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Conference Paper: Neural origin of the interhemispheric functional connectivity loss after complete corpus callosotomy

TitleNeural origin of the interhemispheric functional connectivity loss after complete corpus callosotomy
Authors
Issue Date2013
PublisherInternational Society for Magnetic Resonance in Medicine (ISMRM).
Citation
The 21st Annual Meeting & Exhibition of the International Society for Magnetic Resonance in Medicine (ISMRM 2013), Salt Lake City, UT., 20-26 April 2013. In Society of Magnetic Resonance in Medicine Proceedings, 2013, v. 21, p. 3267 How to Cite?
AbstractPreviously, a case study reported that complete transection of the corpus callosum induced loss of interhemispheric correlations in resting-state functional connectivity MRI (RSfcMRI). However, the results were limited by the lack of any electrophysiological recordings. Therefore, it could not be excluded that the loss of interhemispheric correlations in RSfcMRI might arise due to non-neuronal physiological modulations. In this study, intra-cortical electroencephalography (EEG) signals were recorded in the complete corpus callosotomy rats to understand the neural origin of the loss of interhemispheric correlations in RSfcMRI. The results clearly supported that the loss of interhemispheric correlations in RSfcMRI reflects the changes in spontaneous brain activity and its coherence. More importantly, the results strongly suggested that resting-state spontaneous fluctuations have strongest correlation with delta oscillations. (Abstract by ISMRM)
DescriptionElectronic Poster Session: Functional MRI (neuro) - Resting State Connectivity: Methods
Persistent Identifierhttp://hdl.handle.net/10722/191652
ISSN

 

DC FieldValueLanguage
dc.contributor.authorChan, RWen_US
dc.contributor.authorZhou, IYen_US
dc.contributor.authorLiang, YXen_US
dc.contributor.authorHu, Yen_US
dc.contributor.authorSo, KFen_US
dc.contributor.authorWu, EX-
dc.date.accessioned2013-10-15T07:14:53Z-
dc.date.available2013-10-15T07:14:53Z-
dc.date.issued2013en_US
dc.identifier.citationThe 21st Annual Meeting & Exhibition of the International Society for Magnetic Resonance in Medicine (ISMRM 2013), Salt Lake City, UT., 20-26 April 2013. In Society of Magnetic Resonance in Medicine Proceedings, 2013, v. 21, p. 3267en_US
dc.identifier.issn1557-3672-
dc.identifier.urihttp://hdl.handle.net/10722/191652-
dc.descriptionElectronic Poster Session: Functional MRI (neuro) - Resting State Connectivity: Methods-
dc.description.abstractPreviously, a case study reported that complete transection of the corpus callosum induced loss of interhemispheric correlations in resting-state functional connectivity MRI (RSfcMRI). However, the results were limited by the lack of any electrophysiological recordings. Therefore, it could not be excluded that the loss of interhemispheric correlations in RSfcMRI might arise due to non-neuronal physiological modulations. In this study, intra-cortical electroencephalography (EEG) signals were recorded in the complete corpus callosotomy rats to understand the neural origin of the loss of interhemispheric correlations in RSfcMRI. The results clearly supported that the loss of interhemispheric correlations in RSfcMRI reflects the changes in spontaneous brain activity and its coherence. More importantly, the results strongly suggested that resting-state spontaneous fluctuations have strongest correlation with delta oscillations. (Abstract by ISMRM)-
dc.languageengen_US
dc.publisherInternational Society for Magnetic Resonance in Medicine (ISMRM).-
dc.relation.ispartofSociety of Magnetic Resonance in Medicine Proceedingsen_US
dc.titleNeural origin of the interhemispheric functional connectivity loss after complete corpus callosotomyen_US
dc.typeConference_Paperen_US
dc.identifier.emailZhou, IY: iriszhou@eee.hku.hken_US
dc.identifier.emailSo, KF: hrmaskf@hku.hken_US
dc.identifier.emailWu, EX: ewu1@hkucc.hku.hk-
dc.identifier.authorityWu, EX=rp00193en_US
dc.identifier.authorityZhou, IY=rp01739en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros226041en_US
dc.identifier.volume21-
dc.identifier.spage3267en_US
dc.identifier.epage3267en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.issnl1065-9889-

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