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Is epileptogenic cortex truly hypometabolic on interictal positron emission tomography?

dc.contributor.authorJuhász, Csabaen_US
dc.contributor.authorChugani, Diane C.en_US
dc.contributor.authorMuzik, Ottoen_US
dc.contributor.authorWatson, Craig E.en_US
dc.contributor.authorShah, Jagdish R.en_US
dc.contributor.authorShah, Aashit K.en_US
dc.contributor.authorChugani, Harry T.en_US
dc.date.accessioned2006-04-19T13:56:17Z
dc.date.available2006-04-19T13:56:17Z
dc.date.issued2000-07en_US
dc.identifier.citationJuhÁsz, Csaba; Chugani, Diane C.; Muzik, Otto; Watson, Craig; Shah, Jagdish; Shah, Aashit; Chugani, Harry T. (2000)."Is epileptogenic cortex truly hypometabolic on interictal positron emission tomography?." Annals of Neurology 48(1): 88-96. <http://hdl.handle.net/2027.42/34882>en_US
dc.identifier.issn0364-5134en_US
dc.identifier.issn1531-8249en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/34882
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=10894220&dopt=citationen_US
dc.description.abstractPositron emission tomography (PET) of glucose metabolism is often applied for the localization of epileptogenic brain regions, but hypometabolic areas are often larger than or can miss epileptogenic cortex in nonlesional neocortical epilepsy. The present study is a three-dimensional brain surface analysis designed to demonstrate the functional relation between glucose PET abnormalities and epileptogenic cortical regions. Twelve young patients (mean age, 10.8 years) with intractable epilepsy of neocortical origin underwent chronic intracranial electroencephalographic monitoring. The exact location of the subdural electrodes was determined on high-resolution three-dimensional reconstructed magnetic resonance imaging scan volumes. The electrodes were classified according to their locations over cortical areas, which were defined as hypometabolic, normometabolic, or at the border between hypometabolic and normal cortex (metabolic “border zones”) based on interictal glucose PET. Electrodes with seizure onset were located over metabolic border zones significantly more frequently than over hypometabolic or normometabolic regions. Seizure spread electrodes also more frequently overlay metabolic border zones than hypometabolic regions. These findings suggest that cortical areas with hypometabolism should be interpreted as regions mostly not involved in seizure activity, although epileptic activity commonly occurs in the surrounding cortex. This feature of hypometabolic cortex is remarkably similar to that of structural brain lesions surrounded by epileptogenic cortex. Cortical areas bordering hypometabolic regions can be highly epileptogenic and should be carefully assessed in presurgical evaluations. Ann Neurol 2000;48:88–96en_US
dc.format.extent2754578 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherJohn Wiley & Sons, Inc.en_US
dc.subject.otherNeurologyen_US
dc.subject.otherNeuroscienceen_US
dc.titleIs epileptogenic cortex truly hypometabolic on interictal positron emission tomography?en_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPsychiatryen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationotherDepartment of Pediatrics, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MI ; Department of Neurology, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MIen_US
dc.contributor.affiliationotherDepartment of Pediatrics, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MI ; Department of Radiology, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MIen_US
dc.contributor.affiliationotherDepartment of Radiology, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MIen_US
dc.contributor.affiliationotherDepartment of Neurology, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MIen_US
dc.contributor.affiliationotherDepartment of Neurology, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MIen_US
dc.contributor.affiliationotherDepartment of Neurology, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MIen_US
dc.contributor.affiliationotherDepartment of Pediatrics, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MI ; Department of Neurology, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MI ; Department of Radiology, Children's Hospital of Michigan Detroit Medical Center, Wayne State University School of Medicine, Detroit, MI ; Pediatric Neurology/PET Center, Children's Hospital of Michigan, 3901 Beaubien Boulevard, Detroit, MI 48201en_US
dc.identifier.pmid10894220en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/34882/1/13_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/1531-8249(200007)48:1<88::AID-ANA13>3.0.CO;2-3en_US
dc.identifier.sourceAnnals of Neurologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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