| pubmed-article:19699059 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19699059 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:19699059 | lifeskim:mentions | umls-concept:C0014544 | lld:lifeskim |
| pubmed-article:19699059 | lifeskim:mentions | umls-concept:C0013819 | lld:lifeskim |
| pubmed-article:19699059 | lifeskim:mentions | umls-concept:C0025519 | lld:lifeskim |
| pubmed-article:19699059 | lifeskim:mentions | umls-concept:C0524466 | lld:lifeskim |
| pubmed-article:19699059 | lifeskim:mentions | umls-concept:C0032863 | lld:lifeskim |
| pubmed-article:19699059 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19699059 | pubmed:dateCreated | 2009-11-5 | lld:pubmed |
| pubmed-article:19699059 | pubmed:abstractText | EEG power and high frequency activity in the seizure onset zone has been increasingly considered for its relationship with seizures in animal and human studies of epilepsy. We examine the relationship between quantitative EEG measures and metabolic imaging in epilepsy patients undergoing intracranial EEG (icEEG) analysis for seizure localization. Patients with mesial temporal lobe epilepsy (MTLE) and neocortical epilepsy (NE) were studied. Metabolic imaging was performed with MR spectroscopic imaging using N-acetyl aspartate (NAA) and creatine (Cr). All data were acquired from the mesial temporal lobe such that a direct comparison of the same anatomical regions between the two groups could be performed. While no difference was seen in the total power recorded from the mesial temporal lobe, the MTLE group had significantly greater power in the high frequency bands. There was a significant positive exponential relationship between total icEEG power with NAA/Cr in MTLE, R=+0.84 and p<0.001, which was not seen in NE. There was also a significant negative relationship between fractional gamma power with NAA/Cr in MTLE, R=-0.66 and p<0.02, also not seen in NE. These data argue that within the seizure onset zone, the tight correlation between total power and NAA/Cr suggests that total electrical output is powered by available mitochondrial function. These data are also consistent with the hypothesis that high frequency activity is an abnormal manifestation of tissue injury. | lld:pubmed |
| pubmed-article:19699059 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19699059 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19699059 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19699059 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19699059 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:19699059 | pubmed:issn | 1872-6844 | lld:pubmed |
| pubmed-article:19699059 | pubmed:author | pubmed-author:SpencerD DDD | lld:pubmed |
| pubmed-article:19699059 | pubmed:author | pubmed-author:SpencerS SSS | lld:pubmed |
| pubmed-article:19699059 | pubmed:author | pubmed-author:HetheringtonH... | lld:pubmed |
| pubmed-article:19699059 | pubmed:author | pubmed-author:ZaveriH PHP | lld:pubmed |
| pubmed-article:19699059 | pubmed:author | pubmed-author:PanJ WJW | lld:pubmed |
| pubmed-article:19699059 | pubmed:copyrightInfo | 2009 Elsevier B.V. All rights reserved. | lld:pubmed |
| pubmed-article:19699059 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19699059 | pubmed:volume | 87 | lld:pubmed |
| pubmed-article:19699059 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19699059 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19699059 | pubmed:pagination | 18-24 | lld:pubmed |
| pubmed-article:19699059 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
| pubmed-article:19699059 | pubmed:meshHeading | pubmed-meshheading:19699059... | lld:pubmed |
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| pubmed-article:19699059 | pubmed:meshHeading | pubmed-meshheading:19699059... | lld:pubmed |
| pubmed-article:19699059 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19699059 | pubmed:articleTitle | Intracranial EEG power and metabolism in human epilepsy. | lld:pubmed |
| pubmed-article:19699059 | pubmed:affiliation | Department of Neurosurgery, Yale University School of Medicine, New Haven, CT 06520, USA. jullie.pan@yale.edu | lld:pubmed |
| pubmed-article:19699059 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19699059 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19699059 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
