A population-based study of risk of epilepsy after hospitalization for traumatic brain injury. Epilepsia

Department of Medicine, Division of Biostatistics & Epidemiology, Medical University of South Carolina, Charleston, South California 29425, USA.
Epilepsia (Impact Factor: 4.57). 10/2009; 51(5):891-8. DOI: 10.1111/j.1528-1167.2009.02384.x
Source: PubMed


This study was undertaken to determine the risk of developing posttraumatic epilepsy (PTE) within 3 years after discharge among a population-based sample of older adolescents and adults hospitalized with traumatic brain injury (TBI) in South Carolina. It also identifies characteristics related to development of PTE within this population.
A stratified random sample of persons aged 15 and older with TBI was selected from the South Carolina nonfederal hospital discharge dataset for four consecutive years. Medical records of recruits were reviewed, and they participated in up to three yearly follow-up telephone interviews.
The cumulative incidence of PTE in the first 3 years after discharge, after adjusting for loss to follow-up, was 4.4 per 100 persons over 3 years for hospitalized mild TBI, 7.6 for moderate, and 13.6 for severe. Those with severe TBI, posttraumatic seizures prior to discharge, and a history of depression were most at risk for PTE. This higher risk group also included persons with three or more chronic medical conditions at discharge.
These results raise the possibility that although some of the characteristics related to development of PTE are nonmodifiable, other factors, such as depression, might be altered with intervention. Further research into factors associated with developing PTE could lead to risk-reducing treatments.

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Available from: Anbesaw W Selassie, Oct 13, 2014
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    • "In a large populationbased study (N = 1961), persons identified as having depression at discharge have been found to be almost twice as likely to develop PTE [26]. In the same study, participants with three or more chronic comorbid conditions, such as cardiovascular disease or diabetes, at discharge had increased risk of PTE [26]. "
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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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    • "One of the sequelae of TBI is the development of posttraumatic epilepsy (PTE). In a population-based study, the cumulative incidence of PTE in the first three years after hospitalization per 100 persons was 4.4 for mild TBI, 7.6 for moderate TBI, and 13.6 for severe TBI (Ferguson et al., 2010). The risk of PTE is especially high in the military, where the incidence can be up to 53% after penetrating head trauma (Raymont et al., 2010). "
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    ABSTRACT: Posttraumatic epilepsy (PTE) has been modeled with different techniques of experimental traumatic brain injury (TBI) using mice and rats at various ages. We hypothesized that the technique of controlled cortical impact (CCI) could be used to establish a model of PTE in young adult rats. A total of 156 male Sprague-Dawley rats of 2-3 months of age (128 CCI-injured and 28 controls) was used for monitoring and/or anatomical studies. Provoked class 3-5 seizures were recorded by video monitoring in 7/57 (12.3%) animals in the week immediately following CCI of the right parietal cortex; none of the 7 animals demonstrated subsequent spontaneous convulsive seizures. Monitoring with video and/or video-EEG was performed on 128 animals at various time points 8-619 days beyond one week following CCI during which 26 (20.3%) demonstrated nonconvulsive or convulsive epileptic seizures. Nonconvulsive epileptic seizures of >10s were demonstrated in 7/40 (17.5%) animals implanted with 2 or 3 depth electrodes and usually characterized by an initial change in behavior (head raising or animal alerting) followed by motor arrest during an ictal discharge that consisted of high-amplitude spikes or spike-waves with frequencies ranging between 1 and 2Hz class 3-5 epileptic seizures were recorded by video monitoring in 17/88 (19%) and by video-EEG in 2/40 (5%) CCI-injured animals. Ninety of 156 (58%) animals (79 CCI-injured, 13 controls) underwent transcardial perfusion for gross and microscopic studies. CCI caused severe brain tissue loss and cavitation of the ipsilateral cerebral hemisphere associated with cell loss in the hippocampal CA1 and CA3 regions, hilus, and dentate granule cells, and thalamus. All Timm-stained CCI-injured brains demonstrated ipsilateral hippocampal mossy fiber sprouting in the inner molecular layer. These results indicate that the CCI model of TBI in adult rats can be used to study the structure-function relationships that underlie epileptogenesis and PTE.
    Epilepsy research 10/2015; 117:104-116. DOI:10.1016/j.eplepsyres.2015.09.009 · 2.02 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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