Post-traumatic seizure

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Post-traumatic seizures (PTS) are seizures that result from traumatic brain injury (TBI), brain damage caused by physical trauma. PTS may be a risk factor for post-traumatic epilepsy (PTE), but a person who has a seizure or seizures due to traumatic brain injury does not necessarily have PTE, which is a form of epilepsy, a chronic condition in which seizures occur repeatedly. However, "PTS" and "PTE" may be used interchangeably in medical literature.[1]

Seizures are usually an indication of a more severe TBI.[1] Seizures that occur shortly after a person suffers a brain injury may further damage the already vulnerable brain. [2] They may reduce the amount of oxygen available to the brain,[3] cause excitatory neurotransmitters to be released in excess, increase the brain's metabolic need, and raise the pressure within the intracranial space, further contributing to damage.[2] Thus, people who suffer severe head trauma are given anticonvulsant medications as a precaution against seizures.[3]

Around 5 to 7% of people hospitalized with TBI have at least one seizure.[4] PTS are more likely to occur in more severe injuries, and certain types of injuries increase the risk further. The risk that a person will suffer PTS becomes progressively lower as time passes after the injury. However, TBI survivors may still be at risk over 15 years after the injury.[5] Children and older adults are at a higher risk for PTS.

Classificaiton

PTS can further be divided into immediate PTS, also called impact seizures,[3] seizures occurring within 24 hours of injury; early PTS, with seizures between a day and a week after trauma; and late PTS, with seizures more than one week after trauma.[6] Early PTS occur at least once in about 4 or 5% of patients hospitalized with TBI, and late PTS occur at some point in 5% of them.[6] Of all seizures that occur within the first four weeks of head trauma, about 10% occur after the first week.[5]

Immediate and early seizures, which are thought to be a direct reaction to the injury, likely result from different pathophysiological factors than do late seizures, which are believed to result from damage to the cerebral cortex by excitotoxicity and iron from blood.[2]

Prevention

Shortly after TBI, patients are given anticonvulsant medication, because seizures that occur early after trauma can increase brain damage through hypoxia[3] excessive release of excitatory neurotransmitters, increased metabolic demands, and raises pressure within the intracranial space.[2] Prevention of early seizures differs from that of late seizures, because the aim of the former is to prevent damage caused by the seizures, whereas the aim of the latter is to prevent epileptogenesis, or the restructuring of neural circuits within the brain in a way that leads to seizures.[3] Strong evidence from clinical trials suggests that antiepileptic drugs given within a day of injury prevent seizures within the first week of injury, but not after.[4] Anticonvulsants may be ineffective for both early and late seizures in children.[4] Anticonvulsants are commonly given to prevent PTS in the time shortly after TBI, but no treatment is widely accepted to prevent the development of epilepsy.[3] A 2003 review of medical literature found phenytoin to be preventative of early, but probably not late PTS.[7]

For these reasons, antiepileptic drugs are recommended only for patients for a short time after head trauma to prevent immediate and early seizures.[8] The American Academy of Physical Medicine and Rehabilitation recommends that antiepileptics be used prophylactically for early, but not late, seizures.[1] For unknown reasons, prophylactic use of antiepileptic drugs over a long period is associated with an increased risk for seizures.[1]

Assessment and treatment

Medical personnel aim to determine whether a seizure is caused by a change in the patient's biochemistry, such as hyponatremia.[2] Neurological examinations and tests to measure levels of serum electrolytes are performed.[2]

Not all seizures that occur after trauma are PTS; they may be due to a seizure disorder that already existed, which may even have caused the trauma.[9] In addition, post-traumatic seizures are not to be confused with a concussive convulsions, which may immediately follow a concussion but which are not actually seizures and are not a predictive factor for epilepsy.[10]

Neuroimaging is used to guide treatment. Often, MRI is performed in any patient with PTS, but the less sensitive but more easily accessed CT scan may also be used.[11]

Antiepileptic drugs that may be given intravenously shortly after injury include phenytoin, sodium valproate, carbamazepine, and phenobarbital.[2] Antiepileptic drugs do not prevent all seizures in all seizure patients.[5] However, phenytoin and sodium valproate usually stop seizures that are in progress.[2]

Prognosis

It is unknown exactly how long after a TBI a person is at higher risk for seizures than uninjured people, but estimates have suggested lengths of 10 to over 15 years.[5] For most people with TBI, seizures do not occur after three months,[6] and only 20 to 25% of people who suffer TBI have PTS more than two years after the injury.[6] However, moderate or severe TBI still confers a high risk for PTS for up to five years after the injury.[4]

In one quarter of people with seizures from a head trauma, medication controls them well.[1]

Risk of developing PTE

Early PTS, while not necessarily epileptic in nature, are a risk factor for PTE.[12] However, occurrence of PTS does not mean that development of epilepsy is certain to occur.[13] About 3% of patients with no early seizures develop late PTE; this number rises to 25% in those who do have early PTS, and the distinction is even greater if other risk factors for developing PTE are excluded.[13] Seizures that occur immediately after an insult are commonly believed not to confer an increased risk of recurring seizures, but evidence from at least one study has suggested that both immediate and early seizures may be risk factors for late seizures.[5]

