Journal
NEUROLOGY
Volume 75, Issue 10, Pages 904-911Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181f11c06
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Funding
- Pfizer Inc. (Neuroscience Research Grant)
- National Health and Medical Research Council of Australia (NHMRC)
- Dowd Foundation
- UCB
- Janssen-Cilag EMEA
- Eli Lilly and Company
- NHMRC, Health Research Council of New Zealand
- University of Melbourne
- Jack Brockhoff Foundation
- Perpetual Charitable Trustees
- American Epilepsy Society
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Objectives: We used EEG-fMRI to study epileptiform activity in a cohort of untreated children with typical absence seizures (AS). Our aim was to identify cortical and subcortical regions involved in spike and wave events and to explore the timing of activity in these regions. Methods: Eleven children with AS confirmed on video-EEG underwent EEG-fMRI. An eventrelated analysis of epileptiform activity was performed. Regions of interest (ROIs), identified in the event-related analysis, were used to study the time course of the blood oxygen level-dependent (BOLD) signal prior to and immediately following events of interest in these ROIs. Results: Group analysis confirmed positive BOLD in the thalamus and negative BOLD in the lateral and mesial parietal lobe, caudate nuclei, and additionally the brainstem reticular formation. The event-related time course differed between the thalamus, the parietal cortex, and the pons and caudate nuclei. In the subcortical structures, BOLD signal change occurred at, or immediately after, electrographic onset. Importantly, in the parietal cortex, but not in other cortical regions, there was a subtle BOLD signal increase for 10 seconds prior to the onset of epileptiform activity. Conclusions: In children with typical AS, we have confirmed a core network of structures involved in generalized epileptiform activity that includes the reticular structures of the brainstem. Furthermore, we have identified changes in parietal BOLD signal which precede the onset of epileptiform activity, suggesting the parietal cortex has a role in the initiation of epileptiform activity. Neurology (R) 2010; 75: 904-911
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