Long-term risk of epilepsy after traumatic brain injury in children and young adults: A population-based cohort study

Department of Neurology, Aarhus University Hospital, Aarhus, Denmark.
The Lancet (Impact Factor: 45.22). 03/2009; 373(9669):1105-10. DOI: 10.1016/S0140-6736(09)60214-2
Source: PubMed


The risk of epilepsy shortly after traumatic brain injury is high, but how long this high risk lasts is unknown. We aimed to assess the risk of epilepsy up to 10 years or longer after traumatic brain injury, taking into account sex, age, severity, and family history.
We identified 1 605 216 people born in Denmark (1977-2002) from the Civil Registration System. We obtained information on traumatic brain injury and epilepsy from the National Hospital Register and estimated relative risks (RR) with Poisson analyses.
Risk of epilepsy was increased after a mild brain injury (RR 2.22, 95% CI 2.07-2.38), severe brain injury (7.40, 6.16-8.89), and skull fracture (2.17, 1.73-2.71). The risk was increased more than 10 years after mild brain injury (1.51, 1.24-1.85), severe brain injury (4.29, 2.04-9.00), and skull fracture (2.06, 1.37-3.11). RR increased with age at mild and severe injury and was especially high among people older than 15 years of age with mild (3.51, 2.90-4.26) and severe (12.24, 8.52-17.57) injury. The risk was slightly higher in women (2.49, 2.25-2.76) than in men (2.01, 1.83-2.22). Patients with a family history of epilepsy had a notably high risk of epilepsy after mild (5.75, 4.56-7.27) and severe brain injury (10.09, 4.20-24.26).
The longlasting high risk of epilepsy after brain injury might provide a window for prevention of post-traumatic epilepsy.

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    • "Additional definitions related to PTE revolve around the degree of head trauma. Many investigators currently use the following: (1) mild TBI (loss of consciousness less than 30 min and no skull fracture); (2) moderate TBI (loss of consciousness more than 30 min and less than 24 h, with or without skull fracture); and (3) severe TBI (loss of consciousness greater than 24 h, with contusion, hematoma, or skull fracture) [19] [20]. "
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    ABSTRACT: Post-traumatic epilepsy continues to be a major concern for those experiencing traumatic brain injury. Post-traumatic epilepsy accounts for 10-20% of epilepsy cases in the general population. While seizure prophylaxis can prevent early onset seizures, no available treatments effectively prevent late-onset seizure. Little is known about the progression of neural injury over time and how this injury progression contributes to late onset seizure development. In this comprehensive review, we discuss the epidemiology and risk factors for post-traumatic epilepsy and the current pharmacologic agents used for treatment. We highlight limitations with the current approach and offer suggestions for remedying the knowledge gap. Critical to this pursuit is the design of pre-clinical models to investigate important mechanistic factors responsible for post-traumatic epilepsy development. We discuss what the current models have provided in terms of understanding acute injury and what is needed to advance understanding regarding late onset seizure. New model designs will be used to investigate novel pathways linking acute injury to chronic changes within the brain. Important components of this transition are likely mediated by toll-like receptors, neuroinflammation, and tauopathy. In the final section, we highlight current experimental therapies that may prove promising in preventing and treating post-traumatic epilepsy. By increasing understanding about post-traumatic epilepsy and injury expansion over time, it will be possible to design better treatments with specific molecular targets to prevent late-onset seizure occurrence following traumatic brain injury.
    Seizure 12/2015; 33:13-23. DOI:10.1016/j.seizure.2015.10.002 · 1.82 Impact Factor
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    • "The pathophysiology of acute seizures after traumatic brain injury may be related to increased intracranial pressure as well as elevated lactate– pyruvate ratio suggestive of prolonged metabolic distress [6]. In a large population based study from Denmark, the risk of seizures following traumatic brain injury is estimated to be 2.2–7.4 times higher depending on severity of injury; and this risk remains high even after 10 years of injury [7]. In another retrospective cohort study from the US, patients with TBI were 22 times more likely to die from seizures as compared to an age and sex matched general population [2]. "

    Seizure 11/2015; 32:16-22. DOI:10.1016/j.seizure.2015.08.005 · 1.82 Impact Factor
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    • "Epilepsy is a well-documented sequel to traumatic brain injury (TBI) [1] [2] [3] [4] [5] [6] [7] [8] [9] [10]. However, epilepsy can lead to TBI; the incidence of epilepsyinduced TBI depends on the type of epilepsy and the degree of seizure control [11] [12] [13] [14]. "
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    ABSTRACT: While traumatic brain injury (TBI) can lead to epilepsy, individuals with preexisting epilepsy or seizure disorder (ESD), depending on the type of epilepsy and the degree of seizure control, may have a greater risk of TBI from seizure activity or medication side effects. The joint occurrence of ESD and TBI can complicate recovery as signs and symptoms of TBI may be mistaken for postictal effects. Those with ESD are predicted to experience more deleterious outcomes either because of having a more severe TBI or because of the cumulative effects of repetitive TBI. We conducted a case-control study of all emergency department visits and hospital discharges for TBI from 1998 through 2011 in a statewide population. The severity of TBI, repetitive TBI, and other demographic and clinical characteristics were compared between persons with TBI with preexisting ESD (cases) and those without (controls). Significant differences in proportions were evaluated with confidence intervals. Logistic regression was used to examine the association of the independent variables with ESD. During the study period, 236,164 individuals sustained TBI, 5646 (2.4%) of which had preexisting ESD. After adjustment for demographic and clinical characteristics, cases were more likely to have sustained a severe TBI (OR=1.49; 95% CI=1.38-1.60) and have had repetitive TBI (OR=1.54; 95% CI=1.41-1.69). The consequences of TBI may be greater in individuals with ESD owing to the potential for a more severe or repetitive TBI. Seizure control is paramount, and aggressive management of comorbid conditions among persons with ESD and increased awareness of the hazard of repetitive TBI is warranted. Furthermore, future studies are needed to examine the long-term outcomes of cases in comparison with controls to determine if the higher risk of severe or repetitive TBI translates into permanent deficits.
    Epilepsy & Behavior 01/2014; 32C:42-48. DOI:10.1016/j.yebeh.2013.12.035 · 2.26 Impact Factor
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