Abstract

A spectrum of neuropsychiatric abnormalities caused by portosystemic venous shunting occurs in hepatic encephalopathy (HE) patients with or without liver dysfunction. It is not completely clear how the astrocyte swelling leads to glial-neuronal dysfunction, and how the symptoms are manifested in HE. A major goal of this work is to review the current status of information available from the existing magnetic resonance (MR) modalities including MR imaging (MRI) and MR Spectroscopy (MRS) as well as other modalities in the understanding the pathogenesis of HE. First, we discuss briefly neuron-histopathology, neurotoxins, neuropsychological and neurophysiological tests. A short review on the progress with single-photon emission computed tomography (SPECT) and positron emission tomography (PET) is then presented. In the remaining part of the manuscript, the following topics pertinent to understanding the pathogenesis of HE are discussed: MRI, diffusion tensor imaging (DTI), one-dimensional MRS based single- and multi-voxel based spectroscopic imaging techniques and two-dimensional MRS.

Highlights

  • As the term implies, ‘Hepatic Encephalopathy’ is a neuropsychiatric complication primarily due to liver dysfunction, which in turn, could be due to hepatocellular failure and/or portosystemic shunting (Fraser and Arieff, 1985; Trzepacz et al 1991)

  • acute-on-chronic liver failure (ACLF) is defined as an acute deterioration of liver function in patients with previously well-compensated chronic liver disease following acute hepatitis A or E superimposed on underlying liver cirrhosis (Nath et al 2008)

  • Whether there is not enough glutamine synthesis in astrocytes to detoxify ammonia or enough accumulation in the astrocytes, the MR Spectroscopy (MRS) peaks, which represent a mixture of Gln and Glu at the magnetic field strengths used in the clinic, do show an increase in all forms of liver disease, i.e. acute liver failure (ALF), chronic liver disease (CLD, and acute-on-chronic liver failure (ACLF)

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Summary

Introduction

As the term implies, ‘Hepatic Encephalopathy’ is a neuropsychiatric complication primarily due to liver dysfunction, which in turn, could be due to hepatocellular failure and/or portosystemic shunting (Fraser and Arieff, 1985; Trzepacz et al 1991). Catafau et al have shown via Tc-99m-HMPAO-SPECT, hypoperfusion in the left prefrontal cortex (including the anterior cingulate gyrus) when compared with healthy controls.

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