Abstracts

Rationale: A lesion is not present in ~50% of cases of focal epilepsy, which is associated with a less favorable prognosis for surgical treatment. In this work, we are testing the hypothesis that the seizure onset zone (SOZ) in focal epilepsy is more functionally connected to the broader irritative zone and to propagation pathways. To measure functional connectivity (FC), we have used the fMRI-based approach of resting state fMRI which determines how different brain regions are functionally connected or co-activated. Methods: We used fMRI analysis to construct FC maps of the SOZ, as determined from intracranial EEG (icEEG), in patients with focal non-lesional epilepsy undergoing a presurgical evaluation. FC maps derived from the SOZ were obtained in epilepsy patients (n=10) and matched controls. FC maps in patients were derived by placing a 5mm ROI over the location of the most active electrode within the SOZ and in the homologous region of a matched control. These maps consist of all voxels whose BOLD time signal is significantly correlated with the time course of the SOZ ROI. Analysis of intracranial EEG recordings is also used to determine the electrodes with interictal epileptiform discharges (IEDs) comprising the irritative zone. MNI coordinates of the electrodes with IEDs, from each patient, are then overlayed on the FC maps from SOZ and its homologous region in each patient-control pair. Each electrode is assigned a 1mm spherical ROI and the ROIs are then assessed for overlap with fMRI FC map. A group comparison is then performed of the normalized percentage of overlap. Results: After the generation of the SOZ maps, the relationship between the maps and the irritative zone is assessed. We scanned and pre-processed ten patients and matched controls. We performed this preliminary analysis in two patients and their controls. Patient 1, with non-lesional mesial frontal lobe epilepsy, had 25 out of 33 (76%) IED electrode sites overlap with the FC map (figure); compared to 24 out of 33 (73%) electrode overlaps with the control map (1.04 normalized to control). Patient 2, with non-lesional temporal lobe epilepsy, had 7 out of 40 electrodes overlap (18%); compared with 12 out of 40 (30%) in the matched control (0.6 normalized to control). The attached figure shows sites of IEDs, represented by colored small squares, overlayed on the FC derived from the SOZ in this patient (Patient 1) with non-lesional mesial frontal lobe epilepsy. Conclusions: Our initial hypothesis of increased connectivity of the SOZ with the broader irritative zone in focal non-lesional epilepsy does not appear to be supported in this small preliminary sample. It is possible that the SOZ may be more connected to a subset of a broader, multifocal irritative zone (the one that comprises the SOZ). Alternatively, there may indeed be less interictal connectivity within these regions, despite their epileptogenicity, as determined using this fMRI measure of network integrity. We plan to expand this analysis to 10 patients in each group by the time of abstract presentation. We also plan to perform a similar analysis of the seizure propagation network with the hypothesis that seizures spread to areas that are functionally connected with the SOZ. fMRI maps of epileptiform activity could potentially be applied clinically to help predict areas of seizure propagation. Funding: TTR pilot award to KMK as part of the CTSA award at UTHSCSA