Journal
EPILEPSIA
Volume 53, Issue 4, Pages 622-630Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1528-1167.2011.03385.x
Keywords
Idiopathic generalized epilepsy; EEG-fMRI; Absence seizure; BOLD; Default mode network
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Funding
- Fondazione Cassa di Risparmio di Modena,'' Modena, Italy
- Emilia-Romagna Region, Italy
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Purpose: Electroencephalographyfunctional magnetic resonance imaging (EEG-fMRI) coregistration has recently revealed that several brain structures are involved in generalized spike and wave discharges (GSWDs) in idiopathic generalized epilepsies (IGEs). In particular, deactivations and activations have been observed within the so-called brain default mode network (DMN) and thalamus, respectively. In the present study we analyzed the dynamic time course of blood oxygen leveldependent (BOLD) changes preceding and following 3 Hz GSWDs in a group of adolescent and adult patients with IGE who presented with absence seizures (AS). Our aim was to evaluate cortical BOLD changes before, during, and after GSWD onset. Methods: Twenty-one patients with IGE underwent EEG-fMRI coregistration. EEG-related analyses were run both at the single-subject and at group level (random effect). The time-course analysis was conducted for 3 s time windows before, during, and after GSWDs, and they were included until no further BOLD signal changes were observed. Key Findings: Fifteen patients (nine female, mean age 28 years) had GSWDs during EEG-fMRI coregistration (262 total events, mean duration 4 s). Time-course group analysis showedBOLDincrements starting approximately 10 s before GSWD onset located in frontal and parietal cortical areas, and especially in the precuneus-posterior cingulate region. AtGSWDonset, BOLDincrements were located in thalamus, cerebellum, and anterior cingulate gyrus, whereas BOLD decrements were observed in the DMNregions persisting until 9 s after onset. Significance: Hemodynamic changes (BOLD increments) occurred in specific cortical areas, namely the precuneus/ posterior cingulate, lateral parietal, and frontal cortices, several seconds before EEG onset of GSWD. A dysfunction of these brain regions, some of which belongs to the DMN, may be crucial in generating GSWDs in patients with IGE.
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