{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T15:12:51Z","timestamp":1792681971907,"version":"4.5.0"},"reference-count":27,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2014,7,22]],"date-time":"2014-07-22T00:00:00Z","timestamp":1405987200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2014,9]]},"abstract":"Summary<\/jats:title>\n \n Objectives<\/jats:title>\n \n Metabolic imaging studies, such as positron emission tomography (\n PET<\/jats:styled-content>\n ), allow for an assessment of physiologic functioning of the brain, and [\n 18<\/jats:sup>\n F<\/jats:styled-content>\n ]fluoro\u20102\u2010deoxyglucose (\n FDG<\/jats:styled-content>\n )\u2013\n PET<\/jats:styled-content>\n is now a commonly used technique in presurgical epilepsy evaluations. Focal interictal decreases in glucose consumption are often but inconsistently concordant with the ictal onset area, and the underlying mechanisms are poorly understood. The current study tests the hypothesis that areas of glucose hypometabolism, determined by\n FDG<\/jats:styled-content>\n \u2010\n PET<\/jats:styled-content>\n , are associated with mitochondrial dysfunction in patients with medically intractable epilepsy associated with isolated focal cortical dysplasia (\n FCD<\/jats:styled-content>\n ).\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Measures of electron transport chain (\n ETC<\/jats:styled-content>\n ) functioning and mitochondrial abnormalities (\n ETC<\/jats:styled-content>\n complex biochemistry, protein kinase B subtype 1 (Akt1), glial fibrillary acidic protein (GFAP)) were assessed in surgical resection specimens that had hypometabolic abnormalities and those that were normal on\n FDG<\/jats:styled-content>\n \u2010\n PET<\/jats:styled-content>\n . Determination of\n FDG<\/jats:styled-content>\n \u2010\n PET<\/jats:styled-content>\n abnormalities was based on coregistration of statistical parametric mapping (\n SPM<\/jats:styled-content>\n ) results with postsurgical images.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Twenty\u2010two patients (11 male, 11 female; mean age at the time of surgery 10.5\u00a0\u00b1\u00a04.4\u00a0years), with pathologically confirmed\n FCD<\/jats:styled-content>\n , were included in this retrospective review. Complex\n IV<\/jats:styled-content>\n function was found to be significantly reduced in areas of hypometabolism (p\u00a0=\u00a00.014), whereas there was a trend toward a significant reduction in complex\n II<\/jats:styled-content>\n and\n III<\/jats:styled-content>\n function in areas of hypometabolism (p\u00a0=\u00a00.08, p\u00a0=\u00a00.059, respectively). These decreases were independent of cortical dysplasia severity (p\u00a0=\u00a00.321) and other clinical epilepsy measures.\n <\/jats:p>\n <\/jats:sec>\n \n Significance<\/jats:title>\n \n This study suggests an association between glucose hypometabolism and reduced mitochondrial complex\n IV<\/jats:styled-content>\n functioning, which is independent of the degree of cortical dysplasia. This supports the role of cellular energy failure as a potential mechanism for intractable epilepsy.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/epi.12731","type":"journal-article","created":{"date-parts":[[2014,7,22]],"date-time":"2014-07-22T16:41:33Z","timestamp":1406047293000},"page":"1415-1422","source":"Crossref","is-referenced-by-count":48,"title":["Cerebral glucose hypometabolism is associated with mitochondrial dysfunction in patients with intractable epilepsy and cortical dysplasia"],"prefix":"10.1111","volume":"55","author":[{"given":"Jeffrey R.","family":"Tenney","sequence":"first","affiliation":[{"name":"Division of Neurology Cincinnati Children's Hospital Medical Center Cincinnati Ohio U.S.A"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leonid","family":"Rozhkov","sequence":"additional","affiliation":[{"name":"Division of Neurology Cincinnati Children's Hospital Medical Center Cincinnati Ohio U.S.A"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Horn","sequence":"additional","affiliation":[{"name":"Division of Neurology Cincinnati Children's Hospital Medical Center Cincinnati Ohio U.S.A"},{"name":"Department of Mathematical Sciences University of Cincinnati Cincinnati Ohio U.S.A"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lili","family":"Miles","sequence":"additional","affiliation":[{"name":"Division of Pathology Cincinnati Children's Hospital Medical Center Cincinnati Ohio U.S.A"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael V.","family":"Miles","sequence":"additional","affiliation":[{"name":"Division of Neurology Cincinnati Children's Hospital Medical Center Cincinnati Ohio 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