Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10321
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dc.contributor.authorBriellmann, Regula Sen
dc.contributor.authorMark Wellard, Ren
dc.contributor.authorMasterton, Richard A Jen
dc.contributor.authorAbbott, David Fen
dc.contributor.authorBerkovic, Samuel Fen
dc.contributor.authorJackson, Graeme Den
dc.date.accessioned2015-05-15T23:44:17Z
dc.date.available2015-05-15T23:44:17Z
dc.date.issued2007-02-01en
dc.identifier.citationEpilepsia; 48(2): 315-23en
dc.identifier.govdoc17295625en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/10321en
dc.description.abstractPatients with refractory temporal lobe epilepsy (refractory TLE) often have hippocampal sclerosis (HS). However, some HS patients have less-severe, drug-responsive epilepsy (mild TLE). We investigated the pattern of MR changes in these two HS groups.We acquired a 3D volumetric sequence, T(2) relaxation times (T2) and proton MR spectroscopy (MRS) in 41 HS patients (24 refractory TLE, 17 mild TLE) and 60 controls. Hippocampal volumes were measured bilaterally. T2 was measured in the hippocampus, amygdala, thalamus, in the white matter of the anterior temporal lobe (ATL), and in the frontal lobe. The temporal lobe MRS established concentrations of N-acetylaspartate (NAA), choline, creatine, myoinositol and glutamine/glutamate.The degree of hippocampal volume loss and hippocampal T2 increase was not different between the two HS groups. However, in refractory TLE, the T2 signal in the ipsilateral ATL was increased, and the ipsilateral NAA concentration was reduced (p < or = 0.05).In this group of HS patients, the degree of HS was not related to the clinical course, possibly reflecting the common cause of epilepsy. In contrast, refractory TLE patients had pronounced white matter changes and metabolite disturbance in the ipsilateral temporal lobe. These abnormalities may indicate the refractory nature of the epilepsy.en
dc.language.isoenen
dc.subject.otherAdulten
dc.subject.otherAspartic Acid.analogs & derivatives.metabolismen
dc.subject.otherCholine.metabolismen
dc.subject.otherCreatine.metabolismen
dc.subject.otherEpilepsy, Temporal Lobe.diagnosis.metabolismen
dc.subject.otherFemaleen
dc.subject.otherFunctional Lateralityen
dc.subject.otherGlutamic Acid.metabolismen
dc.subject.otherGlutamine.metabolismen
dc.subject.otherHippocampus.metabolism.pathologyen
dc.subject.otherHumansen
dc.subject.otherMagnetic Resonance Spectroscopy.statistics & numerical dataen
dc.subject.otherMaleen
dc.subject.otherPrognosisen
dc.subject.otherSclerosis.pathologyen
dc.subject.otherSeverity of Illness Indexen
dc.subject.otherTemporal Lobe.metabolism.pathologyen
dc.titleHippocampal sclerosis: MR prediction of seizure intractability.en
dc.typeJournal Articleen
dc.identifier.journaltitleEpilepsiaen
dc.identifier.affiliationBrain Research Institute, Austin Health, Heidelberg West, Australiaen
dc.identifier.doi10.1111/j.1528-1167.2006.00932.xen
dc.description.pages315-23en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/17295625en
dc.type.austinJournal Articleen
local.name.researcherAbbott, David F
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.grantfulltextnone-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptEpilepsy Research Centre-
crisitem.author.deptNeurology-
crisitem.author.deptNeurology-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
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