{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T15:21:01Z","timestamp":1791386461504,"version":"4.3.3"},"reference-count":28,"publisher":"Cambridge University Press (CUP)","issue":"6","license":[{"start":{"date-parts":[[2014,12,2]],"date-time":"2014-12-02T00:00:00Z","timestamp":1417478400000},"content-version":"unspecified","delay-in-days":1127,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Can. J. Neurol. Sci."],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:sec id=\"S0317167100012518_abs1\"><jats:title>Background:<\/jats:title><jats:p>Repetitively discharging neurons in epileptic foci have a high energy requirement that might be demonstrated histochemically as increased mitochondrial enzymatic activity in brain resections for epilepsy in children.<\/jats:p><\/jats:sec><jats:sec id=\"S0317167100012518_abs2\"><jats:title>Materials and Methods:<\/jats:title><jats:p>Frozen sections were studied histochemically of 10 brain resections from 7 epileptic children, 2 months to 17 years of age. None had mitochondrial disease. Three patients had tuberous sclerosis (TS) or hemimegalencephy (HME). Tissues included hippocampus and neocortex. Oxidative enzymes were studied for respiratory chain complexes I, II, IV, using the muscle biopsy protocol. In addition, immunoreactivities of \u03b1-B-crystallin and transmission electron microscopy (EM) were performed.<\/jats:p><\/jats:sec><jats:sec id=\"S0317167100012518_abs3\"><jats:title>Results:<\/jats:title><jats:p>Oxidative activities were variable in adjacent neurons within a field: a minority were intense, adjacent to neurons with weaker mitochondrial activity exhibiting poor contrast of the soma because of similar oxidative activity in surrounding neuropil. Endothelium of vessels uniformly exhibits strong activity. Alpha-B-crystallin reactivity was strong at these foci. EM confirmed an abundance of neuronal mitochondria with normal cristae. In TS and HME, many dysplastic neurons showed intense activity; balloon cells had sparse activity.<\/jats:p><\/jats:sec><jats:sec id=\"S0317167100012518_abs4\"><jats:title>Conclusions:<\/jats:title><jats:p>Histochemistry of mitochondrial oxidative enzymes reveals scattered and clustered neurons with stronger activities than others at epileptic foci. Such intensely staining neurons may be functionally \u201chypermetabolic\u201d but they do not signify mitochondrial disease. Individual intensely stained neurons might be epileptogenic, but do not denote an epileptogenic field in the same manner as \u03b1-B-crystallin, which also was strongly reactive in these foci.<\/jats:p><\/jats:sec>","DOI":"10.1017\/s0317167100012518","type":"journal-article","created":{"date-parts":[[2014,12,12]],"date-time":"2014-12-12T15:09:56Z","timestamp":1418396996000},"page":"909-917","source":"Crossref","is-referenced-by-count":22,"title":["Mitochondrial \u201cHypermetabolic\u201d Neurons in Paediatric Epileptic Foci"],"prefix":"10.1017","volume":"38","author":[{"given":"Harvey B.","family":"Sarnat","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura","family":"Flores-Sarnat","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Walter","family":"Hader","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luis","family":"Bello-Espinosa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"56","published-online":{"date-parts":[[2014,12,2]]},"reference":[{"key":"S0317167100012518_ref009","doi-asserted-by":"publisher","DOI":"10.1111\/j.1399-0004.2009.01236.x"},{"key":"S0317167100012518_ref008","doi-asserted-by":"publisher","DOI":"10.1055\/s-2008-1076737"},{"key":"S0317167100012518_ref024","doi-asserted-by":"publisher","DOI":"10.1007\/s10545-008-0841-x"},{"key":"S0317167100012518_ref005","doi-asserted-by":"publisher","DOI":"10.1016\/j.freeradbiomed.2004.08.021"},{"key":"S0317167100012518_ref004","doi-asserted-by":"publisher","DOI":"10.1097\/00019052-200204000-00009"},{"key":"S0317167100012518_ref019","doi-asserted-by":"publisher","DOI":"10.1111\/j.1471-4159.1959.tb13179.x"},{"key":"S0317167100012518_ref003","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.56.10.1340"},{"key":"S0317167100012518_ref011","first-page":"3","article-title":"Mitochondrial dysfunction and oxidative stress in seizure-induced neuronal cell death","volume":"19","author":"Chuang","year":"2010","journal-title":"Acta Neurol Taiwan"},{"key":"S0317167100012518_ref002","first-page":"193","article-title":"Mitochondrial encephalomyopathy of mixed MELAS type","volume":"324","author":"Bertrand","year":"1996","journal-title":"Folia Neuropathol"},{"key":"S0317167100012518_ref025","doi-asserted-by":"publisher","DOI":"10.1177\/0883073809352888"},{"key":"S0317167100012518_ref015","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1167.2005.01014.x"},{"key":"S0317167100012518_ref006","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.00222.2006"},{"key":"S0317167100012518_ref007","doi-asserted-by":"publisher","DOI":"10.1111\/j.1528-1167.2007.01341.x"},{"key":"S0317167100012518_ref020","unstructured":"Miles L , Miles MV , Horn PS , DeGrauw AJ , Wong BL , Bove KE . 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