{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T19:44:42Z","timestamp":1789155882880,"version":"build-2803163510"},"reference-count":17,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,6,28]],"date-time":"2004-06-28T00:00:00Z","timestamp":1088380800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2004,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Benign rolandic epilepsy (BRE) is considered to be a genetically determined idiopathic partial epilepsy. We studied twins with BRE and compared the concordance with a twin sample of idiopathic generalized epilepsy (IGE). All eight BRE pairs (six monozygous [MZ], two dizygous [DZ]) were discordant. MZ pairwise concordance was 0 (95% confidence interval [CI], 0\u20130.4) for BRE compared with 0.7 (95% CI, 0.5\u20130.9) for 26 IGE MZ pairs. Our data suggest that conventional genetic influences in BRE are considerably less than for IGE, and other mechanisms need to be explored. Ann Neurol 2004;56:129\u2013132<\/jats:p>","DOI":"10.1002\/ana.20153","type":"journal-article","created":{"date-parts":[[2004,6,28]],"date-time":"2004-06-28T13:08:02Z","timestamp":1088428082000},"page":"129-132","source":"Crossref","is-referenced-by-count":41,"title":["Is benign rolandic epilepsy genetically determined?"],"prefix":"10.1002","volume":"56","author":[{"given":"Lata","family":"Vadlamudi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A. 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