Perinatal adversities and risk of epilepsy after traumatic brain injury: A Danish nationwide cohort study.
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ABSTRACT: Objectives
Traumatic brain injury (TBI) and perinatal adversities such as low gestational age at birth, low birth weight, low Apgar, and being born small for gestational age are well-established risk factors for epilepsy. We examined whether perinatal adversities modified the risk of epilepsy after TBI in a nationwide cohort study of Danish singletons born from 1982 to 2011.Materials and methods
We categorized perinatal adversities as a composite measure of preterm delivery, low birth weight, low Apgar score, or being born small for gestational age. Cox regression and competing risk regression were used to estimate the risk of epilepsy after TBI according to such perinatal adversities. The study included 1,715,095 singletons (51.1% males). The mean age at end of follow-up was 19.3 years (Interquartile range [IQR] = 12.1-26.3). During follow-up, 85,636 persons (58.2% males) sustained a TBI and 18,064 developed epilepsy (50.7% males), of whom 1329 persons had a preceding TBI.Results
The hazard ratio (HR) of epilepsy in persons with perinatal adversities was 1.19 (95% confidence interval [CI] 1.15-1.24), compared to persons without. The HR of epilepsy in persons with TBI was 2.31 (95% CI 2.18-2.45) compared to persons without TBI, but this risk was not modified by perinatal adversities (p = 0.2460).Conclusions
Perinatal adversities and TBI both increased the risk of epilepsy, but the risk of epilepsy after TBI was not modified by these perinatal adversities.
SUBMITTER: Lolk K
PROVIDER: S-EPMC9311430 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundTraumatic brain injury (TBI) has been associated with dementia. The questions of whether the risk of dementia decreases over time after TBI, whether it is similar for different TBI types, and whether it is influenced by familial aggregation are not well studied.Methods and findingsThe cohort considered for inclusion comprised all individuals in Sweden aged ?50 years on December 31, 2005 (n = 3,329,360). Diagnoses of dementia and TBI were tracked through nationwide databases from 1964 until December 31, 2012. In a first cohort, individuals diagnosed with TBI (n = 164,334) were matched with up to two controls. A second cohort consisted of subjects diagnosed with dementia during follow-up (n = 136,233) matched with up to two controls. A third cohort consisted of 46,970 full sibling pairs with discordant TBI status. During a mean follow-up period of 15.3 (range, 0-49) years, 21,963 individuals in the first cohort (6.3% with TBI, 3.6% without TBI) were diagnosed with dementia (adjusted odds ratio [OR], 1.81; 95% confidence interval [CI], 1.75-1.86). The association was strongest in the first year after TBI (OR, 3.52; 95% CI, 3.23-3.84), but the risk remained significant >30 years (OR, 1.25; 95% CI, 1.11-1.41). Single mild TBI showed a weaker association with dementia (OR, 1.63; 95% CI, 1.57-1.70) than did more severe TBI (OR, 2.06; 95% CI, 1.95-2.19) and multiple TBIs (OR, 2.81; 95% CI, 2.51-3.15). These results were in general confirmed in the nested case-control cohort. TBI was also associated with an increased risk of dementia diagnosis in sibling pairs with discordant TBI status (OR, 1.89; 95% CI, 1.62-2.21). A main limitation of the present study is the observational design. Thus, no causal inferences can be made based on the associations found.ConclusionsThe risk of dementia diagnosis decreased over time after TBI, but it was still evident >30 years after the trauma. The association was stronger for more severe TBI and multiple TBIs, and it persisted after adjustment for familial factors.
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Project description:Post-traumatic epilepsy accounts for 10-20% of symptomatic epilepsy in the general population and 5% of all epilepsy. During the last decade, an increasing number of laboratories have investigated the molecular and cellular mechanisms of post-traumatic epileptogenesis in experimental models. However, identification of critical molecular, cellular, and network mechanisms that would be specific for post-traumatic epileptogenesis remains a challenge. Despite of that, 7 of 9 proof-of-concept antiepileptogenesis studies have demonstrated some effect on seizure susceptibility after experimental traumatic brain injury, even though none of them has progressed to clinic. Moreover, there has been some promise that new clinically translatable imaging approaches can identify biomarkers for post-traumatic epileptogenesis. Even though the progress in combating post-traumatic epileptogenesis happens in small steps, recent discoveries kindle hope for identification of treatment strategies to prevent post-traumatic epilepsy in at-risk patients.
