Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/28220
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dc.contributor.authorKhlif, Mohamed Salah-
dc.contributor.authorWerden, Emilio-
dc.contributor.authorBird, Laura J-
dc.contributor.authorEgorova-Brumley, Natalia-
dc.contributor.authorBrodtmann, Amy-
dc.date2021-11-27-
dc.date.accessioned2021-12-07T02:50:52Z-
dc.date.available2021-12-07T02:50:52Z-
dc.date.issued2022-07-
dc.identifier.citationJournal of magnetic resonance imaging : JMRI 2022; 56(1): 273-281en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/28220-
dc.description.abstractThe structural integrity of hippocampal subfields has been investigated in many neurological disorders and was shown to be better associated with cognitive performance than whole hippocampus. In stroke, hippocampal atrophy is linked to cognitive impairment, but it is unknown whether the hippocampal subfields atrophy differently. To evaluate longitudinal hippocampal subfield atrophy in first year poststroke, in comparison with atrophy in healthy individuals. Cohort. A total of 92 ischemic stroke (age: 67 ± 12 years, 63 men) and 39 healthy participants (age: 69 ± 7 years, 24 men). A3 T/T1-MPRAGE, T2-SPACE, and T2-FLAIR. FreeSurfer (6.0) was used to delineate 12 hippocampal subfields. Whole hippocampal volume was computed as sum of subfield volumes excluding hippocampal fissure volume. Separate assessments were completed for contralesional and ipsilesional hippocampi. A mixed-effect regression model was used to compare subfield volumes cross-sectionally between healthy and stroke groups and longitudinally between 3-month and 12-month timepoints. False discovery rate at 0.05 significance level was used to correct for multiple comparisons. Also, a receiver operating characteristic (ROC) curve analysis was performed to assess differentiation between healthy and stroke participants based on subfield volumes. There were no volume differences between groups at 3 months, but there was a significant difference (P = 0.027) in whole hippocampal volume reduction over time between control and stroke ipsilesionally. Thus, the ipsilesional whole hippocampal volume in stroke became significantly smaller (P = 0.035) at 12 months. The hippocampal tail was the highest single-region contributor (22.7%) to ipsilesional hippocampal atrophy (1.19%) over 9 months. The cornu ammonis areas (CA1) subfield volume reduction was minimal in controls and stroke contralesionally but significant ipsilesionally (P = 0.007). CA1 volume significantly outperformed whole hippocampal volume (P < 0.01) in discriminating between stroke participants and healthy controls in ROC curve analysis. Greater stroke-induced effects were observed in the ipsilesional hippocampus anteriorly in CA1 and posteriorly in the hippocampal tail. Atrophy of CA1 and hippocampal tail may provide a better link to cognitive impairment than whole hippocampal atrophy. 2 TECHNICAL EFFICACY STAGE: 3.en
dc.language.isoeng-
dc.subjectFreeSurferen
dc.subjectatrophyen
dc.subjecthippocampal subfieldsen
dc.subjectneurodegenerationen
dc.subjectstrokeen
dc.titleAtrophy of Ipsilesional Hippocampal Subfields Vary Over First Year After Ischemic Stroke.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of Magnetic Resonance Imaging : JMRIen
dc.identifier.affiliationEastern Cognitive Disorders Clinic, Box Hill Hospital, Monash University, Box Hill, Victoria, Australiaen
dc.identifier.affiliationThe Florey Institute for Neuroscience and Mental Health, University of Melbourne, Melbourne, Australiaen
dc.identifier.affiliationMelbourne School of Psychological Sciences, University of Melbourne, Melbourne, Australiaen
dc.identifier.affiliationNeurologyen
dc.identifier.affiliationDepartment of Neurology, Royal Melbourne Hospital, Parkville, Victoria, Australiaen
dc.identifier.doi10.1002/jmri.28009en
dc.type.contentTexten
dc.identifier.orcid0000-0002-0096-434Xen
dc.identifier.orcid0000-0002-4763-1980en
dc.identifier.orcid0000-0001-7073-725Xen
dc.identifier.orcid0000-0002-9244-2900en
dc.identifier.orcid0000-0001-9466-2862en
dc.identifier.pubmedid34837426-
local.name.researcherBrodtmann, Amy
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
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