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.

Download full-text


Available from: Jakob Christensen, Oct 01, 2015
162 Reads
  • Source
    • "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]. "
    [Show abstract] [Hide abstract]
    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
  • Source
    • "Because our methods and definition of PTE closely align with those of Kharatishvili et al. (2006), it is reassuring that our finding that 30–52% of rats given severe LFPI displayed either spontaneous seizures and/or epileptic discharges are similar to those reported by this group (Kharatishvili et al., 2006). This is also consistent with rates of PTE in patients following TBI (Englander et al., 2003; Frey, 2003; Christensen et al., 2009), and supports the use of LFPI in rats to model and study PTE. However , it is important to acknowledge that some workers in the field would question the relevance of brief seizures, even when lasting longer than 5 s, recorded in rodents postexperimental TBI to human posttraumatic epilepsy (Dudek & Bertram, 2010). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Purpose: Posttraumatic epilepsy (PTE) occurs in a proportion of traumatic brain injury (TBI) cases, significantly compounding the disability, and risk of injury and death for sufferers. To date, predictive biomarkers for PTE have not been identified. This study used the lateral fluid percussion injury (LFPI) rat model of TBI to investigate whether structural, functional, and behavioral changes post-TBI relate to the later development of PTE. Methods: Adult male Wistar rats underwent LFPI or sham injury. Serial magnetic resonance (MR) and positron emission tomography (PET) imaging, and behavioral analyses were performed over 6 months postinjury. Rats were then implanted with recording electrodes and monitored for two consecutive weeks using video-electroencephalography (EEG) to assess for PTE. Of the LFPI rats, 52% (n = 12) displayed spontaneous recurring seizures and/or epileptic discharges on the video-EEG recordings. Key findings: MRI volumetric and signal analysis of changes in cortex, hippocampus, thalamus, and amygdala, (18) F-fluorodeoxyglucose (FDG)-PET analysis of metabolic function, and behavioral analysis of cognitive and emotional changes, at 1 week, and 1, 3, and 6 months post-LFPI, all failed to identify significant differences on univariate analysis between the epileptic and nonepileptic groups. However, hippocampal surface shape analysis using large-deformation high-dimensional mapping identified significant changes in the ipsilateral hippocampus at 1 week postinjury relative to baseline that differed between rats that would go onto become epileptic versus those who did not. Furthermore, a multivariate logistic regression model that incorporated the 1 week, and 1 and 3 month (18) F-FDG PET parameters from the ipsilateral hippocampus was able to correctly predict the epileptic outcome in all of the LFPI cases. As such, these subtle changes in the ipsilateral hippocampus at acute phases after LFPI may be related to PTE and require further examination. Significance: These findings suggest that PTE may be independent of major structural, functional, and behavioral changes induced by TBI, and suggest that more subtle abnormalities are likely involved. However, there are limitations associated with studying acquired epilepsies in animal models that must be considered when interpreting these results, in particular the failure to detect differences between the groups may be related to the limitations of properly identifying/separating the epileptic and nonepileptic animals into the correct group.
    Epilepsia 05/2013; 54(7). DOI:10.1111/epi.12223 · 4.57 Impact Factor
  • Source
    • "The seizure rate was slightly lower in the phenytoin group (p < 0.001). Epilepsia ILAE posttraumatic epilepsy among these patients is low, approaching that of the general population (Annegers et al., 1998; Christensen et al., 2009). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Traumatic brain injury (TBI) is a potentially preventable cause of epilepsy. Increasing incidence among army personnel and the high incidence among children and young people raise concern. This article presents a review of selected studies dealing with the risks of TBI and the risk of posttraumatic epilepsy in humans. The incidence of persons admitted to hospital with TBI has decreased in developed countries in recent years. However, there is little change in TBI-associated deaths, and the decrease in hospitalization may merely reflect that more people with head injury are cared for on an outpatient basis. It is clear that epilepsy is a frequent consequence of brain injury, even many years after the injury. However, several well-controlled studies have been unable to identify therapies that prevent the development of epilepsy after TBI. Posttraumatic epilepsy has significant implications for the affected individuals, family, and society. Despite several interventions used to prevent posttraumatic epilepsy, the only proven "intervention" to date is to prevent TBI from occurring.
    Epilepsia 09/2012; 53 Suppl 4(s4):43-7. DOI:10.1111/j.1528-1167.2012.03612.x · 4.57 Impact Factor
Show more