{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,16]],"date-time":"2026-07-16T16:24:35Z","timestamp":1784219075846,"version":"3.55.0"},"reference-count":51,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2020,9,18]],"date-time":"2020-09-18T00:00:00Z","timestamp":1600387200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["K23\u2010NS092923"],"award-info":[{"award-number":["K23\u2010NS092923"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01NS115868"],"award-info":[{"award-number":["R01NS115868"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2020,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Childhood epilepsy with centrotemporal spikes (CECTS) is a common, focal, transient, developmental epilepsy syndrome characterized by unilateral or bilateral, independent epileptiform spikes in the Rolandic regions of unknown etiology. Given that CECTS presents during a period of dramatic white matter maturation and thatspikes in CECTS are activated during non\u2013rapid eye movement (REM) sleep, we hypothesized that children with CECTS would have aberrant development of white matter connectivity between the thalamus and the Rolandic cortex. We further tested whether Rolandic thalamocortical structural connectivity correlates with spike rate during non\u2010REM sleep.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Twenty\u2010three children with CECTS (age = 8\u201015\u00a0years) and 19 controls (age = 7\u201015\u00a0years) underwent 3\u2010T structural and diffusion\u2010weighted magnetic resonance imaging and 72\u2010electrode electroencephalographic recordings. Thalamocortical structural connectivity to Rolandic and non\u2010Rolandic cortices was quantified using probabilistic tractography. Developmental changes in connectivity were compared between groups using bootstrap analyses. Longitudinal analysis was performed in four subjects with 1\u2010year follow\u2010up data. Spike rate was quantified during non\u2010REM sleep using manual and automated techniques and compared to Rolandic connectivity using regression analyses.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Children with CECTS had aberrant development of thalamocortical connectivity to the Rolandic cortex compared to controls (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.01), where the expected increase in connectivity with age was not observed in CECTS. There was no difference in the development of thalamocortical connectivity to non\u2010Rolandic regions between CECTS subjects and controls (<jats:italic>P<\/jats:italic>\u00a0=\u00a0.19). Subjects with CECTS observed longitudinally had reductions in thalamocortical connectivity to the Rolandic cortex over time. No definite relationship was found between Rolandic connectivity and non\u2010REM spike rate (<jats:italic>P\u00a0<\/jats:italic>&gt;\u00a0.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Significance<\/jats:title><jats:p>These data provide evidence that abnormal maturation of thalamocortical white matter circuits to the Rolandic cortex is a feature of CECTS. Our data further suggest that the abnormalities in these tracts do not recover, but are increasingly dysmature over time, implicating a permanent but potentially compensatory process contributing to disease resolution.<\/jats:p><\/jats:sec>","DOI":"10.1111\/epi.16681","type":"journal-article","created":{"date-parts":[[2020,9,18]],"date-time":"2020-09-18T07:15:42Z","timestamp":1600413342000},"page":"2500-2508","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["Persistent abnormalities in Rolandic thalamocortical white matter circuits in childhood epilepsy with centrotemporal spikes"],"prefix":"10.1111","volume":"61","author":[{"given":"Emily L.","family":"Thorn","sequence":"first","affiliation":[{"name":"Department of Neurology Massachusetts General Hospital Boston Massachusetts USA"},{"name":"Elson S. Floyd College of Medicine Washington State University Spokane Washington USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren M.","family":"Ostrowski","sequence":"additional","affiliation":[{"name":"Department of Neurology Massachusetts General Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dhinakaran M.","family":"Chinappen","sequence":"additional","affiliation":[{"name":"Department of Neurology Massachusetts General Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jin","family":"Jing","sequence":"additional","affiliation":[{"name":"Department of Neurology Massachusetts General Hospital Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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Martinos Center for Biomedical Imaging Charlestown Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark A.","family":"Kramer","sequence":"additional","affiliation":[{"name":"Department of Mathematics and Statistics Boston University Boston Massachusetts USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7670-9313","authenticated-orcid":false,"given":"Catherine J.","family":"Chu","sequence":"additional","affiliation":[{"name":"Department of Neurology Massachusetts General Hospital Boston Massachusetts USA"},{"name":"Harvard Medical School Boston Massachusetts 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