Hepatic encephalopathy

  • Patients with liver dysfunction
  • Cirrhosis, portal hypertension, portal systemic shunts, acute liver failure
  • MRI demonstrates CNS increase in certain substances that are normally metabolized by the liver
  • MRI
    • T1 high signal in globus pallidum due to excess manganese
    • Elevated glutamate/glutamine peak with decreased myo-inositol and choline on spectroscopy. This is due to hyperammonemia
    • T1 high signal in anterior pituitary
    • White matter abnormalities due to hyperammonemia: magnetization transfer ratio significantly low in normal appearing brain white matter. T2 FLAIR hyperintensities with increased diffusivity. Restoration of liver function reverses these findings
    • Acute encephalopathy: bilateral T2/FLAIR hyperintensities with restricted diffusion involving cortical grey matter – insular cortex and cingulate gyrus. Perirolandic and occipital cortex spared. Thalami, posterior limb internal capsule, periventricular white matter and dorsal brain stem also involved. Cytotoxic edema due to hyperammonemia can cause intracranial hypertension and severe brain injury
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Chen, Hua-Jun, et al. “Brain dysfunction primarily related to previous overt hepatic encephalopathy compared with minimal hepatic encephalopathy: resting-state functional MR imaging demonstration.” Radiology 266.1 (2013): 261-270.

Inoue, Etsuo, et al. “Portal-systemic encephalopathy: presence of basal ganglia lesions with high signal intensity on MR images.” Radiology 179.2 (1991): 551-555.

Naegele, Thomas, et al. “MR imaging and 1H spectroscopy of brain metabolites in hepatic encephalopathy: time-course of renormalization after liver transplantation.” Radiology 216.3 (2000): 683-691.