You are here

Article Text

Article menu
Download PDFPDF
Epilepsy
Short report
Quantitative epileptiform burden and electroencephalography background features predict post-traumatic epilepsy
  1. Yilun Chen1,
  2. Songlu Li1,
  3. Wendong Ge2,
  4. Jin Jing2,
  5. Hsin Yi Chen1,
  6. Daniel Doherty1,
  7. Alison Herman1,
  8. Safa Kaleem3,
  9. Kan Ding4,
  10. Gamaleldin Osman5,
  11. Christa B Swisher3,
  12. Christine Smith6,
  13. Carolina B Maciel1,6,
  14. Ayham Alkhachroum7,8,
  15. Jong Woo Lee9,
  16. Monica B Dhakar10,
  17. Emily J Gilmore1,
  18. Adithya Sivaraju1,
  19. Lawrence J Hirsch1,
  20. Sacit B Omay11,
  21. Hal Blumenfeld1,
  22. Kevin N Sheth1,
  23. Aaron F Struck12,13,
  24. Brian L Edlow2,
  25. M Brandon Westover2,
  26. Jennifer A Kim1
  1. 1 Neurology, Yale School of Medicine, New Haven, Connecticut, USA
  2. 2 Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA
  3. 3 Neurology, Duke University School of Medicine, Durham, North Carolina, USA
  4. 4 Neurology, UT Southwestern Medical Center, Dallas, Texas, USA
  5. 5 Neurology, Henry Ford Health System, Detroit, Michigan, USA
  6. 6 Neurology, University of Florida College of Medicine, Gainesville, Florida, USA
  7. 7 Neurology, University of Miami Miller School of Medicine, Miami, Florida, USA
  8. 8 Neurology, Jackson Memorial Hospital, Miami, Florida, USA
  9. 9 Neurology, Brigham and Women's Hospital, Boston, Massachusetts, USA
  10. 10 Neurology, Emory University School of Medicine, Atlanta, Georgia, USA
  11. 11 Neurosurgery, Yale School of Medicine, New Haven, Connecticut, USA
  12. 12 Neurology, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA
  13. 13 Neurology, William S Middleton Memorial Veterans Hospital, Madison, Wisconsin, USA
  1. Correspondence to Dr Jennifer A Kim, Neurology, Yale School of Medicine, New Haven, CT 06520, USA; jennifer.a.kim{at}yale.edu

Abstract

Background Post-traumatic epilepsy (PTE) is a severe complication of traumatic brain injury (TBI). Electroencephalography aids early post-traumatic seizure diagnosis, but its optimal utility for PTE prediction remains unknown. We aim to evaluate the contribution of quantitative electroencephalograms to predict first-year PTE (PTE1).

Methods We performed a multicentre, retrospective case–control study of patients with TBI. 63 PTE1 patients were matched with 63 non-PTE1 patients by admission Glasgow Coma Scale score, age and sex. We evaluated the association of quantitative electroencephalography features with PTE1 using logistic regressions and examined their predictive value relative to TBI mechanism and CT abnormalities.

Results In the matched cohort (n=126), greater epileptiform burden, suppression burden and beta variability were associated with 4.6 times higher PTE1 risk based on multivariable logistic regression analysis (area under the receiver operating characteristic curve, AUC (95% CI) 0.69 (0.60 to 0.78)). Among 116 (92%) patients with available CT reports, adding quantitative electroencephalography features to a combined mechanism and CT model improved performance (AUC (95% CI), 0.71 (0.61 to 0.80) vs 0.61 (0.51 to 0.72)).

Conclusions Epileptiform and spectral characteristics enhance covariates identified on TBI admission and CT abnormalities in PTE1 prediction. Future trials should incorporate quantitative electroencephalography features to validate this enhancement of PTE risk stratification models.

  • EPILEPSY
  • TRAUMATIC BRAIN INJURY
  • EEG

https://doi.org/10.1136/jnnp-2022-329542

Statistics from Altmetric.com

    Request Permissions

    If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

    View Full Text

    Footnotes

    • Twitter @YilunChen_, @neurologyrules, @AAlkhachroum, @JennKimMDPHD

    • Contributors YC, JAK, MBW and EJG contributed to the study design. SL, HYC, DD, AH, SK, KD, GO, CBS, CS, CBM, AA, JWL, MBD, EJG, AS, LJH, SBO, HB, KNS, AFS, BLE, MBW and JAK contributed to data acquisition. YC, SL, WG, JJ, MBW and JAK contributed to data analysis. YC, JAK, EJG, HB and MBW contributed to drafting and revising the manuscript. All authors contributed to editing and approval of the manuscript.

    • Funding KD received funding from the National Institute on Aging (NIA) (R34AG061304) and the National Institute of Neurological Disorders and Stroke (NINDS) (R01NS117904) of the National Institutes of Health (NIH). CS and CBM acknowledge the University of Florida Integrated Data Repository (IDR) and the UF Health Office of the Chief Data Officer for providing the analytic data set for this project. CS and CBM were supported by the National Center for Advancing Translational Sciences (NCATS) of the NIH under University of Florida Clinical and Translational Science Awards (UL1TR000064, UL1TR001427). CBM received funding from the American Heart Association (AHA). AA is supported by NCATS of the NIH through an institutional KL2 Career Development Award from the Miami Clinical and Translational Science Institute (UL1TR002736). MBD received funding from the NINDS of the NIH and the American Epilepsy Society. EJG received funding from NIH (R01NS117904). AFS received funding from the NINDS under the NIH (R01NS111022) and Ceribell. BE received funding from the NINDS (R21NS109627, RF1NS115268) and the Office of the Director (DP2HD101400) of the NIH, the James S. McDonnell Foundation, and the Tiny Blue Dot Foundation. MBW received funding from the Glenn Foundation for Medical Research, the American Federation for Aging Research (Breakthroughs in Gerontology), the American Academy of Sleep Medicine Strategic Research Award, and the NINDS (R01NS102190, R01NS102574, R01NS107291) and the NIA (RF1AG064312, R01AG062989, R01AG073410) of the NIH. JAK received funding from the NINDS (R25N065743, K23NS112596-01A1, R01NS117904), the American Academy of Neurology Clinical Research Training Scholarship, the AHA and the Bee Foundation.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.