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Brain magnetic resonance spectroscopy in episodic hepatic encephalopathy
Authors:Laia Chavarria  Juli Alonso  Rita García-Martínez  Macarena Simón-Talero  Meritxell Ventura-Cots  Clara Ramírez  Maria Torrens  Víctor Vargas  Alex Rovira  Juan Córdoba
Affiliation:1.Liver Unit, Hospital Vall d''Hebron, Barcelona, Spain;2.Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, Madrid, Spain;3.Departament de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Spain;4.Magnetic Resonance Unit (IDI), Department of Radiology, Hospital d''Vall Hebron, Barcelona, Spain;5.Biochemistry Unit, Hospital Vall d''Hebron, Barcelona, Spain
Abstract:Brain magnetic resonance (MR) study has shown metabolic abnormalities and changes in water distribution of the brain tissue that may relate to the pathogenesis of hepatic encephalopathy (HE). We designed a study to investigate the disturbances in brain water and metabolites during episodic HE using a 3-T MR scanner. Cirrhotic patients with different grades of HE underwent MR during hospitalization (n=18). The MR was repeated at 6 weeks'' follow-up (n=14). The results were compared with those of a group of healthy volunteers (n=8). During episodic HE, brain diffusion-weighted imaging showed a high apparent diffusion coefficient (ADC) (12% to 14%) that decreased during follow-up (−1% to −4%). These disturbances were accompanied by high glutamine (581%), low choline (−31%), and low myo-inositol (−86%) peaks on MR spectroscopy. In overt HE, patients showed high glutamine that decreased during follow-up (−22%). In addition, these patients exhibited a rise in plasma S100 beta and enlargement of brain white-matter lesions. In conclusion, several disturbances detected by MR support the presence of impaired brain water homeostasis during episodic HE. Although astrocytes have a major role in this condition, brain edema during episodic HE may be extracellular and does not appear to be directly responsible for the development of neurologic manifestations.
Keywords:acute hepatic encephalopathy, blood–  brain barrier, glutamine, leukoaraiosis, spectroscopy
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