| S-EPMC3996118 | biostudies-literature
Project description:ObjectiveTraumatic brain injury (TBI) is common and associated with a marked increased risk of developing epilepsy. Animal studies indicate that treatment with selective serotonin reuptake inhibitors (SSRIs) may increase the risk of epilepsy after TBI. The aim of this study was to investigate whether use of SSRIs modifies the risk of epilepsy after TBI.MethodsThis was a cohort study of 205,715 persons, who suffered a TBI in Denmark from 1996 to 2013. For each person with TBI, we matched 10 reference persons (N = 2,057,150) who were alive on the day of TBI and who had the same age and gender but had no history of TBI. We used a stratified Cox regression to calculate the relative risk of epilepsy after TBI for persons exposed to TBI, SSRI or both after adjustment for income, civil status, medical and neurological comorbidities, severe mental disease, and substance abuse.ResultsThe risk of epilepsy was 5.61 times higher for persons who used SSRI at time of TBI (adjusted Hazard Ratio (aHR): 5.61 (95% CI: 4.88; 6.45)), 3.23 times higher for persons who had a TBI but did not use SSRI at time of TBI (aHR: 3.23 (95% CI: 3.12;3.35)), and 1.31 times higher for persons who used SSRI but had no TBI (aHR: 1.31 (95% CI: 1.18; 1.45)) compared to persons unexposed to both TBI and SSRI.ConclusionsThis large population based cohort study showed that people using SSRI at the time of a TBI had higher risk of developing epilepsy compared to people not using SSRI at the time of TBI. The results are in line with those of animal studies and calls for further studies to evaluate whether the association is due to SSRIs or to the underlying disease (e.g. depression or anxiety).
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| S-EPMC7558982 | biostudies-literature
Project description:IntroductionThe impact of life-course traumatic brain injury (TBI) on dementia is unclear.MethodsWithin the Swedish Twin Registry (STR), 35,312 dementia-free twins were followed for up to 18 years. TBI history was identified via medical records. Data were analyzed using generalized estimating equation (GEE) and conditional logistic regression.ResultsIn multi-adjusted GEE models, the odds ratio (OR, 95% confidence interval [CI]) of dementia was 1.27 (1.03-1.57) for TBI at any age, 1.55 (1.04-2.31) for TBI at 50 to 59 years, and 1.67 (1.12-2.49) for TBI at 60 to 69 years. Cardiometabolic diseases (CMDs) increased dementia risk associated with TBI at age 50 to 69 years. The ORs in GEE and conditional logistic regression did not differ significantly (P = .37).DiscussionTBI, especially between ages 50 and 69 years, is associated with an increased risk of dementia, and this is exacerbated among people with CMDs. Genetic and early-life environmental factors may not account for the TBI-dementia association.
| S-EPMC10078668 | biostudies-literature
Project description:IntroductionTraumatic brain injury (TBI) is an occupational health hazard of military service. Few studies have examined differences in military occupational categories (MOC) which take into consideration the physical demands and job requirements across occupational groups.MethodsThis study was approved by the University of Texas Health Science Center at Houston Institutional Review Board. Data for this cross-sectional study were obtained from the Naval Health Research Center's Millennium Cohort Study, an ongoing DoD study. Univariate analyses were employed to calculate frequencies and proportions for all variables. Bivariate analyses included unadjusted odds ratios (OR) and 95% CI for the association between all variables and TBI. Multivariable logistic regression was used to calculate adjusted ORs and 95% CIs to assess the association between MOC and TBI, adjusted for potential confounders: sex, race/ethnicity, rank, military status, branch of service, before-service TBI, and panel. Logistic regression models estimated odds of TBI for each MOC, and stratified models estimated odds separately for enlisted and officer MOCs.ResultsApproximately 27% of all participants reported experiencing a service-related TBI. All MOCs were statistically significantly associated with increased odds of service-related TBI, with a range of 16 to 45%, except for "Health Care" MOCs (OR: 1.01, 95% CI 0.91-1.13). Service members in "Infantry/Tactical Operations" had the highest odds (OR: 1.45, 95% CI 1.31-1.61) of service-related TBI as compared to "Administration & Executives." Among enlisted service members, approximately 28% reported experiencing a service-related TBI. Among enlisted-specific MOCs, the odds of TBI were elevated for those serving in "Infantry, Gun Crews, Seamanship (OR: 1.79, 95% CI 1.58-2.02)," followed by "Electrical/Mechanical Equipment Repairers (OR: 1.23, 95% CI 1.09-1.38)," "Service & Supply Handlers (OR 1.21, 95% CI 1.08-1.37)," "Other Technical & Allied Specialists (OR 