Table 4

Neuroimaging patterns in hepatic encephalopathy

Hepatic encephalopathy
 CTUsually normal
  • ▸ T1 hyperintensities in the globus pallidus and, less frequent, in the substantia nigra and the midbrain tegmentum

  • ▸ FLAIR and DWI hyperintense thalami, posterior limbs of the internal capsule, periventricular region, dorsal brain stem and diffuse cortical involvement in 1 study of 20 patients

  • ▸ In acute hepatic encephalopathy the widespread grey matter changes on FLAIR and DWI are often reversible, in contrast to anoxic-ischaemic encephalopathy

  • ▸ Connectivity: decreased in the caudate of the anterior/middle cingulate gyrus; increased in the caudate of the left motor cortex; reduced between the putamen and the anterior cingulate gyrus, right insular lobe, inferior frontal gyrus, left parahippocampal gyrus and the anterior lobe of the right cerebellum; increased between the putamen and right middle temporal gyrus

  • ▸ Increased glutamate/glutamine ratio and low myoinositol and choline on MRS

  • ▸ Diminished choline and elevated glutamate/glutamine ratio in the parieto-occipital cortex on MRS

  • ▸ High blood flow in the cerebellum, basal ganglia and cerebral cortex

  • ▸ Alteration of striatal D2-receptor binding and dopamine reuptake

  • ▸ Hypoperfusion of the superior and middle frontal gyri, and inferior parietal lobules

  • ▸ Increased peripheral benzodiazepine binding sites prefrontal and striatal in patients with cirrhosis

  • DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery; MRS, MR spectroscopy; PET, positron emission tomography; SPECT, single-photon emission CT.