Risk factors

The chances that a person will suffer PTS are influenced by factors involving the injury and the person. The largest risk for PTS is penetrating head trauma, which carries a 35 to 50% risk of seizures within 15 years.[2] If a fragment of metal remains in within the skull after injury, the risk of both early and late PTS may be increased.[5] Head trauma survivors who abused alcohol before the injury also at higher risk for developing seizures.[4] People with the ApoE-ε4 allele may also be at higher risk for late PTS.[1]

Risks for late PTS include a torn dura mater, focal neurological deficits,[6] hydrocephalus, reduced blood flow to the temporal lobes of the brain,[1] brain contusions and subdural hematomas.[5] Post-traumatic amnesia (PTA) that lasts for longer than 24 hours after the injury is a risk factor for both early and late PTS.[1] Up to 86% of people who have one late post-traumatic seizure have another within two years.[5]

Epidemiology

File:Pts bar graph by severity.svg
The relative risk of PTS increases with the severity of injury.[2]

Research has found that the incidence of PTS varies widely based on the population studied; it may be as low as 4.4% or as high as 53%.[5] Of all TBI patients who are hospitalized, 5 to 7% have PTS.[4] PTSs occur in about 3.1% of traumatic brain injuries, but the severity of injury affects the likelihood of occurrence.[6] The most important factor in whether a person will develop early and late seizures is the extent of the damage to the brain.[2] More severe brain injury also confers a risk for developing PTS for a longer time after the event.[4] One study found that the probability that seizures will occur within 5 years of injury is in 0.5% of mild traumatic brain injuries (defined as no skull fracture and less than 30 minutes of PTA or loss of consciousness, abbreviated LOC); 1.2% of moderate injuries (skull fracture or PTA or LOC lasting between 30 minutes and 24 hours); and and 10.0% of severe injuries (cerebral contusion, intracranial hematoma, or LOC or PTA for over 24 hours).[14] Another study found that the relative risk of seizures is 1.5 in mild (defined as PTA or LOC for less than 30 minutes), 2.9 in moderate TBI (LOC lasting between 30 minutes and 1 day), and 17.2 in severe TBI (cerebral contusion, subdural hematoma, or LOC for over a day; image at right).[2]

Immediate seizures have an incidence of 1 to 4%, that of early seizures is 4 to 25%, and that of late seizures is 9 to 42%.[2]

Age influences the risk for PTS. Early seizures up to twice as frequently in children as they do in their adult counterparts.[5] As age increases, risk of early and late seizures decreases; one study found that early PTSs occurred in 30.8% of children age 7 or under, 20% of children between ages 8 and 16, and 8.4% of people who were over 16 at the time they were injured.[5][15] In one study, children under age five with trivial brain injuries (those with no LOC, no PTA, no depressed skull fracture, and no hemorrhage) suffered an early seizure 17% of the time, while people over age 5 did so only 2% of the time.[5] People over age 65 are also at greater risk for developing PTS after an injury.[1][5]

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 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.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 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.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 Iudice A, Murri L (2000). "Pharmacological Prophylaxis of Post-Traumatic Epilepsy". Drugs. 59 (5): 1091–1019. PMID 10852641.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 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.
  5. 5.00 5.01 5.02 5.03 5.04 5.05 5.06 5.07 5.08 5.09 5.10 5.11 5.12 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. 6.0 6.1 6.2 6.3 6.4 6.5 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. Chang BS, Lowenstein DH (2003). "Practice Parameter: Antiepileptic Drug Prophylaxis in Severe Traumatic Brain Injury: Report of the Quality Standards Subcommittee of the American Academy of Neurology". Neurology. 60 (1): 10–16. PMID 12525711.
  8. Beghi E (2003). "Overview of Studies to Prevent Posttraumatic Epilepsy". Epilepsia. 44 (Supplement 10): 21–26. PMID 14511391.
  9. Kushner D (1998). "Mild Traumatic Brain Injury: Toward Understanding Manifestations and Treatment". Archives of Internal Medicine. 158 (15): 1617–1624. PMID 9701095.
  10. Ropper AH, Gorson KC (2007). "Clinical Practice. Concussion". New England Journal of Medicine. 356 (2): 166–172. doi:10.1056/NEJMcp064645. PMID 17215534.
  11. Posner E, Lorenzo N (October 11, 2006). "Posttraumatic Epilepsy". Emedicine.com. Retrieved on 2008-02-19.
  12. 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.
  13. 13.0 13.1 Chadwick D (2005). "Adult Onset Epilepsies". E-epilepsy - Library of articles, National Society for Epilepsy.
  14. D'Ambrosio R, Perucca E (2004). "Epilepsy After Head Injury". Current Opinion in Neurology. 17 (6): 731–735. PMID 15542983.
  15. Asikainen I, Kaste M, Sarna S (1999). "Early and Late Posttraumatic Seizures in Traumatic Brain Injury Rehabilitation Patients: Brain Injury Factors Causing Late Seizures and Influence of Seizures on Long-Term Outcome". Epilepsia. 40 (5): 584–589. doi:10.1111/j.1528-1157.1999.tb05560.x. PMID 10386527.