1.21, 95% CI 1.02-1.43)," "Health Care Specialists (OR 1.19, 95% CI 1.04-1.36)," and "Communications & Intelligence (OR: 1.16, 95% CI 1.02-1.31)," compared to "Functional Support & Administration." Among officer service members, approximately 24% reported experiencing a service-related TBI. After adjustment the odds of TBI were found to be significant for those serving as "Health Care Officers" (OR: 0.65, 95% CI: 0.52-0.80) and "Intelligence Officers" (OR: 1.27, 95% CI: 1.01-1.61).ConclusionsA strength of this analysis is the breakdown of MOC associations with TBI stratified by enlisted and officer ranks, which has been previously unreported. Given the significantly increased odds of service-related TBI reporting within enlisted ranks, further exploration into the location (deployed versus non-deployed) and mechanism (e.g., blast, training, sports, etc.) for these injuries is needed. Understanding injury patterns within these military occupations is necessary to increase TBI identification, treatment, and foremost, prevention.Results highlight the importance of examining specific occupational categories rather than relying on gross categorizations, which do not account for shared knowledge, skills, and abilities within occupations. The quantification of risk among enlisted MOCs suggests a need for further research into the causes of TBI.
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Project description:BackgroundDue to the potential consequences of post-traumatic epilepsy (PTE) exacerbating secondary injury following traumatic brain injury (TBI), the use of antiepileptic drugs (AEDs) is an accepted option for seizure prophylaxis. However, there is only a paucity of data that can be found regarding outcomes surrounding the use of AEDs. The purpose of this retrospective study is to evaluate whether the prophylactic administration of AEDs significantly decreased the incidence of PTE, when considering the severity of TBI.MethodsAll trauma patients who had been newly diagnosed with TBI from January 1, 2010 to December 31, 2017 were retrospectively analyzed. Statistical comparisons were made using the chi-square test, Mann-Whitney U test, and Cox regression modeling. After excluding any exposed subjects with no appropriate match, patients who had received AED prophylaxis were matched by propensity score with those who did not receive AEDs. All of the TBI populations were followed up until June 30, 2018.ResultsWe identified 1316 patients who met the inclusion and exclusion criteria in our matched cohort through their propensity scores, where 138 patients had been receiving prophylactic AEDs and 138 patients had not. Baseline characteristics were similar in gender, age, Glasgow Coma Scale (GCS) scores, and risk factors of PTE including skull fracture, chronic alcoholism, subdural hematoma, epidural hematoma, and intracerebral hematoma. After adjusting for those risk factors, the relative incidence of seizure was not statistically significant in either of the groups (p = 0.566).ConclusionIn our cohort analysis, AED prophylaxis was ineffective in preventing seizures, as the rate of seizures was similar whether patients had been receiving the drugs or not. We therefore concluded that the benefits of routine prophylactic anticonvulsant therapy in patients with TBI need to be re-evaluated.
| S-EPMC7526576 | biostudies-literature
Project description:BackgroundTraumatic brain injury (TBI) is an important cause of death and disability worldwide. The relationship between TBI and kidney diseases is largely unknown.MethodsWe aimed to determine whether TBI is associated with long-term adverse renal outcomes. We performed a nationwide, population-based, propensity score-matched cohort study of 32,152 TBI patients and 128,608 propensity score-matched controls. Data were collected by the National Health Insurance Research Database of Taiwan from 2000 to 2012. Our clinical outcomes were chronic kidney disease (CKD), end-stage renal disease (ESRD) and the composite endpoint of ESRD or all-cause mortality.ResultsThe incidence rate of CKD was higher in the TBI than in the control cohort (8.99 vs. 7.4 per 1000 person-years). The TBI patients also showed higher risks of CKD (adjusted hazard ratio [aHR] 1.14, 95% confidence interval [CI] 1.08-1.20; P < 0.001) and composite endpoints (aHR 1.08, 95% CI 1.01-1.15; P = 0.022) than the control groups, but the ESRD was not significantly different between the groups. In subgroup analyses, the risks of incident CKD and composite endpoints were significantly raised in TBI patients aged < 65 years and/or without comorbidities. However, the risks of both CKD and composite outcome were little affected by the severity of TBI.ConclusionsTBI has a modest but significant effect on incident CKD and composite endpoint, but not on ESRD alone. TBI patients under 65 are at greater risk of CKD and composite outcome than their older counterparts.
