Abstracts

Rationale: The study of epilepsy can help to understand both normal and abnormal brain physiology. Generalized epileptic events such as absence seizures create neuronal activity changes across the brain which are characterized by spike-and-wave discharge (SWD). Typical large amplitude bilateral SWD are common in absence epilepsy, but are also found in other forms of epilepsy. It is hoped that an extensive understanding of the neuronal activity changes during SWD might lead to improved treatment for absence seizures. Blood oxygen-level dependent (BOLD) fMRI signal change alone cannot fully reveal neuronal activity in the imaged system. Absence seizures are associated with widespread cortical fMRI small increases several seconds before EEG seizure onset and decreases that persist for up to 20 seconds after EEG seizure termination, but the physiological basis for these changes remains unknown. Methods: EEG-fMRI data from children age 6-19 with typical childhood absence seizures were analyzed. fMRI timecourse data was binned into seizures of different durations, then aligned to averaged seizure onset and offset of each time bin. After this, we created a signal processing model of electrical activity by deconvolving the BOLD signal during SWD with the standard hemodynamic response function (HRF) used in SPM. Results: Data from 528 seizures in 34 subjects were analyzed. By deconvolving with canonical HRF, we found activated neural activity before seizures and deactivated neural activity after seizures. The neural activity patterns differed substantially based on anatomical location, with the thalamus showing mainly activity increases and cortical regions showing biphasic increases followed by decreases. Conclusions: If the canonical HRF is correct, then the small increases before seizures and decrease in BOLD fMRI signals following seizures can not be explained by electrical activity during the seizure alone. Conversely, if the BOLD signal is only associated with electrical neural activity during seizure, the canonical HRF is not valid for modeling seizures. Further investigation of neuronal changes before, during and after SWD may lead to a better understanding of the pathophysiology of absence seizures and help guide future treatment. Funding: N/A