Cristina Cudalbu1, Valrie McLin2, Olivier Braissant3, Nicolas Kunz, 14, Yohan van de Looij, 14, Rolf Gruetter5, 6
1Laboratory for Functional and Metabolic Imaging (LIFMET), Ecole Polytechnique Fdrale de Lausanne (EPFL) , Lausanne, Vaud, Switzerland; 2Dpartement de l'Enfant et de l'Adolescent, Unit de Gastroentrologie, Hpatologie et Nutrition, Hpitaux Universitaires de Genve (HUG), Geneva; 3Laboratoire de Chimie Clinique, Dpartement de Pathologie et de Mdecine de Laboratoire, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland; 4Division of Child Growth & Development, University of Geneva, Geneva, Switzerland; 5Laboratory for Functional and Metabolic Imaging (LIFMET), Ecole Polytechnique Fdrale de Lausanne (EPFL), Lausanne, Vaud, Switzerland; 6Departments of Radiology, Universities of Lausanne and Geneva, Switzerland
Chronic liver disease (CLD) is characterized by an array of cognitive and fine motor deficits labeled as hepatic encephalopathy. No in vivo longitudinal Spectroscopic Imaging (1H-SI) or Diffusion Tensor Imaging (DTI) studies were performed in CLD animal models. The aim was to analyze the in vivo alterations in brain osmolytes and brain edema using longitudinal 1H SI and DTI methods at 9.4T. Our preliminary data show that in CLD before the appearance of severe neurological signs, the osmotic imbalance created by the continuous increase of Gln can be compensated by a continuous decrease of other osmolytes with minimal brain edema.