Abstracts

Rationale: Acute symptomatic seizures (ASyS) occur within seven days of acute brain injury. Increases in EEG monitoring reveal an even higher ASyS burden, where ASyS are primarily non convulsive, plus other epileptic patterns (defined here as any pattern known to be associated with seizures). Patients with ASyS are typically discharged on anti-seizure medications (ASMs) and remain treated without appropriate follow up. Many of these patients may not need long term ASMs but there are no clear guidelines for optimal duration of treatment. True risk of developing post-injury epilepsy (PIE) remains uncertain.

Methods: Retrospective cohort study of 83 patients seen in the Post-Acute Symptomatic Seizure (PASS) clinic at Yale New Haven Hospital from 2016 to 2018. All patients either had an ASyS or epileptic EEG patterns within seven days of acute brain injury. Patients with prior known history of epilepsy, unprovoked seizures, those presenting with cardiac arrest, or a new diagnosis of brain tumor were excluded. All patients had a follow up outpatient EEG prior to the clinic visit. Decision to taper ASMs was individualized, and all patients were followed for a period of at least two years from the time of the initial brain injury to assess the risk of epilepsy development.

Results: 130 patients were seen in the PASS clinic. 83 patients met the study inclusion criteria. Median time to first in-person clinic visit was 93 days (IQR 50-176). Median follow up duration was 23.5 (IQR 18.4 – 27.6) months. Figure 1A shows the etiology of the initial injury. Figure 1B displays the evolution of EEG findings. Median time to outpatient EEG was 116 days (IQR 58-204). Duration of outpatient EEG was 1h in 59 (71%) patients and ³24h EEG in 24 (29%) patients. 15/54 (28%) with an initial abnormal EEG had epileptic findings on the outpatient EEG.

18/83 (22%) developed PIE (i.e., at least one late, unprovoked seizure). ASM taper was attempted in 46/83 (55%) patients, of which, five (11%) had seizure recurrence, and all within six months of taper. 13/37 (35%) patients without ASM taper developed PIE. Table 1 shows the univariable analyses of factors associated with PIE. Patients with vascular malformations (p =0.04 [5.9 (1.4-24.78)], those requiring a neurosurgical intervention (p=0.02 [4.16 (1.4-11.45)] and persistence of epileptic abnormalities on outpatient EEG (p=0.003 [6.6(1.08-23.13)] were more likely to develop PIE.

Conclusions: Persistence of epileptic patterns is likely to increase the risk of PIE even when ASMs are not tapered. In our cohort, a toxic metabolic infectious etiology, acute symptomatic clinical seizure at onset, epileptic findings on initial EEG and tapering ASMs were not associated with an increased risk of developing PIE. We provide a proof of concept for an operational PASS clinic, which can address critical knowledge gaps, including optimal ASM duration, long-term significance of epileptic patterns on EEG and risk and timing of PIE development.

Funding: Please list any funding that was received in support of this abstract.: Dr. Sivaraju reports funding from Swebilius grant foundation in support of this abstract.