Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/31061
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dc.contributor.authorAllebone, James-
dc.contributor.authorWilson, Sarah J-
dc.contributor.authorBradlow, Richard C J-
dc.contributor.authorMaller, Jerome-
dc.contributor.authorO'Brien, Terry-
dc.contributor.authorMullen, Saul A-
dc.contributor.authorCook, Mark-
dc.contributor.authorAdams, Sophia J-
dc.contributor.authorVogrin, Simon-
dc.contributor.authorVaughan, David N-
dc.contributor.authorConnelly, Alan-
dc.contributor.authorKwan, Patrick-
dc.contributor.authorBerkovic, Samuel F-
dc.contributor.authorD'Souza, Wendyl J-
dc.contributor.authorJackson, Graeme D-
dc.contributor.authorVelakoulis, Dennis-
dc.contributor.authorKanaan, Richard A A-
dc.date2022-
dc.date.accessioned2022-10-21T04:48:27Z-
dc.date.available2022-10-21T04:48:27Z-
dc.date.issued2022-10-
dc.identifier.citationSeizure 2022; 101: 244-252en
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/31061-
dc.description.abstractTo explore the cortical morphological associations of the psychoses of epilepsy. Psychosis of epilepsy (POE) has two main subtypes - postictal psychosis and interictal psychosis. We used automated surface-based analysis of magnetic resonance images to compare cortical thickness, area, and volume across the whole brain between: (i) all patients with POE (n = 23) relative to epilepsy-without psychosis controls (EC; n = 23), (ii) patients with interictal psychosis (n = 10) or postictal psychosis (n = 13) relative to EC, and (iii) patients with postictal psychosis (n = 13) relative to patients with interictal psychosis (n = 10). POE is characterised by cortical thickening relative to EC, occurring primarily in nodes of the cognitive control network; (rostral anterior cingulate, caudal anterior cingulate, middle frontal gyrus), and the default mode network (posterior cingulate, medial paracentral gyrus, and precuneus). Patients with interictal psychosis displayed cortical thickening in the left hemisphere in occipital and temporal regions relative to EC (lateral occipital cortex, lingual, fusiform, and inferior temporal gyri), which was evident to a lesser extent in postictal psychosis patients. There were no significant differences in cortical thickness, area, or volume between the postictal psychosis and EC groups, or between the postictal psychosis and interictal psychosis groups. However, prior to correction for multiple comparisons, both the interictal psychosis and postictal psychosis groups displayed cortical thickening relative to EC in highly similar regions to those identified in the POE group overall. The results show cortical thickening in POE overall, primarily in nodes of the cognitive control and default mode networks, compared to patients with epilepsy without psychosis. Additional thickening in temporal and occipital neocortex implicated in the dorsal and ventral visual pathways may differentiate interictal psychosis from postictal psychosis. A novel mechanism for cortical thickening in POE is proposed whereby normal synaptic pruning processes are interrupted by seizure onset.en
dc.language.isoeng
dc.subjectCortexen
dc.subjectEpilepsyen
dc.subjectInterictal psychosisen
dc.subjectPostictal psychosisen
dc.subjectPsychosisen
dc.titleIncreased cortical thickness in nodes of the cognitive control and default mode networks in psychosis of epilepsy.en
dc.typeJournal Articleen_US
dc.identifier.journaltitleSeizureen
dc.identifier.affiliationMelbourne Neuropsychiatry Centre, University of Melbourne and Melbourne Health, Melbourne, Australiaen
dc.identifier.affiliationDepartment of Neuroscience, Alfred Hospital, Monash University, Melbourne, Australiaen
dc.identifier.affiliationNeuropsychiatry Unit, Royal Melbourne Hospital, Melbourne, Victoria, Australiaen
dc.identifier.affiliationTurning Point, Eastern Health, Victoria, Australiaen
dc.identifier.affiliationThe Florey Institute of Neuroscience and Mental Healthen
dc.identifier.affiliationGraeme Clark Institute, University of Melbourne, Melbourne, Australiaen
dc.identifier.affiliationPsychiatry (University of Melbourne)en
dc.identifier.affiliationSt Vincent's Hospital, Melbourne, Victoria, Australiaen
dc.identifier.affiliationComprehensive Epilepsy Programen
dc.identifier.affiliationDepartment of Medicine, St Vincent's Hospital, The University of Melbourne, Australiaen
dc.identifier.affiliationANU College of Health and Medicine, Australian National University, Canberra, Victoria, Australiaen
dc.identifier.affiliationMonash Alfred Psychiatry Research Centre, The Alfred and Monash University, Melbourne, Australiaen
dc.identifier.affiliationMelbourne School of Psychological Sciences, University of Melbourne, VIC, Australiaen
dc.identifier.affiliationRoyal Melbourne Hospital, Melbourne, Victoria, Australiaen
dc.identifier.doi10.1016/j.seizure.2022.09.006en
dc.type.contentTexten_US
dc.identifier.pubmedid36116283
local.name.researcherBerkovic, Samuel F
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptEpilepsy Research Centre-
crisitem.author.deptEpilepsy Research Centre-
crisitem.author.deptNeurology-
crisitem.author.deptNeurology-
crisitem.author.deptThe Florey Institute of Neuroscience and Mental Health-
crisitem.author.deptPsychiatry (University of Melbourne)-
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