Abstracts

Rationale: Several recent studies evaluated BOLD signal distribution in patients with GSWD using EEG/fMRI at 1.5 or 3T. The results of these studies support the notion that GSWD may be the result of interactions within broad cortical and subcortical networks including thalami and frontal and parietal cortices. The goal of this study was to evaluate the BOLD signal changes in response to frequent and prolonged bursts of generalized spike and wave discharges (GSWD) using EEG/fMRI at 4T in a patient with late-onset, valproate (VPA)-controlled juvenile absence epilepsy (JAE). Methods: A 28 year old had JAE diagnosed based on a single generalized tonic-clonic seizure at the age of 23 and presence of episodes of “staring” since mid-teenage years. At the time of the EEG/fMRI the patient received a combination of low-dose lamotrigine and topiramate. Subsequently, she was switched to VPA with complete normalization of the EEG. 400 EPI whole brain volumes were acquired with concurrent EEG at 4T with TR=1.8s and an interscan interval of 3.0s. EPI and ballistocardiographic artifact EEG artifacts were removed using Scan 4.3.3 software (Compumedics USA, Inc). Statistical parametric mapping of event-related BOLD response was performed in SPM5. FMRI data corresponding to events were convolved with a canonical hemodynamic function; subsequent analysis using General Linear Model was performed. Head motion parameters were included as nuisance variables; cluster size ≥ 10 was imposed. Results: Four prolonged bursts of GSWD were recorded (2-4s each; 36 GSWD). Bilateral activations were observed in frontal, thalamic, and occipital regions (T > 3), while deactivation was principally present bilaterally in the parietal lobe (T < -3). These thresholds correspond to uncorrected p < 0.001. Representative slices of a functional activation map for a single subject are shown in Figure. Conclusions: This is the first report of absence seizures imaged with EEG/fMRI at 4T The patterns of BOLD signal changes are similar to changes observed in previous studies at lower MR field and support network involvement in the generation and propagation of GSWD. Support: NIH K23 NS052468 to JPS