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Assistant Professor of Clinical Neurology, Weill Cornell Medical College
Dr. Pargeon reports no financial relationships relevant to this study.
SYNOPSIS: Following traumatic brain injury, early (first five days after injury) epileptiform abnormalities on EEG were seen more commonly in patients with subsequent post-traumatic epilepsy (PTE), compared to controls, and were found to be a significant and independent predictor of PTE. The presence of subdural hemorrhage was the only other independent predictor of PTE.
SOURCE: Kim JA, Boyle EJ, Wu AC, et al. Epileptiform activity in traumatic brain injury predicts post-traumatic epilepsy. Ann Neurol 2018;83:858-862.
Traumatic brain injury (TBI) is a significant cause of morbidity and mortality for both adults and children, with about 12% resulting in hospitalization or death.1 Post-traumatic seizures can be a relatively common complication, affecting up to 20% of patients, especially those with more severe injuries requiring surgery and those of younger age.1 Patients with acute TBIs commonly are placed on prophylactic anti-seizure drugs (ASD), but duration of treatment is often unclear, as is which patients will go on to develop post-traumatic epilepsy (PTE). Kim et al sought to determine if epileptiform abnormalities (EAs) seen on initial EEG and other demographics could be used as early predictors for development of PTE within the first year after TBI.
The authors retrospectively reviewed records for adult patients presenting with TBI from 2011-2015 to a single tertiary care center in the northeastern United States (Massachusetts General Hospital). All patients underwent EEG monitoring during their initial admission for TBI. Twenty-five consecutive patients were identified who developed PTE, defined as at least one seizure in the two to 12 months post-TBI. Twenty-five age-matched controls also were identified with comparable TBIs (as determined by similar Glasgow Coma Scale [GCS] at admission), but without PTE by one year. EAs on EEG were classified by a standardized nomenclature and were as follows: seizures, sporadic epileptiform discharges (EDs), lateralized or generalized periodic discharges (LPDs or GPDs), and lateralized rhythmic delta activity. The authors also recorded the incidence of generalized rhythmic delta activity, as well as polymorphic generalized and focal slowing, but none of these were considered EAs. The timing of target EEG activity was noted relative to the day of TBI onset. Finally, the authors calculated associations between PTE and certain demographic variables, including age, gender, admission GCS, and the presence of intracranial hemorrhage delineated by type (intraparenchymal, subdural, epidural, or subarachnoid).
Overall, patients with subsequent PTE were monitored longer on EEG, relative to controls. Acute EAs also were nearly twice as common in patients with PTE (64% vs. 36%) when controlling for the presence of subdural hemorrhage (SDH), making EAs a significant and independent predictor of PTE (odds ratio, 3.16).1 More specifically, when looking at the types of EAs, only EDs showed a significant association with PTE, as did focal slowing, although the latter was not classified as an EA. EDs, when observed, often were seen early, with about half seen at five days or sooner after the TBI. Early seizures and LPDs showed positive associations with PTE development, but neither were statistically significant. The only demographic variable found to be significantly associated with later PTE was the presence of SDH. In fact, the authors found that SDH and EAs, specifically EDs, independently contributed to the risk of developing PTE without a relationship to one another, suggesting these were “independent causal factors.”1
Kim et al demonstrated a significant association for patients with TBI and SDH for later development of PTE, which has been reported previously. However, this study also suggests that early EAs, particularly EDs, are significantly and independently associated with later PTE, which has not been reported previously. In addition, although not considered an EA, polymorphic focal slowing was significantly associated with later PTE. The authors point to prior evidence demonstrating EEG slowing in areas where the blood-brain barrier was disrupted associated with TBI, more commonly seen in patients with PTE, compared to those who did not develop later seizures.2 However, the key for the associated EAs is that these often were seen early, within the first five days after the TBI in the Kim et al study, so early EEG monitoring could be used to diagnose and even predict patients with TBI at higher risk for later PTE.
One of the limitations of this study is that the sample sizes were small, with only 25 patients included in each group, which likely limited the ability to see effects for relatively infrequent entities, such as LPDs and early seizures, both of which showed a positive association with PTE but were not statistically significant. Further, the authors set their defined period for development of PTE at up to one year after TBI, but some patients in the control group still may have developed PTE after this mark. The authors acknowledged this may not capture all patients with eventual PTE, but believed this would capture the highest risk period.2 However, the authors of another recent study found an incidence of post-traumatic seizures up to 20.5% by five years after injury.1 Regardless, Kim et al hope to use EAs as an early biomarker for designing more cost-effective studies for evaluating epileptogenesis in patients with TBIs.
Financial Disclosure: Neurology Alert’s Editor in Chief Matthew Fink, MD; Peer Reviewer M. Flint Beal, MD; Executive Editor Leslie Coplin; Editor Jonathan Springston; and Editorial Group Manager Terrey L. Hatcher report no financial relationships relevant to this field of study.