Original Article

Journal of Cerebral Blood Flow & Metabolism (2009) 29, 891–902; doi:10.1038/jcbfm.2009.12; published online 25 February 2009

The effect of ethanol on human brain metabolites longitudinally characterized by proton MR spectroscopy

Armin Biller1,2,3, Andreas J Bartsch1,3, György Homola1, László Solymosi1 and Martin Bendszus2

  1. 1Department of Neuroradiology, University of Wuerzburg, Wuerzburg, Germany
  2. 2Department of Neuroradiology, University of Heidelberg, Heidelberg, Germany

Correspondence: Dr A Biller, Department of Neuroradiology, University of Heidelberg, Im Neuenheimer Feld 400, 69198 Heidelberg, Germany. E-mail: armin_biller@med.uni-heidelberg.de

3These authors contributed equally to this work.

Received 6 June 2008; Revised 20 January 2009; Accepted 22 January 2009; Published online 25 February 2009.

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Abstract

The effect ethanol exerts on the human brain has not yet been addressed by longitudinal magnetic resonance (MR) spectroscopic experiments. Therefore, we longitudinally characterized cerebral metabolite changes in 15 healthy individuals by proton magnetic resonance spectroscopy (1H-MRS) subsequent to the ingestion of a standard beverage (mean peak blood alcohol concentration (BAC): 51.43plusminus10.27 mg/dL). Each participant was examined before, over 93.71plusminus11.17 mins immediately after and 726.36plusminus94.96 mins (12.11plusminus1.58 h) past per os alcohol exposure. Fronto-mesial and cerebellar ethanol concentrations over time were similar as determined by the LCModel analysis of spectral data. Alcohol-induced changes of fronto-mesial creatine, choline, glucose, inositol and aspartate levels for 5.79plusminus2.94 mins upon ingestion as well as cerebellar choline and inositol levels for 8.64plusminus2.98 mins past exposure. Closely associated with ethanol concentrations, supratentorial creatine, choline, inositol and aspartate levels decreased after ethanol administration, whereas glucose levels increased. Similarly, infratentorial choline and inositol concentrations were negatively correlated with ethanol levels over time. There were no changes in N-acetyl-aspartate levels upon alcohol exposure. Furthermore, no influence of ethanol on brain water integrals was detected. Ethanol consumption may directly increase oxidative stress and the neuronal vulnerability to it. In addition, our results are compatible with ethanol-induced cell membrane modifications and alternative energy substrate usage upon alcohol exposure.

Keywords:

alcohol, brain, cerebral metabolism, proton MR spectroscopy

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