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dc.contributor.authorTenney, Jeffrey R.
dc.contributor.authorDuong, Timothy Q.
dc.contributor.authorKing, Jean A.
dc.contributor.authorFerris, Craig F.
dc.date2022-08-11T08:08:49.000
dc.date.accessioned2022-08-23T16:09:23Z
dc.date.available2022-08-23T16:09:23Z
dc.date.issued2004-05-18
dc.date.submitted2009-01-13
dc.identifier.citationEpilepsia. 2004 Jun;45(6):576-82. <a href="http://dx.doi.org/10.1111/j.0013-9580.2004.39303.x">Link to article on publisher's site</a>
dc.identifier.issn0013-9580 (Print)
dc.identifier.doi10.1111/j.0013-9580.2004.39303.x
dc.identifier.pmid15144421
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32682
dc.description.abstractPURPOSE: EEG-triggered functional magnetic resonance imaging (fMRI) was used to identify areas of brain activation during spontaneous spike-and-wave discharges (SWDs) in an epileptic rat strain under awake conditions. METHODS: Spontaneous absence seizures from 10 WAG/Rij rats were imaged by using T2*-weighted echo planar imaging at 4.7 Tesla. fMRI of the blood-oxygenation-level-dependent (BOLD) signal was triggered based on EEG recordings during imaging. Images obtained during spontaneous SWDs were compared with baseline images. RESULTS: Significant positive BOLD signal changes were apparent in several areas of the cortex and several important nuclei of the thalamus. In addition, no negative BOLD signal was found in any brain area. CONCLUSIONS: We have shown that EEG-triggered BOLD fMRI can be used to detect cortical and thalamic activation related to the spontaneous SWDs that characterize absence seizures in awake WAG/Rij rats. These results draw an anatomic correlation between areas in which increased BOLD signal is found and those in which SWDs have been recorded. In addition, no negative BOLD signal was found to be associated with these spontaneous SWDs. We also demonstrated the technical feasibility of using EEG-triggered fMRI in a genetic rat model of absence seizure.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15144421&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1111/j.0013-9580.2004.39303.x
dc.subjectAnimals; Brain; Brain Mapping; Cerebral Cortex; Disease Models, Animal; *Electroencephalography; Epilepsy, Absence; *Magnetic Resonance Imaging; Male; Neural Pathways; Oxygen; Rats; Rats, Wistar; Thalamic Nuclei
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleFMRI of brain activation in a genetic rat model of absence seizures
dc.typeJournal Article
dc.source.journaltitleEpilepsia
dc.source.volume45
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1240
dc.identifier.contextkey693150
html.description.abstract<p>PURPOSE: EEG-triggered functional magnetic resonance imaging (fMRI) was used to identify areas of brain activation during spontaneous spike-and-wave discharges (SWDs) in an epileptic rat strain under awake conditions.</p> <p>METHODS: Spontaneous absence seizures from 10 WAG/Rij rats were imaged by using T2*-weighted echo planar imaging at 4.7 Tesla. fMRI of the blood-oxygenation-level-dependent (BOLD) signal was triggered based on EEG recordings during imaging. Images obtained during spontaneous SWDs were compared with baseline images.</p> <p>RESULTS: Significant positive BOLD signal changes were apparent in several areas of the cortex and several important nuclei of the thalamus. In addition, no negative BOLD signal was found in any brain area.</p> <p>CONCLUSIONS: We have shown that EEG-triggered BOLD fMRI can be used to detect cortical and thalamic activation related to the spontaneous SWDs that characterize absence seizures in awake WAG/Rij rats. These results draw an anatomic correlation between areas in which increased BOLD signal is found and those in which SWDs have been recorded. In addition, no negative BOLD signal was found to be associated with these spontaneous SWDs. We also demonstrated the technical feasibility of using EEG-triggered fMRI in a genetic rat model of absence seizure.</p>
dc.identifier.submissionpathgsbs_sp/1240
dc.contributor.departmentDepartment of Psychiatry
dc.contributor.departmentCenter for Comparative Neuroimaging
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages576-82


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