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Elevated Lactate and Alkalosis in Chronic Human Brain Infarction Observed by 1H and 31P MR Spectroscopic Imaging
Author(s) -
James W. Hugg,
Jeff H. Duijn,
Gerald B. Matson,
Andrew A. Maudsley,
Jay S. Tsuruda,
Deborah Gelinas,
Michael W. Weiner
Publication year - 1992
Publication title -
journal of cerebral blood flow and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.167
H-Index - 193
eISSN - 1559-7016
pISSN - 0271-678X
DOI - 10.1038/jcbfm.1992.104
Subject(s) - alkalosis , brain infarction , medicine , chemistry , nuclear medicine , acidosis , ischemia
The goal of this study was to investigate lactate and pH distributions in subacutely and chronically infarcted human brains. Magnetic resonance spectroscopic imaging (MRSI) was used to map spatial distributions of 1 H and 31 P metabolites in 11 nonhemorrhagic subacute to chronic cerebral infarction patients and 11 controls. All six infarcts containing lactate were alkalotic (pH i = 7.20 ± 0.04 vs. 7.05 ± 0.01 contralateral, p < 0.01). This finding of elevated lactate and alkalosis in chronic infarctions does not support the presence of chronic ischemia; however, it is consistent with the presence of phagocytic cells, gliosis, altered buffering mechanisms, and/or luxury perfusion. Total 1 H and 31 P metabolites were markedly reduced (about 50% on average) in subacute and chronic brain infarctions ( p < 0.01), and N-acetyl aspartate (NAA) was reduced more (∼75%) than other metabolites ( p < 0.01). Because NAA is localized in neurons, selective NAA reduction is consistent with pathological findings of a greater loss of neurons than glial cells in chronic infarctions.

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