The aim of this retrospective analysis is to quantitatively examine pre- and post-transection spike (PrTSB/PoTSB) as measured by ECoG, and their correlation with long-term seizure outcomes.

Multiple hippocampal transections (MHT) are an effective treatment option for dominant mesial temporal lobe epilepsy (DmTLE), providing the benefit of preserved verbal memory.^1-6 Few studies have analyzed PrTSB and PoTSB via intra-operative electrocorticography (ECoG) and their relationship with long-term seizure outcome.^4-6  

All cases of drug-resistant DmTLE status-post MHT with or without partial temporal lobe resection/amygdalectomy at our center from 2008-2016 were examined. Pre- and post-MHT ECoG epochs were analyzed for spike burden and correlated with post-op seizure outcome for at least 2 years. Cases with incomplete ECoG data or poor outpatient follow-up were excluded.

6 out of 21 MHT cases were analyzed after applying inclusion/exclusion criteria. The PoTSB was significantly reduced by 45-100% compared to PrTSB (mean PrTSB 20.5±14.6 spikes/min, PoTSB  3.5±4.3 spikes/min, p=0.03). All patients were clinically seizure-free for >2 years in the absence of external triggers (ET). Two patients experienced recurrence of seizures without ET (2y, 3y), two after medication weaning (16m, 6y), one after medication non-compliance (9 years), and one after intoxication. Using Spearman correlation coefficient, a strongly positive correlation was found between spike reduction after MHT and duration of seizure freedom (0.5147). Strong negative correlations (-0.6088) were found between absolute PrTSB and duration of seizure freedom as well as between absolute PoTSB and duration of seizure freedom (-0.6377) in absence of ET.

Our study demonstrates a significant reduction in hippocampal spike burden after MHT and a strong correlation between spike reduction and duration of seizure freedom. This supports the hypothesis that the likely mechanism of seizure freedom after MHT is the disruption of the longitudinal hippocampal circuit, which is required for synchronization & emergence of the epileptic activity.