Epidemiology of Post-traumatic Epilepsy and Its Risk Factors: An Analysis of U.S. Health Insurance Claims Data, 2006-2012 Público
De Grauw, Xinyao Guo (2016)
Published
Abstract
BACKGROUND: About 1.7 million people experience a medically attended traumatic brain injury (TBI) each year in the United States. The occurrence of early seizures (wthin seven days after head injury) is a recognized complication. Chronic post-traumatic epilepsy (PTE) is a disabling life-long outcome of TBI. The purpose of this study is to examine the incidence of PTE and early seizure; the probability of developing PTE within 9 years after TBI, the risk factors associated with PTE, and the prevalence and duration of anti-epileptic drugs (AEDs) use among individuals with PTE.
METHODS: Using the MarketScan Commercial Claims and Encounters and Medicare Supplemental (CC&M) data set, we examined new TBI patients between 2006 and 2012. We examined the incidence of early seizure and the cumulative incidence of PTE among TBI patients. We examined the probability of developing PTE within nine years among TBI patients with risk factors (age, gender, TBI severity, early seizure, and AED use). We conducted univariate and multivariable survival analysis to obtain estimates of crude and adjusted hazard ratios (cHRs, aHRs) of PTE and 95% confidence intervals by constructing Cox proportional hazard model among TBI cases. We estimated the prevalence and durations of AE use among TBI patients.
RESULTS: The annual incidence of early seizure stayed at 0.5%. A total of 8,704 individuals with TBI experienced early seizures. The cumulative incidence of PTE increased with the severity. Most patients with TBI (92.4%) were not prescribed any AED. Of those who received AEDs, about 97% stopped their use within 90 days. Gender was not associated with PTE. The risk of PTE significantly increased with age and TBI severity, and decreased with the duration of AED use (p<0.05). The risk of PTE for individuals with early seizures was 18-times higher than those without early seizures (cHR=18.1; 95% CI: 17.3, 18.9). The probability of developing PTE among individuals with early seizures on clonazepam or gabapentin was significantly lower than that for those without AED. Among age 15-45 year olds, aHR for clonazepam was o.48 and for gabapentin was 0.29 (p<0.05). Among age 45 and older, aHR for clonazepam was 0.33 and for gabapentin was 0.26 (p<0.05). The probability of developing PTE was significantly lower among those without early seizure on acetazolamide compared to those who did not use AED (aHR: 0.45, p<0.05).
CONCLUSIONS: We found that nearly 1% of individuals with TBI developed PTE over one year and more than 10% developed PTE over three years. Most of the individuals did not receive AED after TBI. Most of individuals who received a prescription stopped their AED use within 90 days. Clonazepam and gabapentin appeared to prevent PTE in the individuals with early seizures. There was no evidence suggesting AEDs helped to prevent PTE in the individuals without early seizure, with possible exception of acetazolamide. With the possible exception of clonazepam, gabapentin and acetazolamide, this analysis provides no evidence that prophylactic AED use is effective in decreasing the risk of PTE. However, further studies may be needed to test the efficacy of acetazolamide in preventing PTE.
Table of Contents
CHAPTER 1: INTRODUCTION….……………………….......1
Background of Problem…………………………………….....1
Goal of Study……………………………………………...........3
Research Questions……………………………...................4
Importance of Study…………………………………………...4
CHAPTER 2: LITERATURE REVIEW…………...…………..6
Introduction………………………………………………........6
Occurrence of TBI. …………………………………………....6
Incidence of early seizures and PTE after TBI. …….......7
Risk factors of PTE…………………………………………..…8
Prevention of PTE by using AEDs after TBI…………......9
Conclusion……………………………………………………...11
CHAPTER 3: METHODS……….…………………………….12
Data source……………………………………………………..12
Study population………………………………………………12
Outcome ……...….…………………………………………….14
Primary predictor…. …………………………………………14
Co-variables…………………………………………………….14
Statistical analysis…………………………………………….14
CHAPTER 4: RESULTS………..………………………………16
CHAPTER 5: DISCUSSION..………………………………...19
Strength and Limitation……………………………………..24
Public Health Implications and Conclusion……………..25
REFERENCES…...………………………………………………27
TABLE 1………………………………………………………….29
TABLE 2………………………………………………………….29
TABLE 3…………………………………………………………..31
TABLE 4 ..………………………………………………………..31
TABLE 5. ………………….……………………………………..34
TABLE 6 .…………………………………………………………35
TABLE 7…………………………………………………………..36
TABLE 8 A……………………………………………………….38
TABLE 8 B………...…………………………………………….39
FIGURE 1…………………………………………………………41
APPENDIX A…...………………………………………………42
APPENDIX B…...………………………………………………42
APPENDIX C…...………………………………………………42
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