Corticothalamic Modulation during Absence Seizures in Rats: A Functional MRI Assessment

Purpose: Functional magnetic resonance imaging (fMRI) was used to identify areas of brain activation during absence seizures in an awake animal model. Methods: Blood‐oxygenation‐level–dependent (BOLD) fMRI in the brain was measured by using T2*‐weighted echo planar imaging at 4.7 Tesla. BOLD imaging...

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Published inEpilepsia (Copenhagen) Vol. 44; no. 9; pp. 1133 - 1140
Main Authors Tenney, Jeffrey R., Duong, Timothy Q., King, Jean A., Ludwig, Reinhold, Ferris, Craig F.
Format Journal Article
LanguageEnglish
Published 350 Main Street , Malden , MA 02148 , U.S.A Blackwell Science Inc 01.09.2003
Blackwell
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Summary:Purpose: Functional magnetic resonance imaging (fMRI) was used to identify areas of brain activation during absence seizures in an awake animal model. Methods: Blood‐oxygenation‐level–dependent (BOLD) fMRI in the brain was measured by using T2*‐weighted echo planar imaging at 4.7 Tesla. BOLD imaging was performed before, during, and after absence seizure induction by using γ‐butyrolactone (GBL; 200 mg/kg, intraperitoneal). Results: The corticothalamic circuitry, critical for spike–wave discharge (SWD) formation in absence seizure, showed robust BOLD signal changes after GBL administration, consistent with EEG recordings in the same animals. Predominantly positive BOLD changes occurred in the thalamus. Sensory and parietal cortices showed mixed positive and negative BOLD changes, whereas temporal and motor cortices showed only negative BOLD changes. Conclusions: With the BOLD fMRI technique, we demonstrated signal changes in brain areas that have been shown, with electrophysiology experiments, to be important for generating and maintaining the SWDs that characterize absence seizures. These results corroborate previous findings from lesion and electrophysiological experiments and show the technical feasibility of noninvasively imaging absence seizures in fully conscious rodents.
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ISSN:0013-9580
1528-1167
DOI:10.1046/j.1528-1157.2003.61002.x