| S-EPMC5308784 | biostudies-literature
Project description:ObjectivesIt is unclear whether kidney disease is a risk factor for developing dementia. We examined the association between kidney disease and risk of future dementia.Design and settingNationwide historical registry-based cohort study in Denmark based on data from 1 January 1995 until 31 December 2016.ParticipantsAll patients diagnosed with kidney disease and matched general population cohort without kidney disease (matched 1:5 on age, sex and year of kidney disease diagnosis).Primary and secondary outcome measuresAll-cause dementia and its subtypes: Alzheimer's disease, vascular dementia and other specified or unspecified dementia. We computed 5-year cumulative incidences (risk) and hazard ratios (HRs) for outcomes using Cox regression analyses.ResultsThe study cohort comprised 82 690 patients with kidney disease and 413 405 individuals from the general population. Five-year and ten-year mortality rates were twice as high in patients with kidney disease compared with the general population. The 5-year risk for all-cause dementia was 2.90% (95% confidence interval: 2.78% to 3.08%) in patients with kidney disease and 2.98% (2.92% to 3.04%) in the general population. Compared with the general population, the adjusted HRs for all-cause dementia in patients with kidney disease were 1.06 (1.00 to 1.12) for the 5-year follow-up and 1.08 (1.03 to 1.12) for the entire study period. Risk estimates for dementia subtypes differed substantially and were lower for Alzheimer's disease and higher for vascular dementia.ConclusionsPatients diagnosed with kidney disease have a modestly increased rate of dementia, mainly driven by vascular dementia. Moreover, patients with kidney disease may be underdiagnosed with dementia due to high mortality and other comorbidities of higher priority.
| S-EPMC8543681 | biostudies-literature
Project description:AbstractObjectivesAn estimated 14-23% of patients with traumatic brain injury (TBI) incur multiple lifetime TBIs. The relationship between prior TBI and outcomes in patients with moderate to severe TBI (msTBI) is not well delineated. We examined the associations between prior TBI, in-hospital mortality, and outcomes up to 12 months after injury in a prospective US msTBI cohort.MethodsData from hospitalized subjects with Glasgow Coma Scale score of 3-12 were extracted from the Transforming Research and Clinical Knowledge in Traumatic Brain Injury Study (enrollment period: 2014-2019). Prior TBI with amnesia or alteration of consciousness was assessed using the Ohio State University TBI Identification Method. Competing risk regressions adjusting for age, sex, psychiatric history, cranial injury and extracranial injury severity examined the associations between prior TBI and in-hospital mortality, with hospital discharged alive as the competing risk. Adjusted HRs (aHR (95% CI)) were reported. Multivariable logistic regressions assessed the associations between prior TBI, mortality, and unfavorable outcome (Glasgow Outcome Scale-Extended score 1-3 (vs. 4-8)) at 3, 6, and 12 months after injury.ResultsOf 405 acute msTBI subjects, 21.5% had prior TBI, which was associated with male sex (87.4% vs. 77.0%, p=0.037) and psychiatric history (34.5% vs. 20.7%, p=0.010). In-hospital mortality was 10.1% (prior TBI: 17.2%, no prior TBI: 8.2%, p=0.025). Competing risk regressions indicated that prior TBI was associated with likelihood of in-hospital mortality (aHR=2.06 (1.01-4.22)), but not with hospital discharged alive. Prior TBI was not associated with mortality or unfavorable outcomes at 3, 6, and 12 months.ConclusionsAfter acute msTBI, prior TBI history is independently associated with in-hospital mortality but not with mortality or unfavorable outcomes within 12 months after injury. This selective association underscores the importance of collecting standardized prior TBI history data early after acute hospitalization to inform risk stratification. Prospective validation studies are needed.Level of evidenceIV.Trial registration numberNCT02119182.
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