doi: 10.3174/ajnr.A1139
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American Journal of Neuroradiology 29:1612-1621, October 2008
© 2008 American Society of Neuroradiology
Review Article
MR Imaging Findings in Hepatic Encephalopathy
a Magnetic Resonance Unit (Institut de Diagnostic per La Imatge), Department of Radiology, Hospital Universitari Vall d'Hebron, Barcelona, Spain
b Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Madrid, Spain
c Liver Unit, Department of Internal Medicine, Hospital Universitari Vall d'Hebron, Barcelona, Spain
d Department of Medicine, Autonomous University of Barcelona, Cerdanyola del Vallès, Spain
Please address correspondence to Alex Rovira Cañellas, MD, Unitat de Ressonància Magnètica, Servei de Radiologìa, Hospital Universitari Vall d'Hebron, Pg. Vall d'Hebron 119–129, Barcelona 08035 Spain; e-mail: alex.rovira{at}idi-cat.org
SUMMARY: The term hepatic encephalopathy (HE) includes a spectrum of neuropsychiatric abnormalities occurring in patients with liver dysfunction. Most cases are associated with cirrhosis and portal hypertension or portal-systemic shunts, but the condition can also be seen in patients with acute liver failure and, rarely, with portal-systemic bypass and no associated intrinsic hepatocellular disease. Although HE is a clinical condition, several neuroimaging techniques, particularly MR imaging, may eventually be useful for the diagnosis because they can identify and measure the consequences of central nervous system (CNS) increase in substances that under normal circumstances, are efficiently metabolized by the liver. Classic MR imaging abnormalities include high signal intensity in the globus pallidum on T1-weighted images, likely a reflection of increased tissue concentrations of manganese, and an elevated glutamine/glutamate peak coupled with decreased myo-inositol and choline signals on proton MR spectroscopy, representing disturbances in cell-volume homeostasis secondary to brain hyperammonemia. Recent data have shown that white matter abnormalities, also related to increased CNS ammonia concentration, can also be detected with several MR imaging techniques such as magnetization transfer ratio measurements, fast fluid-attenuated inversion recovery sequences, and diffusion-weighted images. All these MR imaging abnormalities, which return to normal with restoration of liver function, probably reflect the presence of mild diffuse brain edema, which seems to play an essential role in the pathogenesis of HE. It is likely that MR imaging will be increasingly used to evaluate the mechanisms involved in the pathogenesis of HE and to assess the effects of therapeutic measures focused on correcting brain edema in these patients.