Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/32707
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dc.contributor.authorBalfroid, Tom-
dc.contributor.authorWarren, Aaron E L-
dc.contributor.authorDalic, Linda J-
dc.contributor.authorAeby, Alec-
dc.contributor.authorBerlangieri, Salvatore U-
dc.contributor.authorArcher, John S-
dc.date2023-
dc.date.accessioned2023-04-21T00:55:23Z-
dc.date.available2023-04-21T00:55:23Z-
dc.date.issued2023-03-30-
dc.identifier.citationEpilepsy Research 2023; 192en_US
dc.identifier.issn1872-6844-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/32707-
dc.description.abstractLennox Gastaut syndrome (LGS) can be conceptualised as a "secondary network epilepsy", in which the shared electroclinical manifestations reflect epileptic recruitment of a common brain network, despite a range of underlying aetiologies. We aimed to identify the key networks recruited by the epileptic process of LGS using interictal 2-deoxy-2-(18F)fluoro-D-glucose positron emission tomography (18F-FDG-PET). Group analysis of cerebral 18F-FDG-PET, comparing 21 patients with LGS (mean age = 15 years) and 18 pseudo-controls (mean age = 19 years), studied at Austin Health Melbourne, between 2004 and 2015. To minimise the influence of individual patient lesions in the LGS group, we only studied brain hemispheres without structural MRI abnormalities. The pseudo-control group consisted of age- and sex-matched patients with unilateral temporal lobe epilepsy, using only the hemispheres contralateral to the side of epilepsy. Voxel-wise permutation testing compared 18F-FDG-PET uptake between groups. Associations were explored between areas of altered metabolism and clinical variables (age of seizure onset, proportion of life with epilepsy, and verbal/nonverbal ability). Penetrance maps were calculated to explore spatial consistency of altered metabolic patterns across individual patients with LGS. Although not always readily apparent on visual inspection of individual patient scans, group analysis revealed hypometabolism in a network of regions including prefrontal and premotor cortex, anterior and posterior cingulate, inferior parietal lobule, and precuneus (p < 0.05, corrected for family-wise error). These brain regions tended to show a greater reduction in metabolism in non-verbal compared to verbal LGS patients, although this difference was not statistically significant. No areas of hypermetabolism were detected on group analysis, although ∼25 % of individual patients showed increased metabolism (relative to pseudo-controls) in the brainstem, putamen, thalamus, cerebellum, and pericentral cortex. Interictal hypometabolism in frontoparietal cortex in LGS is compatible with our previous EEG-fMRI and SPECT studies showing that interictal bursts of generalised paroxysmal fast activity and tonic seizures recruit similar cortical regions. This study provides further evidence that these regions are central to the electroclinical expression of LGS.en_US
dc.language.isoeng-
dc.subjectEpileptic encephalopathyen_US
dc.subjectExecutive control networken_US
dc.subjectFrontoparietal control networken_US
dc.subjectLGSen_US
dc.subjectPositron Emission Tomographyen_US
dc.titleFrontoparietal 18F-FDG-PET hypo-metabolism in Lennox-Gastaut syndrome: Further evidence highlighting the key network.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleEpilepsy Researchen_US
dc.identifier.affiliationDepartment of Pediatric Neurology, Hôpital Universitaire des Enfants Reine Fabiola (HUDERF), Université Libre de Bruxelles (ULB), Brussels, Belgium.en_US
dc.identifier.affiliationMedicine (University of Melbourne)en_US
dc.identifier.affiliationNeurologyen_US
dc.identifier.affiliationDepartment of Pediatric Neurology, Hôpital Universitaire des Enfants Reine Fabiola (HUDERF), Université Libre de Bruxelles (ULB), Brussels, Belgium.en_US
dc.identifier.affiliationMolecular Imaging and Therapyen_US
dc.identifier.affiliationThe Florey Institute of Neuroscience and Mental Healthen_US
dc.identifier.doi10.1016/j.eplepsyres.2023.107131en_US
dc.type.contentTexten_US
dc.identifier.pubmedid37054522-
dc.description.volume192-
dc.description.startpage107131-
local.name.researcherArcher, John S
item.grantfulltextnone-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptNeurology-
crisitem.author.deptClinical Haematology-
crisitem.author.deptOlivia Newton-John Cancer Wellness and Research Centre-
crisitem.author.deptEpilepsy Research Centre-
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