{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T18:43:02Z","timestamp":1791657782350,"version":"4.3.4"},"reference-count":47,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2022,12,27]],"date-time":"2022-12-27T00:00:00Z","timestamp":1672099200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100014607","name":"Royal Children's Hospital Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100014607","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","award":["GNT1161549"],"award-info":[{"award-number":["GNT1161549"]}],"id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2023,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Favorable seizure outcome is reported following resection of bottom\u2010of\u2010sulcus dysplasia (BOSD). We assessed the distribution of epileptogenicity and dysplasia in and around BOSD to better understand this clinical outcome and the optimal surgical approach.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We studied 27 children and adolescents with magnetic resonance imaging (MRI)\u2010positive BOSD who underwent epilepsy surgery; 85% became seizure\u2010free postresection (median\u00a0=\u00a05.0\u2009years follow\u2010up). All patients had resection of the dysplastic sulcus, and 11 had additional resection of the gyral crown (GC) or adjacent gyri (AG). Markers of epileptogenicity were relative cortical hypometabolism on preoperative <jats:sup>18<\/jats:sup>F\u2010fluorodeoxyglucose (FDG) positron emission tomography (PET), and spiking, ripples, fast ripples, spike\u2013high\u2010frequency oscillation cross\u2010rate, and phase amplitude coupling (PAC) on preresection and postresection electrocorticography (ECoG), all analyzed at the bottom\u2010of\u2010sulcus (BOS), top\u2010of\u2010sulcus (TOS), GC, and AG. Markers of dysplasia were increased cortical thickness on preoperative MRI, and dysmorphic neuron density and variant allele frequency of somatic <jats:italic>MTOR<\/jats:italic> mutations in resected tissue, analyzed at similar locations.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Relative cortical metabolism was significantly reduced and ECoG markers were significantly increased at the BOS compared to other regions. Apart from spiking and PAC, which were greater at the TOS compared to the GC, there were no significant differences in PET and other ECoG markers between the TOS, GC, and AG, suggesting a cutoff of epileptogenicity at the TOS rather than a tapering gradient on the cortical surface. MRI and tissue markers of dysplasia were all maximal in the BOS, reduced in the TOS, and mostly absent in the GC. Spiking and PAC reduced significantly over the GC after resection of the dysplastic sulcus.<\/jats:p><\/jats:sec><jats:sec><jats:title>Significance<\/jats:title><jats:p>These findings support the concept that dysplasia and intrinsic epileptogenicity are mostly limited to the dysplastic sulcus in BOSD and support resection or ablation confined to the MRI\u2010visible lesion as a first\u2010line surgical approach. <jats:sup>18<\/jats:sup>F\u2010FDG PET and ECoG abnormalities in surrounding cortex seem to be secondary phenomena.<\/jats:p><\/jats:sec>","DOI":"10.1111\/epi.17495","type":"journal-article","created":{"date-parts":[[2022,12,17]],"date-time":"2022-12-17T14:47:06Z","timestamp":1671288426000},"page":"348-363","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["Intrinsic and secondary epileptogenicity in focal cortical dysplasia type II"],"prefix":"10.1111","volume":"64","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9894-4610","authenticated-orcid":false,"given":"Emma","family":"Macdonald\u2010Laurs","sequence":"first","affiliation":[{"name":"Department of Neurology Royal Children's Hospital  Parkville Victoria Australia"},{"name":"Murdoch Children's Research Institute  Parkville Victoria Australia"},{"name":"Department of Paediatrics University of Melbourne  Parkville Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6534-2800","authenticated-orcid":false,"given":"Aaron E. 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