{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T13:14:41Z","timestamp":1788614081870,"version":"build-2803163510"},"reference-count":44,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T00:00:00Z","timestamp":1788566400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T00:00:00Z","timestamp":1788566400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100002341","name":"Research Council of Finland","doi-asserted-by":"publisher","award":["358944"],"award-info":[{"award-number":["358944"]}],"id":[{"id":"10.13039\/501100002341","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004012","name":"Jane ja Aatos Erkon S\u00e4\u00e4ti\u00f6","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004012","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia Open"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Focal cortical dysplasia type II (FCDII) is a cortical malformation representing a common cause of surgically treatable drug\u2010resistant epilepsy. We studied whether FCDII disrupts normal structural interhemispheric asymmetry beyond the lesion location and quantified these asymmetries derived from structural magnetic resonance imaging (MRI) between individuals with FCDII and healthy controls (HC) as well as within FCDII subtypes using surface\u2010based morphometry (SBM).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Using an open MRI dataset from University Hospital Bonn, we processed T1\u2010weighted images from HC and individuals with FCDII aged over 15\u2009years at the time of scan. We designed a three\u2010stage workflow consisting of SBM using FreeSurfer, visual inspection of atlas\u2010based cortical parcellations, and lesion projection. We extracted five cortical measures of intensity, thickness, volume, curvature, and surface area from 34 regions of interest (ROIs) and computed unsigned interhemispheric asymmetry indices beyond the lesion location.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The majority of FCDII lesions annotated in the original dataset were located in the frontal lobe (64.0%). Compared to the HC, individuals with MRI\u2010diagnosed FCDII showed significantly reduced unsigned interhemispheric intensity asymmetry across parietal, temporal, and occipital cortices (\n                      <jats:italic>q<\/jats:italic>\n                      \u2009&lt;\u20090.001). We observed an increase in the unsigned interhemispheric volume asymmetry in the lateral orbitofrontal cortex and in the unsigned interhemispheric surface\u2010area asymmetry in the inferior temporal cortex for FCDII compared to HC (\n                      <jats:italic>q<\/jats:italic>\n                      \u2009&lt;\u20090.001). Subtype analyses revealed greater unsigned interhemispheric intensity asymmetry in caudal anterior cingulate and superior temporal cortices in FCDIIb compared with FCDIIa (\n                      <jats:italic>q<\/jats:italic>\n                      \u2009&lt;\u20090.001). Conversely, precentral unsigned surface\u2010area and volume asymmetries were smaller in FCDIIb relative to FCDIIa (\n                      <jats:italic>q<\/jats:italic>\n                      \u2009&lt;\u20090.001). We observed no significant differences for unsigned interhemispheric cortical thickness and curvature asymmetries after multiple\u2010comparison corrections.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Significance<\/jats:title>\n                    <jats:p>SBM\u2010derived interhemispheric asymmetry captures cortical alterations in FCDII beyond the focal lesions. Observed differences in group\u2010level unsigned interhemispheric intensity, volume, and surface\u2010area asymmetry indicated cortical alterations that are consistent with distributed cortical involvement between FCDIIa and FCDIIb. These findings may enhance presurgical evaluation by highlighting cortical areas outside the primary lesion that could contribute to seizure generation and achieving seizure\u2010freedom after the operation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Plain Language Summary<\/jats:title>\n                    <jats:p>Focal cortical dysplasia type II (FCDII) is a malformation of cortical development associated with drug\u2010resistant epilepsies. FCDII may disrupt normal cortical interhemispheric asymmetries which are understudied in focal, extratemporal epilepsies. We discovered that individuals with FCDII display altered structural cortical interhemispheric asymmetries in intensity, volume, and surface area compared to healthy volunteers, with each FCDII subtype exhibiting a distinct pattern of disrupting the natural asymmetries. Since extra\u2010lesional abnormalities may contribute to incomplete seizure control after surgery, these interhemispheric asymmetry findings could provide complementary information for presurgical evaluations.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/epi4.70336","type":"journal-article","created":{"date-parts":[[2026,9,5]],"date-time":"2026-09-05T13:09:48Z","timestamp":1788613788000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Quantifying extra\u2010lesional interhemispheric cortical asymmetry in focal cortical dysplasia type\n                    <scp>II<\/scp>"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8044-3068","authenticated-orcid":false,"given":"Faezeh","family":"Heidari","sequence":"first","affiliation":[{"name":"Department of Neurology, Institute of Clinical Medicine University of Eastern Finland  Kuopio Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6172-7842","authenticated-orcid":false,"given":"Mastaneh","family":"Torkamani\u2010Azar","sequence":"additional","affiliation":[{"name":"A.I. Virtanen Institute for Molecular Sciences University of Eastern Finland  Kuopio Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1048-5860","authenticated-orcid":false,"given":"Jussi","family":"Tohka","sequence":"additional","affiliation":[{"name":"A.I. Virtanen Institute for Molecular Sciences University of Eastern Finland  Kuopio Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2935-5131","authenticated-orcid":false,"given":"Reetta","family":"K\u00e4lvi\u00e4inen","sequence":"additional","affiliation":[{"name":"Department of Neurology, Institute of Clinical Medicine University of Eastern Finland  Kuopio Finland"},{"name":"Kuopio Epilepsy Center Kuopio University Hospital, Full Member of ERN EpiCARE  Kuopio 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