Published in

SAGE Publications, Acta Radiologica, 6(39), p. 701-710, 1998

DOI: 10.3109/02841859809175502



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Proton MR Spectroscopy in Infants with Cerebral Energy Deficiency due to Hypoxia and Metabolic Disorders

Journal article published in 1998 by Harald Kugel ORCID, W. Heindel, B. Roth, S. Ernst, K. Lackner
This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Data provided by SHERPA/RoMEO


Purpose: To investigate the similarities and differences of cellular energy deficiencies due to asphyxia and to impaired oxidative phosphorylation caused by enzyme deficiencies using localized 1H-MR spectroscopy of the brain. Material and Methods: In 35 neonates and infants with a postconceptional age of 36.4–153 weeks, 1H-MR spectra were obtained from the basal ganglia. of the 35 children, 14 served as a control group, 12 suffered from hypoxicischemic disease (HIE), and 9 had congenital enzymatic disorders. Results: Eleven of the 12 children with HIE showed low n-acetyl aspartate (NAA) to trimethylamine (TMA) ratios, indicating neuronal damage. Lactate (Lac) to TMA ratios correlated with the HIE grade. Children with congenital disorders of energy metabolism had NAA/TMA ratios ranging from severely decreased to normal, but 7 of the 9 had high Lac signals, even in brains with normal NAA/TMA. Conclusion: High Lac/TMA even with normal NAA/TMA in children with enzyme deficiencies, in contrast to Lac/TMA that correlates with clinical grade and low NAA/TMA in asphyxic children, hints at different mechanisms of cell damage in the two disease groups.