Abstracts

Rationale: One-third of patients with focal epilepsy suffer from drug-resistant epilepsy. Surgery is the therapy of choice in this patient group; seizure freedom relies on resection of the epileptogenic zone (EZ), the region generating seizures. However, up to 50% of well-selected patients are not seizure-free after surgery, despite invasive exploration with stereo-encephalography (SEEG). One explanation is that the propagation of epileptic activity complicates localization of the EZ. In a previous study, we established a robust method to build patient-specific spike propagation networks using SEEG. However, it remains difficult to develop a complete understanding of spike propagation from SEEG alone; SEEG is unable to sample from the vast majority of the brain and there exist numerous structural pathways that may be responsible for any observed propagation. We may be able to improve our understanding of spike propagation by informing SEEG with white matter tractography, which can non-invasively map structural pathways in the whole brain. We aim to provide evidence that spike propagation is mediated by identifiable white matter tracts.

Methods: From our SEEG database, patients with epilepsy surgery, anatomical MRIs, diffusion MRI, and clinical outcomes were selected. All MRIs were pre-processed using standard pipelines from FreeSurfer. White matter tractography was done using the probabilistic tractography algorithm, iFOD2 (MRtrix3). One-hour segments of SEEG recordings were used to construct patient-specific spike propagation networks based on consistent propagation direction. Spheres (5mm radius) were constructed around each SEEG electrode contact to represent the recording area; these spheres are the basis for our region-of-interest maps. After co-registration between the ROI maps and tractograms we determine the number of white matter tracts between ROIs in all possible pairs of ROIs. ROI pairs for which a significant spike propagation relationship is observed are categorized as Propagation Pairs. The cumulative sum of tracts observed among Propagation Pairs is compared to a random distribution of the sum of tracts seen among all possible pairs (10,000 iterations of groups matched in size to the Propagation Pairs group). We also compare the number of tracts in Propagation Pairs to all possible pairs on a group level, normalizing the number of tracts in each pair with the ROI pair with the highest number of tracts for each patient.

Results: Eight patients met our inclusion criteria. In seven, we observe a significantly greater number of white matter tracts among Propagation Pairs (p < 0.05). On a group level (n = 8), there was a significantly greater number of tracts among Propagation Pairs (0.34) as compared to all ROI pairs (p < 0.01; alpha threshold at a normalized value of 0.22).