, Manju M (2006). "Post-traumatic Epilepsy: An Overview". Clinical Neurology and Neurosurgery. 108 (5): 433–439. doi:10.1016/j.clineuro.2005.09.001. PMID 16225987.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8 4.9 Tucker GJ (2005). "16: Seizures". In Silver JM, McAllister TW, Yudofsky SC. Textbook Of Traumatic Brain Injury. American Psychiatric Pub., Inc. p. 309-321. ISBN 1585621056.
  5. 5.0 5.1 5.2 Frey LC (2003). "Epidemiology of Posttraumatic Epilepsy: A Critical Review". Epilepsia. 44 (Supplement 10): 11–17. doi:10.1046/j.1528-1157.44.s10.4.x. PMID 14511389.
  6. Cuccurullo S (2004). Physical Medicine and Rehabilitation Board Review. Demos Medical Publishing. pp. 68–71. ISBN 1-888799-45-5. Retrieved 2008-02-13.
  7. 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 Iudice A, Murri L (2000). "Pharmacological Prophylaxis of Post-Traumatic Epilepsy". Drugs. 59 (5): 1091–1019. PMID 10852641.
  8. 8.0 8.1 Mazarati A (2006). "Is Posttraumatic Epilepsy the Best Model of Posttraumatic Epilepsy?". Epilepsy Currents. 6 (6): 213–214. doi:10.1111/j.1535-7511.2006.00149.x. PMID 17260063.
  9. Willmore LJ (1990). "Post-traumatic Epilepsy: Cellular Mechanisms and Implications for Treatment". Epilepsia. 31 (Supplement 3): S67–73. PMID 2226373.
  10. 10.0 10.1 10.2 10.3 10.4 10.5 Posner E, Lorenzo N (October 11, 2006). "Posttraumatic Epilepsy". Emedicine.com. Retrieved on 2008-02-19.
  11. 11.0 11.1 11.2 11.3 D'Ambrosio R, Perucca E (2004). "Epilepsy After Head Injury". Current Opinion in Neurology. 17 (6): 731–735. PMID 15542983.
  12. 12.0 12.1 Beghi E (2003). "Overview of Studies to Prevent Posttraumatic Epilepsy". Epilepsia. 44 (Supplement 10): 21–26. PMID 14511391.
  13. 13.0 13.1 13.2 13.3 13.4 13.5 Chadwick D (2005). "Adult Onset Epilepsies". E-epilepsy - Library of articles, National Society for Epilepsy.
  14. Rees PM (2003). "Contemporary Issues in Mild Traumatic Brain Injury". Archives of Physical Medicine and Rehabilitation. 84 (12): 1885–1894. PMID 14669199.
  15. Oliveros-Juste A, Bertol V, Oliveros-Cid A (2002). "Preventive Prophylactic Treatment in Posttraumatic Epilepsy". Revista de Neurolología (in Spanish; Castilian). 34 (5): 448–459. PMID 12040514.
  16. de la Peña P, Porta-Etessam J (1998). "Post-traumatic Epilepsy". Revista de Neurologia (in Spanish; Castilian). 26 (150): 256–261. PMID 9580443.

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