Abstracts

Rationale: Generalized tonic-clonic seizures have devastating consequences for patient safety and quality of life. The mechanisms which prevent or permit secondary generalization of focal seizures are not well understood. Intracranial EEG (icEEG) provides a unique opportunity to study seizure propagation and areas of involvement in secondarily generalized seizures. Our goal was to study icEEG in a relatively homogeneous group of focal temporal lobe seizures to investigate the differences in onset and propagation patterns between seizures that remained focal vs. those with secondary generalization. Methods: A total of 33 seizures were analyzed in 9 patients who met the following criteria for confirmed mesial temporal lobe epilepsy and icEEG data: 1) icEEG-video monitoring with at least 1 secondarily generalized seizure, 2) pathologically proven hippocampal sclerosis, 3) no seizures for at least 1 year after anteromedial temporal lobe resection. Onset of secondary generalization was defined based on icEEG-video data demonstrating behavioral vocalization, facial clonus and tonic head/eye deviation. We obtained data from 16 focal seizures without generalization (FS), and 17 secondarily generalized seizures (GTC). Results: Seizure onset patterns did not differ between FS and GTC, although we did observe differences in later propagation. All seizures started with low voltage fast activity except 3 seizures in one patient (2 FS, 1 GTC), which started with theta-frequency spike discharges. 15 of 33 seizures started from the hippocampus and 18 of 33 seizures (including 4 seizures without hippocampal contacts) started from the non-hippocampal anterior medial temporal lobe contacts, but did not differ between FS and GTC. We observed involvement or more prominent activation of the posterior-lateral temporal regions in GTCs prior to propagation to the other cortical regions, vs. FS which had no involvement or less prominent activation of the posterior lateral temporal cortex. Contacts placed on the occipital lobe, in those patients who had such placement, were not involved at the time of clinical secondary generalization. Conclusions: The posterior-lateral temporal region may serve as an important "gateway" controlling propagation of temporal lobe seizures to other cortical regions. Further quantitative analysis may provide additional insight into the possible role of cortical slow or fast activity, representing inhibitory or excitatory drives, in gating seizure propagation beyond the temporal lobe. Identifying the mechanisms of seizure secondary generalization has important therapeutic implications, and may lead to improved treatments to confine seizure spread.