Cortical and subcortical contributions to absence seizure onset examined with EEG/fMRI

摘要: Abstract In patients with idiopathic generalized epilepsies (IGEs), bursts of spike and wave discharges (GSWDs) lasting ≥ 2 seconds are considered absence seizures. The location the seizures generators in IGEs is thought to involve interplay between various components thalamocortical circuits; we have recently postulated that medication resistance may, part, be related GSWD [Szaflarski JP, Lindsell CJ, Zakaria T, Banks C, Privitera MD. Epilepsy Behav. 2010;17:525–30]. present study hypothesized medication-refractory IGE (R-IGE) continued may locations other than thalamus, as typically seen IGE. Hence, objective this was determine R-IGE using EEG/fMRI. Eighty-three received concurrent EEG/fMRI at 4 T. Nine them (aged 15–55) experienced during were included; all diagnosed R-IGE. Subjects participated up three 20-minute sessions (400 volumes, TR = 3 seconds) performed After removal fMRI ballistocardiographic artifacts, 36 identified. Statistical parametric maps generated for each these correlating BOLD response. Timing differences brain regions tested statistical by modeling onset times shifted relative onsets. Although thalamic responses peaked approximately 6 seconds after seizures, areas including prefrontal dorsolateral cortices showed brief nonsustained peaks occurring ∼ 2 seconds prior maximum peak. Temporal lobe occurred same time peak, a cerebellar peak ∼ 1 second later. Confirmatory analysis averaging cross-correlation cortical interest across corroborated findings. Finally, Granger causality effective connectivity directed from frontal supporting notion earlier involvement. results support our original hypothesis indicate studied, initiated widespread (frontal parietal) sustained subcortical (thalamic) regions, suggesting examined epilepsy propagation thalamus.