Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10103
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dc.contributor.authorChan, Chow Huat Patricken
dc.contributor.authorBriellmann, Regula Sen
dc.contributor.authorPell, Gaby Sen
dc.contributor.authorScheffer, Ingrid Een
dc.contributor.authorAbbott, David Fen
dc.contributor.authorJackson, Graeme Den
dc.date.accessioned2015-05-15T23:26:58Z
dc.date.available2015-05-15T23:26:58Z
dc.date.issued2006-02-01en
dc.identifier.citationEpilepsia; 47(2): 399-405en
dc.identifier.govdoc16499767en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10103en
dc.description.abstractPatients with childhood absence epilepsy (CAE) have normal clinical magnetic resonance imaging (MRI) studies. The presence of abnormalities in corticothalamic networks has been suggested to be the functional basis of absence seizure generation. We assessed whether structural grey and white matter volume changes of these areas occurred in patients with absence seizures by using optimized voxel-based morphometry (VBM).We recruited 13 patients with a clinical and EEG diagnosis of CAE (mean age at examination, 17 +/- 8 years) and compared them with a consecutive series of 109 controls (mean age, 29 +/- 9 years). The 3 tesla MRI examination included a 3D T(1)-weighted sequence, which was analyzed with an optimized VBM protocol using the SPM2 package. The threshold was set at p < 0.05, corrected for multiple comparisons.Compared with controls, CAE patients showed areas of grey matter decrease in both thalami and in the subcallosal gyrus. White matter decrease was found in the extranuclear subcortical area and in the white matter of the basal forebrain. Grey and white matter increase was restricted to small clusters of cortical and subcortical areas.Evidence exists of subcortical grey and white matter volume reduction in CAE patients. Bilateral thalamic atrophy may be either a result of damage from seizures (as in hippocampal sclerosis) or a reflection of a primary underlying pathology as the cause of absence seizures.en
dc.language.isoenen
dc.subject.otherAdolescenten
dc.subject.otherAdulten
dc.subject.otherAtrophyen
dc.subject.otherBrain Mappingen
dc.subject.otherCerebral Cortex.pathologyen
dc.subject.otherDominance, Cerebralen
dc.subject.otherElectroencephalographyen
dc.subject.otherEpilepsy, Absence.pathologyen
dc.subject.otherFemaleen
dc.subject.otherHumansen
dc.subject.otherImage Interpretation, Computer-Assisteden
dc.subject.otherMagnetic Resonance Imaging.statistics & numerical dataen
dc.subject.otherMaleen
dc.subject.otherProsencephalon.pathologyen
dc.subject.otherTemporal Lobe.pathologyen
dc.subject.otherThalamus.pathologyen
dc.titleThalamic atrophy in childhood absence epilepsy.en
dc.typeJournal Articleen
dc.identifier.journaltitleEpilepsiaen
dc.identifier.affiliationBrain Research Institute, Neurosciences Building, Austin Health, Heidelberg West, Victoria 3081, Australiaen
dc.identifier.doi10.1111/j.1528-1167.2006.00435.xen
dc.description.pages399-405en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/16499767en
dc.type.austinJournal Articleen
local.name.researcherAbbott, David F
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
crisitem.author.deptEpilepsy Research Centre-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptNeurology-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
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